Microneurosurgery I (volume. 1)

Microneurosurgery in 4 Volumes

M.G.Yasargil Microsurgical Anatomy of the Basal Cisterns and Vessels of the Brain, Diagnostic Studies, General Operative Techniques and Pathological Considerations of the Intracranial Aneurysms II Clinical Considerations, Surgery of the Intracranial Aneurysms and Results

III Clinical Considerations and Microsurgery of the Arteriovenous Racemose Angiomas

IV Clinical Considerations and Microsurgery of the Tumors Georg Thieme Verlag Stuttgart • New York

Thieme Stratton Inc. New York

V

Acknowledgement

I am deeply indebted to my colleagues Drs. R. D. Smith, P. H. Young and P. J. Teddy for their very capable assistance in writing and reviewing the English manuscript of both volumes. I wish to express my sincere appreciation to Dr. R. D. Smith, New Orleans, who, with the exception of Chapters 6-11, Vol. II, played the initial role of '^Ghostwriter" for the entire manuscript. After detailed discussions with the author concerning the concept and|ayput_of the scheduled monograph and after being presented with the anatomical, pathological, radiological, surgical and clinical aspects, results and statistical material, he composed the primary text for each chapter. Very special thanks go to Dr. P. H. Young, St. Louis, who reviewed and elaborated on the entire manuscript. After detailed discussions and after being presented with statistical material, he also composed the text for Chapters 6-11, Vol. II, and for the figures and illustrations. I am very grateful to Dr. P. J. Teddy, Oxford, who made a final, very careful review of the entire manuscript, made many relevant suggestions and helped to fully restructure the galley-proofs. I appreciate the assistance of Dr. H. J. W. Nauta who wrote the English text concerning the anatomy of perforating arteries, and Dr. Ho and Dr. Slater who elaborated on the English text concerning the anatomy of the middle cerebral artery, Chapter 1, Vol. I. Dr. H.-G. Imhof studied and analyzed Chapter 8, Vol. II. Dr. R. C. Janzer wrote the section of embryology.

Dr. C. Gasser composed Chapter 4, Vol. I, and Dr. M. Curcic, neuroanesthetist since 1977 in my department, reviewed the manuscript and brought it up to date. Mrs. G. Siegenthaler deserves special thanks for her excellent work in controlling the internal medical aspects of treatment. I am very grateful to the assistance of the following colleagues in Zurich, Mrs. M. Fuchs, T. Grauer, M. J. Maraqa, A. Monshi, R. Munch, Mrs. C. Piischel, A. Sarioglu and Mrs. U. Schmid-Sutro for studying the clinical material and presenting some of the statistics. I am convinced that the artistic skills of Mr. P. Roth have enhanced the teaching quality of this publication. The first volume could not have been realized without the generous help of the Institutes of Pathology (Prof. C. Hedinger, Prof. J. R. Riittner, Dr. J. Schneider) and Radiology (Prof. J. Wellauer, Dr. A. Valavanis) and the Department of Surgical Photography (Mr. O. Reinhard) at the University Hospital of Zurich. Very special thanks go to my long-time secretary Mrs. M. Traber who not only typed the whole manuscript, but also performed countless duties related to this project. Finally I would like to thank cordially Dr. h.c. G. Hauff, owner of Georg Thieme Verlag, Stuttgart and his staff especially Mr. R. Zeller and Mr. R. Zepf, for their understanding and cooperation in the preparation and publication of this book.

VI

Preface This book and the succeeding volumes are the product of a rather extraordinary team effort. The team has comprised not only myself and the staff at the University Hospital, Zurich, but also colleagues from all parts of the world too numerous to name who have visited our department for varying lenghts of time over the past sixteen years. Throughout this period all our craniotomies have been performed using microsurgical techniques. The operations have each been displayed on a television monitoring system starting with the drilling of the sphenoid wing and continuing until dural closure. This has allowed close observer participation on every step of the procedure. Discussion during and after surgery and on reviewing the videotapes has stimulated thought, generated research projects and produced many innovative ideas concerning anatomy, clinical problems and techniques which have therefore been constantly evolving throughout the period studied. After carrying out over 4200 microsurgical procedures (1400 for aneurysms, 400 arteriovenous malformations and 2400 cranial and spinal tumors) in the past 16 years I have come to several general conclusions. First, and perhaps the most important, is that in no single case can one totally predict the outcome or peroperative difficulties from either the general or specific condition of the patient or from neuroradiological investigations. Cerebral and extracerebral responses to surgery remain intermittently quite unpredictable and detailed anatomy can only be properly evaluated by microsurgical exploration rather than by X-ray. Secondly, we need to know a great deal more regarding the pathophysiology of events following subarachnoid hemorrhage. In particular we must study the involvement of the cisternal systems, the hemodynamics of the central nervous system, and the reactivity and finer anatomical details of the vessels themselves. It is not only aneurysm location and size which makes for difficult surgery but

the construction of the wall of the sac and the involvement of perforating vessels particularly at the major bifurcations and at the anterior communicating artery. Thirdly, the skill of the individual surgeon still plays a critical role in determining outcome and such skill must embody the concepts of tactic and technique. There is still a common misconception that simply to use a sucker, bipolar coagulation and clips means competence in microsurgery. In fact, these form only the material part of the techniques involved and the real skill has to be learned not just in the operating theatre but by meticulous laboratory training over many months. A further misconception is that the optimally trained microneurosurgeon must have protracted operating experience before he can hope to obtain good results. Previous generations of neurosurgeons have been able to develop their skills by virtue of having large practices but the greatly increased number of trainees today must be provided with modern teaching facilities incorporating slides, tapes and television. A good training in microsurgical technique is no guarantee of success but compared with his macrosurgical colleagues the young neurosurgeon of today should have a much greater opportunity and the distinct advantage of being able to see fine anatomical structures far more clearly. Some colleagues still express doubts as to the real advantage of microsurgery to the patient expecting, for instance, that in some mystical way it may help improve operative results in Grade III-V SAH. The importance and advantages of microtechniques are to be seen best in cases of Grade O-II in whom morbidity rates have, in some hands, reached less than 0.5% even with early operation in many patients. I am convinced that microtechniques are advantageous because they enable one to work in a small gap, minimize trauma to the brain and presumably by reducing retraction and manipulation minimize the "stress"

Preface which may arise in the early days after aneurysmal surgery. I have had the opportunity to develop microsurgical methods and this has led to experience in aneurysm surgery in a considerable number of patients. Over the past three years there has been a gradual decline in the number of cases of ruptured

VII

aneurysm presenting in our clinic. Although this may be due to a variety of factors, I would like to think that the main reason is that colleagues welltrained in microtechniques are now able to successfully take on much of this work themselves. If so, a long-term ambition will have been fulfilled. M. G. Ya$argil

Introduction

Introduction The successful treatment of ity, loss of consciousness, cranial nerve palsies, cerebral aneurysms has become an important contribution by the neu-rosurgeon to patients suffering from cerebrovas-cular disease. The development of an adequate method of treating these lesions demanded first an understanding of the pathogenesis of the lesion itself in order that a diagnosis could be made in life, and subsequently an evolution of the means to perform a delicate surgical procedure that promised both hope for recovery and cure of the lesion. In the 18th century, Morgagni (1761) and Biumi (1778) first described cerebral aneurysms and showed that their rupture might lead to subarachnoid hemorrhage. These observations were not further evaluated until 1859, when Sir William Gull gave recognition to the pathological nature of the lesion with his often quoted statement "Whenever young persons die with ingravescent apoplexy, and after death a large effusion of blood is found, especially if the effusion be over the surface of the brain, in the meshes of the pia mater, the presence of an aneurysm is probable". It is curious that he nevertheless concluded, "Although we may from the circumstances sometimes suspect the presence of aneurysm within the cranium, we have at the least, no symptoms upon which to ground more than a possible diagnosis". The latter half of the 19th century saw considerable investigation into the pathological nature of cerebral aneurysms although clinically, little progress was made. Beadles (1907) addressing the Royal College of Surgeons stated "...the conclusion that I have been forced to draw from a careful study of a large series of cases is, therefore, that it is quite impossible to diagnose an aneurysm of any one of the cerebral arteries except in the most unusual of circumstances. Only two or three have ever been diagnosed in life, and even in these cases it can scarcely be said to have been an absolutely certain diagnosis". Fearnsides (1916) echoed this opinion, although in his analysis of 31 patients who had died of a ruptured cerebral aneurysm, he noted severe headache, nuchal rigid-

hemiparetic syndromes, and papilledema in the clinical histories. It remained for Sir Charles Symonds (1923, 1924) to put together the clinical syndrome of subarachnoid hemorrhage and to stress the importance of ruptured cerebral aneurysm as the most probable etiology. During this era, surgeons occasionally encountered aneurysms during intracranial operations for "tumors" around the sella turcica - a misdiagnosis that can still occur today despite the most advanced radiological methods. Sir Victor Horsley in 1885 is reported to have exposed an aneurysm in the area of the optic chiasm that he treated with bilateral cervical carotid artery ligation (Keen, 1890). Harvey Gushing (1929) in his extensive pituitary tumor experience reported opening an aneurysm and packing it with muscle. More often, though, these lesions were left undisturbed. In such an era of diagnosis by bedside neurological examination combined with investigation only by air contrast encephalography, aneurysms remained lesions that with few exceptions were diagnosed only during incidental operation or at the autopsy table. In 1927, Egas Moniz introduced cerebral angiography to the medical community, and clinicians finally had a method by which cerebral aneurysms could be documented in life. As Dandy (1944) was later forced to admit, "There is no doubt whatever of the excellent demonstrations of aneurysms by this method (cerebral angiography); it is unquestionably the most important, if not the only function that this procedure serves." With the ability to localize the source of subarachnoid hemorrhage, the neurosurgeon could now initiate a coherent plan of operative management. In 1933 Pott brought together the important findings that had been reported in the preceding decade. He presented to the medical and surgical society of Edinburgh a series of eight patients who had undergone angiography with the diagnosis of subarachnoid hemorrhage, describing the location of their aneurysms and reporting his operative

Introduction results. With this work the essential ingredients of cerebral aneurysm surgery were finally defined, i.e. cerebral aneurysms as a common cause of spontaneous subarachnoid hemorrhage, the demonstration of an aneurysm by cerebral angiography, and the possibility of operative treatment for these lesions. Although operations for cerebral aneurysms remained hazardous, reports of intracranial procedures for aneurysm began to appear (Tonnis 1936; McConnell 1937). Krayenbiihl's (1941) monograph described his experience with 31 patients of whom several were treated by carotid ligation and three underwent intracranial procedures. Dandy (1944) subsequently published a series of 108 patients, 30 of whom had undergone intracranial operation. Between 1950 and 1965, neurosurgeons became increasingly committed to the prospect of operative management for cerebral aneurysms. Improvements in operative technique, in anesthesia, and in radiology resulted in many favorable reports of intracranial operative management (Norlen and Olivecrona 1953; Uihlein and Huges 1955; Poppen 1960). However, these reports did not go unchallenged. Other investigators pointed out that the natural history of a ruptured cerebral aneurysm had not been adequately defined and that operations were usually performed only on the more favorable cases; so reports ascribing some benefit to operative treatment might indeed represent only favorable case selection (Magladery 1955; Slosberg 1960; Richardson et al 1966). The difficulty of adequately delineating the natural history of a disease that is both episodic in nature and variable in severity of presentation and that keeps the patient at risk over his lifetime was soon apparent. Nevertheless, considerable progress was made in defining the natural history of intracranial aneurysms and this work will be discussed in the following chapter. With an improved understanding of the nature of cerebral aneurysms, attention could then be directed toward the pathophysiological complications of ruptured aneurysms and the importance of clinical presentation in determining the need and timing of operative therapy. By the middle 1960's it was recognized that the operative management of cerebral aneurysm patients was not producing the significant reduction in morbidity and mortality that had been hoped for. While many neurosurgeons with considerable experience were able to achieve a marked reduction in mortality in favorable cases, larger studies continued to show disappointing mortality and morbidity attending the operative treatment

of these lesions (McKissock et al 1965; Skultety and Nishioka 1966). As a result, other methods of treatment including hypothermia (Botterell et al 1956), proximal occlusion (Logue 1956) coating and wrapping (Dutton 1956; Selverstone 1963) intraluminal thrombosis (Mullan and Dawley 1968) and stereotactic thrombosis (Alksne et al 1965, 1971, 1977, 1980) were tried with varying degrees of success. Along the same lines Serbi-nenko (1974), Debrun et al (1975, 1977, 1981), Taki et al (1979), Mullan et al (1980) and Romo-danov and Shcheglov (1982) used detachable ballon catheters to successfully treat a variety of intracranial aneurysms. It became evident that the morbidity associated with the surgical treatment of aneurysms was to some degree related to a variety of technical difficulties encountered during these procedures, including the close proximity of the lesion to vital structures at the base of the brain, the frequent formation of adhesions between the aneurysm and jhe jT^ejv^jvesse^pgrforating arteries or other adjacent structures, and the propensity of the lesions to rupture during manipulation. To overcome these difficulties it seemed reasonable that the operating microscope and microsurgical methods might prove helpful by allowing more accurate dissection and control of these lesions. The operating microscope would also, perhaps, give the neurosurgeon a. chance to avoid significant brain retraction that all too often produced premature rupture of the aneurysm or created spasm in neighboring small vessels. Additionally the microscope would provide the neurosurgeon with a well-illuminated binocular view of the aneurysm in the depths of a narrow operating field, and when combined with microsurgical techniques, further damage to an already compromised brain would be minimized. Early reports of the application of microsurgical techniques to intracranial aneurysms were not disappointing (Kurze 1964; Adams and Witt 1964; Pool and Colton 1966; Rand and Jannetta 1967). Subsequent series of patients (Guidetti 1973; Adams et al 1976; Pia 1976) operated upon using the microscope confirmed the better results achieved with this method. At a conference in Giessen, Germany in 1977, several distinguished neurosurgeons in the field of aneurysm surgery presented their operative techniques and results (Pia et al 1979). It was apparent then that the benefits of the microsurgical approach to the aneurysm surgery were finally becoming appreciated. Still, the use of the microscope remained individually variable with many aneurysm surgeons employing it only briefly

Introduction during an otherwise classical operation. Therefore .jntelligible_ comparisons of microscopic and classical approaches remained impossible. In 1979 Suzuki reported excellent surgical results in over 1000 aneurysm patients undergoing operation without microsurgical techniques. While there is no question that a few accomplished neu-rosurgeons with a wealth of clinical material can achieve a high standard of operative results with classical or other ^sophisticated approaches to aneurysm surgery, for most neurosurgeons, there nevertheless remains the need of a comprehensive plan of operation fully utilizing the benefits of the microsurgical technique; a plan that incorporates microsurgical principles into the entire procedure from craniotomy to closure. The main principle of microneurosurgery is the ability of the surgeon to perform all the necessary manipulations through a small "key-hole" approach. For the mastery of tactics and techniques of this "key-hole" surgery it is absolutely necessary to be familiar with a new perspective of the anatomy of the cisternal and neurovascular systems. The former techniques of neurosurgery allowed one to perform explorations mainly in subduraltranscerebral approaches whereas the microtechnique enables the neurosurgeon to dissect and expose cerebral aneurysms, arteriovenous malformations and tumors in a natural pathway within the subarachnoidal cisterns, presenting all important surrounding structures, especially the cerebrovascular system in stereoscopic deep sharp focus. The subarachnoidal cisterns are the road-

maps for microneurosurgeons. Taking this very important fact into consideration a chapter of 50 pages in Volume I is devoted to cisternal anatomy. Furthermore, our knowledge concerning the anatomy of the neurovascular system is still not fully completed. Despite the many contributions of the anatomist, pathologist, neurosurgeon and stereotactic surgeon towards an understanding of the cerebral vasculature, the operative microscope provided the microsurgeon with a new approach / for detailed study of the living brain vasculature. ' During microsurgical operations for intracranial' aneurysms, arteriovenous malformations and tumors considerable effort has been made in the present series of patients to delineate the anatomy of the cerebral vasculature in order to familiarize the surgeon with the various anomalous configurations often encountered with other anatomical works. Volume I will present anatomical, neuroradiologi-cal, operative, neuroanesthetic and pathological considerations. The second volume will deal with clinical considerations, early and late results of operated intracranial aneurysms at different locations in 1312 patients, the problems and results in cases with giant and multiple aneurysms, the results of nonoperated cases and finally the complications of aneurysm surgery. Volume III and IV will present microsurgery of arteriovenous malformations and tumors.

Contents Acknowledgement Introduction

1 Operative Anatomy Subarachnoid Cisterns . . . . . . . . . . . . . .

5

Introduction . . . . . . . . . . . . . . . . . . . . . Early Anatomists . . . . . . . . . . . . . . . . . Neuroradiology and Modern Anatomists . . Embryology of Meningeal Development . . . Microneurosurgical Observations . . . . . . . Compartmentalization . . . . . . . . . . . . Intracisternal Arachnoidal Trabeculation . Cisternal Junctions . . . . . . . . . . . . . . . Apposition of Arachnoid and Ependyma . Pathological Thickening and Reduplication of Arachnoid . . . . . . . . . Relationship to Pathological Processes . . Normal Cisternal Anatomy. . . . . . . . Supratentorial Cisterns . . . . . . . . . . . . . . Anterior (Parasellar) . . . . . . . . . . . . . Lateral (Parapeduncular) . . . . . . . . . . . Posterior (Tentorial Notch) . . . . . . . . . Superior (Callosal) . . . . . . . . . . . . . . . Infratentorial Cisterns . . . . . . . . . . . . . . Anterior . . . . . . . . . . . . . . . . . . . . . Lateral . . . . . . . . . . . . . . . . . . . . . . Posterior . . . . . . . . . . . . . . . . . . . . .

5 5 12 13 14 14 20 20 20 23 23 25 26 26 39 46 46 47 47 49 52

Intracranial Arteries. . . . . . . . . . . . . 54 Introduction . . . . . . . . . . . . . . . . . . . . . Internal Carotid Artery . . . . . . . . . . . . . Ophthalmic Artery . . . . . . . . . . . . . . . Superior Hypophyseal Arteries . . . . . . . Posterior Communicating Artery . . . . . . Anterior Choroidal Artery . . . . . . . . . . Dural Artery of Internal Carotid Artery . Middle Cerebral Artery . . . . . . . . . . . . . Superior Lateral Group or Temporal Vessels . . . . . . . . . . . . . . . . Inferior Medial Group or " Lenticulostriate or Striate Vessels" . . . Middle Cerebral Bifurcation . . . . . . . . . Anterior Cerebral Artery Complex ...92 Proximal Anterior Cerebral Artery . . . . Anterior Communicating Artery . . . . . . Distal Anterior Cerebral Artery .... . . . . . Vertebrobasilar System . . . . . . . . . . . . . Vertebral Artery . . . . . . . . . . . . . . . . Basilar Artery . . . . . . . . . . . . . . . . . .

54 56 60 60 60 66 70 72 73 77 84 92 99 116 128 128 131

Perforating Arteries to the Basal Ganglia and Brain Stem

I. Basal Perforation Zones . . . . . . . . . . . 145 la. Anterior Perforated Substance and Extensions: Anterior Perforation Zone . 145 Ib. Posterior Perforated Substance and Extensions: Posterior Perforation Zone . 151 Ic. Pontine Perforation Zone . . . . . . . . 155 Id. Basal Medullary Perforation Zone .. 155 II. Dorsal Perforation Zones . . . . . . . . . . 158

3 General Operative Techniques. . . . .

Ila. Dorsal Midbrain Perforation Zone . lib. Dorsal Thalamic Perforation Zone . Cerebral Veins . . . . . . . . . . . . . . . . . . Parasellar Area . . . . . . . . . . . . . . . . . . . Dorsal Mesencephalic Area . . . . . . . . . . . Ventrolateral Posterior Fossa . . . . . . . . . . The Inferior Surface of the Frontal Lobe . . .

158 162 165 165 165 165 168

2 Diagnostic Studies. . . . . . . . . . . . . Lumbar Puncture . . . . . . . . . . . . . . . . . Xanthochromia . . . . . . . . . . . . . . . . . Uniformity of Blood Concentration . . . . 169 Cellular Changes . . . . . . . . . . . . . . . . 169 Increased Pressure . . . . . . . . . . . . . . . Electroencephalography (EEG) . . . . . . . . Radiological Investigation . . . . . . . . . . . . Background . . . . . . . . . . . . . . . . . . . Plain Skull Radiography . . . . . . . . . . . Pneumoencephalography . . . . . . . . . . . Radioisotopic Brain Scan . . . . . . . . . . . Radioisotopic Cisternography . . . . . . . . Digital Subtraction Angiography . . . . . . Positron Emission Tomography . . . . . . . Nuclear Magnetic Resonance . . . . . . . . Cerebral Angiography . . . . . . . . . . . . . . Method of Angiography . . . . . . . . . . . General Information Derived from Angiography . . . . . . . . . . . . . . . . . . .

169 169

169 170 170 170 170 170 171 171 171 171 171 171 171

172 Specific Technical Details for Given Aneurysms Internal Carotid Artery Aneurysms . . . . 182 Middle Cerebral Artery Aneurysms . . . . 184 Anterior Cerebral-Anterior Communicating Artery Aneurysms . . . . 184 Upper Basilar Artery Aneurysms . . . . . . 187 Vertebrobasilar Aneurysms . . . . . . . . . 187 Diagnostic Difficulties in Cerebral Angiography Anatomical Problems . . . . . . . . . . . . . 188 Inadequate Clinical Information . . . . . . 188 False Positive Angiography (Negative Exploration) . . . . . . . . . . . . 189 Unexpected Location of Aneurysm . . . . 190 Equivocal Angiograms (Positive Exploration) . . . . . . . . . . . . . 192 Discussion . . . . . . . . . . . . . . . . . . . . 193 Multiple Aneurysms with one or more Unrecognized Angiographically . . . . . . 195 Postoperative Angiography . . . . . . . . . 195 Complications of Angiography . . . . . . . 196 Rupture of Aneurysm During Angiography . . . . . . . . . . . . . . . . . . . 198 Computerized Tomography Method of Computerized Tomography . . 199 Information Derived from Computerized Tomography: Identification of Aneurysm . 199 Pitfalls of Computerized Tomography . . . 205 Timing of Radiological Procedures . . . . . . 206 Apparatus and Instruments . . . . . . . . . . . 208 Operating Microscope . . . . . . . . . . . . . . 208 Optical Principles . . . . . . . . . . . . . . . . 208

Lighting System . . . . . . . . . . . . . . . . . Microscope Stand . . . . . . . . . . . . . . . . Accessories to the Microscope . . . . . . . . Microsurgical Instrumentation . . . . . . . . . Stability . . . . . . . . . . . . . . . . . . . . . . Mobility . . . . . . . . . . . . . . . . . . . . . . Post-Operative Care of Instruments . . . . Aneurysm Clips . . . . . . . . . . . . . . . . . Temporary Vascular Clips . . . . . . . . . .

208 210 210 210 211 211 212 212 213

Operating Room Organization. . . . . . . . . 213

Personnel . . . . . . . . . . . . . . . . . . . . . . 213 Operating Room Lay-Out . . . . . . . . . . . . 214 Operative Approach. . . . . . . . . . . . . . . 215 Interfascial Pterional (Frontotemporosphenoidal) Craniotomy . . 215 Position of the Patient . . . . . . . . . . . . . 215 Draping . . . . . . . . . . . . . . . . . . . . . . 217 Incision . . . . . . . . . . . . . . . . . . . . . . 217 Interfacial Temporalis Flap . . . . . . . . . 217 Craniotomy . . . . . . . . . . . . . . . . . . . 220 Other Craniotomies. . . . . . . . . . . . . . . 234 Anterior Paramedian Frontal Craniotomy . . . . . . . . . . . . . . . . . . . 234 Combined Frontal Paramedian and Pterional Craniotomy . . . . . . . . . . . . . 236

Subtemporal Craniotomy . . . . . . . . . . . 237 Lateral Suboccipital Craniotomy . . . . . . 238 Variations . . . . . . . . . . . . . . . . . . . . 239 Occipital Craniotomy . . . . . . . . . . . . . 244 Aneurysm Clipping . . . . . . . . . . . . . . . . 245 Preparation . . . . . . . . . . . . . . . . . . . 245 Microtechniques of Aneurysm Obliteration 260 Stepwise (Staging) Elimination of Aneurysm Sac . . . . . . . . . . . . . . . . . . 260 Efficacy of Clipping . . . . . . . . . . . . . . 263 Summary . . . . . . . . . . . . . . . . . . . . . 264 Alternative Methods of Aneurysm Treatment Cervical Carotid Artery Ligation . . . . . . 265 Intracranical Parent Artery Ligation and Trapping Procedures Aneurysm Ligation . . . . . . . . . . . . . . . 265 Wrapping and Coating Techniques . . . . . 265 Microsurgical Vascular Repair and Anastomosis Induced Thrombosis and Internal Occlusion . . . . . . . . . . . . . . . . . . . . . 266 Special Operative Problems . . . . . . . . . . . 267 Multiple and Bilateral Aneurysms . . . . . 267 Giant Aneurysms . . . . . . . . . . . . . . . . 268 Intraoperative Rupture . . . . . . . . . . . . 269 Intraoperative Vasospasm . . . . . . . . . . 271 Summary of Methods Applied in the Current Series271

5 Pathological Considerations. . . . . .

4 Anesthesia for Microsurgical Procedures in Neurosurgery Introduction . . . . . . . . . . . . . . . . . . . . . 272 Anesthetic Principles and Pharmacological Considerations Preoperative Care . . . . . . . . . . . . . . . 273 Premedication . . . . . . . . . . . . . . . . . . 273 Induction of Anesthesia . . . . . . . . . . . . 273 Maintenance of Anesthesia . . . . . . . . . 274 Brain Relaxation . . . . . . . . . . . . . . . . 274 Postoperative Care . . . . . . . . . . . . . . . . 275 Induced Hypotension . . . . . . . . . . . . . . . 275 Deliberate Hypotension Induced by Halothane . Deliberate Hypotension Induced with Trimetaphan Induced Hypotension with Sodium Nitroprusside Hypothermia . . . . . . . . . . . . . . . . . . . . 277 Vertebro-Basilar Aneurysms . . . . . . . . . . 277 Anesthetic Management of Posterior Fossa Microsurgery in the Sitting Position . . . . . . 277 Premedication . . . . . . . . . . . . . . . . . . 277 Cardiovascular and Respiratory Complications Monitoring and Air Embolism . . . . . . . 278 Cranial Nerve Examination . . . . . . . . . 278 Postoperative Care . . . . . . . . . . . . . . . 278

Epidemiology of Cerebral Aneurysms . . . . 279

Incidence . . . . . . . . . . . . . . . . . . . . . . Classification . . . . . . . . . . . . . . . . . . . . I. Saccular Aneurysms . . . . . . . . . . . . II. Other Types of Cerebral Aneurysms . Infectious (Mycotic) Aneurysms . . . . Traumatic Aneurysms . . . . . . . . . . Dissecting Intracranial Aneurysms . . Arteriosclerotic Ectatic Aneurysms . . Aneurysmal Enlargement . . . . . . . . . . Distribution . . . . . . . . . . . . . . . . . . . . . Location of Cerebral Aneurysms . . . . . .

279 280 280 281 281 282 285 285 295 299 299

Latoatity . . . . . . . . . . . . . . . . . . . . .

299

Age . . . . . . . . . . . . . . . . . . . . . . . . 299 Sex . . . . . . . . . . . . . . . . . . . . . . . . . 300 Multiplicity . . . . . . . . . . . . . . . . . . . . 301 Familial Occurrence of Cerebral Aneurysms 304 Occurrence with a Described Hereditary Syndrome Coarctation of the Aorta . . . . . . . . . . . 304 Ehlers-Danlos Syndrome . . . . . . . . . . . 304 Pseudoxanthoma Elasticum . . . . . . . . . 304 Friedreich's Ataxia . . . . . . . . . . . . . . . 304 Hypertension . . . . . . . . . . . . . . . . . . 304 Fibromuscular Dysplasia . . . . . . . . . . . 305 Occurence without a Described Hereditary Syndrome Associated Vascular Anomalies . . . . . . . . 306 Development Abnormalities . . . . . . . . . 306 Persistent Carotid-Basilar Anastomosis . . 306

Persistent Hypoglossal Artery . . . . . . . . 306 Proatlantal Intersegmental Artery . . . . . 307 Agenesis and Aplasia of the Internal Carotid Artery . . . . . . . . . . . . . . . . . 307 Accessory Middle Cerebral Artery . . . . . 308 Fenestration and Duplication . . . . . . . . 308 Arteriovenous Malformation . . . . . . . . 309 Coincidental Association of Aneurysm and Occlusive Vessel Diseases . . . . . . . . 313 Moya-Moya Disease Associated with Aneurysms Association of Brain Tumor and Cerebral Aneurysm Pathology of Saccular Aneurysm Formation and Rupture . . . . . . . . . . . . . . . . . . . . . 321 Natural History of Ruptured Cerebral Aneurysms Mortality and Morbidity . . . . . . . . . . . 324 Necropsy of Fatal Aneurysm Rupture . . . 325 Spontaneous Thrombosis of Cerebral Aneurysms Pathophysiological Complications of Ruptured Cerebral Aneurysm . . . . . . 334 Hematoma Formation . . . . . . . . . . . . . 334 Subdural Hematoma . . . . . . . . . . . . . . 334 intracisternal Hematoma . . . . . . . . . . . 336 Intracerebral Hematoma . . . . . . . . . . . 336 Intraventricular Hematoma . . . . . . . . . 342 Cerebral Ischemia and Infarction . . . . . . . 342 Vasospasm . . . . . . . . . . . . . . . . . . . . . 343 Prolonged Chronic Spasm or Narrowing of Arteries . . . . . . . . . . . . . . . . . . . . . . 343 Our Observations . . . . . . . . . . . . . . . . 344 Hypothalamic Injury . . . . . . . . . . . . . . 345 Cerebral Edema . . . . . . . . . . . . . . . . . . 345 Ventricular Dilatation and Communicating Hydrocephalus Unexplained Subarachnoid Hemorrhage . . 347

References

Operative Anatomy

1 Subarachnoid Cisterns

Early Anatomists

Introduction Although many of the clinical pathophysiological processes occurring in the subarachnoid space have been well described (i.e. subarachnoid hemorrhage, meningitis, circulatory disturbances of CSF, tumors, AVM's etc.), it is surprising that an accurate topography of the basal cisterns has jnot been adequately worked out.] Knowledge of 1 the neural and vascular contents of each of the basal cisterns is of particular value to the neurosurgeon in the planning and execution of intracranial procedures. The neurosurgeon may chart his intracranial approach like a road map in terms of • the basal cisterns. Many of the subarachnoid cisterns can be considered to be anatomically distinct compartments, but others are not, these being separated from each other by a porous trabeculated wall with various sized openings. Under normal circumstances this permits a continuous exchange of CSF from one compartment to another. These apertures can become plugged and partially or totally obliterated after subarachnoid hemorrhage, infectious meningitis, chemical meningitis, (e.g. craniopharyngioma) spread of malignant cells in the subarachnoid space (e.g. carcinomatous meningitis) and spread of proteinaceous exudate (e.g. meningioma, acoustic neuroma), thus hindering the normal CSF circulation. At surgery the release of CSF from the basal cisterns provides a quick effective reduction of cerebral volume and facilitates the intracranial approach. A good example of this is the opening of the lateral cerebello-medullary cistern prior to exploration of tumors, aneurysms, and angiomas in the cerebello-pontine angle. Similarly, the Sylvian, carotid, chiasmatic and interpeduncular cisterns are opened for approaches to aneurysms and parasellar tumors.

While Galen and Vesalius had made general reference to membranes over the brain in 1555 Blaes (Blasius) is credited with naming of the arachnoid in 1666. Vieussens (1690) noted that the pia and arachnoid existed as two separate membranes, and Ruysch (1697) showed that the arachnoid extended over the convexities of the brain. Pac-chioni (1729) recognized fluid around the brain, but this was considered by others to be a pathological condensation until Cotugno (1770) verified the normal presence of cerebrospinal fluid. In 1802, Bichat proposed that the arachnoid formed a serous cavity similar to the peritoneal cavity. He felt the arachnoid cavity communicated with the ventricular system by extensions of the arachnoid • into the ventricles. Magendie (1822) gave the first modern description of the subarachnoid space as containing cerebrospinal fluid that circulated under pressure and was intercommunicating in all areas. He described the basal cisterns and the extensions of the arachnoid along cranial nerves II, V and VIIVIII. His ideas were accepted by anatomists of the nineteenth century (Kolliker 1850; Virchow 1854; Luschka 1855; Quain 1844), and are generally considered valid today. In 1875, Key and Retzius published a monumental work in which they presented drawings of the subarachnoid space that had been injected with blue dye (Berliner-Blau) to demonstrate the extensions and divisions of the subarachnoid system (Fig 1A). They were able to demonstrate that the subarachnoid space, although intercommunicating, is also compartmentalized. They showed the relationship of the cerebral vessels to the arachnoid and the numerous trabeculae which suspend these vessels from the walls of the cisterns. This outstanding study remains valid today, although an appreciation of the importance of these findings for neurosurgery had to await the introduction of the operating microscope (Figs 1BK)

6

1 Operative Anatomy

Fig 1 A This original figure from the monograph (1875) by Key and Retzius shows the ventricular, arachnoid, and cislernal spaces outlined by Berliner Blue.

Early Anatomists g 1 B This precisely drawn picture depicts a dissection of Tie basal cisternal compart"lents. including the olfactory, gitasmatic. SyMan, carotid, in'.erpedLincular, crural, prepontine. cerebellopontine, and an_terior spinal cisterns.

Fig 1 C Dissection of the interpeduncular cistern with its trabeculae invaginating the pia mater of the ventral pons.

8

1 Operative Anatomy Fig 1 D Dissection of the cerebellopontine, lateral cerebellomeduilary and anterior medullary cisterns.

--.a'

Fig 1 E A perfect depiction of the perimesencephalic cisterns (the interpeduncular, ambient, and quadriqeminal).

\'in !•

Early Anatomists Fig 1 F Incresed density of fibers around the Galenic vein.

FigIG A unique representation of the completely dissected lamina terminalis cistern. Chiasmatic cistern closely surrounding the optic nerves.

9

10

1 Operative Anatomy Fig 1H An illustration of the perioptic cistern, extending along the optic nerve within its sheath.

Fig 1 i Arachnoidal compartments in a sulcus and dense organization of the fibers around the artery.

Early Anatomists - g 1J Arachnoid fibers within the sulcus.

Fig 1 K A microscopic representation of arachnoid trabeculae from the work of Key and Retzius. Arachnoid trabeculae from different areas are composed of differing fiber organizations.

The figures (1 A-K) have been taken from the excellent monograph by Key and Retzius (Stockholm 1875). This two volume masterpiece contains several hundred extremely accurate pictures and it should be consulted for further details.

11

12

1 Operative Anatomy

Neuroradiology and Modern Anatomists j l n 1919 Dandy described the injection of air into ' the lumbar subarachnoid space in order to outline the cerebral ventricles. While it was seen that the basal subarachnoid cisterns were also demonstrated in this manner, attention was primarily fixed on the size and shape of the ventricles. Locke and Naffziger (1924) undertook a corrosion cast study of the subarachnoid cisterns in dogs and humans, and demonstrated the shapes and intercommunications of the subarachnoid space. They gave general names to the subarachnoid cisterns, and admitted that the finer points of the system had probably not been demonstrated by this method. Vital dye studies and a somewhat different classification were reported by Spatz and Stroescu (1934). In 1937, Davidoff and Dyke published a textbook on the normal pneumoencephalogram in which they discussed the shape and extension of the subarachnoid cisterns in some detail. Corrosion casts had displayed the subarachnoid system as freely intercommunicating while fractional pneumoencephalography suggested more j:om-partmentalization of the subarachnoid space. Liliequist (1959) employed both techniques to provide a working normal anatomy of the subarachnoid space. For the most part he used the terminology of Key and Retzius to name the cisterns. Since this monograph, several radiological and anatomical papers have discussed the subarachnoid space (Epstein 1965; Wilson 1972; Lang 1973), but little attention was directed toward the subarachnoid cisterns. The relationship of the fine structure of the subarachnoid cisterns to subarachnoid hemorrhage was discussed by Arutiunov and associates^ 1974), and electron microscopic studies oftne intricate pattern of membranes and fibers which form this system were reported by Andres (1967), Alien and Low (1975), Suzuki et al (1977, 1979), Barrio-nuevo et al (1978), and Julow et al (1979). The anatomical relationship of the dura and arachnoid was disputed for many years (Clara 1953; Pease and Schultz 1958; Ham 1974), until the advent of microsurgical procedures, where the careful elevation of the dura under magnification revealed multiple, fine reticular attachments between the jfeiia and arachnoid.. This observation provided" the impetus_for Schachenmayr and Friede (1978) to develop a technique for the in situ fixation of human meninges in order to finally document the ultrastructure of the dura-arachnoid interface.

Their results refuted the existence of a subdural jjpace (real or potential). They concluded that all disease processes originally thought to exist in this space, occur in a cleavage plane within the innermost layer of cells of the dura (what are termed "dural border cells") (Fig 2)._____________ Many other questions remain to be answered about the structure and function of the leptome-ningeal arachnoid membrane. Unresolved problems, such as the role of epithelial cells and the importance and tensile strength of elastic bands (Fig IK) in the arachnoid need to be studied further, and would be of interest to the neurosur-geon. Some of these questions may eventually find answers in electron microscopic studies of the arachnoid similar to the one described above. Interface layer

DURA MATER Subarachnoid space Dense collagenous Trabecula

Fig 2 Typical relationship existing at the dura-arachnoid interface (For more detail consult the publication by Friede and Schachenmayr, Amer. J. Path. 1978). __

Embryology of Meningeal Development 1 3

Embryology of Meningeal Development The brain and spinal cord are enclosed within membranous structures collectively known as meninges. They are commonly subdivided into Pachymeninx (Dura mater) and Leptomeninx (Arachnoidea and Pia mater). Anatomical organization and development of these different parts of the meninges show considerable species-dependent differences. Findings in other species cannot be extrapolated to humans without reservation. Sensenig (1951) has described 75 human embryos and fetuses at the Carnegie Institute of Embryology most thoroughly, but ultrastructural investigations of the human meningeal development are still lacking. At Carnegie stage XI (gestational age (days) 23-26; 2.5-4.5 mm CR) a single layer of cells is first seen along the lateral aspect of the primitive neural tube. These cells are continuous with and probably derived from the neural crest. This layer participate in the later formation of the intima pia. In stage XII (gestational age (days) 26-30; 3-5 mm CR) vascularization begins in tissues around the neural tube and in stage XV (35-38 days, 7-9 mm CR) the neural tube is completely surrounded by developing vessels. At the same time a loose, sparsely cellular area lying between the neural tube, somites and notochord is descernible. This mesoderm derived tissue is called meninx pri-mitiva. At stage XVI (37-42 days, 8-11 mm CR) the meninx primitiva has surrounded the neural tube. It has contributed to the single cell layer adjacent to the neural tube, which is now continuous and represents the primitive intima pia. Laterally the meninx primitiva is adjacent to the vertebral primordia. At stages XVII-XVIII (42-48 days; 11-17 mm CR) vascular channels penetrate the neural tube, carrying cells of the intima pia and meninx primitiva as their adventitia. At certain sites the second component of the pia mater, the epipial tissue, forms as a stratified cell layer upon the single cell layer of the intima pia. At stage XIX-XX (48-53 days; 16-22 mm CR) the meninx primitiva begins to cavitate. The outermost part of the cavitated meninx primitiva forms a compact layer, which correspond to the dura mater. At this stage, it is in continuity with the perichondrium of the vertebrae, which are already chondrified. At cranial levels, there will never be a separation of these two layers, but in the spinal cord an epidural space begins to form at stage

XXIII (56-60 days; 27-31 mm CR). This corresponds to the end of the embryonic period of development. With the cavitation of the meninx primitiva a primitive subarachnoid space is formed before any arachnoid is identifiable with certainity. The sequence of arachnoid development is much less certain than the above mentioned development of the dura mater and pia mater. From the sparse data available on humans it can be said that it probably develops from the inner aspect of the dura, that it is of mesodermal origin, and that it is the last of the three meninges to differentiate. A recent ultrastructural study (Schachenmayr and Friede 1978) of adult human meninges has shown that there is no subdural space, but a complex tight layer of cells, the interface layer, composed of the innermost portion of the dura mater (the dural border layer) and the outermost portion of the arachnoid (the arachnoid barrier layer) (see Fig 2). The exact embryological development of these ultrastructurally defined subdivisions of dura mater and arachnoidea is not yet elucidated. The formation of the basal cisternae is correlated with a total regression of the arachnoid trabecu-lae. The cisterns are formed by the end of the embryonic stages, at the same time as the foramen of Magendie.

14

1 Operative Anatomy

Microneurosurgical Observations The operating microscope has provided a unique opportunity for the observation of the subarach_noid spacf in vivo under close to physiological conditions with the chance to note fine anatomical details. An important contribution of the operating microscope and microsurgical technique to neurosurgery has been a better understanding of the important role of the subarachnoid cisterns in I the dissection and exposiirePof" cerebTaT d£eu-| rysms, arteriovenous malformations, and tumors. • It has been recognized that the subarachnoid space and, in particular, the cisterns, can provide a natural pathway for dissection that preserves all important brain structures and have an important relationship to the cerebrovascular system. The observations presented here are based on i over 4200 intracranial and spinal procedures and i 200 cadaver dissections performed under the , microscope by the senior author (MGY). During the early stages, there was developed this operative concept of utilizing the subarachnoid cisterns as natural pathways for the surgeon, thus providing easier access to deep brain structures and allowing operation on a variety of pathological lesions. Particular attention was directed toward the topography of the cisterns and associated arachnoidal adhesions and trabeculae in operative approaches to intracranial aneurysms, vascular malformations, and a variety of basal tumors, such as gliomas, meningiomas, neurinomas, craniopharyngiomas, epidermoids, and chordomas. The pathophysiological effects of these processes on the cisterns were carefully observed and recorded on 35 mm slides, movies, video tapes and sketches.

Compartmentalization The traditional view of the subarachnoid space as a freely communicating channel for the flow of cerebrospinal fluid around the cerebral-spinal axis and between the arachnoid and pia is inadequate to explain the findings at operation. The arachnoid partitions the subarachnoid space into relatively discrete chambers. Sheets of arachnoid form the walls of the cisterns whicri_ retard, and perhaps direct the flow of cerebrospinal fluid. Thus the opening of one subarachnoid cistern does not allow the immediate egress of fluid from the adjoining cisterns and collapse the entire sub-arachnoid space. The arachnoid and pia can be considered connective tissue rather than mesothelial elements. This

connective tissue forms fibers and trabeculae that bridge the subarachnoid space and are continuous with the adventitia of vessels within the subarachnoid space. The arachnoid fibers and membranes are in fact, noted to be regularly thicker and tougher where the arteries pass through the trabeculated wall from one cisternal compartment to another. ____________________. These barriers to cerebrospinal fluid flow are seen in numerous locations, providing a rationale for naming them as individual subarachnoid cisterns. For example, at pneumoencephalography air is often prevented from ascending into the subarachnoid space around the optic chiasm by a well developed bridge of arachnoid (Liliequist 1959) thus forming a wall between cisterns differentiated as interpeduncular and chiasmatic (Key and Ret-zius 1875; Epstein 1965). Undoubtedly the more fragile cisternal boundaries are partially destroyed by corrosion techniques, and autopsy studies are limited by the difficulty in avoiding disruption of the subarachnoid system on removing the brain and by autolysis after death. Microsurgical operations have thus provided a new, previously unobtainable look at the Compartmentalization of the , basal subarachnoid cisterns as they remain distended with cerebrospinal fluid and to some extent' remain in their natural physiological state. It is to • be expected that the degree of competence of the walls between cisterns varies with the individual patient and with the effects of the disease process. In addition some cisterns are easily accessible for observation while others can be only partially explored at operation. Some correlation with radiological information is therefore required to develop an overall concept of Compartmentalization within the subarachnoid space (Figs 3A-C, 4A-B).

Microneurosurgical Observations

15

iry cistern————-^ Premedullary cistern-Fig 3 A Schematic representation of the cisterns in lateral view, which can also be demonstrated on contrast CTscan.

16

1 Operative Anatomy

Fig 3B-C Schematic representation of the basal cisterns as observed during microsurgical procedures and inforrnalin-fixed brains. B The relationship between the basal cisterns (Arabic numbers) and the cranial nerves {Roman numerals).

1 Olfactory cistern 2a Callosal cistern 2b Lamina terminalis cistern 3 Chiasmatic cistern 4 Carotid cistern 5 Sylvian cistern 6 Crural cistern

7 Interpeduncular cistern

8 9 10 11

Ambient cistern Prepontine cistern Superior cerebellar-pontine cistern Inferior cerebeliar-pontine cistern (lateral cerebellomedullary) 12 Anterior spinal cistern 13 Posterior spinal cistern

Microneurosurgical Observations

ant.cho. a. p.c.{P,)

V.a. PICA

A.sp.

3C The relationship between the basal cisterns (Arabic numbers) and the ventral cerebral arterial system.

A

= A! + A2 + Anterior communicating artery

ex MCA ICA p.co.a. ant.cho.a. p.c. (PT)

B = = = = =

Middle cerebral artery Internal carotid artery posterior communicating artery anterior choroidal artery posterior cerebral artery

sea compl AICA V.a. PICA A.sp.

= = = = =

superior cerebellar artery Basilar artery anterior inferior cerebellar artery Vertebral artery posterior inferior cerebellar artery anterior spinal artery

17

18

c

1 Operative Anatomy

D Fig 4 A-D Perioptic and basal cistern visualized by computed tomography with dye injection.

Microneurosurgical Observations 1 9

ICA

sup.tr. MCA MCABi.

Fig 4 E

Schematic representation of the basal cistern seen on Fig 4 A-D.

A3 ICA sup.tr. MCA MCABi. inf.tr. MCA ant.ch. p.co.A.

= = = = = = =

A2 segment Internal carotid artery superior trunk of MCA MCA Bifurcation inferior trunk of MCA anterior choroidal artery posterior communicating artery

P!

P2

= P, segment = P2 segment

Hip.

= Hippocampus

Ba.Bi.

= Basilar Bifurcation

Pa

= P3 segment

P«

= PA segment

20

1 Operative Anatomy

Intracisternal Arachnoidal Trabeculation Numerous connective tissue strands bridge the subarachnoid space adhering to, and supporting, the vessels and nerves within the cisterns (Fig 5AE). The cisterns vary in the strength and density of these trabeculae. Key and Retzius (1875) presented the relationship of the arachnoid trabeculae to cerebral vessels in elaborate detail. Mayet (1965) found neural elements including complicated nerve endings within the arachnoid and arachnoid trabeculae of the cisterna magna of man. The shape of these nerve endings in the arachnoid was variable but complex end formations such as knobs, loops, varicosities, and fine baskets up to 1 mm in length were found in the trabeculae. It was concluded that these nerve endings might convey information about the cere-brospinal fluid pressure. Arutiunov et al (1974) described similar nerves within the trabeculae and felt that they might relate to cerebral vasospasm. Hirano and associates (1976) found capillaries in the arachnoid trabeculae of the rat, and tiny vessels over the posterior wall of the cisterna magna have been seen in man during microneurosurgical operations (see Figs 5B and 35).

Cisternal Junctions There are some areas where several cisterns come together. At these points there are though reinforcements of the arachnoid fibers that hold the neural and vascular structures firmly_in position. These areas are important surgical landmarks and provide a key to understanding the subarachnoid space. The cisterns will be discussed in detail in the following pages, but the junction points will be mentioned briefly here: Parasellar Area Above the internal carotid artery bifurcation is a confluence of the carotid, chiasmatic, olfactory, lamina terminalis, Sylvian, crural and interpeduncular cisterns. Thickened bands of arachnoid run across the origins of the anterior and middle cerebral arteries from the area of the olfactory trigone to the lateral optic nerve and mesial temporal lobe. Additional thickened fibers are closely applied between the posterior communicating artery and oculomotor nerve as both pierce the interpeduncular cistern, and between the anterior choroidal artery and the mesial temporal lobe as the carotid and crural cisterns meet. This forms a triangle of firm arachnoid fibers joining the posterior communicating artery, anterior choroidal artery, and oculomotor nerve.

Foramen of Luschka At the foramen of Luschka is a confluence of the lateral cerebellomedullary, cerebellopontine, premedullary and prepontine cisterns and the lateral recess of the fourth ventricle. The flocculus of the cerebellum is just above this junction and the choroid plexus of the fourth ventricle is frequently visible. The pontomedullary sulcus is medial and from this point cranial nerves VII and VIII run superolaterally, while cranial nerves IX and X run inferolaterally. Pineal Area Above the pineal gland is a confluence of the superior cerebellar, quadrigeminal, ambient, pericallosal and velum interpositi cisterns. This is near the area of the tentorial notch posterior to the quadrigeminal plate. The posterior cerebral and superior cerebellar arteries approach the midline in this area, and the internal cerebral veins, basal veins of Rosenthal, pericallosal veins, and occipital veins converge to form the great vein of Galen.

Apposition of Arachnoid and Ependyma In certain areas of the brain, the subarachnoid space and ventricular system are in close approximation. Knowledge of these areas helps in understanding the general plan of the subarachnoid space, and may be of some therapeutic importance. \ Lamina Terminalis The lamina terminalis cistern and the third ventricle are separated by this thin membrane which contains also neural elements. A small venous plexus is usually found in this area (Duvernoy et al 1969). Choroid Fissure The crural cistern and the temporal horn of the laterale ventricle are separated only by the arachnoid and a single pial layer as the anterior and lateral posterior choroidal arteries enter the temporal horn to supply the choroid plexus. Velum Interpositum The cistern of the velum interpositum is separated from the third ventricle by arachnoid and ependyma and contains the medial posterior choroidal arteries and the internal cerebral veins.

Microneurosurgical Observations Fig 5 A Operative photograph (right pterional approach) demonstrating the numerous trabeculae that extend from the arachnoid over the frontoorbital gyrus to gain attachment to the orbital dura. These are normally present in many areas but can be appreciated only after the most delicate dural opening.

Fig 5B Membranous arachnoidal layer between the frontoorbital gyrus and orbital dura (arrows). Note: this membrane has its own micro-vasculature.

Fig 5C Operative photograph (supracerebellar approach) showing innumerable trabeculae that suspend the cerebellar vermis.

21

221 Operative Anatomy Fig 5D Operative photograph illustrating the more delicate trabeculae extending from the anterior quadrangular lobule to the tentorium.

Fig 5 E Operative photograph (right Sylvian cistern) demonstrating numerous trabeculae that suspend the middle cerebral artery (M) within the cistern. Microscissors (sc) are seen over the artery. Arachnoidal membrane over Sylvian fissure (arrows).

Microneurosurgical Observations

Foramen of Luschka The lateral recess of the fourth ventricle opens into the lateral cerebellomedullary cistern as described above. Again a fine incomplete membrane is present separating the ventricle from the cistern. Foramen of Magendie The fourth ventricle opens in the midline into the cisterna magna. A thin membrane separating the ventricle from the cistern has been observed.

Pathological Thickening and Reduplication of Arachnoid There are two important changes in the arachnoid which the surgeon may encounter during operations for cerebral aneurysm. First, hemorrhage leads to staining and thickening of the arachnoid making visualization of structures and dissection more difficult. Second, with aneurysm growth, reduplications of the arachnoid are encountered as the aneurysm carries the arachnoid of its original cistern against the arachnoid of adjacent cisterns. Thus the aneurysm becomes invested with the arachnoid of neighboring cisterns. This allows tension to be transmitted to the fundus of the aneurysm even when dissection is being carried out some distance away, but it also provides an invaluable plane of dissection to allow easier separation of the aneurysm from adjacent structures.

23

Relationship to Pathological Processes If the arachnoid cisterns are to be utilized as a plane of dissection to separate pathological lesions from the brain, cranial nerves, and vascular system, the precise relationship of these lesions to the arachnoid must be appreciated. Such a relationship for various lesions is outlined diagrammatically in Fig. 6A-C for the sellar area, although the general concepts are valid throughout the intracranial cavity and spinal canal. Processes that originate outside the dura will with growth indent the dura and be separated from normal neural and vascular structures by the dura and the arachnoid (Fig 6A). Such lesions include pituitary adenomas, osteomas, chordomas, chon-dromas, glomus jugulare tumors, and epidural metastases. Processes arising between the dura and arachnoid will be invested with various reduplications of the subarachnoid cisterns depending on the particular location (Fig 6B). These lesions are primarily meningiomas and schwannomas such as acoustic neuroma. Most important to the present discussion are those lesions that arise within the subarachnoid cisterns (Fig 6C). With growth, these lesions encroach upon adjacent cisterns and become invested with various reduplications of arachnoid. These arachnoid layers are the planes by which the lesion can be separated from adjacent structures and removed. Such lesions include subarachnoid cysts, craniopharyngiomas, exophytic gliomas, dermoids, epidermoids, and of course, cerebral aneurysms and arteriovenous malformations.

24

1 Operative Anatomy

Fig6A-C Schematic representation of the relationship between the parachiasmal cisterns and expanding masses in the area. Cisterns (blue), dura mater (green), skull (black). A Pituitary adenomas, osteomas, chordomas and glomus tumors arise in the epidural space and are covered by both dural and arachnoid membranes (A-,). B Meningiomas and schwannomas originate in the subdu-ral space and extend subdurally, but epiarachnoidally. They are covered by two or more cisternal layers depending on the number of cisterns traversed (B,). C Craniopharyngiomas, optic and hypothalamic gliomas, AVMs, and aneurysms arise wilhin the cisternal spaces, If confined to a single cistern, they are covered by a single cisternal layer only (d).

Normal Cisternal Anatomy

25

Normal Cisternal Anatomy In describing and naming the subarachnoid cisterns, certain limitations present themselves: 1) While most of the cisterns can be almost completely explored at microneurosurgical operations, only portions of some cisterns are available for inspection. 2) During exploration the jlimsy walls of some cisterns may be torn with only minimal retraction, thereby altering the normal topography. 3) In other cases cisternal walls may be deficient as part of a pathological process or as the usual anatomical variation. 4) Embryological studies are still incomplete concerning development of the subarachnoid cisterns, so the basis for any current categorization is only empirical.

With these limitations in mind, a concept of the subarachnoid space is presented that attempts as accurately as possible to describe what has actually been observed at operation. The structures are placed into surgically relevant groups, and an easily understood nomenclature is employed. The cisterns are divided into two major groups supratentorial and infratentorial (Table 1), both for convenience and to parallel neurosurgical approaches.

Table 1 Subarachnoid Cisterns I. Supratentorial Cisterns A) Anterior (parasellar) 1) Carotid cistern 2) Chiasmatic cistern 3) Lamina terminalis cistern 4) Olfactory cistern 5) Sylvian cistern B) Lateral (parapeduncular) 1) Crural cistern 2) Ambient cistern (anterior part) C) Posterior (tentorial notch) 1) Quadrigeminal cistern 2) Velum interpositum cistern D) Superior (callosal) 1) Corpus callosum cistern - anterior portion 2) Corpus callosum cistern - posterior portion 3) Hemispheric cistern II. Infratentorial Cisterns A) Anterior 1) Interpeduncular cistern 2) Prepontine cistern 3) Premedullary cistern B) Lateral 1) Ambient cistern (posterior part) 2) (Superior) cerebellopontine cistern 3) Inferior cerebellopontine or lateral cerebellomedullary cistern C) Posterior 1) Cisterna magna 2) Superior cerebellar cistern D) Superior 1) Vermian cistern 2) Hemispheric cistern

26

1 Operative Anatomy

Supratentorial Cisterns Anterior (Parasellar) Carotid Cistern

This cistern, described radiologically by Lewtas and Jefferson (1966) and by Wackenheim and associates (1973) is bordered superiorly by the dura over the anterior clinoid process and the orbitofrontal lobe, and inferiorly by the cavernous sinus (Figs 7, 8A-B). The arachnoid does not follow the internal carotid artery into the cavernous sinus nor is it attached to the anterior cfmoid process. There are one or two millimeters of jiaked internal carotid artery which are between the investment of the carotid cistern and the dura of the cavernous sinus. Medially the cistern shares

a wall with the chiasmatic cistern and laterally is bounded by the mesial temporal lobe and the free margin of the tentorium. Opening the carotid cistern does not always release cerebrospinal fluid from the chiasmatic and interpeduncutar cisterns, justifying its designation as a separate cistern. The cistern is relatively free of trabeculated fibers except around the origins of the posterior communicating and anterior choroidal arteries which have their own sleeves of arachnoid within the carotid cistern (Figs 9A-D, 10). The inferior part of the carotid cistern and superior part of the mterpeduncufar cistern are in apposition sometimes creating a single (Lilie-quist's) membrane, which may be thick or thin -but normally forming two separate layers. The carotid cistern may sometimes extend 1-2 cm deep inferiorly.

cistern cistern

Pco.A.

Carotid cistern Ant. ch. A.

Ambient

cistern Crural cistern Sylvian cistern

Interpeduncular Chiasmatic Olfactory cistern Callosal cistern Lamina terminalis cistern Fig 7 Schematic representation of the parachiasmal and neighboring cisterns as encountered during the pterional approach. Chiasmatic cistern contains Chiasm (Ch) and stalk (st) Carotid cistern contains Carotid artery (C) and branches

Lamina terminalis cistern contains Anterior communicating and A, segment

Sylvian cistern contains Middle cerebral artery (M) Olfactory cistern contains Olfactory tract Interpeduncular cistern contains Basilar artery (B) and branches Crural cistern contains Anterior choroidal artery (Ant. ch. A.) Ambient cistern contains P2 segment of posterior cerebral Oculomotor nerve (III) has its own sleeve of arachnoid.

Supratentorial Cisterns

Fig 8A-B The parachiasmatic cisterns as recognized under the operating microscope from the pterional approach. 1 Sylvian cistern with middle cerebral artery 2 Olfactory cistern (base) with olfactory tract 3 Carotid cistern with internal carotid artery 4 Interpedunojlar cistern (lateral recessj with posterior communicating artery 5 Crural cistern with anterior choroidal artery 6 Chiasmatic cistern with chiasm 7 Lamina terminalis cistern with anterior cerebral and

27

anterior communicating artery 8 Callosal cistern (ant, part) with distal anterior cerebral artery A2

28

1 Operative Anatomy

Fig 9 A Operative photograph (right pterional approach) pointing out the proximal Sylvian and carotid cisterns (Ca-C) already partially exposed (arrows).

Fig 9 B The opened arachnoidal membrane over the right internal carotid artery. Strong membranous fibers at the proximal part of the Sylvfan fissure between the fronto-orbital and temporal gyrus (arrows).

Fig 9C The proximal limit of the carotid cistern with ophthalmic artery (arrows). Vasa vasorum over the sclerotic right internal carotid artery.

Fig9D Vasa vasorum over the sclerotic right internal carotid artery. Large sclerotic ophthalmic artery (arrow) also with vasa vasorum. Compression of the right optic nerve without clinical signs and symptoms.

Supratentorial Cisterns

29

Fig 10 Schematic drawing of the superiorly opened carotid cistern showing the posterior communicating artery entering the lateral recess of the interpeduncular cistern, while the anterior choroidal artery (arrow) is entering the crural cistern.

Especially important relationships of the carotid cistern are to the posterior communicating artery, dorsum sellae, oculomotor nerve, and interpeduncular cistern, since aneurysms commonly arise fromjhe lateral wall of the internal carotid artery and involve these structures. The arachnoid of the cistern is easily separated from the anterior cli-noid process and anterior cavernous sinus, is not attached to the free edge of the tentorium, and is contiguous with the_ mterpeduncular cistern^ Nevertheless a sleeve of arachnoid around the origin of the posterior communicating artery is in some cases densely adherent to the dura over the posterior clinoid process, and the artery may lie in a sulcus within the dorsum sellae. This accounts for much of the difficulty encountered in isolating some inferiorry directed posterior communicating artery aneurysms and is responsible for their often sudden rupture when attempts are made to place a clip before adequate division of the adherent bandsjFigs 11-131__________________ A second point of aracrmoidal reinforcement is where the posterior communicating artery penetrates the interpeduncular cistern and the oculo-

motor nerve with its own arachnoidal sheath, Jeaves the cistern to enter the dura of the cavernous sinus. Dense arachnoid trabeculations often bind the artery and nerve at this point. A final area of dense arachnoid fibers is between the carotid and crural c^ierns and the uncus of the temporal lobe, where the anterior choroidal artery leaves the carotid cistern to enter the crural cistern. These regularly observed areas of thickened arachnoid bind the posterior communicating and anterior choroidal arteries and oculomotor nerve firmly and must be divided sharply to gain mobility during dissection. Additional areas of thickening are similarly present at the bifurcation of the internal carotid artery, but these are discussed with the lamina terminalis and Sylvian cisterns as they relate primarily to these cisterns. ______ ! The carotid cistern contains the supraciinoid~por-tion of the internal carotid artery, the origins of ophthalmic, posterior communicating and anterior choroidal arteries, small arteries to thg_gp_tic_ jierves and pituitary stalk, a small but regularly seen artery to the dura over the anterior clinoid process (see Figs 11A and 47A-C), and variably

30

1 Operative Anatomy

Fig 11A Operative photograph of the opened carotid cistern: d = dural artery, posterior communicating artery (arrow 1) , anterior choroidal artery (arrow2).

Fig 11 B Operative photograph of the lateral portion of the right carotid cistern demonstrating the posterior communicating artery (arrow 1 ) , the oculomotor nerve (III), the anterior choroidal (arrow 2) and uncal arteries.

Fig 12 The arachnoidal sleeve (arrow) encasing the right oculomotor nerve (III) has been opened in this operative photograph.

Fig 13 The left oculomotor nerve (III) and its arachnoidal sleeve within the interpeduncular cistern as seen (arrow) from a dorso-lateral approach in the sitting position after the removal of a meningioma from the upper cerebellopon-tine angle. The basilar artery is well seen (Ba).

Supratentorial Cisterns

31

Fig 1 4 A The chiasmatic cistern has been partially opened on the right side in this operative photograph. The roof of the cistern is closely applied to the dorsal surface of the optic nerves and chiasm, as demonstrated by the dissecting forceps (arrow). Fig14B Subchiasmal part of the chiasmatic cistern, seen between the right internal carotid artery and the optic nerve (arrow). Fig 1 4 C Pituitary stalk after opening of the chiasmatic cistern (arrow).

/present frqntqorbital veins which lie just overjhe J internal carotid artery and drain into the sphenoj parietal sinus. "~™ ~' Chiasmatic Cistern (Cisterna Chiasmatica) This cistern encloses the subarachnoid space, around the optic nerves and chiasm. Superiorly it is tightly adherent to the superior surface of the optic nerves and chiasm and caudal to this contiguous with the inferior part of the lamina termina-lis cistern (Fig 14A-C)._______________ Interiorly it shares a common wall with the interpeduncular cistern, this thick arachnoid joining the chiasmatic and interpeduncular cisterns being called "Liliequist's membrane" (Fig 15A-D). Anteroinferiorly it extends to the infundibulum and pituitary stalk and is bounded by the diaphragma sellae. When the diaphragma is incom-

petent, the chiasmatic cistern may send extensions inside the sella. Often a remarkable density of arachnoid fibers bind the inferior surface of the optic nerves to the pituitary stalk, sometimes completely enclosing the stalk in the form of a collar. Anteriorly the cistern is limited by the limbus sphenoidale except at the optic foramina where short extensions of the subarachnoid space follow _the optic nerves into the orbit./ Laterally the cistern shares a common wall with the carotid The chiasmatic cistern contains the optic nerves, pituitary stalk, and numerous small internal carotid branches to both structures. The ophthalmic artery enters the chiasmatic cistern within the optic canal.

32

1 Operative Anatomy

Fig 1 5 A The inferior border of carotid and superior border of the interpeduncular cistern is composed of tough trabecular fibers (also known as Lillequist's membrane) as seen through the opened carotid cistern, beneath the right carotid artery (ICA) in this operative photograph.

Fig 15 B Sugero-medial wall of Liliequist's membrane is opened (arrow) between the right optic nerve and right internal carotid artery.

Fig 1 5 C Inferior wall of carotid cistern and superomedial wall of Liliequist's membrane are separately seen (arrow).

Fig 1 5 D Lateral perspective to the stalk (arrow 1 ) . Pathway of the right P-, segment (arrow 2).

Supratentorial Cisterns

Fig 16 Schematic drawing of the lamina terminalis cistern containing both anterior communicating artery and branches.

Lamina Terminalis Cistern (Cisterna Laminae Cinerae Terminalis) This cistern is defined primarily by the anterior / cerebral arteries (Fig 16). Its anteroinfcriorjirmt is the superior surface of the optic chiasm where it is contiguous with the chiasmatic cistern. Anterosuperiorly the rostrum of the corpus callosum covers the cistern. The posterior boundary is jhe lamina_ terminalis^; Extensions laterally enclose !each anterior cerebral artery with the anterior 'perforated substance above and the optic chiasm below, before the cistern joins several cisterns above the internal carotid artery bifurcation, it Thickened bands of arachnoid running from the olfactory area to the optic nerve demarcate the most lateral limit of the cistern. These form a jtunnel through which the anterior cerebral artery |must pass on leaving the carotid and entering the lamina terminalis cistern (Figs 17-19)

33

and proximal part of A2 segment and

In the center of the cistern dense, but very fragile trabcculatcd fibers _arc present running between the anterior communicating artery and the lamina terminalis (Fig 20). Near the origins of the frontopolar arteries, similar thickened arachnoidal bands bind the A2 segments of the anterior cere bral arteries to each other. Finally, throughout the anterior extension of the cistern in the interhemisphcric fissure, short tough fibers connect both re_ctus^gyri. __________ _________ The lamina terminalis cistern contains the anterior cerebral arteries, medial striate branches (the recurrent artery of Heubner), the anterior com municating artery complex, arteries to the hypothalamus, the most proximal A2 segments of the anterior cerebral arteries, frontoorbital arteries, and occasionally the origin of the frontopolar arter ies. Anterior communicating and anterior cerebral veins also lie within the cistern (Figjl^______

34

1 Operative Anatomy

Fig 1 7 A Opening of the lateral part of the right lamina terminalis cistern.

Fig 1 8 A The proximal portion of this right A, segment is nearly strangulated by similar trabeculations as seen at operation (arrow), su = sucker.

Fig 17B In this operative photograph, the right carotid and Sylvian cisterns have been opened. The entrance of the right A, segment into the lateral part of the lamina terminalis cistern is marked by the presence ofjough trabeculae (arrow) extending betwen the optic and~olfactory nerves. ~

Fig 1 8 B After opening of the arachnoidal fibers over the right A, segment.

Supratentorial Cisterns

35

Fig 20 Numerous trabeculae and a few small perforating vessels suspending the anterior cerebral artery complex within the lamina terminalis cistern in a formalin-fixed specimen. These fibers are easily disrupted during dissection and thus are seldom recognized at operation. A = Anterior cerebral artery, ArSegment.

Fig 1 9 A In this operative photograph, the right portion of the chiasmatic cistern has been opened. At the tip of the sucker (su) is the edge of the left gyrus rectus (gr). Fig 1 9 B Left wing of the lamina terminalis cistern seen from the right sided pterional approach. I. A1 = left A, segment, H = left Heubner's artery, CH = chiasm, r. A1 = right A, segment. Fig 1 9 C Left internal carotid artery (ICA) seen from the right sided pterional approach. Op = optic nerves, left A, and M, segment.

36

1 Operative Anatomy

OL.

Fig 21 Bilateral medial orbitofrontal arteries (arrows) arising from the A2 segments and disappearing into the olfactory sulci beneath the olfactory tracts (OL.) in this formalin-fixed specimen and coming to the surface of (small arrows) lateral to the right olfactory tract. Ch = Chiasm.

Olfactory Cistern This cistern is formed by the arachnoid over the olfactory tract between the orbital gyri laterally and the gyrus rectus medially. The olfactory sulcus between the gyri may be several (usually 5-10) millimeters deep with the cistern expanding slitlike into the sulcus (Fig 22). Inferiorly it is bounded rostrally by the floor of the anterior fossa including the cribriform plate of the ethmoid bone and caudally by the chiasmatic cistern. Posteriorly it joins several other cisterns above the internal carotid artery bifurcation. The olfactory cistern contains the olfactory bulb and tract, parts of frontoorbital and olfactory arte^_ jies^ their branches, and several frontobasal veins. The frontoorbital artery characteristically dips into the olfactory cistern as it passes laterally across the orbital surface of the frontal lobe.

Fig 22 Basal view of the right olfactory cistern following retraction of the tract (arrow 1) in a formalin-fixed specimen. The olfactory cistern extends to a depth of 1-2 cm and within it the medial orbito-frontal artery (arrow 2) divides. Its branches leave the cistern on its lateral border (arrows 3).

Sylvian Cistern (Cisterna Fossae Sylvii, Cisterna Fissurae Lateralis) This cistern is transitional between the basal cisterns and the subarachnoid space over the convexities. The most medial and inferior extent of the Sylvian cistern is at the origin of the middle cerebral artery from the internal carotid (Fig 23). Thickened bands of arachnoid completely enclose the origin of the middle cerebral as it arches from the area of the olfactory trigone on the lateral orbitobasal frontal lobe to the mesiobasal temporal lobe (see Fig 9B). These form a tunnel through which the middle cerebral artery passes before entering the Sylvian fissure. Slightly more distal there are very often numerous frontotemporal

Supratentorial Cisterns

Fig 23

37

Schematic drawing of the proximal part of the Syivian cistern containing the M-, segment and branches.

fibers within the Syivian cistern, crossing over the artery and almost forming a second membrane on top of the artery. The cistern narrows superiorly as the frontal and temporal lobes approach each other over a length of 15-20 mm. The width of the cistern is usually about 0.5-1.0 cm on the surface. In some cases however, the ftwnftrf sad temporal lobes are closely approximated on the surface thereby covering the substance of the cistern (Fig 24A-B). For this reason the Syivian cistern and its investing arachnoid can be categorized as follows:

Category \ 2 3 4

dsiernal Size Large Small Large Small

Arachnoidal Characteristics Transparent + Fragile Transparent + Fragile Thickened + Tough Thickened +JTqugh_

Microsurgical dissections of the Syivian cistern during the pterional operative approach are increasingly more difficult as the category of cistern increases according to the above classification. Thus the exposure of a category 3 cistern is quite tedious, but certainly easier than that of a category 4, post-meningitic cistern, which is almost impossible.

38

1 Operative Anatomy

Tern.

Fig 24A-B The variations of the width of the proximal Sylvian cistern and the position of the middle cerebral artery (M). Tem. = Temporal lobe, Fr. = Frontal lobe.

B Fig 25 A-B The proximal part of the lateral fronto-orbital gyrus (Fr.) herniating into the temporal lobe (Tem.). M = Middle cerebral artery (A). The proximal part of the superior temporal gyrus herniating into the lateral fronto-orbital gyrus (B).

Supratentorial Cisterns Rarely is the cistern clearly visible on the surface. Usually the lateral orbital gyrus firmly indents the temporal lobe inside the proximal Sylvian fissure thereby compressing the cistern, pushing it laterally, and concealing its deeper portion (Fig 25A-B). At the limen insulae the cistern enlarges to encompass the middle cerebral artery bifurcation. Thickened arachnoid fibers are present over the origins of both major trunks. These trunks diverge in a gentle curve and then reapproximate after 10 to 15 mm, still within the cistern. Numerous arachnoid trabeculae stretch between the two trunks as they diverge, and as the trunks recon-verge they are again covered with these thickened arachnoid fibers. Over the insula, the cistern is large, even though it appears small on the surface. Scattered arachnoid fibers course across the cistern and they are reinforced around the middle cerebral branches as the arteries exit from the Sylvian fissure. The Sylvian cistern contains the middle cerebral artery and the origins of the lenticulostriate, tem-poropolar and anterior temporal arteries, the middle cerebral artery bifurcation and the origins of the major branches. The superficial and deep Sylvian veins (with insular branches) are also within the cistern.

bral peduncle and the interpeduncular cistern, and its lateral boundaries are supratentonally the mesial temporal lobe and infratentorially the lobu-lus quadrangularis of the cerebellum. Inferiorly it shares an arachnoid wall with the cerebellopontine cistern. Anteriorly the cistern is related to the crural cistern. It has yet to be determined whether the lateral posterior choroidal artery must cross a cisternal wall to gain access to the crural cistern. The anterior choroidal and posterior lateral choroidal arteries enter the choroidal fissure within a few millimeters of each other. There is a superior extension of each ambient cistern which was named the wing of the ambient cistern by Liliequist (1959). This includes that portion of the cistern which extends from the I uncus of the temporal lobe, over the pulvinar of the thalamus, and anteromedially to the area of the velum interpositum near the foramen of Monro. The ambient cistern contains segments of the posterior cerebral artery, numerous arteries to the midbrain from both PCA's, and the basal vein of Rosenthal. The superior cerebellar artery and the trochlear nerve have their own arachnoid sleeves around the peduncle.

Lateral (Parapeduncular) Crural Cistern The crural cistern (see Fig 11A-B) lies between the parahippocampal gyrus _and the cerejjral peduncle. The cistern extends to the carotid • cistern anteriorly and lies on top of the interpeduncular cistern with the ambient cistern lateroposterior.|The crural cistern is clearly demarcated from the carotid and interpeduncular cisterns between the anterior choroidal and posterior communicating arteries./t has been recently possible at operation (selective hippocampectomy) to clearly separate the cistern posteriorly and infe-riorly from the ambient and interpeduncular _cisterns.jThe importance of this cistern lies in the valuable surgical plane it establishes between the anterior choroidal and posterior communicating arteries. The crural cistern contains the anterior choroidal and medial posterior choroidal arteries and the basal vein of Rosenthal. Ambient Cistern (Gisterna Ambiens) This cistern covers the lateral aspect of the mesencephalon and is both supra- and infratentorial justifying its inclusion in both categories (Figs 26A-D, 27A-J). Its medial boundary is the cere-

39

40

1 Operative Anatomy Fig 26A Schematic drawing of the right parapeduncular cistern (right subtemporal approach}.' ~~ " '"

Fig 26 B The right parapeduncular cistern; posterior cerebral artery within the ambient cistern, superior cerebellar artery has its own sleeve as has the trochlear nerve (IV). The anterior choroidal (cho) artery is seen in the opened crural cistern. Ill - oculomotor nerve, sea = superior cerebellar artery, P2 = P2 segment.

Supratentorial Cisterns

Fig 27A

The right lateral portion of the

Fig 26C Operative photograph of the right parapeduncu-lar cistern. Fig 26D The right lateral wing of the interpeduncular cistern seen on the operative photograph after elevation of the tentorial edge by forceps (Fore.) sea = right superior cerebe/lar artery. right carotid cistern (ICA) has been opened (arrows) following retraction of the temporal pole to reveal the posterior communicating artery (pco), tuberomammillary artery (tu) and anterioT choroidal artery (cho). Ill = oculomotor nerve.

41

42

1 Operative Anatomy Fig 27 B Lateral portion of the right carotid cistern, superolateral part of the interpeduncular cistern and the beginning of thejimlbient cistern (arrows) are 6pe~riedTfh~= thalamoperforating vessels.

Fig 27 C The P! segment and the perforating vessels from the P, and P2 segments of the posterior cerebral artery can be better seen (th), before the P2 segment enters the ambient cistern.

Supratentorial Cisterns Fig27D The right posterior communicating artery, tuberomammillary artery (tu) and the arachnoidal membrane (arrows) at the beginning of the ambient cistern.

Fig 27 E Following a right selective amygdalo-hippocampectomy, the crural and ambient cisterns have been opened, revealing: - the P2 segment of the posterior cerebral artery, as well as the anterior cho-, roidal artery (cho). op = optic tract.

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44

1 Operative Anatomy Fig 27 F The parapeduncular section of the ambient cistern is opened. The P2 segment and branches are better seen. The superior cerebellar artery (sea) is seen within its own arachnoidal sleeve.

Fig 27 G The end of the posterior cerebral artery P2 segment as it branches into temporal and parieto-occipital arteries (P3) and the posterior lateral choroidal artery (arrows) as it enters the choroid plexus.

Supratentorial Cisterns Fig 27 H The parieto-occipital branches (Pr, Oc) of the P3 segment and temporal branch (Te) after removal of a temporobasal astrocytoma.

Fig 27 i The trochlear nerve leaving the quadrigeminal cistern and entering its own sleeve along the tentorial edge.

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46

1 Operative Anatomy

Posterior (Tentorial Notch) Quadrigeminal Cistern (Cisterna Venae Magnae Galeni) This cistern (Fig 28A-C) is jpmewhat arbitrarily divided from the ambient cistern. The vein of Galen has well-developed, sometimes dense arachnoid attachments which form a clear boundary dorsally. Laterally, however, it has been difficult to demarcate this area because any retraction quickly ruptures the arachnoid membranes and there are no specific anatomical structures defining the limits of the cistern. The anterior limits of the cistern are the dorsal mesencephalon, the quadrigeminal plate, and the pineal gland. Posteriorly arachnoid is attached to the tentorium and extends from the splenium of the corpus callosum inferiorly to the lingula of the cerebellar vermis, above the anterior medullary velum of the fourth ventricle. The cistern is contiguous superiorly with the velum interpositum cistern and laterally with the ambient cisterns. The quadrigeminal cistern contains the medial posterior choroidal arteries, the great vein of Galen, the terminal portions of its tributaries, and the internal cerebral, basal, pericallosal, and occipital veins. The origins of the posterior pericallosal arteries and the continuation of the posterior cerebral arteries are also contained within this cistern. Velum Interpositum Cistern This small cistern extends from the habenular commissure to the foramen of Monro (see Fig 3C). It is located beneath the splenium of the corpus callosum above the velum interpositum, with the roof of the third ventricle below. Anteriorly it is beneath the fornix, converging to a point at the foramen of Monro. It lies between the pulvinar thalami, the arachnoid margins blending with the tela chorioidea. Posteriorly there is no clear distinction from the quadrigeminal cistern. The cistern contains the medial posterior choroidal artery, the splenothalamic branches of the pericallosal arteries, and the internal cerebral veins.

Superior (Callosal) Corpus Callosum Cistern - Anterior Portion (Cisterna Corpus Callosi, Cisterna Fissurae Interhemisphaerica) This cistern extends from .he falx cerebri medially to the pia over the cingulate gyri laterally (see Fig 3C). Anteriorly the cistern follows the falx to the

Fig 28A-B Quadrigeminal and Galenic cisterns; original drawing from the work of Key and Retzius (1875). Fig 28C Operative view of the quadrigeminal cistern (supracerebellar approach).

Infratentorial Cisterns

47

crista galli and joins the lamina terminalis cistern near the rostrum of the corpus callosum. Although there are reinforced arachnoidal fibers at the branching of the pericallosal and callosomarginal arteries, no distinct division of the corpus callosum cistern has been noted, and the arbitary division of this cistern into anterior and posterior portions is merely for convenience in discussing regional anatomy. The cistern contains the pericallosal arteries, and the origins of the frontopolar and callosomarginal arteries. Small anterior cerebral veins may be present sometimes making connections with the inferior sagittal sinus. Corpus Callosum Cistern - Posterior Portion Beyond the branching of the callosomarginal and pericallosal arteries, the corpus callosum cistern is narrower as the falx conies closer to the corpus callosum. Arachnoid forming the roof of the cistern is suspended from the inferior margin of the falx. Inferiorly the cistern joins the quadrigeminal and velum interpositum cisterns at the end of the splenium. The posterior portion of the corpus callosum cistern contains the pericallosal arteries which may end anywhere between the gyrus precuneus and the foramen of Monro. When the pericallosal arteries are not long, posterior pericallosal arteries arise from the parietooccipital branch of the posterior cerebral artery and run forward in the corpus callosum cistern. This cistern also contains the posterior pericallosal veins.

Fig 29 Dissection of a formalin-fixed brain demonstrating the interpeduncular (arrow 1) and prepontine (arrow 2) cisterns.

Infratentorial Cisterns Anterior Interpeduncular Cistern As the cerebral peduncles emerge from between the two optic tracts, they converge to enter the pons so that the subarachnoid space between them forms a cone-shaped cul-de-sac occupying the interpeduncular fossa. This is the most posterior recess of the interpeduncular cistern. The roof of the cistern is formed by the inferior surface of the mesencephalon and the lower diencephalon, the posterior perforated substance, and the mammillary bodies. The anteroinferior boundary is the clivus, and laterally tEe~cisfern joins the ambient cistern inferiorly and superiorly is limited by the carotid and crural cisterns and the mesial temporal lobes (Figs 29,

The anteroposterior wall of the interpeduncular cistern is especially well-developed. It stretches like a curtain from one mesial temporal surface to another and is fused with the chiasmatic cistern around the infundibulum and pituitary stalk. This membrane was described by Key and Retzius (1875) but j§ commonly referred to as, Liliequist's membrane (Liliequist 1959). Following subarachnoid hemorrhage, this arachnoid membrane may become thickened and create ajoculation of cerebrospinal fluid in the interpeduncular and prepontine area. Opening of this membrane at operation almost always results in \he escape of some cerebrospinal fluid, even in the presence of profuse lumbar drainage.

48

1 Operative Anatomy

Fig 30A-B Diagonal arachnoidal membranes along the inferior border of the interpeduncular cistern as seen in a formalinfixed specimen, on both, right (A) and left (B) sides. The arachnoid trabeculae crossing the cistern (B).

The inferior aspect of the cistern extends in a tine to the cerebellopontine cistern. Just above the triangular shape down to the middle portion of the level of this artery a plane separates this cistern basilar artery. The origins of the superior cerebel- superiorly from the interpeduncular cistern. The lar arteries lie within the interpeduncular cistern lateral extent of the prepontine cistern is limited as there is no significant arachnoid membrane by bilateral arachnoid membranes that form the between these arteries and the posterior cerebral medial walls of the cerebellopontine cisterns. The arteries, but at the level of the third nerve the inferior arachnoidal wall of the cistern is thickened superior cerebellar arteries acquire their own as the vertebral arteries join to form the basilar arachnoid sleeves and the Pj segments enter the artery beneath the pontomedullary sulcus. The ambient cistern (see Figs 26 and 27). The cistern contains the basilar artery, the origin of the interpeduncular cistern contains the upper 1A of the anterior inferior cerebellar artery, and the entire basilar artery and the origins of the posterior free course of the abducens nerve from the pons to cerebral and superior cerebellar arteries, medial Dorello's canal. posterior choroidal and thalamogeniculate arteries, and their branches, the basal veins of Rosenthal, and the oculomotor nerves. The oculomotor nerves Premedullary Cistern (Anterior Medullary can be seen to have their own distinct sleeve of Cistern) arachnoid when leaving the cistern. This cistern extends superiorly from the pontomedullary sulcus over the ventral aspect of the Prepontine Cistern medulla to the upper cervical area inferiorly. It is This cistern lies between the anterior surface of limited anteriorly by the clivus. The lateral extenthe pons and the clivus surrounding the basilar sion of the cistern is not as great as the vertebral artery (see Figs 29, 30A). Arachnoidal fibers arteries and hypoglossal nerves are in the adjacent encircling the anterior inferior cerebellar artery lateral cerebellomedullary cistern. The cistern denote the passage of this artery from the preponcontains the anterior spinal artery and the anterior medullary vein.

50

1 Operative Anatomy

Fig 32 A-C Operative photographs of the right cerebellopontine angle revealing: A The lateral cerebello-medullary or inferior cerebellopontine cistern containing cranial nerves IX, X, and XI (arrows). B The inferior cerebello-pontine cistern has been opened revealing cranial nerves IX, X, and XI, while nerves VIII and VII remain hidden within the upper cerebello-pontine cistern (arrow). C Both upper und lower cerebello-pontine cisterns have now been opened revealing cranial nerves VII, VIM, IX, X and XI, along with dense interposing trabeculae and a loop of anterior inferior cerebellar artery (arrow).

Laterally the cistern extends along the posterior petrous portion of the temporal bone entering the internal auditory meatus and extending outwards into Meckel's cave. Posteriorly the cistern is covered by the posterior quadrangular and superior semilunar lobulus of the anterior cerebellar hemisphere. Medially the flocculus is immediately posterior to the cerebellopontine cistern (Fig 32AC). Operative and cadaver observations show that the trigeminal nerve has its own cisternal sleeve which is separate from, but which forms a recess into the cerebellopontine cistern (Fig 33). This situation is analogous to the oculomotor nerve in the interpeduncular cistern, which carries

its own arachnoid sheath and is separate from the cistern. Anatomically, however, leaving the trigeminal nerve within the cerebellopontine cistern simplifies the topographical concept and leads to no particular change in operative planning or dissection (Fig 34A-B). The cerebellopontine cistern contains the anterior inferior cerebellar artery and the auditory artery if this has an independent origin, cranial nerves V, VII and VIII, and the lateral pontomesencephalic vein. The superior petrosal vein (Dandy vein) lies just outside the cistern except medially where it is located between the superior wall of the cerebellopontine cistern and the recess of the trigeminal nerve.

1 Operative Anatomy

52

Lateral Cerebellomedullary Cistern (or Inferior Cerebellopontine Cistern) This lateral cerebellomedullary cistern lies anterior and lateral to the medulla (see Figs 31-33). Its anterosuperior border is the sulcus between the medulla and the pons. Arachnoid over cranial nerves IX, X, and the cranial portion of XI separate this cistern from the cisterna magna dorsally and from the cerebellopontine cistern superiorly. Ventrally a less clear arachnoid sheet separates the cistern from the premedullary cistern. The cistern extends from the pontomedullary sulcus superiorly to the foramen magnum inferiorly, and reaches laterally along the occipital bone with short sleeves into the jugular and hypoglossal foramina accompanying the respective nerves. The cistern contains the vertebral artery, the origin of the posterior inferior cerebellar artery, the retroolivary and lateral medullary veins, and cranial nerves IX, X, XI and XII.

Posterior Cisterna Magna (Cisterna Cerebellomedullaris Dorsal is) As the dorsal spinal subarachnoid space opens into the intracranial cavity through the foramen magnum, it widens into a large cistern, the cisterna magna. This cistern is limited anteriorly by the dorsal surface of the upper spinal cord and lower medulla, and extends to the posterior medullary velum. Superiorly in the midline it runs beneath the vermis between the tonsils to communicate with the fourth ventricle at the foramen of Magendie, forming a cephalad extension of the cistern called the vallecula (Fig 34 C). Dorsally over the vermis the cistern has a variable i_^ VJl. \JX*1JL»

VJ

>"*il

*»»*.""»

fr^M. n.TU.13

„».»,.

_ ——— -_ _ _ ———

———_ . _

„

-_-_

_

-

expansion depending to some degree on the development of the falx cerebelli. It usually ends near the lobulus pyramis of the vermis but may extend all the way up the tentorium. Posteriorly, the cistern conforms to the inner table of the occipital bone except in the midline where the falx cerebelli partially divides the cistern. Laterally over the cerebellum, the cistern is limited by the fusion of the arachnoid to the pia and laterally over the brainstem by the arachnoid over the bulbar nerves forming the lateral cerebellomedullary cistern. Numerous tough trabeculae are seen in the cisterna magna stretching between the dorsal medulla and the posterior arachnoidal wall of the cistern. Similar fibers arch between the medulla, the cerebellar tonsil and the ipsilateral posterior

Fig 34 C Median suboccipital craniotomy. Arachnoidal membrane of the cisterna magna with vascularization of the membrane.

inferior cerebellar artery. Often a median sheet of arachnoid divides the cistern into sagittal halves, and at the level of Q-C2 two additional paramedian septi are formed and extend to the level of Tu_i2, thereby dividing the dorsal spinal subarachnoid space into several distinct compartments (Key and Retzius 1875). This cistern contains the inferior vermian branches of the posterior inferior cerebellar arteries and the median tonsillar veins. Several small vessels including draining veins between the medulla and overlying dura are adherent to the dorsal wall of the sinus.

Superior Cerebellar Cistern This cistern covers the superior vermis and blends laterally with the subarachnoid space over the cerebellar hemispheres. Anteriorly it meets the tentorium and the quadrigeminal and ambient cisterns. The cistern contains the terminal branches of the superior cerebellar arteries and the superior cerebellar and vermian veins (Table 2).

JSupra- and Infratentorial Cisterns | Table 2 Summary of anatomical relationships within various cisterns Cistern

Artery

Vein

Nerve

Internal carotid artery Origin ophthalmic artery Origin posterior communicating artery Artery to the dura of anterior clinoid Origin of anterior choroidal artery,

Occasionally fronto-orbital vein draining to sinus sphenoparietale or to basilar vein

None

Optic venous plexus

Optic nerves Pituitary stalk Olfactory nerve

Parasellar area Carotid

branches to the stalk and optic nerve Chiasmatic Olfactory

Hypophyseal arteries Chiasmal arteries Olfactory artery

Medial fronto-orbital artery Lamina terminalis

Anterior cerebral artery (A,-A2) Anterior communicating artery Proximal medial striate artery Recurrent artery of Heubner Perforating branches (to chiasma)

Olfactory vein Orbital veins Anterior cerebral vein Lamina terminalis venous plexus Orbital veins

None

Medial fronto-orbital artery (origin) Olfactory artery (origin) Distal anterior cerebral artery (A2) Frontopolar artery (origin) Callosomarginal artery (origin) Middle cerebral artery (M,)

Anterior cerebral vein

None

None

Anterior choroidal artery

Superficial middle cerebral veins Deep middle cerebral veins Basal vein of Rosenthal

Basilar artery (upper)

Pontomesencephalic veins

Oculomotor nerve

Lateral pontomesencephalic vein Basal vein of Rosenthal

Trochlear

Vein of Galen

Trochlear origin

Medial posterior choroidal artery Splenothalamic artery Dorsal (posterior) callosal artery Superior cerebellar artery (distal)

Internal cerebral veins

None

Precentral cerebellar vein Superior vermian veins

None

Corpus callosum (posterior) Posterior fossa

Posterior pericallosal arteries

Pericallosal veins

None

Cisterna magna Premedullary Prepontine

PICA (distal)

Inferior vermian vein

C,-C2

Anterior spinal artery Basilar artery AICA (origin) Perforating arteries

Median medullary vein Pontine veins

Abducens

Lateral cerebello-

Vertebral artery

Inferior petrosal vein

Glossopharyngeal

medullary

PICA (origin)

Anterior portion corpus callosum Sylvian _ __ Crural Interpeduncular

and its branches

None

Posterior cerebral artery (origin) P, Thalamoperforating arteries Med. posterior choroidal artery (origin) Quadrigeminal artery

Dorsal mesencephalon Ambient j

Posterior cerebral artery (P2-P3)

Quadrigeminal

Posterior cerebral artery (P4)

Superior cerebellar artery Lateral posterior choroidal artery (origin) Quadrigeminal artery Quadrigeminal artery

Velum interpositum

Superior cerebellar

Cerebellopontine (inferior) Cerebellopontine (superior) Superior vermian and hemispheric cistern

Occipital veins

Vagus

AICA and its branches

Superior petrosal vein Lateral recessus vein

Medial and lateral terminal branches of superior

Branches to the tentorial dura and straight sinus, branches to the precentral cerebellar veins

cerebellar artery

Accessory Hypoglossal Facial Vestibular Trochlear Trigeminal

53

54

1 Operative Anatomy

Intracranial Arteries Introduction The initial descriptions of the cerebral vasculature were produced by anatomists such as Thomas Willis, who in 1664 laid the framework for cerebral vascular anatomy (Fig 35 A). During the next two centuries, the fascination of the anatomists in the field of cerebral vasculature was reflected in the work of the pathologists. Textbooks such as those by Quain (1844), Luschka (1867), Henle (1868), and Duret (1874) and the description of the mesencephalic arteries by Alezais and d'Astros (1892) laid the foundation for the present-day understanding of the cerebral Fig 35A Ventral aspect of the brain and basal circle of arterial circulation. In 1872, Heubner recognized the need circulation as envisaged by Willis and published in 1664, for a more detailed description of the cerebral drawing by Sir Christopher Wren. arteries and with infusion techniques detailed many of the smaller cerebral arteries including the one that bears his name. Windle (1884, 1888) reported anomalies and variations in the cerebral vasculature in 200 cadaver examinations and Lazorthes et al 1956, Lazorthes 1959, 1961; pointed out the scant literature available on that Krayenbuhl and Ya§argil 1959; Baptista 1963; subject. Westberg 1963; Ostrowski et al 1964; Kaplan and Over the next several decades, increased attention Ford 1966; Ahmed and Ahmed 1967; Gillilan was paid to the anatomy of the cerebral vessels 1968; Stephens and Stilwell 1969; Wollschlaeger and their distinct distribution areas, and neurolo- and Wollschlaeger 1970; Krips and Kleihues 1971; gists in particular, began to define clinical syn- Waddington 1974; Newton and Potts 1974; Ya§ardromes associated with particular vascular territories gil et al 1975; Dunker and Harris 1976; Marino (DeVriese 1905; Testut 1904; Fawcett and 1976; Perlmutter and Rhoton 1976; Lazorthes et Blachford 1906; Looten 1906; Beevor 1907; Ayer al 1976; Schlesinger 1976; Salamon and Huang 1907; Aitken 1909; Kramer 1912; Stopford 1916; 1976; Duvernoy 1978; Brunner 1978; Lang and Shellshear 1920, 1921, 1927; Foix and Hillemand Brunner 1978; Lang 1979; Rhoton et al 1979) 1925; Bonne 1926; Adachi and Hasebe 1929; (Fig35B-C). Critchley 1930; DeAlmeida 1933; Kleiss 1941/42). It will become obvious to the careful reader that Anomalies in the circle of Willis were also noted (Lautard 1893; Longo 1905; Blackburn 1907; wide discrepancies exist among many of the anaBusse 1921; Hansenjager 1927; Slany 1938) and tomical descriptions (Fig 35B-C). developmental (Padget 1944, 1948) and phyloge- However, it must be realized that many of the netic (Abbie 1933/34; Watts 1934) aspects dis- topographical observations from both past and cussed. present work are based on fundamental differenWith the advent of arteriography and the active ces. As previously stated, these studies have been treatment of cerebral aneurysms, important con- performed by anatomists, pathologists, neuroratributions were made by the neuroradiologists and diologists, and surgeons, each with a different neurosurgeons. The relationship of aneurysms to perspective and each utilizing a different method anomalies of the circle of Willis was described. of examination. Among other things, the effects (Wilson et al, 1954; Stehbens 1963; Riggs and of formal fixation, latex perfusion, high pressure Rupp, 1963). In addition the introduction of ste- contrast injection, coexistant intracranial pathology reotactic surgery renewed interest in the fine ana- including vasospasm, (whether non-operative or tomy of the cerebral vasculature. (Kaplan 1950; surgically induced) CO2 levels, the examiners degree of precision etc., must be taken into considKaplan et al 1954; von Mitterwallner 1955; eration.

Introduction

Fig 35B

Circle of Willis at skull base (Clara).

( 1 ) Anterior communicating a. (2) Posterior communicating a. (3) Anterior choroidal a. (4) Pontine ramus. . (5) Basilara. (6) Anterior spinal a.

(7) Vertebral a.

(8) Posterior spinal a. (9) Cristagalli. (10) Anterior cerebral a. (10a) Pericallosal a. (11) Ophthalmic a. ( 1 2 ) Middle cerebral a. (13) Posterior cerebral a. (14) Superior cerebellar a. (15) Labyrinthine a. ( 1 6 ) Anterior inferior cerebellar a. (1 7 ) Middle inferior cerebellar a. ( 1 8 ) Posterior inferior cerebellar a. (19) Great foramen (From Krayenbuhl, H., M. G. Yasargil: Cerebral Angiography, 2nd Ed. Thieme, Stuttgart 1982)

Fig 35C (1) (2) (3) (4) (5) (6)

(7)

55

A contemporary drawing of the Circle of Willis.

Internal carotid artery Anterior choroidal artery Plexus A, segment Anterior communicating artery Heubner's artery MT segment

(8) Vertebral artery (9) Basilar artery

(10) P2 segment

(11) Posterior inferior cerebellar artery (12) Anterior inferior cerebellar artery (13 /1 4) Pontine branches (15) Superior cerebellar artery (16) Posterior communicating artery (From Kahle, W., H. Leonhardt, W. Platzer: Color Atlas and Textbook of Human Anatomy, Vol. III. Thieme, Stuttgart 1978)

56

1 Operative Anatomy

It is vital that the microsurgeon should have a sound knowledge of cerebrovascular anatomy in order that all brain vessels be preserved at surgery. At first, the idea that the _trainee should acquire such a detailed anatomical knowledge, especially of the arterial perforators, is formidable^ However, as this study shows, a pattern emerges that can easily be mastered and applied in the operating room. The fundamental concept is that any given area of the brain requires a blood supply that is fairly constant from one patient to another, and hence the arterial supply is constant. The difference between patients is in the size of the vessels, which can vary greatly and often with one or more dominating (socalled "hyperplastic"). This size difference may be so great that it appears that the primary feeding artery for a given region varies from brain to brain. However, when the underlying pattern is understood, a basic picture emerges. In aneurysm surgery, the need for detailed knowledge of cerebrovascular anatomy reaches its height. Preoperatively, the surgeon plans an approach based on his basic knowledge of the arrangement of the vascular tree. Using angio-grams, he can work out the relationship of the neck of the aneurysm to the vessels, in particular the perforators, in the vicinity. Should the aneurysm rupture, he has a plan based on his anatomical knowledge, of how to deal with the situation in a controlled fashion. Similar principles apply to tumor surgery. The surgeon works out the distortion of the normal vascular pattern pre-operatively. At surgery, he recognizes the normal vasculature and then works towards the tumor, dealing with all tumor surface vessels as though they were distorted brain vessels, until he can prove otherwise. Armed with a full vascular knowledge, the operator approaches surgery with complete command of the situation; a confidence that is frequently repaid by excellent post-operative results.

Internal Carotid Artery The intracranial internal carotid artery begins as the vessel exits from the carotid canal at the apex of the petrous pyramid. At this point the artery is just medial to the Gasserian ganglion and may be separated from it by only a dural sleeve. As it passes upward, forward and medially over the foramen lacerum, the vessel reaches the lower lateral portion of the posterior sella turcica and enters the cavernous sinus.

The intracavernous portion of the artery follows a somewhat tortuous course with the vessel first ascending for a short distance along the posterolateral aspect of the sella turcia. It then curves anteriorly continuing along the lateral aspect of the sella and enters the carotid sulcus. As it approaches the anterior portion of the sella, it then curves upward and medially and continues in this direction to emerge from the cavernous sinus infero-medial to the anterior clinoid process.____ This segment of the carotid artery has traditionally been considered to lie within the cavernous sinus, encased in venous blood, and studies by Bedford (1966) and Harris and Rhoton (1976) support this ' concept. However Parkinson (Parkinson and Shields 1974) maintains that the cavernous sinus is not a simple, single venous channel but actually a trabeculated plexus of veins. He believes that in this intricate maze of venous channels, the carotid artery and the other components of the sinus are each compartmentalized and separated from con-tact with venous blood by sinus endothelium.____ Branches of the intracavernous carotid artery have been studied by Bernasconi and Cassinari (1956), de la Torre and Netsky (1960), Schnurer and Stattin (1963), Parkinson (1964), Pribram et al (1966), Wallace et al (1967), Hacker and Alonso (1968), Lehrer (1970), Manelfe et al (1974), Wollschlaeger and Wollschlaeger (1974), Harris and Rhoton (1976) and Lang (1979). The meningohypophyseal trunk (dorsal main stem) is a constant vessel arising from the dorsal aspect of the artery near the beginning of its anteriorly directed segment. Branches include tentorial (supplying the mass of the tentorium and its petrous attachment), dorsal meningeal (supplying the dura of the dorsum sellae and clivus), and inferior hypophyseal (supplying the posterior "pituitary). A second vessel regularly arises further distally along the cavernous carotid artery called the artery of the inferior cavernous sinus (lateral main stem). It supplies branches to the nervous components of the cavernous sinus, its wall, the Gasserian ganglion and the surrounding dura in the floor of the middle fossa, and the free edges of the tentorium. Final branches of the cavernous carotid termed capsular arteries by McConnel (1953) ramify both anterior and posterior to the pituitary in the dural floor of the sella. However, these vessels were found by Harris and Rhoton in only 28 per cent of specimens.

Internal Carotid Artery

57

The persistent primitive trigeminal artery occurs with a frequency of 0.1-0.2 per cent (Rupprecht and Scherzer 1959; Madonick and Ruskin 1962; Krayenbiihl and Yas,argil 1965; Lie 1968). This artery arises from the intracavernous carotid artery proximal to the meningohypophyseal trunk (Parkinson and Shields 1974). The vessel passes posteriorly through the cavernous sinus and emerges at the dorsum sellae where it curves medially and enters the basilar artery between the superior and anterior inferior cerebellar arteries (see Figs 238239). As the carotid artery emerges from the cavernous sinus infero-medial to the anterior clinoid, it enters the dura and carotid cistern. The anterior clinoid process can cover the proximal, supra-clinoid internal carotid artery and the origin of its proximal vessels to a variable degree and may even indent the internal carotid at this point (Newton and Potts 1974). The artery then passes upward, posteriorly, and slightly laterally towards its bifurcation and is within the carotid cistern for its entire course. The length, caliber, direction, and tortuosity of this vessel varies and its termination at the bifurcation, although usually occurring inferior to the anterior perforated substance, may occur as high as the Sylvian fissure. The artery is immediately lateral to the optic nerve and may course parallel to it, or it may describe a convex or concave curve in relation to the nerve. At times this tortuosity of the artery will severely indent the nerve as it enters the optic canal (see Fig 9C-D), but no clinical syndrome has been recognized from this. This relationship of the supraclinoid carotid artery and optic nerve is particularly important in frontotemporal exposures to the basilar artery bifurcation (see chapter 3). Vasa vasorum normally are present along the internal carotid artery only to the point of origin of the ophthalmic artery, but can also extend to the level of the bifurcation when atherosclerotic changes are present in the vessel wall (see Fig 9C). An autonomic plexus covers the artery (Fig 36). The diameter of the proximal intracavernous carotid artery varies between 3.3-5.4 mm while the proximal supraclinoid portion measures 2.4—4.1 mm (Wollschlaeger et al 1967).__________ Unilateral and bilateral instances of hypoplasia of the internal carotid artery have been reported (Hyrtl 1848; Orr 1906; Schmeidel 1930; Tondury 1934; Priman and Christie 1959; Van den Zvan and "Fossen 1962; Brihaye and Dhaene 1962;

Fig 36 The autonomic plexus covering the right carotid artery as seen at operation.

Fields et al 1966; Lie 1968; Smith et al 1969; Lhermitte et al 1968; Steimle et al 1969; Teal et al 1973d). In the present series, the right and left carotid arteries were of equal size in all cases except in two; in one of these an anomalous short right common carotid artery and an aneurysm at the left internal carotid artery bifurcation were seen (Fig 37A-B) and in the other case an aplasia of the internal carotid artery was seen (see p. 308) (Fig 38A-F). Several examples of bilateral aplasia have been reported (Fisher 1913: da Silva 1936; Wolff 1944; Keen 1946: Fields et al 1965: Hills and Sament 1968; Lie 1972; Dilenge 1975; Rosen et al 1975; Teal et al 1980). No examples of fenestra-tion or duplicated carotid arteries have been reported. Aplasia of the left internal carotid artery associated with an aneurysm of the anterior communicating artery, a transverse carotid anastomosis at the base of the skull and 8 other cases have been published by Huber (1980). A transsellar intracavernous intercarotid collateral artery was associated with agenesis of the internal carotid artery in a case of Staples (1979).

58

1 Operative Anatomy

Fig 37A-B Arteriograms revealing (A) an anomalous short right common carotid artery (black arrows), (B) aneurysm at the left internal carotid bifurcation and A, segment (white arrows).

Fig 38A-F Two unusual cases: Fig 38A A ruptured saccular aneurysm (large arrow) at the junction of the P, and P2 segments of the right posterior cerebral artery (left vertebral injection) and spontaneous visualization of the right middle cerebral artery (small arrow).

Internal Carotid Artery

59

I Fig 38B Filling of the right middle cerebral artery through the right P, segment by left vertebral injection (arrow). The right internal carotid artery is aplastic.

Fig 38 C The operative findings are expressed diagrammatically. Dotted lines indicate the aplasia of the right ICA and the right A, segment. The right MCA originating from the right P-|-P2 corner.

Fig 38D Another patient with an aneurysm of the anterior communicating artery showed aplasia of the right internal carotid artery. Fig 38 E The right middle cerebral artery (arrow) is spontaneously visualized by vertebral angiography.

Fig38F The operative findings in diagrammatic form. The right ICA is aplastic. The right MCA originating from the right P1-P2 corner. Black arrow indicates the blood flow from right P, segment to the right distal internal carotid artery and its branches.

60

1 Operative Anatomy

The branches of the supracavernous internal caro tid artery include the ophthalmic artery, several small superior hypophyseal arteries arising from the infero-medial carotid and supplying the pitu'itary stalk, anterior pituitary lobe, and chiasm, the posterior communicating artery arising from the infero-lateral carotid, the anterior choroidal artery and occasionally 2-3 smaller branches to the area of the uncus arising from the distal infero-lateral carotid, a commonly present, small artery to the dura of the anterior clinoid arising from the supero-medial carotid, and finally the terminal branches - the anterior and middle cerebral arter ies. ______

Ophthalmic Artery The ophthalmic artery is the first major branch of the internal carotid artery and is the only large branch directed medially. The ophthalmic artery usually arises from the antero-medial (53.6%) or supero-medial (31.5%) surfaces of the carotid artery (Hayreh 1974). The exact site of origin is somewhat variable as attested by Hayreh and Dass (1962) who studied 168 specimens. In 83 per cent the origin of the artery was in the subdural space just at the point where the carotid artery enters the dura after leaving the cavernous sinus. In 2 per cent it arose just proximal to this point so the artery was partially subdural and partially extradural. In 7.5 per cent it originated even further proximally, so that it was intracavernous and completely extradural. In the remaining 6.5 per cent, it arose within the most anterior portion of the carotid cistern within 1 mm of its most anterior portion. The initial course of the ophthalmic artery is intimately related to the body of the sphenoid and to the proximal part of the suprachiasmatic internal carotid artery to which it is frequently adherent for some distance (Hayreh 1974). The artery most frequently lies within the subdural space for its entire intracranial course attached to the undersurface of the optic nerve by a loose meshwork of connective tissue. The artery is infero-medial to the nerve in 43 per cent of cases, directly inferior in 37 per cent, infero-lateral in 16 per cent, or rarely directly medial or lateral in 2 per cent each (Hayreh and Dass 1962). As it enters the optic canal beneath the optic nerve (infero-lateral 25.9 per cent, directly inferior 32.7 per cent, inferomedial 41.4 per cent - Hayreh and Dass 1962), it pierces the optic nerve dural sheath to lie between this sheath and the periosteum of the optic canal. As it courses through the optic canal, the ophthalmic artery lies infero-lateral (84.5%) or infero-

medial (15.5%) to the optic nerve (Hayreh and Dass 1962). Shortly after penetrating the orbit, the artery crosses over (82.6%) or under (17.4%) the nerve to continue a more medial course. The entire orbital course, branches, anastomoses, and anomalies of the ophthalmic artery are beyond the scope of this book. Interested readers should consult Hayreh in Newton and Potts 1974, Chapter 61, for a detailed description of these topics. The diameter of the ophthalmic artery varies between 1.0 and 2.0 mm. No cases of duplication or aplasia were seen in the present series, but in one case an artery was noted to originate from the ophthalmic, course with the optic nerve, and penetrate the anterior perforated substance. The topographical anatomy of the ophthalmic artery has been discussed by Bock and SchwarzKarsten (1955), Hayreh and Dass (1962), Hayreh (1974) and Vignaud et al (1972). A complete list of references is given by Hayreh (1974) and Lang (1979). Radiological anatomy has been studied by Bregeat et al (1952), Decker and Schlegel (1957), Di Chiro (1961), Dilenge et al (1965), Salamon et al (1965), Vignaud et al (1975), Lasjaunias et al (1975), Huber (1975).

Superior Hypophyseal Arteries Several small but constant arteries leave the infero-medial internal carotid artery and course beneath the optic nerves through the carotidjmd chiasmatic cisterns to supply the pituitary stalk, tuber cinereum, anterior lobe of the pituitary, and inferior surface of the optic nerves and chiasm (Stephens and Stilwell 1969). These arteries anastomose with similar vessels from the opposite side and with the inferior hypophyseal branches to form a longitudinally oriented vascular plexus around and along the stalk - the hypophyseal portal system. The visualization of this plexus of vessels is helpful at surgery in identifying the pituitary stalk.

Posterior Communicating Artery The posterior communicating artery takes origin from the infero-lateral wall of the supraclinoid internal carotid artery within a few millimeters (2-8 mm) of the anterior portion of the carotid cistern. From its origin at the internal carotid artery to the point where it leaves the carotid cistern by piercing the interpeduncular cistern, the posterior communicating artery does not lie freely within the cistern, but is encased in a sleeve of arachnoid that is adherent to a similar sleeve encasing the oculomotor nerve. As with most

Internal Carotid Artery

PcoA = P-]

c

PcoA > PI

B

D

PcoA

2nd PCA

Fig 39A-D Variations between the posterior communicating artery and P, segment. A Posterior communicating artery and P, are equal. B P, is larger. C Posterior communicating artery is larger. D A second posterior cerebral artery (arrow).

intracranial arteries, it is further stabilized by bands of arachnoid suspending it from the walls of the cisterns. As the artery courses posteriorly to join the posterior cerebral artery, impasses close to the dura overlying the posterior clinoid process. In some cases it may be adherent to the dura in this region over a few millimeters or it may even lie in a sulcus within the process. These attachments of the artery may at times hinder attempts to mobilize the vessel during aneurysm operation. The calibre of the posterior communicating artery is highly variable. Dilenge (1962) found the artery to be larger than 2 mm in 38.7 per cent of cases, between 1-2 mm in 41.5 per cent, and less than 1 mm in 18.9 per cent. In children a greater proportion of large calibre postcommunicating arteries are seen (38.5-75%) as compared to adults (829%), suggesting that this vessel diminishes in size with increasing age (De Vriese 1905; Padget 1944). In 67.5 per cent of cases the posterior communicating artery is Ys to '/2 the size of the corresponding posterior cerebral artery. However

61

in 8.0 per cent of cases the posterior communicating artery is of similar calibre to the posterior cerebral artery and in 24.5 per cent it is actually larger (Fig 39A-D). In these situations (PcoA > PCA), the proximal portion of the posterior cerebral artery (P^ is often hypoplastic, thereby demonstrating a persistence of the fetal type of circulation (Table 3). Hypoplasia of the posterior communicating artery is not at all infrequent and multiple cases of apla-sia have been described. The incidence of aplasia varies from 3-11 per cent for unilateral cases and 0.3-1.5 per cent for bilaterally absent vessels (Windle 1888; Stopford 1916; Fettermann-Moran 1941; Padget 1944). Other variations of the posterior communicating including duplication and fenestration of the vessel have been presented by Hasebe (1928), Kleiss (1941), Dandy (1944), von Mitterwallner (1955), Alpers et al (1959), Wells (1960), Riggs and Rupp (1963), Kaplan and Ford (1966), Krayenbiihl and Ya§argil (1968), Wollschlaeger et al (1969), Ozaki et al (1977), Saeki and Rhoton (1977), and Lang and Brunner (1978). In the present series three cases of duplication of the posterior communicating artery were seen at operation (Figs 40-42). In these cases the artery that originated distally did not join the posterior cerebral artery but coursed independently along the medial-basal temporal lobe and functioned as a temporal artery. One such a case was also encountered during 200 cadaver brain dissections (see Fig 42C). Similar cases were described by Windle (1888) who found one (1 case) or two (1 case) vessels arising from the internal carotid artery in the position of the posterior communicating artery; "In one case two arteries sprang from the internal carotid artery in the position normally occupied by the posterior communicating artery. Instead however, of joining the posterior cerebral artery, they passed to the under surface of the temporo-sphenoidal lobe which they supplied. A few filaments from each of these anastomosed with slender twigs from the posterior cerebral artery." Dandy (1944) also describes this variation. Wollschlaeger and Wollschlaeger (1974) in: Newton and Potts, p. 1178, describe two main branches of the posterior cerebral artery which may arise separately. In this variation the temporo-occipital branch arises from the internal carotid artery and the parieto-occipital branch from the basilar artery. Also in this series one case of fenestration of the posterior communicating artery and two cases of another unusual variation were seen (Fig 43A-C).

62

1 Operative Anatomy Fig 40 A Left lateral angiograms demonstrating a second posterior cerebral artery (arrows) arising just proximal to the anterior choroidal artery and ending in the medialbasal occipital pole.

Fig 40 B AP view of the second posterior cerebral artery. It does not give rise to parieto-occipital branches.

Fig40C Operative picture of the left second posterior cerebral artery (arrows 12). Anterior choroidal artery (arrow 3).

Internal Carotid Artery

63

Fig 41 A-C A second posterior cerebral artery that ends in the parieto-occipital lobe and does not give any temporal branches. A AP angiogram showing the distal supply of the second posterior cerebral artery (arrows). B Vertebral angiogram portraying the terminations of the real right posterior cerebral artery that gives only temporal branches (arrow). C Operative photograph of two posterior cerebral arteries (arrows 1 and 2), anterior choroidal artery (arrow 3).

64

1 Operative Anatomy

Fig 42 A A rare variation of the Circle of Willis observed in a formalin-fixed brain. The right P,-P2 junction is duplicated as in the anterior communicating artery. The left fronto-polar and Heubner's arteries have a common trunk, as do the left lateral fronto-orbital and lateral striate arteries. Fig 42B Another unusual anomaly showing two right posterior cerebral arteries joined by a bridge and 3 Aa segments. Again the left lateral fronto-orbital and striate arteries have a common trunk. Fig 42 C An example of two completely separate right posterior cerebral arteries.

Table 3 Variations of the posterior communicating artery in 200 cadaver brains (400 hemispheres) Left

Right

Total

(%)

Aplasia

unilateral bilateral

6 -

.

2

8

2.0 67.5%

Hypoplasia

unilateral bilateral

112 .

62

174

43.5 22.0

88

Equal to P,

unilateral bilateral Hyperplasia (larger than P,)

7 12

unilateral bilateral

29

13

20

5.0 3.0 32.5%

53

16

82

20.5 4.0

Fenestration

unilateral bilateral

2 -

2

0.5 -

1 -

1

0.25 -

Duplication

unilateral bilateral

Internal Carotid Artery

65

Fig 43A-C An unusual case of a posterior communicating artery aneurysm. A Schematic representation of the posterior communicating artery aneurysm arising on a fenestrated posterior communicating artery, B Lateral angiogram showing the aneurysm but failing to show the complexity of the situation. C Operative photograph showing the fenestrated posterior communicating artery (arrow 1) and the coagulated aneurysm neck (arrows 2).

The posterior communicating artery has along its course 2-10 branches that generally begin about 2-3 mm from the origin of the artery and run posteroinferiorly and medially into the interpe-duncular cistern. Perlmutter and Rhoton (1976) found that more of these branches are located on the anterior half of the artery in 54 per cent of cases, on the posterior half in 25 per cent and are equally distributed in the other 21 per cent. These branches were called the "anterior thalamoperfo-rating arteries" by Westberg (1966) and supply the

inferior optic chiasm, optic tract, tuber cinereum, mammillary bodies, subthalamus, posterior jiypothalamus, and the anterior and vertebral portion of the thalamus. Most of these branches are quite variable in size and may branch early or run a long course, except one larger vessel that regularly passes in front of the mammillary bodies and then penetrates the brain (see Fig 44, p. 66). This artery was designated the "premammillary" by Stephens and Stilwell (1969) and Perlmutter and Rhoton (1976) and the "thalamotuberal

66

1 Operative Anatomy

Fig 44 Tubero-mammillary (premammillary) (2), other perforating branches of the posterior communicating artery (1), and the anterior choroidal artery (3) are well seen.

artery" by Haymaker (1969) and Foix and Hillemand (1925a). In the present series, this vessel was identified in all cases (Fig 44). In only one instance was this vessel seen to arise directly from the internal carotid artery. The mammillary bodies themselves are supplied by either these branches from the posterior communicating artery or from branches of the proximal posterior cerebral artery (P^. In 65 per cent of cases each mammillary body is supplied by ipsilateral vessels, in 23 per cent by bilateral arteries, and in 12 per cent of cases both are supplied by one side (Putz and Poisel 1974). Dunker and Harris (1976) described some nutriment of these structures by proximal anterior cerebral branches (A,). Even when the posterior communicating artery is hypoplastic, rather stout penetrating branches may be seen to exit from the artery. In the present experience, no branches to the temporal lobe were seen to originate from the posterior communicating artery. In one case an artery originated from the posterior communicating artery and coursed toward the crural cistern, but this probably represented an anomalous origin of the anterior choroidal from the posterior communicating artery. Further details about the topography of the posterior communicating artery can be found in the work of Zeal and Rhoton (1978).

Anterior Choroidal Artery The anterior choroidal artery arises 2-5 mm (1.19.0 mm, Rhoton et al 1979) distal to the posterior communicating artery and 2-5 mm

(2.0-8.0 mm, Rhoton et al 1979) proximal to the carotid bifurcation from the infero-lateral aspect of the internal carotid artery. In every case except one in the present series, the anterior choroidal artery arose as the first infero-lateral branch of the internal carotid artery after the posterior communicating artery. In one case, the posterior communicating and anterior choroidal arteries were seen to arise from exactly the same level with the former from the medial-inferior wall and the latter from the lateralinferior wall. It is surprising that Carpenter et al (1954) and Rhoton et al (1979) found branches between the posterior communicating and anterior choroidal arteries in 10 and 32 per cent of cases respectively. Rhoton describes these branches as most frequently terminating in the optic tract, medial temporal lobe, and posterior perforate substance. In our cases, we found branches emerging from the intero-medial wall of the internal carotid artery between the posterior communicating and the anterior choroidal arteries and supplying the optic tract and posterior perforate substance that could represent the vessels described by Rhoton. However, branches tojhe medial-basal temporal lobe in our experience always originate from the infero-lateral internal ' carotlcTTfista/ to^the anterior choroidal artery. Without exception the second infero-lateral branch of the internal carotid artery after the posterior communicating artery is the anterior choroidal artery or arteries. When duplicated one or more trunks of the anterior choroidal artery occur. The uncal artery is always distal to the anterior choroidal artery or may originate from the lateral wall of the proximal middle cerebral artery (Waddington 1979). As mentioned under the posterior communicating artery, in one case from the present series, an anterior choroidal artery may have originated from the posterior communicating artery but this was not verified (Figs 45A-E, 46A-G). The calibre of the anterior choroidal artery varies from 0.5-1.5 mm (0.7-2.0 mm, Rhoton 1979). In 70 per cent of cases in the present series, the anterior choroidal artery aros^^s_a_singlejrunk that usually then divided either immediately or within 2-5 mm into two trunks. In 30 per cent of cases in the present series, the anterior_chprpidal_ artery arose as 2-4 independent vessels/ Saeki and Rhoton (1977) found a single trunk in 96 per cent of 100 brains and Rhoton et al (1979) found only single trunks in 50 brains. Several authors have found the anterior choroidal artery to occasionally arise from the bifurcation of the internal carotid artery, from the middle cerebral artery, or from

Internal Carotid Artery

Fig 45A-E Variations of the anterior choroidal and uncal "arteries (u). " "————————————— A Three separate arteries originating from internal carotid artery. B Uncal artery originates from middle cerebral artery. C Uncal artery originates from anterior choroidal artery. D Uncal artery originates from internal carotid artery. E Anterior choroidal artery originates from posterior communicating artery (extremely rare). Fig 46A-G Variations of the anterior choroidal and uncal arteries as seen at operation. A Right anterior choroidal (arrow) and uncal (u) arteries arising from the common trunk. B Right anterior choroidal (2) and uncal (u) arteries arising independently at the same level. Posterior communicating artery (1). C Separated origin of anterior choroidal artery ( 1 ) and uncal artery (u). PcoA = posterior communicating artery.

67

68

1 Operative Anatomy

46 D Three separate branches (black arrow) of the anterior choroidal and uncal arteries. White arrow indicates the posterior communicating artery.

E Tubero-mammillary artery (arrow 1) , anterior choroidal artery (arrow 2), uncal artery (arrow 3). PcoA = posterior communicating artery.

F Left pterional approach: Posterior communicating artery (1), anterior choroidal artery (2), uncal artery (3), large proximal lateral striate artery (4). M = middle cerebral artery.

G Anterior choroidal artery (1), uncal artery (2), temporal pole artery (3) in a case with an AVM of the temporal pole, tu = tuberomammillary artery.

Internal Carotid Artery

69

Table 4 Arteries with origin at the anterior choroidal artery Anatomic studies in cadavers

No. of arteries examined

ICA

ICB

MCA

PcoA

AchA absent

Bevoor 1907

174

100%

-

-

-

-

Carpenter et al 1 954

60

76.6%

3.3%

1 1 .7%

6.7%

1 .7%

Von Mitterwallner 1955

360

97.0%

L. 0.3% R. 0.0%

L. 2.0% R. 0.5%

L. 2.0% R. 1 L. 1 .2% R. 1 .6% .6%

Otomo 1 965

778

99.2%

0.4%

-

0.4%

-

Herman et al 1 966

74

85%

7%

8%

-

-

Saeki and Rhoton 1977

100

100%

-

-

-

-

Rhoton et al 1979

50

98.0%

-

-

2.0%

-

Own 1982

200

99.5%

_

_

0.5%

_

. Angiographic studies Sjogren 1956

88%

2.0

3.0

Cooper 1954

92%

%

%

the anterior communicating artery (Table 4). In the present series of over 2000 operative exposures in this area and 200 cadaver brain examinations by the senior author (MGY), the anterior choroidal artery was seen to arise only from the internal carotid artery in every case but one.____ From its origin, the anterior choroidal artery passes postero-medially in the carotid cistern to reach the optic tract postero-lateral to the posterior communicating artery. At this point it diverges from the posterior communicating artery and follows in the general direction of the optic tract between the mesial temporal lobe and the cerebral peduncle to enter the crural cistern. If the artery arises as two separate vessels or as a single trunk that divides into two vessels, one of them, the uncal artery ramifies immediately to supply the uncus piriform cortex, the postero-medial amygdala, the anterior hippocampal and dentate gyri and the tail of the caudate nucleus. The other generally larger vessel continues in the crural cistern as the main anterior choroidal artery with proximal branches that supply the inferior aspect of the optic chiasm, the posterior % of the optic tract, the medial 2 segments of the globus pallidus, the genu of the internal capsule, the middle '/i of the cerebral peduncle, the substantia nigra, upper parts of the red nucleus, a portion of the subthalamus, and a lateral portion of the ventral anterior and ventral lateral thalamic nuclei (Abbie 1932). The main anterior choroidal artery then courses through the wing of the ambient cistern to enter the choroidal fissure and join the choroid plexus of the temporal horn. Branches of this portion of the anterior choroidal artery supply the antero-

lateral half and hilum of the lateral geniculate body, the inferior half of the posterior limb of the internal capsule, the retro-lenticular portion of the internal capsule and the optic radiations. The anterior choroidal artery supplies the choroid plexus of the lateral ventricle in association with the posterior lateral choroidal artery. The anatomy and distribution of the anterior choroidal artery have been discussed by Abbie (1933), Carpenter et al (1954), Morello and Cooper (1955), Mounier-Kuhn et al (1955), von Mitterwallner (1955), Sjogren (1956), Otomo (1965), Herman et al (1966), Wollschlaeger et al (1969), Goldberg (1974), Theron (1976), Saeki and Rhoton (1977), Rhoton et al (1979), and Lang (1979). A marked reciprocal relationship between the arterial distribution areas of the anterior choroidal artery and surrounding branches of the internal carotid, posterior cerebral, posterior communicating, and middle cerebral arteries has been noted (Rhoton et al 1979). Rich anastomoses between branches of these major vessels permit inter-changeability in their distribution of blood such that if one is smaller than usual, others are larger than normal to compensate. This phenomenon has been noted in the present series of patients but not studied. Other than duplicated or triplicated anterior choroidal arteries, there usually are no additional branches of the infero-lateral internal carotid artery between the anterior choroidal artery and the bifurcation. However in one case from the present series, an anterior temporal artery took origin proximal to the bifurcation, and in another case an accessory middle cerebral artery arose

70

1 Operative Anatomy

from the infero-lateral wall of the internal carotid artery just distal to the anterior choroidal artery origin.

Dural Artery of Internal Carotid Artery A consistent small branch arises from the superomedial aspect of the internal carotid_artery 3 to 5 mm proximal of the bifurcation and courses to the dura in the area of the anterior clinoid process (Fig 47A-F). Rarely this artery may arise from

the anterior cerebral artery (Aj), and in one case bilateral symmetrical branches of the anterior cerebral arteries (Aj) ran to the limbus sphenoidale. Retraction may blanch this artery so it appears only to be a strand of arachnoid, and when accidentally avulsed from the parent artery it may be a source of unrecognized bleeding, especially after a local sympathectomy and the application of papaverine to the internal carotid artery.

Fig 47A-C Operative photographs (right pterional approach) illustrating a small but regular branch (arrow) of the internal carotid artery, leaving its distal, superomedial wall and supplying the dura over the anterior clinoid (A).

B Dural branch of internal carotid artery (arrow).

C Rarely this branch arises from the A, segment (arrow).

продолжение

Internal Carotid Artery продолжение Fig47D Dural artery (arrow) to the tuberculum sellae arising from the right A, segment. Fig47E Dural artery (arrow) to the area of the tuberculum sellae arising from the left A, segment. Fig 47F An unusual branch (arrows) of the right A, segment to a vascular network within the prechiasmatic arach-noidal membrane.

71

74

1 Operative Anatomy

polar temporal artery is enlarged one might expect to see that the anterior temporal artery is hypoplastic or absent. It is then the enlarged polar temporal artery supplying both the polar temporal and anterior temporal regions. Occasionally, during surgical dissection one may observe that both the polar temporal and anterior temporal arteries may be hypoplastic or absent and their cortical areas are supplied by a single large middle temporal branch that arises from the inferior trunk of the M2 bifurcation (Fig 51). Infrequently a single large cortical branch arises at the site of the hypoplastic or absent polar temporal or anterior temporal arteries (Figs 52A-H). It is very important to be aware of these different patterns along the superior lateral wall of the Mj segment, both at angiography and at the time of surgery. These different anatomical patterns can lead to_confusion of the position of the true middle cerebral artery bifurcation. The examples cited in Fig 52A-E, are referred to as examples of the false early bifurcation occurring along the superior lateral MI segments. If the position of the true bifurcation is mistaken, it is understandable to find that the length of the Mt segment has been incorrectly identified as being 0 to 30 mm in length.

Fig 51 Variation of the M, segment with no branches arising from its lateral wall. The polar-temporal and anterior temporal branches originate instead from the inferior trunk ofM2.

Fig 52A False bifurcation (giving the impression of an early true bifurcation) due to the presence of a larger than normal polartemporal branch from the lateral wall of the proximal M-, segment. This temporal artery may give rise to multiple temporal lobe branches as depicted in this diagram. ___.

Fig 52 B Similar situation with the temporal artery arising more distally on the M-, segment.

Middle Cerebral Artery

2 \A) 3 Fig 52C Variations of the origin of the temporal trunk: (1) from ICA, (2) from proximal M,, (3) from distal M,.

Fig 52 D AP angiograms showing a false early bifurcation due to the origin of a large right temporal artery from the most proximal MI segment (arrow 1). The left temporal artery is small (arrow 2).

Fig 52 E Operative photograph showing the false (arrow 1) and true (arrow 2) bifurcations.

75

76

1 Operative Anatomy

Fig 52F A large temporal artery trunk arising from the internal carotid artery (arrow). The lenticulostriate arteries arising from M-,.

Fig 52G Left sided carotid angiogram of the same case showing normal anatomy of middle cerebral artery, the lenticulostriate artery arising from distal M,.

Fig 52 H Operative diagram of an unique example of another large temporal artery trunk arising from the internal carotid artery (arrow) in a case with ruptured aneurysm of the anterior choroidal artery.

Middle Cerebral Artery

Inferior Medial Group or "Lenticulostriate or Striate Vessels" The inferior medial group of vessels along the Mj segment are the striate arteries which number 215. At their origin they form "vascular loops" on their way to supply the sub-cortical areas of the brain after entering the lateral two-thirds of the anterior perforated substance (Newton and Potts 1974; Ring 1974; Leeds 1974; Lang and Brunner 1978). Since they originate on the inferior surface of the Mj segment it is necessary to gently retract this segment of the artery in order to observe the sites of origin of these arteries.] The striate vessels supply the substantia innominata, the lateral portion of the anterior commissure, most of the putamen, the lateral segment of the globus pallidus, the superior half of the int. capsule and adjacent corona radiata, and the body and head (except the antero-inferior portion^ of the caudate nucleus (Stephens and Stilwell 1969). In our experience three patterns of origin of the striate arteries from the Mt segment have been observed. Most frequently, occurring 40 per cent of the time, we observed that all the striate arteries arose from one single large artery, a stem, artery that then divided after 2-10 mm into many branches (Fig 53A). Two other patterns of striate origin were seen each in 30 per cent of the cases. These patterns consisted either of two large parallel arteries that immediately divided to give off the numerous branches of the striate group (Fig 53B), or numerous small twigs (10-15) of striate arteries that arose directly from the whole inferior medial Mj segment (Fig 53C).

Fig 53A-C Variation in the origin and number of proximal and distal lateral lenticulostriate arteries. A A large and small proximal trunk side by side. B Two large proximal trunks. C Multiple small arteries arising along the whole infero-medial wall of the M, segment.

77

The striate arteries have never been seen to arise from the superior or lateral aspect of M1. In most cases, these vessels arise from the infero-medial aspect of the Mj segment, along either its proximal, mid-portion, or distal segments or along the proximal middle cerebral trunks distal to the bifurcation (M2 segment). Generally they can be separated into proximal, middle and distal groups. Lang et al (1979) found that the striate branches often arose from several areas. Proximal Mj branches were seen in 71 per cent, mid-portion branches in 86 per cent, distal Mj branches in 44 per cent, proximal M2 branches in conjunction with M] branches in 41 per cent and proximal M2 branches only in 14 per cent.

78

1 Operative Anatomy

Thus the striates originate from one or a combination of the following 5 zones: 1) Proximal segment of Mj 2) Mid-portion of M1 3) Distal segment of Mj, bifurcation 4) Superior trunk of M2 5) Inferior trunk of M2 (Fig 54). In the present experience, the major stem(s) of the striates arose from the superior or inferior trunk of M2 in 10 per cent of cases (Figs 55-60). Fig 54 The 5 origins of the Jatera^ proximal and distal lenticulostriate arteries arisingIrorrTthe proximal ( 1 ) or distal (2) M, segment, from the Mt bifurcation (3), or from the superior (4) or inferior (5) trunks of the M2 segment. Combinations of the above are also seen especially distal M, and proximal M2 origins for these branches.

Fig 55 Angiographic demonstration of the lateral distal striate arteries arising from the superior trunk of the left M2 segment (arrow).

Fig 56A-D Aneurysm of the left middle cerebral artery bifurcation with the lateral distal striates (arrow) arising from the superior trunk of the M2 segment (A) angiogram, (B) operative diagram.

Middle Cerebral Artery

Fig 56 C-D Other examples of the lateral distal striate arteries arising from the M2 segment.

Fig 57A-D Examp1eofalargelateralstriate(arrow)arising from the right proximal M, segment (A) operative photograph, (B) schematic diagram.

79

80

1 Operative Anatomy

Fig 57 C Operative photograph of a right carotid bifurcation aneurysm (arrow 1) and a large proximal lateral striate artery (arrow 2).

Fig 57D Operative photograph of a left carotid bifurcation aneurysm. H = Heubner's artery. Arrows = proximal lateral striate arteries.

Fig 58 Operative photograph of multiple distal lateral striate arteries arising from the most distal portion of the right M, segment at the bifurcation (arrow 1) and from the superior trunk of M2 (arrow 2).

Middle Cerebral Artery

A

81

B

Fig 59A-B The right middle cerebral artery bifurcation as seen at operation from behind showing several large distal lateral striates (arrows) arising just below the bifurcation (A) and (B) after elevation of the superior trunk (arrow).

Fig 60 Operative photograph of the left middle cerebral (M) artery showing the origin of several distal lateral striate arteries from the most distal portion of M, (arrow).

82

1 Operative Anatomy

An important variation of the origin of the lenticulostriates occur in the other 3 per cent of cases. In this instance the striate vessels arise either from a large single lateral fronto-orbital branch or from a common stem with the lateral fronto-orbital artery. The usual origin of the lateral fronto-orbital artery is either from the superior trunk of M21-10 mm after the bifurcation or as a common stem with the prefrontal artery from the superior trunk (Figs 61A-C, 62A-C). However, when associated with the striate vessels the lateral orbito-frontal artery originates from the infero-medial aspect of M1. When this anatomical arrangement occurs and especially if the lateral fronto-orbital artery is large, one can be misled into believing that this is the area of the bifurcation. Some aneurysms may arise in this area and the surgeon must be aware of the possible striate topography as these vessels are often hidden by the aneurysm neck (Fig 63AD).

In the current series, no regular branches originating from M! and coursing to the frontal-orbital cortex and anastomosing with the medial frontal-orbital branches of A2 were ever seen. This arrangement was described by Lang (1979) as occurring in 6 per cent of cases, but represents the association of the orbitofrontal artery and striates described above. It is important to keep in mind all of the possible variations of striate origin to avoid injury to this most important group of vessels during surgical exploration in this area. The vascular territory of the striate arteries will be discussed later in this chapter. There is a reciprocal relation between each of the proximal and distal striate branches of the Mj segment, proximal and distal striate branches of the A, segment and between the Al and Mj striate arteries.

B ii.

Fig 61 A-C Schematic (A) and angiographic (B) demonstrations of the right distal lateral striates and the lateral fronto-orbital arteries arising as a common trunk (arrow), (C) operative photograph.

1

2

Fig 62A Relation of lateral fronto-orbital, lateral striate and prefrontal arteries: 1 Separate origin of the lateral fronto-orbital artery from M2 2 Common trunk of lateral fronto-orbital ( 1 ) and prefrontal arteries from M2(2).

3 Common origin of lateral fronto-orbital ( 1 ) artery together with lateral striate artery from M,. 4 Common origin of lateral striate, lateral fronto-orbital ( 1 ) and prefrontal arteries (2) from M,.

Middle Cerebral Artery

Fig 62B The variation may give the impression of an early bifurcation. ,

Fig 62C Common trunk as seen in the angiogram. Arrow indicates the lateral striate artery.

83

84

1 Operative Anatomy Fig 63A-D Operative photographs of the left middle cerebral artery demonstrating an aneurysm at the origin of the lateral fronto-orbital artery (arrow) from M, (A) and its relationship to the distal lateral striate branches (small arrows) of the lateral fronto-orbital artery (large arrow) (C). Schematic representations of A (B) and C (D).

Middle Cerebral Bifurcation The true bifurcation of the proximal middle cerebral artery (Mj) always occurs at the high point of the limen insulae (see Fig 48). The portion of the middle cerebral artery distal to the bifurcation -the M2 segment - is composed of two trunks, the superior and inferior trunks. Distal to the bifurcation, the trunks turn postero-superior to reach the surface of the insula, thereby describing a more or less pronounced curve called the genu. The area of the bifurcation may also be described as forming an "Omega" pattern because of the trunk's initial divergent but then convergent courses.

Arachnoid fibers stretch between both trunks like ajiarp. The major trunks diverge at the bifurcation, but reapproximate in the Sylvian fissure after 10 to 22 mm. The inferior trunk is frequently under the temporal operculum and may not be identified, especially if early branching of the superior trunk is accepted as the principal bifurcation. The majority of arterial branches near the bifurcation are large and occasionally the same diameter as the superior and inferior trunks. When large branches arise from either the superior or inferior trunks in close proximity to the bifurcation, an

Middle Cerebral Artery

Fig 64A-D The superior or inferior M2 trunks may divide just after the bifurcation giving the false impression of a trifurcation (arrow) as seen diagrammatically (A-B), angio-graphically (C), and intraoperatively (D).

85

86

1 Operative Anatomy

Fig 65A An early division of both superior and inferior M2 trunks may also occur giving the false impression of a quadrification.

impression of a "pseudo-trifucation" or "pseudoquadrification" may be given (Figs 64A-D, 65AB). When precisely dissected these usually represent superior or inferior trunk bifurcations immediately adjacent to the true bifurcation. However_LangJ_1979) has reported that in 20 per cent of cases a trifurcation, tetrafurcatlcmTbr even pentafurcation is present. Similarly Gibo et al (1981) found a true bifurcation in 78 per cent, a trifurcation in 12 per cent, and a division into 5 or more trunks in 10 per cent of cases. There was also a misinterpretation in the monograph of Krayenbuhl and Ya§argil (1965) analysing the carotid angiograms of 1000 cases, that a right-sided trifurcation was found in 43 per cent, a left-sided one in 65 per cent, a tetrafurcation in 16 per cent, and a pentafurcation in 3 per cent. An awarness of these possible patterns is important during aneurysm surgery dissection since the majority of middle cerebral artery aneurysms arise at the true branching point of the middle cerebral artery. Distal to the bifurcation, the trunks of the middle cerebral artery pass over the insula and distribute cortical branches to the lateral frontal, parietal, occipital, and temporal lobes. According to Gibo et al (1981) the superior trunk is dominant in 28 per cent of cases, the inferior is larger in 32 per cent, both trunks are of equal calibre in 18 per cent, and multiple trunks of various sizes are found in 22 per cent.

Fig 65B Operative photograph of the right middle cerebral artery with pseudo-quadrification (arrows).

The arterial branches from the superior trunk usually supply the regions of the inferior frontal cortex, the frontal opercular cortex, the parietal and central sulcus territories. The branches from the inferior trunk generally supply the middle temporal cortex, the posterior temporal cortex, the temporal occipital regions as well as the angular and posterior parietal regions. _________ 'Named peripheral branches of the middle cerebral group include lateral orbitof rental, pref rental, frontoopercular, precentral, central sulcus, angular, and posterior temporal arteries. Discussion of these arteries is beyond the scope of this book, but the reader is referred to excellent descriptions by Gabrielle et al (1949), Duroux et al (1952), Vlahovitch et al (1968), Waddington and Ring (1968), Salamon (1973), Salamon and Huang (1976), Michotey (1972), Waddington (1974), Szikla et al (1977), Huber (1979), Lang (1979), and Gibo et al _ At times anomalies were observed in this study. They were not encountered frequently, but must be considered. A fenestration of the middle cerebral artery was seen in two of one hundred cadaver dissections and in three angiographical examinations and surgical dissections for aneurysms (Figs 66A-C, 67AB). When present it occurred near the origin of the middle cerebral artery. Three cases were also radiographically identified by Iro et al (1977).

Middle Cerebral Artery

87

Fig 66 A—C Examples of fenestrated right distal M, segments. A Angiogram. B Intraoperative photograph (arrows). C Diagram.

продолжение

88

1 Operative Anatomy

Fig 67A Fenestration of the left M, segment (arrow). Fig 67B Schematic illustration of the operative finding of fenestration of M, and A, segments with aneurysm of anterior communicating artery, before clipping (1) and after clipping (2).

Two cases of accessory middle cerebral artery were seen (Fig 68A-D). Both occurred at the Aj-A2 junction opposite the anterior communicating artery. This duplication also gave the origin to the Heubner branch. In another four cases the accessory MCA arose from the proximal Al (Fig 69A-B), and in two cases bilaterally (Fig 70A-B). In another case it arose from the internal carotid artery distal to the anterior choroidal artery (Ya§argil and Smith 1977). Crompton (1962) described ten cases (2.9%) of accessory middle cerebral arteries originating from the internal carotid artery distal to the anterior choroidal artery and one case of this vessel originating from the junction of the A, and A2 segments of the anterior cerebral artery. Jain (1964) found accessory middle cerebral arteries in nine of three hundred brains (30%), with one bilateral and noted it arising from the internal carotid in two cases and the anterior cerebral artery in eight cases.

B There were two cases in which there was no right internal carotid artery. In this situation the middle cerebral artery arose from the posterior cerebral artery (see Fig 38A-F). In only one patient a unique variation was observed with a coiled inferior trunk (Fig 71A-B). Finally, we would like to mention that on no occasion have we ever identified the anterior choroidal artery arising from the proximal Ml segment as stated to occur in 11.4 per cent by Carpenter et al (1954). We have only identified the uncal artery arising in 70 per cent of the cases from the internal carotid artery and 30 per cent of the cases from the proximal M1 segment. It is our belief that it was probably the uncal artery which was mistaken for the anterior choroidal artery in Carpenter's study. Finally we have seen two cases in which the uncal artery was large giving off a branch supplying the temporal polar area.

Middle Cerebral Artery

89

Fig 68A Accessory middle cerebral arteries arising from the A!-A2 junction (large distal medial striate artery gives rise to the accessory MCA). B Accessory middle cerebral artery arising from the A!-A2 junction associated with an aneurysm of the anterior communicating artery and circular stenosis of the proximal M, segment. C Right carotid angiogram with partial stenosis of middle cerebral artery (arrow). D Left carotid angiogram showing an aneurysm of the anterior communicating artery (arrow 1) and accessory middle cerebral artery (arrow 2).

90

1 Operative Anatomy

Fig 69A-B Accessory middle cerebral artery arising from the right proximal part of A, at a spot where a large proximal A, perforator is usually present. A AP angiogram showing the origin of the lateral striate (arrow 2) and lateral fronto-orbital (arrow 3) arteries from this vessel 1. B Diagrammatic representation of A. Fig 69C Symmetrical anomaly on the left with larger branch from left A, (arrow).

Fig 70A-D Another example of bilateral accessory middle cerebral arteries arising from the right (A) and left (B) A, segments (arrow), intraoperative photograph (C); Pr = large proximal medial striate artery gives rise of the accessory middle cerebral artery. Arrow 1 = right A, segment, arrow 2 = right accessory middle cerebral artery.

Middle Cerebral Artery

91

Fig 70D Schematic representation of the origin ot the ace. MCA. Origin from lateral A, (1) , origin from A,-A2 junction (2). The ace. MCA is striped.

Fig 71A-B Unique variation of the right M2 segment in a case with bilobular aneurysm of the middle cerebral artery bifurcation (arrow): the enlarged inferior trunk is_coiled (Mg). A Angiogram (arrow indicates the aneurysm and coiling of inferior trunk). B Operative photograph (arrow indicates clipped aneurysm).

92

1 Operative Anatomy

Anterior Cerebral Artery Complex Proximal Anterior Cerebral Artery (Synonyms: precommunicating segment, "Aj segment") The anterior cerebral artery is generally the smaller of the two arteries leaving the internal carotid artery bifurcation (71%), although it may be equal in size to the middle cerebral artery (24%) or it may be larger in caliber than the middle cerebral (5%) especially if the opposite A1 is aplastic or very hypoplastic.) The size of the anterior cerebral artery is usually 1.0-3.0 mm but hypoplastic (< 1.0 mm) and very hypoplastic (< 0.5 mm) arteries are frequently seen. Angiographically demonstrat-_ed aplasia is almost never confirmed at surgery. The artery courses medially and often somewhat anteriorly, to the interhemispheric fissure, passing over the optic nerves and chiasm with a slightly posterior convex curve to join the contralateral anterior cerebral artery through the anterior communicating artery .1 As the artery leaves the internal carotid artery bifurcation it is crossed by thick-ened bands of arachnoid coursing from the olfactory trigone to the lateral part of the optic nerve and forming a tunnel through which the artery enters the lamina terminalis cistern. (The exact course of the artery is somewhat variable as it may loop underneath the orbitofrontal lobe so its junction with the anterior communicating artery may be quite anterior. Fig 72A-F Variations between the perforating branches of the M, and A, segments are constant. One may distinguish proximal lateral ( 1 ) and proximal distal (2) branches of MCA which are called 'lateral lenticulo-striate arteries" in the literature. The proximal A, perforators (3) are j neglected in the literature or called "medial lenticulostriate arteries", whereas the distal A, perforator (4) is well known as Heubner's artery. These vessels have a reciprocal relationship between the size and distribution not only concerning 1 and 2, or 3 and 4, but also between the groups 1-2 and 3-4. If one or two of these arteries are hypo- or dysplastic, then the others are larger and vice versa. Note also that 3 and 4 may give rise to frontopolar and assessory middle cerebral arteries.

Several small perforating arteries arise along the infero-posterior aspect of the proximal anterior cerebral artery (Aj segment). These arteries do not usually arise directly from the internal carotid artery bifurcation, but rather 2-5 mm distal. They are more frequent and larger in the lateral anterior cerebral area beneath the anterior perforated substance, jit "has been shown that these perforating arteries supply the septum pellucidum, the medial portion of the anterior commissure, the pillars of the fornix, the optic chiasm, the paraolfactory area, the anterior limb of the internal capsule, the anterior-inferior part of the striatum and the anterior hypothalamus (Critchley 1930; Abbie 1933/34; Lazorthes et al 1956; Ostrowski et al 1964; Dunker and Harris 1976; Perlmutter and Rhotonl976). As with most small perforating arteries, there is commonly (46%) a stem vessel that originates from the proximal anterior cerebral artery in this location and runs a recurrent course for several millimeters before dividing into several fine arteries that penetrate the brain substance. In most cases this vessel is of smaller caliber than the recurrent artery of Heubner, but courses with Heubner's artery to the medial anterior perforated substance. On occasion, especially if the lateral striate arteries are small, this vessel may be quite large, even larger than Heubner's artery, and supply branches to the lateral parts of the anterior perforated substance (Figs 72A-F, 73A-G).

1 Lateral proximal striate arteries of MCA 2 Lateral distal striate arteries of MCA

3 Medial proxima\ striate arteries 4 Medial distal striate (Heubner's) artery.

Anterior Cerebral Artery Complex

Fig72B-F

B If the lateral striate arteries (1 and 2) are aplastic or hypoplastic, the medial proximal striate (3) and Heubner's (4) arteries are well developed. C The large medial proximal striate artery (3) also gives rise to Heubner's artery (4). D The large medial proximal striate artery (3) gives rise to Heubner's (4) and fronto-polar arteries (Fp). E The large medial proximal striate artery (3) gives rise to the accessory middle cerebral artery and lateral striate arteries (2). F Unique case with large fronto-polar arising from the proximal lateral striate artery (1) (see Fig 74A).

93

94

1 Operative Anatomy

Fig73A-G Operative photographs of: A A large right proximal medial striate artery originating from a large A, segment (arrow). A, larger than M,. B A large right proximal medial striate artery (arrow). C A hypoplastic right A, segment giving rise to several small perforators (arrow 1 ) , two large medial striates (arrows 2-3), and Heubner's artery (H) D A large right proximal medial striate (arrow) originating from a hypoplastic A, segment.

In four cases from the present series, both this vessel and the recurrent artery of Heubner had a common origin from the proximal anterior cerebral artery, while in 2 cases this vessel, Heubner's artery, and a frontopolar artery all arose from a common stem in this location. In one case a large vessel arose in place of an aplastic A, segment and penetrated the brain alongside a normal Heubner's artery. In one case this artery gave origin to the large frontopolar artery (Fig 74A-B).

Anterior Cerebral Artery Complex

95

Fig73E-G E The right Heubner's and fronto-polar arteries (arrow 2), and proximal medial striate branches (arrow 1) all arising from a common trunk of A,. F The right Heubner's artery (H) arising from the proximal A, segment and running a recurrent course with very small proximal medial striate branches from the more proximal A, (arrow). G A hypoplastic right A, segment ending as a proximal medial striate (arrows). No connection to the anterior communicating artery. Fig 74 A The large left frontopolar artery (arrow) arises at the same level as the proximal medial striate artery of A,. The left carotid angiogram gives the impression of a duplication of the left anterior cerebral artery.

96

1 Operative Anatomy

Fig 74 B Schematic representation of the origin of medial fronto-orbital (1) and fronto-polar (2) arteries. 1 Separate origin from A2. 2 Common origin of medial fronto-orbital together with fronto-polar artery. 3 Common origin of 1 x 2 and Heubner's artery (H) from A,-A2 junction. 4 Common origin from proximal A!

Fig 75 Unusual origin of the proximal A, perforator (medial proximal striate artery) from the antero-inferior wall of A, (usually arising from the superior wall). Notice also the common origin of the lateral striates of the M, segment and the lateral fronto-orbital artery in this operative diagram.

This important vessel and these variations have not been previously recognized by dissection of the area (Dunker and Harris 1976, Perlmutter and Rhoton 1976). It may represent the accessory artery of Charcot described by previous investigators (Wollschlaeger and Wollschlaeger 1969). In one case this artery originated from antero-inferior wall of A! segment (Fig 75).

Anterior Cerebral Artery Complex

Inequality of the proximal anterior cerebral arteries (AI segments) has been reported to occur in 7 per cent (Riggs and Rupp 1963), 8 per cent (Kleiss 1941/42), 25 per cent (von Mitterwallner 1955), and 46 per cent (Adachi and Hasebe 1929) of unselected cases. In the senior author's (MGY) angiographic studies, cadaver dissection, and operative experience (Table 5), the incidence of proximal anterior cerebral artery inequality is quite variable depending on the mode of examination and the definition as to what degree of size difference is significant. These variations may be due to the effects of pressure injection at angiography, the consequences of formal fixation in cadaver specimens, or the effects of operative or subarachnoid hemorrhage induced vasospasm. Similarly the incidence of A1 size differences visualized at surgery would diminish if only marked differences (> 1.0 mm) were counted instead of more minor variations. Kwak and Suzuki (1979) reported hypoplasia of AI in 68.1 per cent of cases with an aneurysm of the anterior communicating artery. Patients with an aneurysm of the anterior communicating artery in the present series showed some inequality of the Aj segments in 80 per cent of cases, with the left larger in 51.2 per cent and the right larger in 26.6 per cent (Fig 76A-B). Other less frequent anomalies of the proximal anterior cerebral artery in the present series included aplasia on the right side in 5 cases (severe hypoplasia < 0.1 mm in 3 cases and true aplasia in 2 cases), aplasia on the left side in 4 (severe hypoplasia in 2 cases and true aplasia in 2 cases), fenestration in 9 cases (right Al 5 cases, left At - 4 cases), duplication in 1 case (left AI) and an extremely short Al segment (R.)

in one case (Fig 77). In another case (craniopharyngioma), the left anterior cerebral artery coursed beneath the ipsilateral optic nerve as has been reported by Nutik and Dilenge (1976) and Bosma (1977). Isherwood and Dutton (1969) presented two cases of the anterior cerebral artery arising just above the ophthalmic artery in one case bilaterally. Eight similar cases were collected by Nutik and Dilenge (1976). Other authors have reported the incidence of aplasia of the proximal anterior cerebral artery to be between 1-2 per cent (Windle 1888; Padget 1944; von Mitterwallner 1963). Duplications of the A, segment have been described by Perlmutter and Rhoton (1976) (2 cases) and Windle (1888) (1 case). No cases of bilateral aplasia have been reported.

Table 5 Anomalies and variations of A, segments. Neuroradiological observations 1965/1968 7305 Cadaver brains

Both A, equal

58 %

Left A, larger

22 %

Right A, larger Severe 14 % 4 hypoplasia Aplasia

% 1.3%

200 Angiographies

41.5% 36.0%

21 .0% 41.3% 1.0% (right/left) 0.5% (right)

97

Operative observations 375 cases 20.0% 51 .2% 26.6% 1 .3% 1.1%

98

1 Operative Anatomy Fig 76A-B Variations of the anterior communicating artery complex with equal and unequal A, segments. A A hidden aneurysm of the anterior communicating artery (white arrow) with equal sized A, segments (black arrows). B An aneurysm of the anterior communicating artery (white arrow) with hypoplasia of the right A! segment (black arrow).

Fig 77 AP arteriogram revealing a very short right A^ segment (arrow) with distortion of the entire anterior communicating artery complex and an anterior communicating artery aneurysm situated over the olfactory tract.

Anterior Cerebral Artery Complex

99

or midportion. Section of the vessel showed that the lumen was traversed by a trabeculated^parEmbryologically, the anterior communicating titition that bound the arterial walls and narrowed artery develops from a multichanneled vascular the lumen perhaps functioning as a valve. Similar network which coalesces to a variable degree by anatomical studies have been reported by Busse the time of birth (Padget 1944). As classically (1921), Adachi and Hasebe (1929). De Almeida conceived, this short artery unites the paired ante- (1931), Kleiss (1941/42), von Mitterwallner (1955), rior cerebral arteries in the lamina terminalis and Perlmutter and Rhoton (1976) (Figs 82A-D, cistern to provide an important anastomotic channel 83A-C, see also Fig 97). Aplasia of the anterior for collateral circulation through the circle of communicating artery was not observed either in Willis. Direction of blood flow through the artery the cadaver dissections or operative cases, but would depend on slight variance in pressure extreme hypoplasia (< 0.1 mm) was seen in 3 between the anterior cerebral arteries of each cadaver brains (1.5%) and 5 operative cases side. (1.3%). In one cadaver brain there was no anterior The anterior communicating artery is commonly communicating artery as the two anterior cerebral between 0.1-3 mm long. Its normal caliber is arteries were fused in the prechiasmatic region (Fig between 1.0-3.0 mm, but hypoplastic (0.5-1.0 84). Duplications were seen frequently (Table 6, mm), very hypoplastic (0.1-0.5 mm), or even see Fig 81A-B), and in the aneurysm cases, the hyperplastic (> 3 mm) vessels are not infrequently lesion could originate from either the primary or seen. By definition, the normal anterior communi- secondary vessel. cating artery is one that connects two Aj segments of equal size. As previously discussed, this occurred in only 20 per cent of anterior communicating aneurysm cases, as in most cases a large A, segment divided into the two distal anterior cerebral arteries (A2) and the anterior communicating artery in such cases could only be defined by the entry point of the hypoplastic contralateral At segment.]Wilson et al (1954) found that 85 per cent of anterior communicating aneurysms were associated with hypoplasia of one At segment and attributed the formation of an aneurysm in these instances to resultant hemodynamic abnormalities. This concept has been supported by Stehbens (1963) and Suzuki and Ohara (1978).________ Overall, the anterior communicating artery probably exists as a single channel in about 75 per cent of cases (von Mitterwallner 1955). In other cases a spectrum of anomalies exists between the multichanneled network of the embryo and the single anterior communicating artery. Busse (1921) examined 400 cadaver brains using a binocular microscope and recorded 227 variations in the anterior communicating artery. These included duplications and triplications, fenestrations, reticular patterns, and loops and bridges (Fig 78A-C) which indent the artery and may function as valves. These were also seen under the operating microscope in examinations of cadaver brains by the senior author (Figs 79A-D, 80A-E, 81A-D). In 14 of 200 brains (7%), the anterior communicating artery was strictured and deviated in its lateral

Anterior Communicating Artery

100

1 Operative Anatomy

Table 6 Variations of the anterior communicating artery recorded in our own and in other series Windle 1888

Perlmutter/ Rhoton 1976

Own ( Cadaver brains :ases Operations

200 cases*

50 cases

200 cases

375 cases

One AcoA

159 (79.5%)

60%

1 1 4 (57%)

224 (59.7%)

Aplasia Fusion short unpaired long (1 A2) Hypoplasia 0.1-0.2 mm 0.3-1.0 mm 1.1-1.5 mm Normal 1 .5-3.0 mm Hyperplasia > 3 mm

2 (one A,)

7

-

-

8 1

? 7

5 3

4 8

? ? ? ? ?

? 7 ? 7 ?

2 4 8 90 2

4 5 11 186 6

Duplication one very small 0.1-0.2 mm one small 0.3-1.0 mm both equal

14 (7%)

30%

41 (20.5%)

84 (22.4%)

7 ? ?

7 ? ?

8 15 18

22 27 35

Triplication

7 (3.5%)

10%

37 (18.5%)

57 (15.2%)

one very small two very small three equal triangular bridges

? ? ? ?

7 ? ?

12 6 1 18

27 18 3 9

Network

-

-

8 (4%)

10 (2.7%)

200

375

* ( 1 9 1 in original work)

9

Fig 78 Variations of the anterior communicating artery as described by Busse ( 1 9 2 1 ) . (From Busse, O.: Virchows Arch, path. Anat. 229: 178-206, 1 9 2 1 ) .

Anterior Cerebral Artery Complex

59 years 9

47 years 9

55 years

82 years d

13 years 9

59 years

44 years 9

43 years 9

63 years d

28 years 9

6 months 6

42 years

37 years 9

36 years 9

59 years 9

86 years <S

45 years

9 years 9

49 years 145), larger amounts of oral fluids are prescribed accompanied by furosemide for salt diuresis. For analgesia we use pentazocine (30 mg i.m. every 4 hours) for adults. Pentazocine is a strong analgesic from the group of morphine antagonists but causes less respiratory depression than morphine. Ambulation and physiotherapy is started the first postoperative day, and as a result atelectasis and venous thrombosis are rarely seen. However, mobilization is delayed in those patients who have undergone early (days 1-7) surgery, particularly if there is any subjective complaint of dizziness or faintness on assuming the upright posture (see Vol. II). The patient's status is monitored continuously by the neurosurgeon, the internist and the anesthesiologist.

275

Induced Hypotension Operative bleeding during microsurgical procedures is generally minimal, but occurs to varying degrees. The aim of lowering blood pressure during surgery is not only to reduce bleeding, but to avoid the rupture of coagulated aneurysms. A dry surgical field certainly improves the working condition for the surgeon and offers the patient a better chance for a good result, even though the techniques of induced hypotension are not without their inherent danger. During the last three decades different methods have been used to induce controlled hypotension. In 1946 Gardner produced hypotension , by blood letting / through an arteriotomy. In 1950 Enderby introduced the technique of ganglionic blockade to produce hypotension. Later, deep halothane anesthesia alone was used to induce hypotension. A list of the most commonly used drugs and their action to induce hypotension is as follows: Halothane, by vasodilatation combined with a variable degree of myocardial depression Trimetaphan, by ganglion blockade Sodium nitroprusside, by direct vasodilation of the vessels. There is a paucity of published data regarding the optimal degree of hypotension for neurosurgical patients. From our experience over the last 4 years (600 cases) of providing deliberate hypotension with sodium jiitroprusside we recommend that the mean arterial blood pressure not be lowered below 40 mm Hg in normotensive and not below twothirds of the preoperative value in hypertensive patients. Below a mean arterial blood pressure of 30 mm Hg Finnerty et al (1954) found signs of cerebral ischemia in normotensive individuals. Although we do not hesitate to lower arterial blood pressure drastically for a few minutes to support an essential step in the operation, we see no need for the routine use of profound hypotension. For this reason good communication between the anesthetist and surgeon is of particular importance.

Deliberate Hypotension Induced by Halothane Halothane may be a useful agent to lower blood pressure in neurosurgical procedures. However, one must be aware that halothane is a potent vasodilator and if a patient is not hyperventilated it may increase brain bulk and thus raise the intracranial pressure. Theoretically, one could lower blood pressure with halothane beyond the levels at which autoregulation is able to maintain cerebral blood flow thus decreasing brain bulk and improving

276

4 Anesthesia for Microsurgical Procedures in Neurosurgery

operating conditions. However, one of the dose dependent effects of halothane besides a reduction in stroke volume and cardiac output is an increase in right atrial pressure (Prys Roberts et al 1974) thereby expanding the cerebral venous system and the brain bulk. Thus this procedure cannot be recommended without reservations.

Deliberate Hypotension Induced with Trimetaphan Ganglion blocking agents, such as trimetaphan, block sympathetic vasoconstriction, opening the peripheral vascular bed and thereby reducing blood pressure (Enderby 1950). Trimetaphan also relaxes capacitance vessels and blocks other sympathetic reflexes. Thus, cardiac output is slightly reduced. Trimetaphan inactivates the pupillary reflexes and may interfere with the postoperative neurological evaluation of the patient. At the University of Zurich up to 1974 we performed hundreds of controlled hypotensive episodes with trimetaphan (0.1% solution). The initial dose for an adult is about 3 mg per minute (i.e. 60 drops per minute), but to maintain hypotension the drip is reset to 1 mg per minute (i.e. 20 drops per minute). The combination of halothane and trimetaphan is particularly effective in achieving a desirable level of hypotension due to the suppression of vasomotor responses.

Induced Hypotension with Sodium Nitroprusside Sodium nitroprusside (SNP; Na2FeCN5 -NO • 2H2O) was first isolated in 1849 and its pharmacological effect was described in 1886 by Hermann. In 1929 Johnson differentiated its hypotensive action from its toxic action, which was regarded to be similar to sodium cyanide. Johnson's suggestions for the therapeutic application of the hypotensive effects of SNP remained unnoticed until 1950 when Page (1951) confirmed these findings and described the clinical use of SNP. In some centers SNP has been used to produce deliberate hypotension since 1962 (Tinker and Michenfelder 1976). SNP acts by direct vasodilation: it dilates the peripheral resistance vessels as well as the peripheral capacitance vessels, thereby pooling the blood and reducing not only the afterload but also the preload of the heart (Moraca et al 1962). Heart rate increases initially but returns slowly back to normal. Renal blood flow is maintained or increased, but coronary blood flow is reduced (Wang et al 1977). The potential toxicity of SNP is

now recognized and is the result of cyanide released from the nitroprusside molecule (Wang et al 1977). Cyanide is then converted to thiocyanate via the rhodanase system (Wiedemann 1976). For detecting the development of cyanide toxicity the best indicators are the pH and lactate levels as well as the levels of plasma cyanide and thiocyanate (Wiedemann 1976). SNP is supplied as a 50 mg lyophilized dry powder and it has to be dissolved with 5% glucose. Since it is sensitive to light it must be shielded with aluminium foil. To initiate hypotension with SNP Tinker and Michenfelder (1976) recommend titrating the dose between 0.5 to 1.5 meg per kg per minute. The total intraopera-tive dose should not exceed 3-3.5 mg per kg (Wiedemann 1976). Lawson et al (1976) showed that there is a relation between age, weight and required dose of SNP, and formulated a nomogram to easily estimate the quantity of SNP needed. From 1975-1978 we performed over 300 controlled hypotensions with SNP. In analyzing 138 cases we found the necessary amount of SNP averaged 2.44 + 1.1 SD meg per kg per minute. These findings agree with the data of Stoelting et al (1977) who found in his series a need for 2.4 + 1.1 meg per kg per minute SNP for profound hypotension. However, in another analysis of 153 cases we found 15 cases in which the demand for SNP was of 6.54 + 1.24 meg per kg per minute. To explain this we postulated that the phenomenon of tachyphylaxis probably occurred and from this data the incidence of tachyphylaxis might be as high as 10%. SNP is a very potent and fast acting antihyperten-sive drug. Since it produces hypotension by direct arteriolar vasodilation independent of the auton-omic nervous system (Schlant et al 1963) there is no available antidote. However, its duration of action is so short that it has to be administered by continous infusion, so its hypotensive effect is reversed merely by discontinuing the drip. It can be convenient to give a 0.01% solution at about 4 drops per minute, but in our department we use a 0.1% solution with a perfusor pump starting with 1 meg per kg per minute. At 30 minute intervals we check the blood gases to detect the occurrence of acidosis and to prevent hypoxia. In some cases of AVM we have induced profound hypotension with SNP for over 48 hours without any sign of cyanide intoxication or renal failure. However, in such cases it is advisable to check cyanide and thiocyanate levels routinely (the plasma cyanide should not exceed 300 n mol%) and, if necessary, to initiate therapy with hydroxy-cobalamine. Routinely, a second hypotensive agent (clonidine hydrochloride or dihydrallazin) is administered as

Anesthetic Management of Posterior Fossa Microsurgery in the Sitting Position

the SNP is being tapered to prevent a sudden reflex rise in blood pressure.

Hypothermia

277

Anesthetic Management of Posterior Fossa Microsurgery in the Sitting Position

(Aneurysms of the vertebral artery. PICA, vertebral junction, AICA) In our department the sitting position is used for all posterior fossa surgery, since it provides the best surgical access to the operation field and improves venous drainage (Albin et al 1976). Conversely, the sitting position can present the following dangerous complications: Postural hypotension (Michenfelder et al 1969; Michenfelder 1975; Hunter 1975; Albin et al 1976). Air embolism (Michenfelder et al 1969; Michenfelder 1975; Hunter 1975; Albin et al 1976; Michenfelder et al 1972). Cardiac arrhythmias (Michenfelder et al 1969; Michenfelder 1975; Hunter 1975; Albin et al 1976) Deterioration of the O? saturation by changes in the ventilation/perfusion ratio (Eckenhoff et al 1963). Faced with these problems anesthesiologists may fear the sitting position. However, according to the Vertebro-Basilar Aneurysms literature (Albin et al 1976, 180 cases) as well as to In surgery of vertebro-basilar aneurysms the ques- our own experience (over 500 cases, most of them tion arises as to the advantage of spontaneous tumors and AVM's) there is no increased mortality ventilation as a reliable monitor of brain stem associated with this position. The anesthesia for the function. Authors who have used this method sitting position is given according to the guidelines report alterations in cardiac rhythm, blood for microsurgical anesthesia already described in pressure and respiration as valuable warning sig- this chapter. One can minimize the complications nals of excessive manipulation in the region of the of the sitting position by taking additional measures: brain stem. Spontaneous breathing as an alternative to controlled ventilation is not used in our clinic because we give priority to optimal conditions for both Premedication patient and surgeon which we believe are offered by neurolept-anesthesia with moderate hyperven- To avoid pooling of the venous blood in the lower tilation. Problems which can arise in spontaneously extremities, the legs are wrapped with elastic breathing patients (coughing, respiratory efforts, bandages. Atropine sulfate (0.01 mg i.m.) is given hypoventilation etc.) do not occur. Therefore thirty minutes before the induction of anesthesia to anesthetic management in surgery of vertebro- prevent unwanted vago-mimetic responses as well basilar aneurysms is no different from that for as to increase heart rate in patients with intracranial pressure related bradycardia. In such patients other vascular lesions. the use of morphine or drugs with a morphine-like action must be totally avoided since they may cause a profound and persistent respiratory depression (Hunter 1975). The electrolyte status in these patients who may have repeated emesis with a related hypochloremic alkalosis should be closely monitored. Under hypothermic conditions the brain can safely tolerate the cessation of perfusion for a predictable time corresponding to the degree of cooling. Since the fifties this method has been applied with enthusiastic and disappointing results. Although its property of protecting the brain is beyond dispute its value in neurosurgery remains controversial. Indeed, there is little evidence that the outcome of surgery, which also depends on many other factors, has been improved by this method. We have had only limited experience with hypothermia (one basilar aneurysm and a few cases of arterio-venous malformation) and have never used the technique routinely. The technique is currently rarely employed. Moreover, constant advances in microsurgical techniques have developed to a degree that the use of hypothermia with its potential risks is not imperative.

278

4 Anesthesia for Microsurgical Procedures in Neurosurgery

Cardiovascular and Respiratory Complications The upright position can seriously affect the cardiovascular status of the patient (Millar 1972; Martin 1970). The effect of gravity and the alphareceptor blocking effect of anesthetics (e.g. halothane, ethrane, droperidol etc.) produce a decrease in systemic blood pressure due to venous pooling. For this reason we wrap the legs with bandages. The pressure transducer for continuous intraarterial blood pressure measuring is mounted at the level of the head to accurately monitor the intracranial arterial pressure. Otherwise the pressure measured at the heart level must be reduced by 2 mm Hg for every inch of vertical height above the heart. To avoid hypoxia due to the reduced ventilation/perfusion ratio of the lungs in the upright position (Eckenhoff et al 1963), the patients are ventilated with 50% oxygen and nitrous oxide.

performed as an intraoperative functional test. The following cranial nerves can be examined in this manner: A) Vagus - Bradycardia, hypotension B) Trigeminal - Bradycardia, hypertension (sensory); Jaw jerk (motor) C) Facial - Twitch of face or platysma, salivation D) Accessory - Shoulder shrug.

Postoperative Care The postoperative treatment of patients who have had posterior fossa surgery does not differ from those who have had supratentorial surgery; however, the competency of the larynx must be carefully proved since its innervation may have been disturbed.

Monitoring and Air Embolism Routine monitoring consists of continous direct arterial and venous blood pressure recording, display of a standard ECG lead on an oscilloscope, intermittent arterial blood gas analysis, and continuous auscultation of the heart sounds ("jTullwheel" murmers in case of air embolism) with an ultrasonic device (Doppler) (Michenfelder et al 1972). The microphone of this device is placed over the right atrium. The tip of central venous catheter has to be precisely in the right atrium to allow the aspiration of air in case of embolism. The correct position of the catheter is controlled prior to the operation by a chest radiograph or by an intravascular ECG (Martin 1970; Hufnagel 1976). The frequency of air embolism can be as high as 25% (Albin et al 1976), but serious consequences can be minimized by early diagnosis and prompt treatment (Michenfelder et al 1972). Therefore adequate monitoring in the sitting position cannot be accomplished without a Doppler air bubble detector and a previously inserted right atrial catheter (Albin et al 1976).

Cranial Nerve Examination The use of the sitting position for posterior fossa surgery also enables the anesthesiologist to monitor the slightest surgical manipulation of certain cranial nerves such as the vagus, so as to prevent associated cardiac arrhythmias and inadvertent nerve injury (Giessen 1976). Similarly the stimulation of other nerves such as the facial can be

Продолжение

Продолжение

5

279

Pathological Considerations

Epidemiology of Cerebral Aneurysms Incidence The incidence of cerebral aneurysms has been the subject of several large autopsy reports (McDonald and Korb 1939; Richardson and Hyland 1941; Housepian and Pool 1958; Jellinger 1977). In the general population the incidence of intracranial aneurysms is about 1 per cent which corresponds to their average frequency in large autopsy statistics (Heidrich 1972), although their incidence in various postmortem series ranges from 0.2-9 per cent (Jellinger 1979). More recent studies have tended to show an increasing incidence of cerebral aneurysms with the suggestion that a more careful examination of the cerebral arteries at autopsy has led to a greater number of aneurysms found. Stehbens (1963a) found an incidence of 5.6 per cent in his autopsy series. Evaluating 7,650 autopsies in patients over 10 years old, McCormick and Nofziger (1965) found 153 patients with aneurysms (2.0%), 127 ruptured and 26 unruptured. However in an addendum to their report, they noted that of 197 recent autopsies, 17 (8.6%) had cerebral aneurysms with only five of these ruptured. By inclusion of aneurysms less than 2 mm in diameter, Hassler (1961) found an incidence of 16 per cent ruptured and unruptured lesions. The clinical incidence of cerebral aneurysms is equally difficult to assess. Some large studies group all subarachnoid hemorrhage patients together when speaking of cerebral aneurysm, while others fail to consider unruptured aneurysms which may have presented through mass effect, intracerebral hemorrhage, or carotid artery - cavernous sinus fistula. The most accurate study of incidence of ruptured cerebral aneurysm is probably that of Pakarinen (1967) who related the confirmed cases of subarachnoid hemorrhage to the population of Helskini. He found an incidence of 15.7 per 100,000 per year. The incidence of subarachnoid

hemorrhage caused by verified aneurysm was 10.3 per 100,000 per year. In about 20 per cent of cases, a source of subarachnoid hemorrhage could not be found, and undoubtedly some of these cases had undisclosed ruptured aneurysms. Van der Werf (1972) reported the incidence of subarachnoid hemorrhage in the Netherlands to be 10 per 100,000 per year, and Rasmussen and associates (1980) found an incidence jrf_3_.4 patients per 100,000 per year admitted to neurosurgical departments in Denmark with verified ruptured cerebral aneurysm. An analysis of statistics from Switzerland for the past 13 years shows: From January, 1967, to July, 1979 the incidence of subarachnoid hemorrhage caused by operatively or postmortem verified aneurysms was 624/1.1 million population in the Canton of Zurich; 397 patients were admitted to the Neurosurgical Department of the University Hospital of Zurich, whereas 227 patients died before admission, either at home or at the district hospitals of the Canton of Zurich. The autopsy rate for all deaths in Zurich for this time period was about 40 per cent. Autopsies are not performed randomly, however, and it is not justifiable to extrapolate these figures toward 100 per cent population mortality statistic to calculate the total incidence of cerebral aneurysm in the population. For example, younger patients who died suddenly are likely to be routinely autopsied, while older patients who are found dead at home often do not come to autopsy. Government statistics show about 25 to 30 deaths per year in this older population group from subarachnoid hemorrhage, but another 140 deaths per year from intracerebral hemorrhage, less than half of which are associated with hypertension. Undoubtedly, some of this latter group represent ruptured cerebral aneurysms.

280

5 Pathological Considerations

Classification Several types of aneurysm in the central nervous system (CNS) have been described. The traditional classification separates mycotic, luetic, arteriosclerotic and congenital forms. Krauland (1957) distinguished two major types on the basis of morphological description. As the etiology is still not clear, especially the relationship of congenital factors and acquired degenerative changes, it seems to us reasonable to follow this morphological classification with a slight modification. Type I. Saccular or berry aneurysms (99%) 1) Congenital form 2) Acquired degenerative changes a) unknown factors b) mycotic aneurysms, resulting from inflammatory and embolic lesions c) syphilitic aneurysms d) traumatic aneurysms e) dissecting aneurysms

95-98%

0.4-2.5% very rare < 1.0% very rare

II. Fusiform aneurysms (1%) (synonyms: arteriosclerotic aneurysms, sclerotic aneurysms, megadolicho-arteria, serpentine arteries) a) congenital factors b) arteriosclerosis c) a + b combined

Saccular Aneurysms This type accounts for 66-90 per cent of all aneurysms (Dandy 1944; Housepian and Pool 1958; Sugai and Shoji 1968), but 98 per cent in 1116 cases of Suzuki (1979) and 98 per cent in 1012 of our own cases. Size Saccular aneurysms may be divided into three, i.e. small, medium and large (Sugai and Shoji 1968), four (Freytag 1966; Gabor and Potondi 1967), five (Locksley 1966) and even six groups (Housepian and Pool 1958; McCormick and Acosta-Rua 1970). We distinguished in our material:

1) Baby aneurysms (discovered during operative dissections) 2) Small size 3) Medium size 4) Large size 5) Giant aneurysms

(