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Robert De/aunay Rhythm1938. @VGBild-Kunst,Bonn 1993
Neuroradiology
194
3 Neuroradiology
Historical Review
I
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Robert De/aunay Rhythm1938. @VGBild-Kunst,Bonn 1993
Neuroradiology
194
3 Neuroradiology
Historical Review
I
Plain Radiographs Wilhelm Conrad Roentgen was Professor of Physics at the University of Würzburg when he made his discovery of X-rays in 1895. The first X-rays, or radiograph, (of Roentgen's wife's hand) was made in January, 1896. This heralded the era of diagnostic radiology, and Roentgen was awarded the Nobel Prize for Physics in 1901 for his discovery. Skull radiographs, supplemented by chest and, when appropriate, spinal radiography, quickly became part of the investigation of patients with neurological diseases. Not surprisingly, the diagnostic yield was limited. In 1912, Schuller published his detailed monograph on skull radiography, the first substantive work on radiographic changes created by CNS lesions. Plain radiographs still provide useful information in many cases of extrinsic tumors, and in some intrinsic as well (Diethelm and Strnad 1916).
Contrast Encephalography In 1918, the first neuroradiological contrast study was performed when Walter Dandy introduced air ventriculography, replacing ventricular cerebrospinal fluid with air injected directIy through a needle introduced through a burr hole (Dandy 1918). This was followed by his introduction of lumbar pneumoencephalography in 1919.The use of air in the ventric1es and CSF systems proved very useful in imaging the cisternal systems and surface contours of the CNS, and in hydrocephalus, sites of blockage could be accurately localized. With intracranial masses, the type of ventricular displacement and deformity acccurately predicted the side and location of the mass, whether it was tumor, hematoma, or abscess. Between 1920 and 1972, cerebral pneumography was a key investigation method, producing high diagnostic rewards in expert hands. As diagnoses were deduced from indirectIy visualized structural changes within the brain and cisternal systems, interpretation had to be of the highest order. However, tumors not causing such changes could remain undetected.
performing direct intracarotid punctures for other reasons for seven years). In 1948, Seldinger obviated the need for direct carotid puncture procedure, and made cerebral angiography safer and less painful, with the percutaneous transfemoral technique. AIl these technical advances resulted in the widespread use of arteriography in the diagnosis of brain tumors until the introduction of cr scanning in 1972. Not only did this technique permit accurate localization of tumors, their vascularization patterns, and displacement effects, it also provided a confident pathological diagnosis in many cases of meningiomas, gliomas, metastases and hemangioblastomas. At present, arteriography, in selected extrinsic and intrinsic tumors, continues to provide essential information in diagnosis, in surgical planning and in neurointerventional decision making. Considerable improvements in radiological equipment and in contrast less allogenic media have continued right up to the present day. Modern catheter technology has also made angiography much safer and has enabled superselective techniques to be used for both investigation and treatment. The specific indications for angiography, in the management of CNS tumors are comprehensively presented in well knownmonographs on cerebral and spinal arteriography (Newton and Potts 1974, Salamon and Huang 1976, Huber et al. 1979). Even though we have had full access to high-resolution MR scanning for the last five years, we have considered it useful to perform angiography for tumors intimately related to or involved with major arterial feeders or draining veins and sinuses. In these circumstances. arteriography provides detailed information on three aspectsof the vascular system that magnetic resonance angiography (MRA), despite promising advances in quality, cannot yet achieve: the condition of the arteries, veins, and their collaterals (particularIy their dilatation, hyperplasia, stenosis, and ocdusion); the amount of displacement of the arteries and veins.and the quality of flow (slow versus fast, shunts within a tumor). In addition, arteriography is crucial in the evaluation and preoperative embolization of, highly vascular tumors. Venous samplingin suspected ACTH-secreting pituitary adenomas is often usefulin confirming the diagnosis and localization.
Cerebral Angiography Neuroimaging: The next important advance was the introduction of cerebral arteriography by the Portuguese neurologist, Egas Moniz, working in Paris in 1927.Moniz was impressed by the many European misgivings about the safety of ventriculography expressed at a meeting of the Royal Society of Medicine in London in 1924. He set about to find another way of diagnosing cerebral tumors and, in 1926, with his co-worker, Almeida Lima, conducted initial trials on dogs and on a cadaver. Subsequent trials in four patients were failures, but they persevered and demonstrated the first brain tumor in a patient by angiography in 1927. Cerebral angiography, as performed by Moniz, involved bilateral open exploration of the carotid arteries and direct puncture of the common carotid artery, using sodium bromide and later, Thorotrast as contrast agents. Direct percutaneous common carotid puncture for visualization of the cerebral vessels was pioneered in 1936by Loman and Myerson (they had been already
Computed
Tomography
Neuroradiology effectively became neuroimaging on April 19.
1972when Ambrose, a neuroradiologist,showed for the firsttime how it was possible to directly image the brain. In his presentation to the British Institute of Radiology in London, he described"a scanning apparatus which uses crystal detectors and a computer to analyze the information content of a beam of X-rays,andconstruct a tomographic picture from the readings so obtained." The term computed transverse axial tomography (CAT scanning,later simply CT scanning) was given to the technique by Ambrose and Hounsfield (a physicist who produced the original concept andinitial design for the EMI scanner, for which he received the Nobel Prize for Medicine in 1979). Ambrose went on to show how this "new and fundamentally different X-ray method" was 100 times more sensitive than conventional radiographic procedures, and was able to distinguish
Historical Review verysmalldifferencesin tissue density.Apart from normal brain anatomy,it was also possible to appreciate very subtle density differencesbetween normal brain parenchyma, edematous brain, blood,and cerebrospinal fluid, as well as a striking contrast with thehigh-densitybone. Examples of cerebral tumors, intracerebral infarction,and hemorrhage, were immediately discernible. Until this drama tic breakthrough, a diagnosis of suspected pathologywithin the central nervous system had to be indirectly deducedfrom techniques that imaged bone, the ventricles and subarachnoidspaces and blood vessels. Yet even with extensive lesions,when using all the available techniques, it was still not alwayspossible to make a diagnosis, unless the lesion contained abnormalblood vessels, or was associated with edema causing a masseffect.Also, the occasional discrepancy between prominent symptomsand subtle neurological signs often led to an inappropriate neuroradiological search (for example, a posterior fossa lesionrather than a frontallobe tumor). Theintroduction of CT scanning resulted in a rapid decline in the use of isotope brain scanning, diagnostic pneumoencephalography(by 90%) and angiography (by 60%) in neurosurgical unitsin the year following the installation of such a scanner. By 1975,the superiority of CT over all previous studies in the detectionof intracranial tumors was clear (Ambrose 1975). There is no question that the advent of CT scanning marked the most remarkable advance in the investigation of intracranial diseaseso far produced in the twentieth century. At the same time,howevercritical research was being conducted into the applicationsof nuclear magnetic resonance (NMR) in imaging biologicaltissues.
Neuroimaging: MagneticResonanceImaging ThesuccessfulNMR experiments by Purcell and Bloch in 1945 led to the development of NMR spectroscopy in the 1950s and as an indispensableanalytical tool in numerous sciences, 1960s rangingfrom biology and chemistry to solid-state physics. CommercialNMR spectrometers were pioneered in both the Onited Statesand Switzerland by 1958. Odeblad, a Swedish physicist and gynecologist, was the first toapplyNMR spectroscopy in medicine (1955, 1960). He studied theprotons in human milk, saliva, cervical mucus, gingival tissue, andthe eye. The NMR experiments by Cope (1970), and Hazlewood(1971)provided a better understanding of the nature of cell water,and helped confirm the concept (1962) of the existence of intracellularwater as multiple polarized layers adsorbed onto cell proteins.These works formed the basis for current interpretations ofedema. The real breakthrough in NMR technology carne with the inventionof Fourier NMR spectroscopy in 1966 in California by DrW.A. Anderson and Professor Richard Ernst of the Swiss Federal Institute of Technology in Zurich. The use of pulse techniquesand Fourier transformation to boost sensitivity and to increase versatility revolutionized the field. Spectroscopy, especiallyof large organic molecules and of less sensitive nuclei suchascarbon-13,becamefeasible. Damadian (1971) drew attention to the in-vitro observation of differencesin the values of the proton nuclear spin-lattice relaxationTI time in some normal tissues (in the rat), benign
195
tumors (fibroadenomas), and malignant rat tumors. He suggested that spin-echo NMR might be used as a method of discriminating between malignant tumors and normal tissue. His patent application in 1972 "of apparatus and methods for detecting cancer in tissue" was the first proposal of an NMR tumor imaging concept. Weisman (1972) showed that in-vivo recognition of animal tumors was possible with NMR. The necessary concept for imaging with NMR required at least a two-dimensional representation of nuclear density, and Lauterbur (in 1973) was the first to solve the problem. His was a landmark paper, describing the technique for generating twodimensional and three-dimensional images of objects, inciuding living organisms, from NMR signals in magnetic field gradients. Essentially, by applying the linear magnetic field gradient along a number of different directions relative to the object, a number of different one-dimensional profiles are obtained. These could then be combined by computer to give a two-dimensional image of the object, using a method similar to the projection-reconstruction procedures used in CT by Hounsfield in 1972. Lauterbur correctly forecast the potential in vivo application of the technique in the study of tumors. In a later paper, in 1975, he suggested the combination of MRI with high-resolution pulsed Fourier transformation NMR spectroscopy to make possible noninvasive, nondestructive, spatially resolved. chemical analyses of the interiors of objects (magnetic resonance spectroscopy, MRS). Lauterbur's technique was quickly matched by related techniques from other pioneering research groups. At least eight different approaches to image formation were put forward by these groups. Mansfield and Grannell (1973) described NMR "diffraction." Hinshaw (1974), described two further techniques involving time-dependent magnetic field gradients. He advanced the term "spin mapping" in recognition that an NMR image is a map of nuclear spin density and related parameters. In 1976, Hinshaw put forward "the multiple sensitive point method" of image formation by NMR, which was then used in the first NMR ciinical trials in Nottingham. Kumar, Welti and Ernst (1975) carne forward with another approach, conceptually more sensitive, which resulted in the first practical demonstration of two-dimensional NMR spectroscopy. This technique remains one of the most informative in molecular biology, allowing a complete determination of the three-dimensional structure of proteins and nucleic acids in solution. The present-day rapid-sequencing, high-resolution MR images have been a consequence of the development of equipment such as the large magnet with an intense and homogeneous field, extensive radiofrequency equipment (transmitters and receivers), gradient coils, and advanced computer system for the two-dimensional Fourier transformation of extremely large data sets. Supporting control and display units and facilities for digital data storage are also indispensable. The first demonstration of intracranial pathology by nuclear magnetic resonance (NMR) tomography of the brain was produced by Hawkes, Holland, and Moore-physicists-and Worthington, a neuroradiologist, in Nottingham, England in 1980. In the 1990s, high-resolution magnetic resonance imaging (MRI) has become the imaging modality of choice for investigation of central nervous system neoplasms.
196
3 Neuroradiology
Isotope Brain Scanning Radionucleotide imaging of brain tumors was first shown to be of localizing value in the late 1940s. The highest accuracy was achieved in intracranial masses with increased vascularity and edema, such as meningiomas, cerebral abscesses, and metastases (provided the latter were over 2 cm in diameter). Diagnostic accuracy rapidly declined in the case of gliomas and astrocytomas. Thus, the number of false negatives was comparatively high, depending on the type and location of the tumor. In the 1960s, the gamma camera was introduced by Anger, and with the ready availability of isotopes (such as technetium-99) with moderately short half-lives, isotope brain scanning became the least invasive investigation of initial choice for a suspected brain tumor. Di Chiro (1964, 1969) popularized the technique, which reached its zenith between 1970 and 1973. There were three major limitations to brain isotope scanning detecting a tumor. First, a positive result depended on disruption of the blood-brain barrier, or considerable alteration in lesion vascularity. Supratentorial low-grade gliomas were missed in up to 25% of cases (Baker 1976). Second, the lesion had to be greater than 1.5 cm in diameter. Third, the gamma carneras then in use were more sensitive to superficiallesions, and deeply placed central nuclear tumors and tumors in the posterior fossa were frequently missed. False-negative rates of 60% for brainstem tumors and 30% for cerebellar tumors were reported (Burrows 1976).Overall false-negative rates of up to 25% in proved cases of malignant brain tumors were reported by Baker in 1980 from the U. S. National Cancer Institute. In addition, the gross lack of specificity of a positive scan and the lack of information on the secondary effects of the lesion and its internal composition meant that the differential diagnosis often remained broad, including abscess and infarct. This necessitated the routine use of more discriminating, and more invasive, tests (cerebral angiography and pneumoencephalography) to confirm the diagnosis prior to surgery. Conventional radionucleotide studies do remain useful in two situations. Isotope bone scanning is a very sensitive detector of bone destruction, and still merits consideration in patients with suspected metastases, both cranial and extracranial. In cases of CSF rhinorrhea, the intrathecal injection of isotope may often prove the existence of a CSF fistula. When combined with the recovery of positively emitting, previously' placed intranasal pledgets, not only is the diagnosis confirmed, but also the site of origin of the fistula is proven.
Functional Neuroimaging Xenon CT Nonradioactive xenon is an inert gas with an atomic number close to that of iodine, which, when inhaled in sufficient quantity, crosses the blood-brain barrier and remains in the brain for a sufficient time to permit serial CT scans to be performed. Regional cerebral blood flow (rCBF) can be accurately and reproducibly measured, using calculations derived from CT numbers and end-tidal xenon concentrations. Decreased rCBF can be shown in cerebral infarction, transient ischemic attacks, gliomas,
and hypometabolic interictal seizure foci. The major advantages of the xenon CT technique are its high degree of anatomical specificity and its ability to measure the blood-brain partition coefficient in normal and pathological tissue. However, there are enough significant practical, theoretical and biologicallimitations to restrict its widespread use.
Emission Computed Tomography Emission computed tomography in its two forms, positroncomputed tomography (PET) and single photon emission computed tomography (SPECT) combines advances in radionucleotideisotopes with computer technology that permits the mathematical reconstruction of data obtained from multiple projections. Both provide true three-dimensional images of the brain with a maximum resolution of 5.0 mm, and measure concentration of radioactive tracer in nC/ml (Table 3.1). Table 3.1 Neuroimaging: tomographic techniques (alter Di Chiro, Encyclopedia of Neuroscience, Neuroimaging: vol. 2,1990, p. 795-799) Technique
CT
MRI
Property measured
Associated physical parameters
Units
Roentgen ray attenuation coefficient Net transverse nu-
Electron density, atomic number Proton density, T" T2' Ilow Glucose and oxygen utilization rates, blood flow, etc. (depending on radiotracer
HU
0.7mm
Beamhardening
Not relevant
0.3mm
Field inho-
nCi/ml
5.0mm
clear magnetization ECT Concentration 01 (PET, SPECT) radioactive tracer
Maximum resolution
Artilacts engendered
mogeneity
Scatter, attenuation
Positron Emission Tomography Positron emission tomography (PET) is based on the detectionof two high-energy roentgen ray photons that have been emittedas the result of the destruction of a positron. Positrons are produced in a cyclotron from certain radionucleotides with short half-lives. Availability has been limited to research centers, and it remains quite expensive. PET has proved useful in the evaluation of cerebral blood flow, cerebral volume, oxygen transport and metabolism, glucose utilization,amino acid transport and metabolism, and proteinsynthesis. Its role in tumor management has been in the study of functional changes within and around tumors, and the courseof
such changes after treatment. The recent discoveryof a drugthat blocks specific rate-determining steps in brain tumor mitosis (Aston University, ICRF, Plough-Schering) may expand the use of PET from pure research to more routine clinical use.
Current Neuroimaging with CT and MRI
197
SinglePhoton Emission Computed Tomography
Magnetic Resonance Angiography
Singlephoton emission computed tomography (SPECT) is a lowcosttechnique of imaging the three-dimensional distribution of radioisotopes.The technique uses the same kinds of gamma-emittingisotopesroutinelyemployed in most hospital nuclear medicinedepartments,and does not require the availability of an on-sitecycIotron (necessary for PET). SPECT scanning permits the creation of multiplanar tomograms that measure local cerebralbloodvolume,localcerebral blood flow,blood-brain barrier abnormalities,and other cerebral metabolic parameters.
Magnetic resonance angiography (MRA) exploits the fact that cerebral arteries are routinely visible on spin-echo images, due to the flow-void phenomenon. MRA techniques rely on special pulse sequences (sensitive to flow) and on sophisticated processing of the data to give images similar to standard contrast catheter angiograms. The major present applications for MRA are screening for atherosclerotic disease of the extracranial and major intracranial vessels around the circle of Willis. MRA can be used as a screening test for intracranial aneurysms in asymptomatic patients (e. g., family members of patients who have had aneurysms). Recent improvements in the sensitivity and resolution of MRA have been impressive enough for us to use it in the evaluation of certain intracerebral tumors to help decide which of these merit additional study by selective cerebral arteriography. Although intrinsic and extrinsic tumor vessels can be routinely visualized, MRA is of little value in precisely identifying the feeding vessels, and certainly provides no information about the quality (e. g., fragility) of these feeding arteries (see Fig. 3.14, 3.49, 3.48).
CurrentTrends Neuroimaginghas continued to evolve to become a comprehensivediscipline that investigates and displays both normal and abnormal, structural and functional anatomy in the central nervoussystem. Of future importance will be the integration of noninvasivetechniques that precisely demonstrate, to resolutions of 1-3 mm, both structural and functional areas of the brain together.
Echo-planar MRI Magnetic Encephalography Magneticencephalography (MEG) has shown how this precise localizationcan be achieved in the somatosensory and motor areasof the cortex. No doubt the same precision will be achieved withthethreemajorarea componentsof speech.Of more immediate usefulnessare techniques that allow the noninvasive assessmentof alterations in the vascular and CSF systems in and around cerebraltumors,such as magnetic resonance angiography (MRA) andechoplanar MRI.
Echo-planar MRI technology involves the production of ultrafast MRI images (1-2 seconds). It has been used to study real time CSF dynamics and blood flow in vessels and, in addition, may ultimately prove beneficial in the utilization of MRI for the evaluation of cerebral metabolic processes. Unfortunately, it is not inexpensive to adapt it to present MRI imaging capabilities. The need for a high-strength magnet (3.0 Tesla or more) and some uncertainties about the long-term safety may inhibit further clinical development. Future development of fast T2 imaging techniques (3-4 minutes) may prove to have more widespread applicability than echo-planar MRI.
CurrentNeuroimaging with CT and MRI Whilemanyof the problemsof tumor detect~on,localization,and pathologicalcharacterization were solved for extrinsic tumors by the advent of high-resolution CT and MR imaging, especially afterthe introduction of nonionic contrast agents, the pathophysiologicalsignificance of many of the changes seen on MR with intrinsictumors remains uncertain. For neurosurgeons, the sensitivityofcurrent CT and MR in localizing pathology is truly impressive.yet the lack of pathological specificity has been a disappointment.The cIinical history and examination are, and will remain, vital discriminatorsin narrowing the differential diagnosis. To makethe best use of current neuroimaging techniques, close discussionsbetween neuroradiologists, neurosurgeons, and neuropathologistsare more important than ever. Hopefully, parallel developmentsby these associated specialists willlead to a better understandingof tumor pathophysiology (Table 3.2). It is not the intention of this chapter to provide a compendiumof intracranial pathologies and their various radiocharacteristics,but rather to stimulate critical analysesof graphic
how current neuroimaging can be better utilized. Detailed information on these topics and specific lesion characteristics are well reviewed in the literature (Kazner et al. 1988, Bradley et al. 1990) and in current textbooks (Brant-Zawadzki and Norman 1987, Orrison 1989, Higer and Just 1989, Grossman 1990, Chakeres 1991, Dietemann 1993). A higher level of gray /white matter contrast is obtainable with MRI when compared with CT. The degree of anatomical detail shown on the three orthogonal planes is greater with MRI. MRI offers increased sensitivity with earlier detection of smaller lesions in areas previously difficult to image with CT. MRI provides higher-resolution detail of the posterior fossa and skull base. MRI does not have the problems of bone-volume averaging and beam-hardening artifacts that contribute to the false-negative results obtained with CT in these regions. This increased sensitivity of MRI over CT extends to the evaluation of head trauma (Han 1984).
1
198
3 Neuroradiology
Table3.2 Current neuroimaging (CT and MRI)capabilities General aspects Morphologicalchanges Neoplasms: primary and metastatic vascular lesions: aneurysm, AVM,ischemia, hematomas Inlectious diseases White-matterdisease: MS, leukodystrophies, encephalopathies CSF system (hydrocephalus, secondary atrophy) Congenital anomalies Traumatic lesions Location01the lesion Extrinsic Intrinsic(neocerebral, neocerebE¡Jllar,limbic-paralimbic, central nuclei, and intraventricular) Postoperative morphological changes (local and remote) Hematoma Edema Inlarction CSF hygroma and hydrocephalus Completeness 01surgery Residual or recurrent pathological tissue Special aspects: secondary lunctional changes CSF dynamics Hemodynamics Biologicalbehaviour 01the lesi.on Progressive Regressive Inactive Parenchymal dynamics Atrophyand related degenerative changes Tissue intensity changes: perilesional changes ? Biochemical metabolic interactions ? Inliltration01tumor cells Posttreatment effects: surgery, chemotherapy, or radiatiotherapy
Table 3.3 Comparison 01 CT with MRI
Technique Sensitivity Specilicity Spatial resolution Soft-tissue contrast
Blood-brain barrier evaluation Functional capabilities Developed by Ho
CT
MR
First to directly image CNS Limited Fair High
Direct images 01CNS
1) Moderate High-resolution images 01bone Poor gray-white neuroanatomy
2) Limited pathological sensitivity Intravenous con-
trast uselul Poor
Éxcellent Moderate Very high, in three planes 1) Excellent High-resolution images 01bone marrow, CSF spaces, graywhite anatomy, and most gross neuropathology 2) Moderate pathological sensitivity Intravenous gadolinium very uselul Limited
Comparison of CT with MRI During its development, it was predicted that MRI wouldhave three advantages over CT, namely, that (a) MRI scanning usesno ionizing radiation, (b) it requires no moving parts to perform a scan, and (c) multiplanar (axial transverse, coronal, and sagittal) tomograms are easily obtained, since the scanning mechanismis entirely electronic (Holland et al. 1985). The ability of MRI tomography to directly produce coronal and sagittal, as well as axial transverse, images has shown itself today to be the best meansof precise lesion assessment (Table 3.3). In Chapter 2, the importance of identifying the subgyral, gyral, or lobar peduncular origin of the primary location of many intrinsic brain tumors is stressed. Tumors in these locations distort the normal morphology of the brain and make localization difficult. MRI has made this localization much easier. Neurosurgeons, in particular, are most grateful for the specific anatomicallocalization that current MRI, when properly used, is able to provide. Sagittal and axial MRI provides excellent extrinsic tumor imaging detail. Coronal MRI imaging is the most useful image plane inpreoperative localization and surgical planning for intrinsic tumors, as the white-matter peduncular architecture of most gyri can be
most favorably recognized in this planeoFor the frontal and temporal gyri, on the other hand, the horizon~al or sagittal viewsare more helpful. Careful analysis of pre-gadolinium and postgadolinium TI MRI scans in three planes will nearly alwaysprovide the precise anatomical information that is a prerequisite for preoperative surgical planning.
MR Image Selection Unlike CT, MR allows an almost infinite number of manipulations to obtain a diagnostic image and to vary the contrast on images. The choice of independent tissue variables that provide the best contrast on diagnostic evaluations include pro ton density, T ¡-weighted, Tz-weighted, and "flow" -weighted images.The selection of which pulse sequences to use in the evaluation of anysuspected pathology is important not only in eliminating false negatives and in maximizing sensitivity, but is also vital for subsequent correct interpretation. With an initial (diagnostic) study of a suspected tumor, all three types of main sequences (proton density, T,-weighted, and Tz-weighted images) need to be obtained before a study can be regarded as complete. In reality, it is useful to regard each set of images as totally different imaging methods (as different as MRI is from CT), each with its own advantages, disadvantages, and limitations. Therefore, at least three completely different sets of MRI images have to be interpreted using different criteria. In addition to being fully aware of technical variables and limitations, it is especially important for neurosurgeons to realize that artifacts and distortions of real anatomy, especiallyat interfaces, can be significant (Pusey et al. 1986, Kelly 1987). (Table 3.6). With MRI the differences between T,-weighted and Tz-weighted images in various normal and pathological tissues are greater than the variations in proton density. The selectionof various pulse sequences is used to "weight" the images toward TI or Tz data. This forms the basis for the increased sensitivityof MRI. The choice of image sequence parameters can still be critically important in lesion detection (Table 3.4). Some convexity
Current Neuroimaging meningiomas without secondary parenchymal changes can detectionunlessappropriate TI and T2sequences are perescape formed. MRI may underrepresent or overrepresent tissues at interface s betweenCSFand brain parenchyma.The width of sulci is commonly exaggerated, and adjacent gyral surfaces underrepresented. Anatomical resolution is best with TI images, and pathologicalsensitivity greatest with T2 sequences. Image interpretationfollows hnes similar to those used in CT interpretation. Detailedanalyses of geometric factors and 2 tissue contrast factorsare crucial.
MR appearance White 'Increased signal (short) T,W
ContrastMRI
Usefulnessof MRI in Distinguishing VascularMass Lesions from Tumors
199
Table 3.4 Interpretation of T1-weighted and T2-weighted MR images (alter Orrison, Introduction to Neuroimaging, Boston: Little, Brown, 1989, p.87)
Increased signal (long) T2W
Doubts about the sensitivity of CT in identifying tumors promptedAmbrose to develop a contrast agent. The comparison of contrast with noncontrast scans enabled CT to demonstrate tumorneovascularization and alterations in the blood-brain barrier.MRI carne into clinical use before a suitable contrast agent hadbeen developed. The hope was that, with its increased sensitivity over CT and with suitably chosen T2 sequences, a contrast agentwould not be needed. This was not the case. Since 1986, MRI with paramagnetic contrast agents such as Gd-DTPA has increasedthe sensitivity for detection of CNS lesion to a higher leve\.Forexample,compared to a noncontrasted scan, MRI with Gd identifies 15% more metastatic tumors. Contrast MRI is of greathelp in differentiating tumor from perilesional changes. The useofcontrast studies is of major importance when one considers that over 50% of patients with intracranial neoplasms have few localizingsigns and normal neurological examinations.
with CT and MRI
Typical causes
Fat Normal white matter Paramagnetics Lymphoma Chronic hematoma H20 CSF Paramagnetics Edema Inflammation Infarcts Neoplasms Multiple sclerosis Normal gray matter Lymphoma Chronic hematoma
Black or gray Decreased signal (long) T1W
Decreased signal (short) T2W
Ca2+ Blood or CSF flow H20 CSF Edema Inflammation Neoplasms Normal gray matter Lymphoma Ca2+ Blood or CSF Fat White matter Lymphoma Acute hematoma
White: increased signal = short T1' long T2 Black: decreased signal = long T" short T2
this work focuses on brain tumors, vascular lesions can Although sometimespresent as mass lesions. The noninvasive differentiationbetween these two types of pathology is important. MRI is ableto provide far more useful information on the structural and temporal changes associated with hemorrhage and infarction thanCT is.Sometimes even the underlying pathological vascular lesioncan be determined (e. g., AVM or cavernomas). MRI can identify changes associated with subarachnoid hemorrhage, aneurysm,angioma, and occlusive vascular disease. Ischemia, infarction,hematoma (epidural, subdural, intraparenchymal, and interventricular)can also be evaluated.
Functional Studies MRI candefine functional relations between
normal and abnor-
mal tissues better than previous studies. By itself, though, its lack of specificity remains a limitation, especially when attempting to differentiate neoplasms from other disease processes. Current workis aimed at to increasing our functional knowledge of brain tumors. Sodium-gated MRI may provide more information regardingtumor grade and local extension. MRI is very sensitive in displayingperilesional changes, of uncertain significance and conflictinginterpretation. This problem will be further examined below.
Failure of MRI to Detail Surgical Pathophysiology Two other important considerations must be integrated in the synthesis of the final surgical strategy. First, the pathology of the tumor, and second, its functional effects (Iocally, globally and systemically). Unfortunately, these are the two areas where MRI, even with its exquisite sensitivity, has failed to live up to early expectations. This failure has been a particular disappointment and a frustration to surgical decision-making. For many tumors, the specific MR imaging parameters that precisely define pathology (consistenDiffuse
~ Nonsilent ~
Other lactors
Other lactors
Slow
~
>< Malign --
====--=====:
Fast
Operability Yes -
Other lactors
No-
Experience.s capable
~
Adequate
Inexperienced, reler
~
Inadequate
1-11= unchanged, III-IV = changed conscious level
Societal
Hospital
Surgeon's capacity
~
:=-
~
Care I2rovided
-:
Care denied
./
}
Treatment optlons
Treatment Option
323
TreatmentOption Current Treatment Options A tumor may be considered operable but nevertheless not be operatedupon for other therapeutic reasons. If surgery is chosen, additional intervention may be indicated (e. g., adjunctive chemotherapyor radiotherapy. The options available in treating a particulartumor may be determined by the lesion and its effect on thepatient (Table 5.5). Goals.The goals of treatment-be they palliative, ameliorative, or satisfyingly cura tive-are also largely determined by the natureof the lesion and the patient's condition. In general, the ideal,immediate aim of any form of treatment is to effect a completeablation or resolution of the tumor process with no adverseaffects on the structure and function of the CNS. Also the long-termgoal is to prevent, either by surgery alone or in conjunctionwithother modalities, recurrent growth at the same or distant sites(Table 5.6).
Table 5.5 Active treatment
options
lor patients
with CNS neoplasms
Interventional,radiological procedures e. g., embolization 01 tumor arterial supply Pharmacotherapy Palliativeprocedures
Surgery Biopsy Partial
Sub-total removal Complete } Radiotherapy Conventional (external radiotherapy) Local implantation (brachytherapy) Stereotactic Proton beam - Gammaknile (radiosurgery) Chemotherapy Traditional Experimental protocols, including: intracerebra 'nd intra-arterial (withor without blood-tumor barrier modilication, Thermophototherapy Immunotherapy Genetictherapy (investigational)
Ancillaryservices Physical and occupational therapy Psychological and social services Other hospital in-patient and out-patient
services
Table 5.6 Goals 01 surgery The etiology 01neoplasms 01the CNS is unknown. In the case 01benign tumors, surgery is effective. We have to help to patients with palliative therapy. which mayoin the case 01malignant tumor, eventually result in long-term cure. Palliative therapy For increased ICP (decompression, shunt) Tumor surgery Reduction 01tumor mass effect by tumor debulking Cytoreduction and removal 01 necrotic tissue may help to reduce metabolic and biochemical effects 01the tumor This may alter the tumor growth kinetics Re establishment 01imbalanced CNS dynamics, especially 01 CSF dynamics. to help regain normal CSF circulation Reactivation 01 immunological sell-delense 01the CNS and whole body? Reduction 01the pathological effects 01the tumor Prevention 01tumor regrowth Reduction 01the size 01tumor-brain interlace in order to increase the efficacy 01nonsurgical "multimodalitytreatment" (Chemotherapy, immunotherapy, radiotherapy) Avoidance 01iatrogenic damage
Immediatetreatment 01increased intracranial pressure Externaldrainage Shuntprocedure Preoperativeembolization
Combinedtherapy - all 01 the above in various combinations pathologyand situation dictates
Curative surgery. In 1920, Dandy wrote, "There is only one satisfactory form of treatment for brain tumors, i. e., complete operative extirpation of the tumor. It is not conceivable that neoplasms of the brain ever disappear spontaneously or are cured or even benefited by any form of medical therapy." The etiology and pathogenesis of central nervous system neoplasms is stilllargely unknown, and therefore no therapy directed at the cause is currently available. Except for certain benign tumors, our attempts at curative surgery really become only palliative surgery. Still, this frequently results in a long-term remission (or cure), even for some very aggressive lesions. Presently, even with our most sophisticating imaging modalities, the precise amount of tumor that may be safely removed can only be determined at the time of operation. While our aim should always be to safely remove all tumor tissue without damage to the surrounding structures, in many situations this is not realistic. We must, however, not content ourselves too easily with the various forms of palliation, so that possible curative procedures are not even reasonably considered.
as the
324
5 Clinical Considerations
Passive careo Supportive care only (based on the individual patient's condition and lesion) may be appropriate. This may include the amelioration of pain and other symptoms with analgesics,steroids, anticonvulsants, and antidepressants, and psychological and social support of the patient and family. Observation. A delay in the therapeutic decision may be considered for several reasons: a) uncertainty as to the lesion's behavior, b) awaiting a change or improvement in the patient's general condition, and c) the patient's indecision. The relative ease of performing noninvasive CT and MRI does allow the adoption of a conservative approach involving careful follow-up. This is particularly applicable in cases of inactive, nongrowing, or slow-
growing tumors of a benign nature or in slow-growing diffuse gliomas (Case 5.0a-b). This treatment option also involves supportive care, as indicated during the period prior to eventual option selection, or until the clinical process forces a decision (e. g., emergency situations). There are definite exceptions to the practice of observation, including: tumors of foramina of Momo and fourth ventricle masses (all of which may acutely deteriorate), hemorrhagic tumors, tumors producing intractable epilepsy (especially those arising in the limbic and paralimbic areas), cranipharyngiomas, optic gliomas, meningiomas and neurinomas with progressive symptoms, and functional adenomas.
b2 Case 5.0a-b A 38-year-old female who initially suffered a transient left-sided hemiparesis 20 years ago, at the age of 17. She recovered from this with only discrete minimal residual weakness. MRI reveals a lesion within the basal ganglia, with a large cystic lesion situated in between the insula and internal capsule. No progression was demonstrated clinically or by neuroimaging and she remains asymptomatic and very active. Differential diagnosis includes dermoid and ganglioglioma. Since no guarantee could be given to remove the lesion without any additional postb4 operative deficits, she preferred to wait and see.
Treatment Option
325
AppliedMicrosurgery forExtrinsicand Intrinsic Tumors Thedevelopmentof refined microtechniqueshas contributed substantially to the surgical treatment of aneurysms and AVMS.What,then, do we see as the role of microsurgery in the treatmentof CNS tumors? Experienceover the past 26 years, has shown the microsurgical approachto be a very effective and appropriate weapon in the assaulton virtually all forms of extrinsic tumors, permitting dramaticimprovements in operative mortality and morbidity. Extrinsic tumors,particularly those in the region of the cavernous sinus, petrousbone,and parasellar and petroclival areas, seemed for a numberof years to be almost beyond the realm of surgical treatment,evenwiththe applicationof microtechniques.However, by virtueof meticulousanatomical study and persistent refinement ofsurgicalmethods, these once apparently unsurmountable barriersare being eroded. The surgical treatment of these and other basaltumors has become commonplace. Epi- and intradurallesions may be associated with a significantriskof cranialnerve injury.It is important to remember that, if thepatienthas a good chance of being cured of the tumor, or havinga usefullife prolonged, then the loss of unilateral upper cranialnerve function (1- VIII) is acceptable. On the other hand, thelossof ninth and tenth and twelfth cranial nerve function is a serious,life-threatening neurological disability for the patient. Thedecisionto remove large lesions in this area radically,subtotally,or partially should reflect this concern. Microtechnique have permitted the routine complete removalof compact and well demarcated intrinsic tumors from everypart of the brain. The removal of these tumors from even eloquentareas of the CNS is not the problem. This can be done. Usingthe physiological, pathological, radiological, anatomical, and surgical concepts presented in these volumes, the reader shouldapproach these lesions routinely with confident microsurgicalremoval.The problem with the treatment of intrinsic tumors is the nature of the tumor, the biological characteristics of the lesionsthat cause them to extend beyond the limits of microsurgeryand grow again. Even though total tumor-cell removal is not possible with present microsurgical techniques for these lesions,this approach has proved justifiable in terms of improved patientsurvivaland quality of life, and in the production of a bettersubstrate(fewertumor cells) for adjuvant therapy (Table5.8). For diffuse, infiltrating, highly malignant, or end-stage tumors,microsurgical removal can also be good treatment option. Providedthe neurological state is acceptable, it seems entirely reasonableto attempt to increase the longevity (even if for only 3-6 months)in order for the patient to afford better organization of hisor her affairs and to allow time for an adjustment to a limited future.
Table 5.8 Factors to consider in an analysis of the results of glioma surgery Mortality Neurological Morbidity (quantity, quality)
...
'.4
. r'
,
Case 5.38 Another case, but with very similar localization of the tumor within the center 01the pons, elevating the bottom 01the lourth ventricle. The tumor is partiallywell circumscribed, and the ependymallayer is intact. Biopsy was perlormed in another clinic. Histology: anaplastic astrocytoma. Clinicaldala unknown (courtesy 01 Praf. Kleihues, Neurapathologicallnstitute, University01Zurich).
Final Comments
359
Final Comments
Therecent paradigmal changes in the fields of neuroanatomy, neuropathology, neuroradiology, and neurophysiology are presented and discussed in this volume. From this knowledge essential conceptsare yielded, upon which the clinical decision making process andsurgical strategy can be based. The challenge is to evolve new visions,which may break through the present barriers and traditionalways of thinking and forge a new direction. In neuroanatomy we are eminently familiar with the centuryold sectional anatomical descriptions of topography and morphologypresented in a precise but static formo Beyond this it is becomingnecessary to develop a more interactive description of the anatomy of the central nervous system, in order to embrace the various subsystems which continually operate within the brain. This milieu is made up of the dynamic interacting components within the connective fiber tracts, vascular system, CSF pathways, neurotransmitters, immune system, neuroendocrine system,and circumventricular organs system. Only by encompassingall of the various subsystems of the brain, one can develop a more dynamic and definitive, and therefore clinically relevant neuroanatomical concept. Three-dimensional images are presentiy available, and we may soon have the advantage of a fourdimensional picture to include both time and the interwoven nature of these complex neuroanatomical concepts. A dynamic neuroanatomy will provide a basis for our understanding and interpretation of the evolving neuroimaging systems. This will surelyform the basis of the continuing evolution of modern neuroanatomy. From neuropathology we have questioned the reliability of the information given us: not from the interpretation of histopathology, but in understanding the limitations of these proceduresto impart the exact information we require as surgical specialists.We see many other characteristics of tumor systems (not onlyin malignant but also benign tumors), such as aggressiveness, invasiveness,and adhesiveness, which cannot be visualized histopathologically,but which are crucial for the surgeon as well as thepatient. Another consideration is to have reliable markers for delineation of the intrinsic tumor. In the example of intrinsic tumors,observation and experience has shown us that most of these tumors behave essentially like abscesses, in that they displace neuronal fiber systems in the early phase, rather than destroythem. Thus it is possible to often completely remove these lesions.
From neuroradiology we have witnessed an equally large eclectic spectrum of change and are excited about the accessibility and impressive resolution of these electronic photographic representations. While being enthused by the usefulness of this new technology in definition, localization, and demonstration of perilesional affects of tumors upon the brain, we have also demonstrated the limits of this present modern technology (Table 3.6, p. 202, Chapter 3). Again the most significant problem for the neurosurgeon is defining the precise margin of the lesion and understanding the significance of perilesional changes (hyperintensity of white matter) without preconceived assumptions. Furthermore the neurosurgeon should consider that only surgical exploration and dissection can reveal the real construction of a tumor and its relations to the adjacent normal structures. Not even the most sophisticated neuroimaging can demonstrate these characteristics. We all realize that the mechanical effect of tumors upon the brain is insufficient in explaining the many paradoxical situations we encounter within our daily management of patients with CNS tumors. Each generation of neurosurgeons has anecdotally shown that there is no consistent relationship between the size of a particular tumor and the clinical effects it demonstrates in a given patient. Neurophysiologists have now begun to demonstrate the many biochemical factors, which are essential for normal function at a cellular and subcellular level and how they may be influenced or usurped by disease processes such as tumors. The profound effects they bave on the individual disease process is apparent. We now realize that these cases are no longer anecdotal: they can be scientifically documented and presented as part of the CNS tumor disease process. Within this volume there are 184 case presentations, with both pre- and postoperative neuroradiological scans which demonstrate the problems we readily encounter in neuroanatomy, neuropathology, neuroradiology, and neurophysiology. An equal number will be presented in Volume IVE. Innovative concepts and ideas in fundamental and clinical neurosciences are both prerequisites and challenges for us as neurosurgeons. Many of our speciality goals have come to fruition. However, extension of our intuition and insight based on previous knowledge and experience directs us to our goal of providing the best in care for our patients. This has been the intent of Volume IVA. In Volume IVB the special surgical problems of the CNS tumors will be presented. The instrumentation, laboratory training, strategies, tactics, and techniques, as well as the approaches, results, and complications will be discussed and reviewed.
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Neurosurg. 57: 452-458, 1982 Tew,J. M., W. D. Tobler: Present status of lasers in neurosurgery. Adv. Tech. Stand. Neurosurg. 13: 3-36, 1986 lindall, G T., S. C. lindall: Pterional Approach. In: Apuzzo, M. L. J.: Surgery of the Third Ventricle. Williams & Wilkins, Baltimore, London, Los Angeles 1987 (pp. 440-461) Uttley, D., A. Moore, D. J. Archer: Surgical management of midline skull-base tumors: A new approach. J. Neurosurg. 71: 705-710,1989 Vandertop, W. P., H. J. Hoffmann, J. M. Drake, et al.: Focal midbrain tumors in children. Neurosurgery 31: 186-194, 1992 Vorkapic, P., A. Perneczky, M. Tschabitscher, et al.: Transsylvian approach to the tentoríal hiatus-anatomical remarks on Ihe microsurgical exposure. Zbl. Neurochir. 46: 2-10,1985 Voth, D.: Neurosurgery of malignant brain tumors. In: Jellinger, K.: Therapy of Malignant Brain Tumors. Springer, Wien, New York 1987 (pp. 91-129) Wallner, K. E., M. F. Gonzales, M. S. B. Edwards, et al.: Treatment results of juvenile pilocytic astrocytoma. J. Neurosurg. 69: 171-176,1988 Wieser, H. G, M. G. Ya~argil: Selective amygdalohippocampectomy as a surgical treatmen! of mesiobasallimbic epilepsy. Surg. Neurol. 17:445-457,1982 Wilkins, R. H., S. S. Rengachary: Neurosurgery Update 1. Diagnosis, Operative Technique and Neuro-Oncology. McGraw-Hill, Inc.. New York, SI. Louis, San Francisco 1990 Wilson, C. B.: A decade of pituitary microsurgery. The Herbert Olivecrona Lecture. 1.Neurosurg. 61: 814-833, 1984 Wright, J. E., A. A. McNab, W. 1. McDonald: Optic nerve glioma and management of optic nerve tumous in the young. Br. J. Ophthalmol. 73: 973-874, 1989 Ya~argil, M. G: Microsurgery Applied to Neurosurgery. Thieme, Stuttgart 1969 Ya~argil, M. G: Subokzipitale-transmeatale mikrotechnische Exstirpation des AkustikusNeurinomas. In: Naumann, H. H.: Kopf- und Hals-Chirurgie. Thieme, Stuttgart 1976(pp. 545-587) Ya~argil, M. G: Mikrochirurgie der Kleinhirnbrückenwinkel-Tumoren. In: Plester, D.. S. Wende, N. Nakayama: Kleinhirnbrückenwinkel-Tumoren: Diagnostik und Therapie. Springer, Berlin, Heidelberg, New York 1978 (pp. 215-257) Ya~argil, M. G: Microsurgery. AVM of the Brain. Vol. IV. A. Thieme, Stuttgart, New York 1984- I987 Ya~argil, M. G., C. D. Abernathey, A. C. Sarioglu: Microneurosurgical treatment of intracranial dermoid and epidermoid tumours. Neurosurgery 24: 561-569,1989 Ya~argil, M. G, M. Curcic, M. Kis, et al.: Total removal of craniopharyngiomas. Approaches and long-term results in 144 patients. J. Neurosurg. 73: 3-11,1990 Ya~argil, M. G, J. L. Fox: The microsurgical approach to acustic neurinomas. Surg. Neurol. 2: 393-398, 1974 Ya~argil, M. G, R. W, Mortara, M. Curcic: Meningiomas of basal posterior cranial fossa.Adv. Tech. Stand. Neurosurg. 7: 115, 1980 Ya~argil, M. G., A. C. Sarioglu, T. E. Adamson, et al.: Surgical techniques in the management of colloid cySISof the third ventricle. Adv. Tech. Stand. Neurosurg. 17: 133-157, 1990 Ya~argil, M. G., R. D. Smith, J. C. Gasser: Microsurgical approach to acustic neurinomas. Adv. Tech. Stand. Neurosurg. 4: 93-100, 1977 Ya~argil, M. G, P.J. Teddy, P. Roth: Selective amygdalohippocampec!omy. Operative anatorny and surgical technique. Adv. Tech. Stand. Neurosurg. 12:93-123,1985 Ya~argil, M. G., P.J. Teddy, P. Roth: Combined approaches. Surgery of !hird ventricle. Chapter 19. In: M. L. J. Apuzzo: Surgery of the third Ventricle. Williams & Wilkins, Baltimore, London, Los Angeles 1987 (pp. 462-475) Ya~argil, M. G, K. von Ammon, E. Cavazos, et al.: Tumors of the limbic and paralimbic systems. Acta Neurochir. (Wien) 118:40-52,1992 Ya~argil, M. G, K. von Ammon, A. von Deimling, et al.: Central neurocytoma: Histopathological variants and therapeutic approaches. J. Neurosurg. 76: 32-37,1992 Yasui, T., A. Hakuba, S. O. Kim: Trigeminal neurinomas: Operative approach in eight cases.1. Neurosurg. 71: 506-511,1989
I :t.1
I
387
Index Bold numbers refer to figure legends. Vs. (versus) indicates a differential diagnosis.
A
abducens nerve, see nerves abscess effects on CNS, 275 parasplenial area, 232 purulent, temporo-occipital area, 231 thalamus, 306 acoustic neurinoma, 226 cerebellopontine angle, 240, 241, 242,288,290 vs. meningioma, 225 acoustic radiation, 68 adenocarcinoma, occipital, metastatic, 281 adenoleukodystrophy, 245 adenoma occurrence pattern, 149 pituitary, 119, 125 adherence, 147-8 absence, epidermoid tumor, 291 cerebellopontine angle acoustic neurinoma, 241 parachiasmal craniopharyngioma, 239 sphenopetroclival meningioma, 286 adhesiveness, of tumors, 147-8 adjuvant therapy, 153, 296, 306, 335, 359 adults. most common tumors, 119 Ag-NORs (antigen nucleolar organizer regions), 120 AIDS, sequelae, and imaging techniques, 201 allocortex areas, 18 introduction of term, 7 alpha-fetoprotein, 271 amblyopia with epidermoid tumor, 331 with sphenopetroclival meningioma, 327 with third ventricular astrocytoma, 334 amenorrhea, with sphenopetroclival meningioma, 326 y-aminobutyric acid (GABA), 271, 272,273 amygdala ganglioglioma, 161 pilocytic astrocytoma, 186 relationship to basal ganglia, 138 anatomy, 1-14 brain as dynamic unit, 18 cascade structure, 26 centrallobe, 44-7 cerebellum, 81-94 cerebrum, 14-80 MRI correlation, 73-80 concluding summary, 114 frontal lo be, 39-44 gyri, 20-4 and clinical examinations, 24
and imaging techniques, 2 infratentorial, 81-94 inside-out approach, 14,26,27 insular lobe, 53-7 limbic lobe, 57-64 lobar, 39-60 and lobar terminology, 17, 114 and neuroimaging, 114 occipitallobe, 49-51 parietallobe,47-9 sulci, 19-20 and MR imaging, 20 temporal lobe, 52-3 vascular, 95-113 white matter, central zone, 65-8 Anderson, w'A., 195 aneurysm, basilar, 227 angioarchitecture, cerebral venous system, 110 angiogenesis, and tumor pathology, 121 angiography, 148-9,207 cerebral, history, 194 see also MRA angioma, 303 angular gyrus, meningioma, 297 anisocoria, with sphenopetroclival meningioma, 286 anorexia, with optic glioma, 332 anosmia, with meningioma, 236 anterior choroidal artery, supply to projection fibers, 36 anterior commissure, in embryo, 10 antigen nucleolar organizer regions (Ag-NORs),120 antilocalizationalists, 250 apathy with cingulate gyrus glioblastoma, 169 with inoperable neuroectodermal tumor, 357 with meningioma, 217 with parasplenial abscess, 232 apraxia, with insular glioma, 164 arachnoid, and imaging difficulties, 204,205,206 arachnoiditis, and pseudocapsule formation, 204 arbor vitae, cerebellum, anaplastic astrocytoma, 300 archicerebellum, 82 archicortex, insular lobe, 54 archicortical are as, 18 arcuate fibers, 32 area maps, human cortex, 277 Brodmann, 69 Duvernoy, 69 von Economo, 70-2 area postrema, 266, 267 areas, of telencephalon, 18 arginine vasopressin (AVP), 266 arm, ataxia, with brainstem and cerebellar epidermoid tumor, 291 arms, connective inferior frontal gyrus, 22 superior frontal gyrus, 22
PICA,86 and cerebral tissue herniations, 252 medulla oblongata, 106 and medullary hemangioblastoma, 314 territory, 96 territory in cerebellum, 94 pituitary gland, 104 pons, 106,106, 108 posterior cerebral, see PCA above posterior communicating, see PCoA above
Arnold, F., 16 arterial supply corpus callosum, 35 projection fibers, 36 arteries, 95, 95-108 ACA, 96 basal ganglia, 102 and cerebral tissue herniations, 252 internal AChoA
capsule,
103
basal ganglia, 102 internal capsule, 103 thalamus,I03 AICA,86 and cerebral tissue herniations, 252
posterior inferior PICA above
basal ganglia, 102-3 basilar, territory, 96 brainstem, 104, 105 central, 98 central nuclei, 102-3 cerebellar tumors, blood supply, 99-101 cerebellum, 104, 105 cerebral, supply to projection fibers, 36 and cerebral tumors, 99-101 cerebrovascular system, 263 circle of Willis, 263 CNS arteriovenous system, 264 hypothalamus, 104 ICA
internal capsule, 103 medulla oblongata, 106, 107, 108 midbrain, 105, 105, 108 middle cerebral, see MCA above PCA basal ganglia, 103 and cerebral tissue herniations, 252 internal capsule, territory, 96 PCoA
103
basal ganglia, 103 thalamus, 103
see
recurrent (Heubner), putamen, 102 SCA, 86 adherence of meningioma, 286 basal ganglia, 103 pons, 106 territory, 94, 96, 97 in sulci, 98 superior cerebellar, see SCA above thalamus, 103-4 tumor vascularity, 148 white matter, 27 see also mean arterial pressure arteriovenous malformations, 207 effects on CNS, 275 aspiration pneumonia, with pontine cavernoma, 355 association areas, structure, 18 association fibers, 32, 33 in cerebral white matter, 26 cingulum and cerebral cortex, 58 association systems, 6 astrocytoma, 119, 127 anaplastic, 217 fourth ventricle, 353 fronto-orbital region, 184 hippocampus and parahippocampus, 163 inferior and middle frontal gyri, 294
medulla oblongata, 106 pons, 106 territory, 94, 96 angiogenesis, and tumor pathology, 121 anterior cerebral, see ACA above anterior choroidal, see AChoA above anterior inferior cerebellar, see AICA above
globus pallidus, 102 internal capsule, 103 internal carotid, see ICA above internal choroidal, adherence of meningioma, 286 lenticulostriate, 56, 96 leptomeningeal, in sulcus, 98 limbic and paralimbic areas, 136 MCA, 55, 96 basal ganglia, 102 and cerebral tissue herniations,
cerebellar,
252
inferior parietal lo bu le, 159 inoperable, 356, 358 insula, 166 limbic lobe, 168, 339 vs. meningioma, 218 mesencephalon, 308 neocerebral, 154 parahippocampus, 300 posterosuperior frontal gyrus, 180 temporallobe, 161, 280 cystic, posterior cerebellum, 287 diffuse, 175 effects on CNS, 275 fibrillary inferior temporal gyrus, 181 insula, 165 and hamartoma, parahippocampus, 216 hypothalamus, 334 intermediate growth phase, 133 intraventricular, 142 neocerebral, 156
388
Index
occurrence pattern, 149 parietallobe, 335-6 pilocytic, 213, 215 amygdala, 186 with dermoid cyst, 214 infratentorial area, 229, 230 internal capsule, 171, 172 intraventricular, 342, 343 parachiasmal region, 212 pontomesencephalic area, 310 precuneus, 157 retrolenticular region, 173 piloid medulla oblongata, 312, 313 mesencephalon, 309 pleomorphic, 219 temporal lo be, 282 thalamus, 176 astroglial neoplasm, 119 astroglial network, and tumor growth, 132 ataxia with cerebellopontine angle acoustic neurinoma, 241 with infratentorial dermoid tumor, 229 with infratentoriallipoma, 229 with mesencephalic anaplastic astrocytoma, 308 with mesencephalic cavernoma, 305 with multiple lesions, 187 with septal neurocytoma, 182 with tentorial meningioma, 238 aura, olfactory, with meningioma, 237 autonomic function, 267-8 autonomic system, 274 autoregulation, cerebral blood flow, 263-4 AVP (arginine vasopressin), axial sulci, 20 axon, in neurogenesis, 12
266
B Baillarger, lO.E, balance loss with parapineal 225
4 medulloblastoma,
with pontomesencephalic pilocytic astrocytoma, 310 with retrolenticular astrocytoma, 173 barriers, protective, 258 basal ganglia, 14 arterial supply, 102-3 introduction of term, 6 movements, 261 relationship to amygdala encephalon, 138 tumors, 139-42
and pros-
blood-extracellular
fluid barrier, 258
bone scanning, iso tope, 196 borderline, brainstem, 141 borders, of telencephalon, 16 boundaries, of tumors, see demarcation brain action during systole, 261 cortical zones, 127 depictions by Ecker, 5 depictions by Retzius, 6 displacement, case studies, 280-91 divisions, 14,14-15 as dynamic unit, 18 early depictions, 3-4 embryo, 9, 10 fetus, 8, 11 immunomodulation, 274 interaction with tumor, 277 maca que, 138,272 mapping, see are a maps small, see rhinencephalon subdivisions, 15 triune, 126 use of landmarks, 24 venous drainage, 109, 110 brain plate, 8 brain scanning, isotope, 196 brainstem anatomical definition, 14 blood supply, 104, 105 distortion, 282, 283, 336 with angular gyrus meningioma, 297 with middle cranial fossa meningioma, 287 with temporal fossa ganglioglioma, 285 epidermoid tumor, 291 gliomal growth pattern, 140 place in brain structure, 15 tumors, predilection sites, 142 vascular territories, 97 brain structure, history of research, 3-7 brain-tumor interface, 147-8 Broca areas, 41 and neocortical telencephalon, 18 Brodmann areas, 69-70, 126 and cuneus, 50 and lingual gyrus, 50 and neocortical telencephalon, 18 and occipital gyri, 50 and paracentral gyrus, 46 and postcentral gyrus, 47 and temporal gyri, 52 bromodeoxyuridine labeling index, 120 bronchial carcinoma, metastatic, 243 BUDR labeling index, 120 buffering system, intracranial, 254, 258-9 Burdach, E, 4 butterfly lesions, 202
Bell,c., 4 biology CNS tumors, 117 and tumor research, 116 Blalock- Taussig shunt, status after, 306 bias toma, pineal, vs. primitive neuroectodermal tumor, 224 blindness with optic glioma, 332 with sellar optic glioma, 333 see a/so visual deficits blood cerebral flow, 263 circulation in brain, 257 blood-brain barrier, 273 blood-CSF barrier, 258
e cachexia, with intraventricular pilocytic astrocytoma, 342 calcarine sulcus, 10, 19 callosal body, in embryo, 10 callosal fibers, 34 callosal sulcus, 10, 19 capsula extrema, 68 capsula interna, 65, 66 capsula externa, 65, 68 carcinoma, bronchial, metastatic, 243
cascade structure anatomical, 26 white matter, 38 accuracy in tumor localization, 122 cases, suitable, 320 case studies clinical aspects, 326-58 neuroimaging, 209-45 neuropathology, 154-91 neurophysiology, 280-315 categorization of tumors, 122-3 caudate nucleus arterial supply, 102 gliomal growth pattern, 140, 141 cauliflower substructure, cerebral white matter, 26, 27 cautery loop, for tumor removal, 341,346 cavernoma mesencephalon, 305 neocerebral, 157 parietallobule, 303 pons,311,354,355 precentral gyrus, 302 third ven tricle, 188 CBF, see cerebral blood flow cell kinetics, tumors, 120 cellular function unit, 6 cellular response patterns, in CNS, 277 central lo be, 16, 17,45,46,47 anatomy, 44-7 gyri, 46-7 insular surface, 43 projection fibers, 36 central nuclei, tumors, 139-42 central sulcus, 23, 44 continuity rate, 19 in embryo, 9 cerebellar hemispheres, 84-5 cerebellar peduncles, 82, 88, 90, 91-2 cerebellomedullary fissure, 86 cerebellomesencephalic fissure, 86 cerebellopontine angle acoustic neurinoma, 226, 240, 241, 242,288,290 chordoma, 228 differential diagnosis, 225-8 ependymoma, 227 melanoma, 227 meningioma, 225, 226 metastatic carcinoma, 227 cerebellopontine fissure, 86 cerebellum, 14 afferent pathways, 93 anatomy, 81-94 arbor vitae, astrocytoma, 300 arterial supply, 94 blood supply, 104, 105 borders, 85 connections, 92 divisions, 81 efferent pathways, 93 embryogenesis, 8 epidermoid tumor, 291 fissures, 86-7 folia, 89 hemispheres, 84-5 intrinsic tumors, predilective sites, 93,94 lobes and lobules, 81, 82, 82-3 peduncles, 88, 90, 91-2 posterior, cystic astrocytoma, 287 posterior inferior, meningioma, 288 precentrallobule, 88 projection fibers, 90 sulci, 86, 87 surfaces, 83, 84, 84 surgical divisions, 14 vascular terri tories, 97
white matter, 88, 88-93, 90 contents,90 see a/so vermis cerebral blood flow (CBF), 263 autoregulation, 263-4 cerebral cortex, 14 connections to thalamic nuclei, 36 neurophysiology, 250-1 cerebral edema pathophysiology, 255-6 types, 255 cerebral hemispheres, 14,48,56,57 borders, 16 embryogenesis, 8 gyri, 21 cerebrallobes, 16-18 cerebral perfusion pressure (CPP), 263,265,276 cerebrospinal fluid, see CSF cerebrovascular system, 262-5 tumor effects, 265 cerebrum anatomy, 14-80 MRI correlation, 73-80 summary, 69-70 surgical conception, 17 surgical divisions, 14 tumors, symptoms and signs, 251 vascular system, 95-113 veins angioarchitecture, 110 synopsis, 109 white matter, 25, 25-39 children, most common tumors, 119 cholinergic neurotransmitters, 272 cholinergic system, 272 chondroma, occurrence pattern, 149 chordoma, 330 cerebellopontine angle, 228 occurrence pattern, 149 choroid plexus, 266 intraventricular papilloma, 142 chromosome abnormalities, and tumor, 120 chromosomes, abnormal, 153 cingulate fibers, in cerebral white matter, 26 cingulate gyrus, 62, 62 anaplastic astrocytoma, 168 connective arms, 63, 64 giant-cell glioblastoma, 169 mixed oligoastrocytoma, 170 cingulate pole, 62, 63 cingulate region, cytoarchitecture, 63,64 cingulate sulcus, 44, 47 continuity rate, 19 in embryo, 10 circle of WilIis, 263 circumventricular organs (CVOs), 265-7,266 pathophysiology, 267 Clarke and Dewhurst, on history of brain research, 3-7 classification of tumors, history, 116 claustrum, 68 cleavage of tumors, see demarcation clinical considerations, 317-59 clivus, preoperative erosion, 228 CNS (central nervous system), 273-8 arteriovenous system, 264 cellular response to injuries, 277 compartments, 253 disease pathophysiology, 274-7 patterns, 149 spectrum of effects, 275 functional subsystems, 248, 249 imaging, 277 interaction with neurological disease, 276
Index interaction with tumors, 249, 277 neurotransmitters, 273 pathophysiology,274 physiology, general conclusions, 278-9 tumors, see tumors collateral sulcus, continuity rate, 19 colloid cyst, intraventricular, 142 commissural fibers, 32, 33, 34 cascade structure in white matter, 38 in cerebral white matter, 26 coursing with projection fibers, 36 dissection, 37 commissural system, embryogenesis, 10 commissure, anterior, in embryo, 10 compartments, CNS, 253 complete sulci, 20 computed tomography, see CT connective fibers limbic lobe, 57 telencephalon, 32 in white matter sectors, 29 white matter subsystems, 32-8, 33 convergence, loss, with glioblastoma, 223-4 corneal reflex, diminished, with acoustic neuroma, 289 corpus callosum, 34, 34-5, 35 and cingulate gyrus, 63 vascularization, 35 corpus cerebelli, 82 cortex area maps, 69-73 cerebral, 14 cortical are as, functional, 250 cortical blood flow (CoBF), 263 cortical surfaces, 16 corticospinal fibers, cascade structure in white matter, 38 corticospinal tract, internal capsule, 68 corticostriopallidothalamocortical fiber system, 36 corticothalamic-thalamocortical
a
fiber system, 36 CPP, see cerebral perfusion pressure cranial nerves, see nerves craniopharyngioma adherence, 148 epidural, 210 and hypothalamic function, 270 occurrence pattern, 149 parachiasmal, without perilesional changes, 239 third ventricle, 211 crossbrain, see metencephalon CSF (cerebrospinal fluid), 256-62 circulation in brain, 257 and hydrocephalus cIassification, 260 neurons,273 outflow pathways, 257 secretion, 258 CSF pathways, transcerebral, 30 CSF rhinorrhea, and bone scanning, 196 CT (computed tomography), 318 compared with MRI, 198 current neuroimaging, 197-200 emission,196-7 and functional changes, 202 history, 194-5 peritumoral changes, 146 xenon, 196 see a/so PET, SPECT cuneus, 47, 49, 50,51,62 ganglioglioma, 160 curative surgery, 323 cure genuine vs. surgical, 153 surgical, 323
Cushing, H., 318, 319 quoted,258 CVOs, see circumventricular organs cysticercosis, and imaging techniques, 201 cytoarchitecture cingulate region, 63, 64 insular lobe, 54 cytogenetic studies, 153 cytotoxic edema, 255, 255
D
discrepancies, cIinical state vs. neurological deficit, 308-15 di sioca ti o n effect, tumor imaging, caution in interpretation, 208 disorientation with glioblastoma, 223-4 with temporo-occipital purulent abscess, 231 dizziness with amygdala tumor, 161 with encephalomalacia, 235 with incisural meningioma, 222 with infratentorial dermoid tumor, 229 with internal 171
Dandy, w., 194 da Vigevano, G., 3, 4 decision-making cIinical, 319-20, 359 operability, 321-2 time-capability approach, 319 deficits, cIinical, and neuroimaging, 318 demarcation, of tumors, 146-7, 147, 151,206-7 caution in interpretation, 208 deceptiveness, 147 imaging, 203, 204-7 demyelination, CNS, 149 density changes, in imaging, and tumor infiltration, 145 dentate gyrus, 58 dermoid cyst, with pilocytic astrocytoma, 214 dermoid tumor cystic, frontallobe, 292 effects on CNS, 275 infratentorial, 229 occurrence pattern, 149 de Vieussens, R., 3 diabetes insipidus, and pineal tumors, 271 diagnosis, traditional methods, 318 diaphragma sella e, restraining pituitary adenoma, 125 diaschisis, 250 diencephalon, 14 embryogenesis, 8 piloid astrocytoma, 332 place in brain structure, 15 differential diagnosis cerebellopontine angle, 225-8 meningioma vs. glioblastoma, 217-20 neoplastic vs. other disease processes,231-5 neuroimaging, 209-35 parapineal tumors, 221-4 perilesional changes, 235-45 diplopia with acoustic neurinoma, 290 with angular gyrus meningioma, 297 with cingulate gyrus glioblastoma, 169 with cIival chordoma, 330 with fourth ventricular tuberculoma, 233 with fronto-orbital glioblastoma, 167 with infratentoriallipoma, 229 with inoperable tumor, 358 with internal capsule astrocytoma, 171 with intraventricular lesion, 220 with pleomorphic xanthoastrocytoma, 301 with plexus papilloma, 223 with primitive neuroectodermal tumor, 224 with septal neurocytoma, 182
capsule
with parapineal 225
astrocytoma,
medulloblastoma,
with parapineal meningioma, 221 with pilocytic astrocytoma, 213 with primitive neuroectodermal tumor, 224 with temporal fossa anaplastic ganglioglioma, 285 drinking, 270 drowsiness with diencephalic piloid astrocytoma, 332 with thalamic abscess, 306 see a/so fatigue; sleep attacks; somnolence dura and imaging difficulties, 204, 205, 206 not visible on neuroimaging, 210 Duvernoy, area map, human cortex, 69 dysacusis, with limbic lobe astrocytoma, 166 dysarthria with inoperable neuroectodermal tumor, 357 with pilocytic astrocytoma, 172 dysdiadochokinesia with intraventricular astrocytoma, 347 with limbic lobe astrocytoma, 168 with medullary piloid astrocytoma, 312 with parietal glioblastoma, 295 with retrolenticular astrocytoma, 173 dysesthesia facial with cerebellopontine angle chordoma, 228 with cerebellopontine angle melanoma, 227 with cerebellopontine angle meningioma, 225, 226 with endotheliomatous meningioma, 242 with sphenopetroclival meningioma, 329 with limbic lobe astrocytoma, 166 with parietallobule cavernoma, 303 with superior parietallobule tumor, 156 dysmenorrhea, with intraventricular fibrillary meningioma, 341 dysmetria with cerebellar meningioma, 288 with infratentorial dermoid tumor, 229 with parapineal 225
medulloblastoma,
with pontomesencephalic pilocytic astrocytoma, 310 with retrolenticular astrocytoma, 173 with superior temporal gyrus oligoastrocytoma, 299
389
dysphasia with anaplastic astrocytoma, 217 improvement after surgery, 172, 214 with insular glioblastoma, 178 with neocerebral tumor, 159 with parahippocampal anaplastic astrocytoma, 300 with parietal glioblastoma, 295 with parietallobule astrocytoma, 218 with pontine cavernoma, 355 sensorimotor, with insular oligodendroglioma, 335 with sphenopetroclival meningioma, 329 with superior temporal gyrus oligoastrocytoma, 299 with Sylvian fissure meningioma, 235
E eating behavior, 268, 270 echo-planar MRI, 197 Ecker, A., 4 Economo, C. von, 6, 7, 114 area maps, human cortex, 70-2 ectoderm, 8 edema cerebral, pathophysiology, 255-6 cytotoxic, 255, 255 hydrostatic, 256 interstitial, 255, 256 neuroimaging, 200, 243-4 peritumoral,148 and tumor pathology, 121 vasogenic, 255, 255 eloquent areas, lack of expected deficits, case studies, 292-300 embryo, brain, 9, 10 embryogenesis, 8 embryology, 8-13 and cortical structure, 18 encapsulation, of tumor, 147 encephalitis, effects on CNS, 275 encephalography, contrast, history, 194 encephalomalacia, 237 vs. glioma, middle frontal gyrus, 235 encephalon, see brain endbrain, see telencephalon endocrine abnormalities with epidermoid tumor, 331 postoperative, 332 with sellar optic glioma, 333 endotheliomatous meningioma, pontomedullary junction, 242 environmental factors, and primary brain tumors, 119 ependymoma cerebellopontine angle, 227 intraventricular, 142 medulla oblongata, 315 occurrence pattern, 149 epidemiology, 119 CNS tumors, 117 and tumor research, 116 epidermoid tumor, 331 brainstem, 291 cerebellum, 291 effects on CNS, 275 occurrence pattern, 149 epilepsy effects on CNS, 275 focal, with parietallobule cavernoma, 303 with fronto-orbital anaplastic astrocytoma, 184
390
Index
grandmal with diffuse oligoastrocytoma, 175 with inferior temporal gyrus astrocytoma, 181 with multiple lesions, 188, 190 with superior frontal gyrus tumor, 154 with superior temporal gyrus oligodendroglioma, 298 with temporallobe astrocytoma, 161 with temporallobe glioblastoma, 177 with inferior parietallobule tumor, 159 with insular oligodendroglioma, 335 with intraventricular pilocytic astrocytoma, 342 lacksonian with inferior frontal gyrus tumor, 155 with local thrombophlebitis, 307 with precentral cavernoma, 302 with recurrent anaplastic astrocytoma, 180 with limbic anaplastic astrocytoma, 339 with metastatic bronchial carcinoma, 243 with oligodendroglioma, 337 with opercular glioblastoma, 179 partial complex, with temporal lobe astrocytoma, 282 petit mal with cingulate gyrus oligoastrocytoma, 170 with fourth ventricular tuberculoma, 233 with septal oligodendroglioma, 209 with temporallobe xanthoastrocytoma, 162 with temporal fossa anaplastic ganglioglioma, 285 with thalamic astrocytoma, 176 Erasistratus of Alexandria, 3 erb-b 2 oncogene amplification, 120 Ernst, R., 195 examination, 318 exophthalmus, with sphenopetroclival meningioma, 327 external capsule, 65, 68 extraceJlular fluid (ECF), 256 extrinsic tumors biology, 151 categories, 124 definition, 122 demarcation, 204-5 growth patterns, 123-5 and herniation, 253 imaging, 203 vs. in trinsic infratentorial area, 228-30 parachiasmatic area, 209-17 microsurgery, 325 neuropathology, 123-4 sudden aggression, 145 topography, clinical considerations, 321
F facial dysesthesia with cerebeJlopontine doma, 228 with cerebeJlopontine melanoma, 227
angle chorangle
with cerebeJlopontine angle meningioma, 225, 226 with endotheliomatous meningioma, 242 with sphenopetroclival meningioma, 329 facial nerve, see nerves falx, meningioma perilesional changes, 245 vs. tuberculoma, 233 fatigue with internal capsule astrocytoma, 171 with parahippocampal anaplastic astrocytoma, 300 with pulvinar thalami glioblastoma, 183 see a/so drowsiness; sleep attacks; somnolence fetus, brain, 8, 11 fibers, in cerebral white matter, 26
25,
fibrillary astrocytoma, mesencephalon, 351 fibroma, occurrence pattern, 149 fissure of Rolando, 4, 16 fissures cerebeJlar, 82, 86-7 see a/so Sylvian fissure Flechsig, P.E., 6 flocculonodular lobe, 82 flow cytometry, 120 flow voids, MRI, and tumor vascularity, 148 folia, cerebeJlum, 90 food intake, 268, 270 foramen of Magendie, 87 forebrain, see prosencephalon Forel, A., 6 forgetfulness, progressive, with multiple lesions, 186 fornix embryogenesis, variations, 35 fossa
10
middle cranial, meningioma, 287
283,
temporal, anaplastic ganglioglioma, 285 Fourier NMR spectroscopy, 195 fourth ventricle, 87 anaplastic astrocytoma, 353 deviation with pontine cavernoma, 311 displacement, 291 in embryo, 10 lipoma, 229 meduJloblastoma, 352 plexus papilloma, 228 tuberculoma, 233 tumors, 144, 352-3 frontal area, meningioma, 217 frontal gyri, 21, 40 gyrus rectus, 43, 62 variations, 44 inferior, 22, 41, 41 anaplastic astrocytoma, 294 low-grade glioma, 292 meningioma, 293 orbital part, 21, 22 specimen after removal, 43 transverse gyri, 41 triangular part, 21, 22, 294 variations, 42 see a/so opercular medial, 41, 62 middle, 22, 40, 41, 41 anaplastic astrocytoma, 294 glioma vs. encephalomalacia, meningioma, 293 variations, 42 orbital gyri, 43
parietal operculum, oligoastrocytoma, 299 superior, 22, 40, 40, 41, 45 anaplastic astrocytoma, 154, 180 transverse gyri, 41 frontal lo be, 16,17,22 anatomy, 39-44 and Brodmann areas, 69 cystic dermoid tumor, 292 insular surface, 43 MRI anatomical correlation, 78-9 projection fibers, 36 surface, 39 vascularization, 102 frontal poi e, in embryo, 10 frontal sulcus inferior, continuity rate, 19 intermedia te, incidence rate, 19 medial, incidence rate, 19 superior, continuity rate, 19 frontal syndrome, with cystic dermoid tumor, 292 fronto-orbital gyri, variations, 44 fronto-orbital region anaplastic astrocytoma, 184 glioblastoma, 167 frontopontine fibers, casca de structure in white matter, 38 functional disturbances, and hypothalamic disturbance, 270 fusiform gyrus, see temporo-occipital gyrus, lateral
G GABA (y-aminobutyric acid), 271, 272,273 gadolinium DTPA contrast, 199 gait abnormality, with oligoastrocytoma, 299 gait apraxia with cerebeJlar cystic astrocytoma, 287 with cerebeJlopontine angle acoustic neuroma, 289 gait ataxia with brainstem and cerebeJlar epidermoid tumor, 291 with cerebeJlar meningioma, 288 with cerebeJlopontine angle acoustic neurinoma, 290 with diencephalic piloid astrocytoma, 332 with fourth ventricular anaplastic astrocytoma, 353 with fourth ventricular meduJlo-
235
blastoma, 352 with infratentorial pilocytic astrocytoma, 229 with inoperable tumor, 358 with intraventricular pilocytic astrocytoma, 347 with mesencephalic piloid astrocytoma, 309 with third ventricular astrocytoma, 334 galactorrhea, with sphenopetroclival meningioma, 326 GaJl, EJ., 6 ganglioglioma amygdala anaplastic vs. meningioma, 285 temporal fossa, 285 cuneus, 160 occurrence pattern, 149 Gd-DTPA,199 genetic expression, tumors, 120-1 two-hit concept, 126, 153
genu of internal capsule, 66 germinoma, 271 Gerstmann's syndrome with inferior parietallobule tumor, 159 with parieto-occipital cerebral infarction, 234 Glasgow coma score, 259 glial cell, embryogenesis, 12-13 glia limitans, 123 glial systems, 250-4 glioblastoma vs. abscess parasplenial area, 232 parietallobe, 231 diffuse, 174 effects on CNS, 275 fronto-orbital region, 167 giant-ceJl, cingulate gyrus, 169 growth phases intermediate, 132, 133 late, 134 inferior parietallobule, 295 insula,178 vs. meningioma, 217-20 multiple, 184, 185 neuroimmunotherapy, 274 occurrence pattern, 149 peritumoral changes, 146 precuneus, perilesional changes, 244 pulvinar thalami, 183, 345 perilesional changes, 244 vs. purulent abscess, temporooccipital area, 231 superior temporal gyrus, 296 temporal lo be, 177, 284 vs. teratoma, 223-4 glioblastoma multiforme, 119, 121 histologic diagnosis, 183 survival in grade IV, 121 see a/so astrocytoma glioblastomas, adherence, 148 glioma, see tumors and specific tumor types globus paJlidus, arterial supply, 102 glomus tumor, occurrence pattern, 149 Golgi, c., 6,116 granuloma, and imaging techniques, 201 Gratiolet, L.P., 4, 46 gray matter, 14 great horizontal fissure, cerebellum, 86 growth kinetics, tumors, 119-20 gyral convolutions, embryogenesis, 8 gyralsegments,28,28,29 vascularization pattern, 30 gyralsegmentscheme,24 gyri anatomy, 20-4 and clinical examinations, 24 areas for MRI analysis, 73 centrallobe, 46 in cerebral hemisphere, 21 continuum concept, 24 frontallobe, classification, 40 hemispheric, features, 24 interdigitations,21 and lobes, 16, 17 occipital, 49-51 temporallobe, 52 transverse, 23 in frontal sulci, 22 types, 20 vascularization, 102 see a/so specific gyri gyrus rectus, 43, 62 variations, 44
Index
H
hemangioblastoma medulla oblongata, 314 occurrence pattern, 149 hematoma
Haemophilus parainfluenzae, and thalamic abscess, 306 hamartoma, effects on CNS, 275
effects on CNS, 275 thalamus, 304 hemianopsia bitemporal, with epidermoid tumor, 331 with multiple lesions, 187 with optic glioma, 332 with parachiasmal astrocytoma, 212
hamartoma-astrocytoma, parahippocampus, 216 Harvey, W., 112 headache abscess, thalamic, 306 acoustic neurinoma, 226 adenocarcinoma metastatic occipital, 281 temporal poI e, 243 astrocytoma cerebellar cystic, 287 diffuse anaplastic, 179 infratentorial pilocytic, 230 intraventricular pilocytic, 342, 343 limbic lobe, 168 mesencephalic anaplastic, 308 mesencephalic piloid, 309 parietal anaplastic, 335-6, 336 recurrent anaplastic, 180 temporal lo be, 280 cavernoma, pontine, 311, 354 chordoma, clivus, 330 craniopharyngioma, third ventricle, 211 dermoid tumor, infratentorial, 229 encephalomalacia, 235 ganglioglioma, temporal fossa, 285 glioblastoma, 223-4 cingulate gyrus, 169 diffuse, 174 fronto-orbital, 167 multiple, 184 parietal, 231 precuneus, 244 superior temporal gyrus, 296 temporallobe, 284 hemangioblastoma, medullary, 314 hypernephroma, metastatic, 243 intraventricular lesion, 220 lipoma, infratentorial, 229 medulloblastoma, fourth ventricle, 352 meningioma angular gyrus, 297 falx, 245 incisural, 222 middle cranial fossa, 287 parapineal, 221 sphenopetroclival, 286, 328 temporal pole, 244 tentorial, 238 multiple lesions, 186, 187 neurocytoma, intraventricular, 343 oligodendroglioma, 219 limbic, 338 pulvinar, 345 optic glioma, sellar, 333 plexus papilloma, 223 infratentorial, 228 primitive neuroectodermal 176,224
tumor,
telangiectasia, thalamic, 304 xanthoastrocytoma, pleomorphic, 301 hearing deficit acoustic neurinoma, cerebellopontine angle, 290 acoustic neuroma, cerebellopontine angle, 288, 289 with epidermoid tumor, brainstem and cerebellum, 291 with sphenopetroclival meningioma, 329 see a/so tinnitus
with parachiasmal craniopharyngioma, 239 with parieto-occipital cerebral infarction, 234 with pilocytic astrocytoma, 215 with pulvinar glioblastoma, 183 with pulvinar oligodendroglioma, 345 after surgery for fibrillary astrocytoma, 181 with temporal fossa anaplastic ganglioglioma, 285 with temporallobe glioblastoma, 177,284 with tentorial meningioma, 238 hemihypesthesia, with thalamic tela ngiectasia, 304 hemiparesis with cerebral infarction, 234 with insular oligodendroglioma, 335 with intraventricular fibrillary meningioma, 341 with limbic oligodendroglioma, 340 with mesencephalic anaplastic astrocytoma, 308 with mesencephalic cavernoma. 305 with mesencephalic fibrillary astrocytoma, 351 with mesencephalic piloid astrocytoma, 348-9, 350 with pilocytic astrocytoma, 215 with pontomesencephalic pilocytic astrocytoma, 310 postictal with parietal glioblastoma, 295 with precentral cavernoma, 302 with pulvinar thalami glioblastoma, 183, 244 with temporal fossa anaplastic ganglioglioma, 285 with temporo-occipital purulent abscess,231 with thalamic abscess, 306 hemispheres cerebellar,84-5 cerebral, see cerebral hemispheres hemorrhage, acute, case studies, 301-7 Henson's node, 8 herniation, 251-4, 260 extra-axial, 253 frontal areas, 253 intra-axial. 253 severe without neurological deficits, 283 with temporallobe glioblastoma, 284 syndromes, compartments involved, 201 tonsillar, with cerebellar cystic astrocytoma, 287 Heschl's gyri, 21, 23 anaplastic oligodendroglioma, 298 hindbrain, see rhombencephalon hippocampo-mamillo-thalamocingulate circuito 58
hippocampus, 18, 58 anaplastic astrocytoma, 163 embryogenesis, 8 His, w., 6 histology and cortical structure, 18 difficult cases, 188-91 primitive neuroectodermal tumor, 191 histopathology, interpretation, history brain research, 3-7
359
neurodiagnostics, 319 neuroimaging, 194-7 neuropathology, 116 see a/so patient history Hodgkin's disease, 307 human chorionic gonadotropin, 271 Huschke, E., 4, 46 Huxley, T.H., 4, 46 hydrocephalus classification, 260 with mesencephalic anaplastic astrocytoma, 308 with septal neurocytoma. 182 with third ventricle craniopharyngioma, 211 hydrostatic edema, 256 hypacusis, with cerebellopontine angle acoustic neurinoma, 240 hyperdensity, tumor imaging, caution in interpretation, 208 hyperintensity, tumor imaging, caution in interpretation. 208 hypernephroma, metastatic, 243 hypesthesia, facial with cerebellopontine angle acoustic neuroma, 289 with metastatic carcinoma, 227 hypoacusis with cerebellopontine tic neurinoma, 241 with cerebellopontine doma, 228
angle acousangle chor-
with cerebellopontine angle melanoma, 227 with cerebellopontine angle meningioma, 225 with metastatic carcinoma, 227 hypodensity. tumor imaging, caution in interpretation, 208 hypothalamic-limbic connections. 270 hypothalamus, 267-70, 269 arterial supply, 104 astrocytoma, 334 in embryo, 10 and functional disturbances, 270 lateral nuclear area, 270 pathophysiology, 270 regulatory mechanisms, 268 ventromedial nucleus, 270
391
immune response, to tumor growth, 127. 128 immune system, 273-8 pathophysiology, 274 immunohistochemistry, 153 immunomodulation, brain, 274 immunoregulators, 273-4 immunosuppressors, 121 impotence, with third ventricle craniopharyngioma, 211 incontinence, with paracentral gyrus tumor, 157 infarction, cerebral vs. glioma, 234 vs. precentral gyrus tumor, 234 infection, and imaging techniques, 201 infectious disease, CNS, 149 infiltration. of tumors, 144-5 adventitial, 148 infratentorial anatomy, 81-94 infratentorial area dermoid tumor, 229 extrinsic vs. intrinsic tumors, 228-30 lipoma, 229 pilocytic astrocytoma, 229, 230 plexus papilloma, 228 infratentorial structures, cerebral tissue herniations, 252 infundibulum, in embryo, 10 inoperable tumors, 341, 356-8 insula, 23 fibrillary astrocytoma. 165 glioblastoma, 178 mixed glioma, 164 oligodendroglioma, 335, 337 pleomorphic xanthoastrocytoma, 301 posterior, 299 insularlobe, 16,17.54,55 anatomy, 53-7 cytoarchitecture, 54 projection fibers, 36 interbrain, see diencephalon intermediate su1cus, 47 internal capsule, 65, 66-8 arterial supply, 103 genu,66 pilocytic astrocytoma, 171
topography of projection fibers, 67 tumors. case studies, 171-2 vascularization, 68 interparietal superior su1cus, 47 interstitial edema, 256 interstitial fluid, see ISF intracranial buffering system, 258-9 intracranial pressure, see ICP intraparietal su1cus, continuity rateo 19 intraventricular tumors, 142-4,341-7 sites of origin, 143,220 intrinsic tumors, 122-3 biology, 151-3 definition, 123 demarcation, 205 and herniation, 253, 254
lCP (intracranial pressure), 259-62 elevated, 260-2 with intraventricular neurocytoma, 343 and hydrocephalus classification, 260 monitoring. 259 normal, 259-60 pressure-volume curve. 261 thresholds, 260 imaging, density changes, and tumor infiltration, 145 imaging, see neuroimaging immune cells, 273
imaging, 203 initial sites, 130 microsurgery. 325 phylogenetic restriction, 135 predilection sites, 125-7 and primary sulci, 145 resembling abscesses, 359 site of origin, 135 spherical growth, 152 topography, clinical considerations, 321 ischemic infarct, effects on CNS, 275 ISF (interstitial fluid), 256-8 secretion, 257-8 turnover, 256
392
Index
island of Reil, 4 isocortex homotypical, 18 insular lobe, 54 introduction of term, 7 structure, 18
K Kolliker, R.A. von, 4
L lamina terminalis in embryo, 10 organum vasculum, 266-7 landmarks, in brain, 24 language deficit absence, with superior temporal oligodendroglioma, 298 with anaplastic astrocytoma, 217 with frontal gyrus anaplastic astrocytoma, 294 improvement after surgery, 155, 159,172,214 with insular mixed glioma, 164 with limbic lobe astrocytoma, 166, 168 with mesencephalic 305
cavernoma,
with opercular glioblastoma, 179 with parahippocampal anaplastic astrocytoma. 300 with parietal glioblastoma, 295 with parietallobule astrocytoma, 218 with pilocytic astrocytoma, 214 with sphenopetroclival meningioma, 329 with superior temporal gyrus glioblastoma, 296 with Sylvian fissure meningioma, 235 with tentorial meningioma, 238 lateral occipital sulcus, incidence rate,19 lateral ventricle and internal capsule projection fibers, 65, 66 tumors, 143 leakiness, tumor vessels, 148 lesions, see tumors leukemia, and local thrombophlebitis, 307 leukodystrophy, and imaging techniques, 201 limbic area, vascular anatomy. 136 limbic lobe, 16, 17, 18 anatomy, 57-64 and Brodmann's areas, 69 connective fibers. 60 cortical areas, 59 glioma, 338-40 nuclei, 60 projection fibers, 36 semicircular connections, 59 tumors, 136-9 case studies, 161-70 limbic-paralimbic system, cortical and nuclear connections, 137 limiting sulci, 20 lingual gyrus, see temporo-occipital gyrus, medial lingula, cerebellar, 83 lipoma, infratentorial, 229 lip smacking, with amygdala tumor, 161
lobar terminology, 17, 114, 151 inadequacy in neuroimaging, 209 lobes cerebellar. 81, 82-3 cerebral, 16-18 anatomy, 39-60 limbic.18 paralimbic. 18 vascularization, 102 lobules cerebellar. 81. 82, 82-3 parietal,47-8 localizationists, 250 localization system, stereotactic, 24 lues, effects on CNS. 275 lunate sulcus in embryo, 10 incidence rate, 19 Iymphoma B-cell, common location. 201 occurrence pattern, 149 Iymphomas, adherence, 148
perilesional changes, 245 fibrillary, intraventricular, 341 fibroblastic, 222 vs. glioblastoma, 217-20 intraventricular, 142 meningoendotheliomatous, 236 middle and inferior frontal gyri, 293 occurrence pattern, parapineal, 221 without perilesional 238
149 changes, 236,
peritumoral changes, 146 vs. pilocytic astrocytoma, 229 in planum sphenoidale, 125 posterior inferior cerebellum, 288 vs. sarcoma, 222 with severe perilesional 237
M macaque brain, 138, 272 macrophage colony-stimulation tors, 274
falx, 187
fac-
magnetic encephalography, 197 magnetic resonance, see MRA; MRI malignancy, assessing. 120 mamillary body. 58 MAP, see mea n arterial pressure maps. see area maps maxillary pain, with parahippocampal anaplastic astrocytoma, 300 mea n arterial pressure (MAP), 263. 265 medulla oblongata (myelencephalon). 14 arterial supply, 106. 107, 108 in embryo, 10 embryogenesis, 8 ependymoma, 315 hemangioblastoma, 314 piloid astrocytoma, 312, 313 place in brain structure, 15 medullary compression, 229 with cerebellar meningioma, 288 medullary substance, 14 medulloblastoma, 119 fourth ventricle, 352 occurrence pattern, 149 and primitive neuroectodermal tumor, histology, 191 MEG (magnetic encephalography), 197 melanoma, cerebellopontine angle, 227 melatonin, 271 memory loss with intraventricular fibrillary meningioma, 341 with limbic oligodendroglioma, 340 with Sylvian fissure meningioma, 235 with temporal fossa anaplastic ganglioglioma, 285 meningioma, 119 vs. acoustic neurinoma, 225 vs. anaplastic astrocytoma, 218 vs. anaplastic ganglioglioma, temporal fossa, 285 vs. anaplastic oligodendroglioma, histologic diagnosis, 189 angular gyrus, 297 cerebellopontine angle, 225 effects on CNS. 275 endotheliomatous, pontomedullary junction, 242
multiple sclerosis effects on CNS. 275 and imaging techniques, 201 and parieto-occipital cerebral infarction. 234 myc-n oncogene amplification, 120 mydriasis. with pontine cavernoma. 354 myelencephalon, see medulla oblongata myelin, 25 myelinization, in neurogenesis. myelography, 207
13
changes,
sphenoid, 188 sphenopetroclival, 286, 326-9 temporal pole, perilesional changes, 244 vs. tuberculoma, falx, 233 meningiomas, adherence, 147 meningitis, effects on CNS, 275 mesencephalon. 14 anaplastic astrocytoma, 308 arterial supply, 105, 105, 108 cavernoma, 305 compression and distortion, 286 embryogenesis, 8 piloid astrocytoma, 309 place in brain structure, 15 topography of projection fibers. 67,68 tumors, 348-51 mesocortex, areas, 18 metabolic diseases, effects on CNS, 275 metastasis, occurrence pattern. 149 metencephalon, 14 embryogenesis, 8 place in brain structure, 15 Meynert. T., 6 microglia, 276 midbrain, see mesencephalon middle cranial fossa, meningioma, 283,287 migraine with cuneus tumor, 160 with parietallobule cavernoma, 303 with septal neurocytoma, 182 Moniz, E., 194 monoaminergic neurotransmitters, 272 monoclonal antibody Ki-167, 120 Monro-Kellie hypothesis, 277 morphology CNS tumors, 117 of lesions, imaging, 200 motor function loss, with anaplastic astrocytoma, 217 MRA (magnetic resonance angiography), 148, 149, 194,197,207 MRI (magnetic resonance imaging), 318 and anatomy, 114 compared with cr, 198 contrast, 199-200 correlation with cerebral 73-80
and sulcal anatomy, 20 and three-dimensional anatomy, 25 triplanar, 208 and tumor consistency, 147 multicentric tumors. 150-1
anatomy,
disadvantages, 208 echo-planar, 197 functional studies, 199, 200, 202 history, 195 image selection, 198-9 interpreting weighted images, 199 peritumoral changes, 146 recent improvements, 200
N neck pain, with endotheliomatous meningioma, 242 neocerebellum, 82 tumors, 129-35 neocerebral tumors, 129-35 case studies, 154-60 neocortex, histogenesis, 13 nerves abducens (sixth), palsy, 223, 227. 291,310.311.312.330,354 cranial displacement, 291, 329 palsy, 355 facial (seventh), 226 palsy, 291 oculomotor (third) adherence of meningioma, 286 palsy, 213 optic (second), in embryo. 10 trigeminal (fifth) dysfunction, 226 neurinoma, 290 neuroma vs. melanoma. 227 neural plate, 8 neural systems, 250-4 neurendocrine system, 267-71 neurinoma acoustic, 226 cerebellopontine angle, 240, 241,242,290 vs. meningioma, 225 adherence, 148 occurrence pattern, 149 trigeminal, 290 neuroanatomy, and neuroimaging systems, 359 neuroclinical technology, 318-19 neurocytoma intraventricular, 142 septum pellucidum, 182 neurodiagnostics, history, 319 neuroectodermal tumor inoperable, 357 primitive, 176 neuroembryogenesis, 8-11 neuroendocrine system, pathophysiology, 271 neurogenesis, 12, 12-13 neuroglia migration pathway, 30 origin of term, 116 neuroglial cells, 250 neurohypophysis, 266 neuroimaging, 193-245,318 application to CNS tumors, 200-1 case studies, 209-45 cautions for interpretation. 208 current methods, 197-200
Index
cystic changes, 208 diagnostic accuracy, 209 differential diagnosis, 209-35 difficulties, 202-7 overreading, 203 topographic, 203 discrepancies from clinical state, case studies, 308-15 edema, 243-4 four-dimensional, 359 functional changes, 202 history, 194-7 image intensity, 208 interpretation cautions, 208 weighted MRI images, 208 limitations, 202-7 perilesional changes, 235-42 peritumoral changes, 208 postoperative, 201 specificity, 202 summary, 207-9 techniques, 2 tomographic techniques, 196 trends, 197 see u/so Cf; MRI; PET; SPECf neuroimmune system pathway, 38 neuroimmunotherapy, 274 neurological deficit, absent, with temporallobe astrocytoma, 282 neurological diseases, interactions, 274-7 neuroma, acoustic, cerebellopontine angle, 288 neuromodulators, 273 neurons, 250 cerebrospinal fIuid-contacting, 273 cytodifferentiation, 12 embryogenesis, 12-13 introduction of term, 6 morphological 276
diversity
in disease,
neuropathologists, viewpoint on tumors, 121-2 neuropathology, 115-91 features, CNS tumors, 117-19 history, 116 interpretation, 359 specific, 123-44 neuropeptides, 273 neurophysiology, 247-315, 359 case studies, 280-316 outdated ideas, 278 neuroradiology, see neuroimaging neurosurgeons iconoclastic spirit required, 278 viewpoint on tumors, 121-2 neurotransmitters, 272, 272 CNS, 273 pathways, 38 NMR (nuclear magnetic resonance), 195 norepinephrine, 271 NORs (nucleolar organizer 120 nuclear magnetic resonance 195 nucleolar organizer 120
regions), imaging,
regions (NORs),
nystagmus with cerebellopontine angle acoustic neurinoma, 241, 290 with cerebellopontine angle acoustic neuroma, 289 with infratentorial dermoid tumor, 229 with mesencephalic anaplastic astrocytoma, 308 with pontine cavernoma, 354 with pontomesencephalic pilocytic astrocytoma, 310
o observation, as treatment option, 324 occipital gyrus, 21 medial, 49 superior, 49 occipitallobe, 16,17,50,51 anatomy, 49-51 and Brodmann areas, 69 metastatic adenocarcinoma, 281 MRI anatomical correlation, 78-9 projection fibers, 36 vascularization, 102 occipital pole in embryo, 10 tumor, 283 occipitopontine fibers, 68 cascade structure in white matter, 38 occipitotemporal sulcus, continuity rate, 19 oculomotor nerve, see nerves oculomotor paresis, with mesencephalic piloid astrocytoma, 348-9 olfactory cortices, 18 olfactory sulcus, incidence rate, 19 oligoastrocytoma diffuse, 175 falx, 187 mixed, cingulate gyrus, 170 oligodendroglioma anaplastic, 219 vs. atypical meningioma, histologic diagnosis, 189 insula, 335, 337 intermediate growth phase, 132, 133 limbic lobe, 338, J40 middle parietallobule, 158 neocerebral, 155 occurrence pattern, 149 pulvinar thalami, 345 recurrence with glioblastoma, 345 septal region, 209 superior temporal gyrus, 298 oncogenes, 117 amplification, and prognosis, 120 operability, 317-59, 321-4 decision-making, 321-2 perioperative care, 322 operative treatment, decisionmaking, 320-1 opercular part, inferior frontal gyrus, 21,22,23 astrocytoma, 294 glioblastoma, 179 oligodendroglioma, 155 operculated sulci, 20 ophthalmoplegia, with sphenopetroclival meningioma, 328 optic chiasm, in embryo, 10 optic glioma, 123, 332-3 optic nerve, in embryo, 10 optic radiations, 68 displacement, 298 with superior temporal gyrus glioblastoma, 296 orbital gyri, 43 orbital sulci, incidence rate, 19 organ system, circumventricular, 265-7 organum vasculum of lamina terminalis (OVLT), 266, 266-7
p pain arms and legs, with intramedullary ependymoma, 315
aural, with fourth ventricular astrocytoma, 353 maxillary, with parahippocampal astrocytoma, 300 retroauricular, with acoustic neuroma, 288 paleocerebellum, 82 paleocortical areas, 18 palliative treatment, 319, 323, 324 papilledema with diffuse anaplastic astrocytoma, 179 with glioblastoma, 223-4 with infratentorial plexus papilloma, 228 with intraventricular lesion, 220 with intraventricular pilocytic astrocytoma, 342, 343 with meningoendotheliomatous meningioma, 236 with mesencephalic anaplastic astrocytoma, 308 with multiple lesions, 187 with primitive neuroectodermal tumor, 224 with retrolenticular astrocytoma, 173 with septal neurocytoma, 182 with temporallobe glioblastoma, 177 papilloma, intraventricular, choroid plexus, 142 paracentral gyrus, 40, 46, 62 cavernoma, 157 and centrallobe, 44 paracentrallobule, 46 paracentral sulcus, 44 parachiasmal region craniopharyngioma, 239 extrinsic vs. intrinsic tumors, 209-17 pilocytic astrocytoma, 212 parahippocampal gyrus, 61, 61 astrocytoma, 282 glioblastoma, 284 parahippocampus, 18, 51, 53, 62 anaplastic astrocytoma, 163, 300 hamartoma-astrocytoma, 216 paralimbic area, vascular anatomy, 136 paralimbic lo be, 18 tumors, 136-9 parapineal areas glioblastoma, residual, 224 meningioma, 221, 238 fibroblastic, 222 vs. sarcoma, 222 plexus papilloma, anaplastic, 223 tumors, differential diagnosis, 221-4 parasites, 201
and imaging techniques,
parasplenial area glioblastoma vs. abscess, 232 lesion treated by shunt, 309 paraterminal area, 63 paresis arm, with Sylvian fissure meningioma, 235 hand, with frontal gyrus astrocytoma, 294 paresthesia facial with brainstem and cerebellar epidermoid tumor, 291 with cerebellopontine angle acoustic neurinoma, 241, 290 with medullary piloid astrocytoma, 313 with superior temporal gyrus oligoastrocytoma, 299 parietal gyrus, 21
393
parietallobe, 16, 17,49 anatomy, 47-9 astrocytoma, 335-6 and Brodmann areas, 69 glioblastoma vs. abscess, 231 insular surface, 43 local thrombophlebitis, 307 MRI anatomical correlation, 78-9 projection fibers, 36 vascularization, 102 parietallobules, 48, 48 cavernoma, 303 inferior, 23 anaplastic astrocytoma, 159 glioblastoma, 295 middle, oligodendroglioma, 158 superior, astrocytoma, 156 parietal operculum, oligoastrocytoma, 299 parietal peduncles, 47 parieto-occipital fissure, 47 parieto-occipital sulcus, 47 cerebral infarction, vs. glioma, 234 continuity rate, 19 in embryo, 9, 10 parietopontine fibers, 68 cascade structure in white matter, 38 Parinaud syndrome absent, with mesencephalic piloid astrocytoma, 309 with fourth ventricular medulloblastoma, 352 parolfactory area, 62, 63 parolfactory sulcus, anterior, dence rate, 19
inci-
pathogenesis, 119 pathophysiology cerebral edema, 255-6 cerebrovascular system, 265 circumventricular organs, 267 CNS disease processes, 274-7 hypothalamus, 270 immune system, 274 neuroendocrine system, 271 pineal gland, 271 surgical, and MRI, 199 patient history, 318 peduncles cerebellar, 82, 88, 90, 91-2 parietal, 47 periarchicerebral areas, 18 perilesional changes, 146,208 absence acoustic neurinoma, 241, 242, 290 acoustic neuroma, 288 endotheliomatous meningioma, 242 meningiocraniopharyngioma, 239 meningioma, 236, 238 Sylvian fissure meningioma, 235 adenocarcinoma, temporal pole, 243 differential 235-45
diagnostic
problems,
glioblastoma precuneus, 244 pulvinar thalami, 244 imaging, 203-4, 235-45 meningioma meningoendotheliomatous, 236 temporal pole, 244 tuberculoma falx, 233 fourth ventricle, 233 white matter, 245 perioperative care, 322 peripaleocortex, insular lobe, 54 peripaleocortical areas, 18 persona lit y changes
394
Index
with limbic oligodendroglioma, 338 with temporallobe astrocytoma, 280 PET (positron emission tomography),196 and anatomy, 114 phylogenetic recency and initial tumor growth, 126, 128 and intrinsic tumors, 135 limbic and paralimbic are as, 136 physiological subsystems, 248-50 physiological systems, interaction with neurologic diseases, 274-7 pia, and imaging difficulties, 204, 205,206 piloid astrocytoma, mesencephalon, 348-9,350 pineal body, 266 pineal gland, 270-1 pathophysiology, 271 pineal tumors and diabetes insipidus, 271 vs. intraventricular pilocytic astrocytoma, 347 occurrence pattern, 149 pituitary adenoma, 119 growth restrained by diaphragma sellae, 125 pituitary gland, 270 arteries, 104 plexus papilloma anaplastic, 223 infratentorial, 228 occurrence pattern, 149 PNET, see primitive neuroectodermal tumor pneumoencephalography, 207 pons,14 arterial supply, 106, 106, 108 cavernoma, 311 in embryo, 10 tumors, 354-5 see a/so metencephalon pontobulbar area, distortion with acoustic neurinoma, 290 with acoustic neuroma, 288, 289 and postoperative recovery, epidermoid tumor, 291 pontomedullary junction, endotheliomatous meningioma, 242 pontomesencephalic area, pilocytic astrocytoma, 310 postcentral gyrus, 21, 23, 40, 45, 47 and Brodmann areas, 69 and centrallobe, 44 MRI anatomical correlation, 78-9 variations, 46, 47 postcentral sulcus, 23,44, 47, 49 continuity rate, 19 in embryo, 9 posterolateral fissure, cerebellum, 82 postoperative neuroimaging, 201 precentral gyrus, 21, 22, 23, 40, 42, 45,46 and Brodmann areas, 69 cavernoma, 302 and central lo be, 44 MRI anatomical correlation, 78-9 tumor vs. cerebral infarction, 234 variations, 46, 47 precentral sulcus, 23, 44 intermedia te, incidence rate, 19 interruption rate, 19 marginal, incidence rate, 19 precuneus,47,48,62 glioblastoma, perilesional changes, 244 pilocytic astrocytoma, 157 predisposition, genetic, 119 prele.nticular tumors, 134 primitive neuroectodermal tumor, 176
histology, 191 intraventricular,344 vs. pineal blastoma, 224 proisocortex, insular lobe, 54 proisocortical areas, 18 projection fibers, 32, 33, 36-8 cerebellum, 90 in cerebral white matter, 25, 26 coursing with commissural fibers, 36 dissection, 37 internal capsule and basal ganglia, 66 and central nuclei, 66 and lateral ventricle, 65, 66 topography, 67 mesencephalon, topography, 67, 68 sectorial organization, 30 projection systems, 6 proliferation rate, tumors, 120 prosencephalon,14 embryogenesis, 8 place in brain structure, 15 relationship to basal ganglia, 138 proto-oncogenes, 117 pseudocapsule formation, 147, 204 membranes, 205 ptosis with mesencephalic fibrillary astrocytoma, 351 with pontine cavernoma, 354 pulvinar thalami, 68 glioblastoma, 183, 345 perilesional changes, 244 oligodendroglioma, 345 residual glioblastoma, 224 putamen, arterial supply, 102
Q quadrantanopsia, 163, 338 with anaplastic astrocytoma, 217 with parahippocampal anaplastic astrocytoma, 300 with parietal anaplastic astrocytoma, 336 with pilocytic astrocytoma, 214 with pleomorphic xanthoastrocytoma, 301 with retrolenticular astrocytoma, 173 with superior temporal gyrus oligoastrocytoma, 299 with temporallobe astrocytoma, 282 with thalamic telangiectasia, 304 quadrigeminal plate, in embryo, 10 quadriplegia, with pontine cavernoma, 355 qua lit y of life, 320
R radical surgery, 327 radiographs, 194, 207 radiology, see neuroimaging Ram