PRINCIPLES OF NEUROLOGY - PART 6 ppt

CHAPTER 30 / INTRACRANIAL NEOPLASMS 273 TABLE 30-2 Tumors Presenting with Impairment of Mental Function, Headaches, Seizures, or Focal Neurologic Signs: Increased Intracranial Pressure a Late Development Glioblastoma multiforme 20% of all intracranial tumors, 55% of all (anaplastic astrocytoma) gliomas; mainly cerebral but may affect all parts of brain and cord, widely infiltrative; survival about 12 months in most cases Astrocytomas 25–30% of cerebral gliomas; in adults, (low grade) common sites are cerebral hemispheres; in children, brainstem and cerebellum; slowly growing, tendency to form cysts; survival for many years Oligodendroglioma 5–7% of intracranial gliomas; frontal lobes are most common sites; slowly growing; survival for many years if low-grade Ependymoma Common sites are fourth ventricle (particularly in children), conus medullaris, and filum terminale; survival depends on degree of anaplasia Meningioma 15% of all primary intracranial tumors; highest incidence in seventh decade; more frequent in women; common sites are sylvian region, superior parasagittal surfaces, olfactory groove, lesser wing of sphenoid, tuberculum sellae, cerebellopontine angle, spinal canal; very slow growing; symptoms depend on tumor site Primary cerebral May arise in any part of the brain lymphoma (monofocal or multifocal), often near lateral ventricle, usually in adult life; lymphocytes, mononuclear and tumor cells often found in CSF; immunosuppressed patients at risk, particularly those with AIDS; median survival less than 30 months Metastatic carcinoma Three main patterns; (1) skull and dura, from carcinoma of breast and prostate, and multiple myeloma; may compress spinal cord, cranial nerves, and pituitary; (2) brain, one or several cerebral or other foci, from lung, breast, melanoma, colon, kidney; (3) meningeal carcinomatosis or leukemic infiltration of leptomeninges and cranial and spinal nerve roots; average survival 3 months with meningeal carcinomatosis; patients with bony metastases survive longer 4777 Victor Ch 30 p268-276 6/11/01 3:04 PM Page 273 Each of the tumors that causes hydrocephalus or a specific regional syndrome requires a special combination of surgical and radiation therapy. PARANEOPLASTIC DISORDERS This is a group of neurologic disorders that occur in patients with car- cinoma or other types of neoplasia, without invasion or compression of the nervous system itself. Presumably, tumors that induce these effects elaborate enzymes, hormones, or antibodies or dispose the patient to a viral agent capable of invading or cross-reacting with the nervous sys- tem. The most familiar of these remote effects and the chapters in which they are discussed are listed below: 1. Polyneuropathy (Chap. 45) 2. Polymyositis or dermatomyositis (Chap. 48) 3. Myasthenic-myopathic syndrome of Lambert-Eaton (Chap. 52) 4. Carcinomatous cerebellar degeneration and myoclonus-opsoclonus syndrome 274 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE TABLE 30-3 Tumors Causing Mainly Increased Intracranial Pressure and Hydrocephalus, Focal or Lateralizing Signs Less Conspicuous Medulloblastoma and Mainly in children 4 to 8 years; begins with cystic astrocytoma of listlessness, vomiting, headaches; later, cerebellum squint, ataxic gait, falling, and papilledema Ependymoma and Clinical syndrome similar to papilloma of choroid medulloblastoma but more protracted; plexus two-thirds of patients present with increased ICP, others with vomiting, dysphagia, paresthesias of extremities, vertigo, head tilt Hemangioblastoma of Dominant inheritance; retinal angioma cerebellum (von Hippel– and polycythemia often conjoined; may Lindau disease) develop multiple spinal cord lesions and syringomyelia Pinealoma (includes Onset in adolescence and adulthood; pineal germinoma symptoms and signs of increased ICP; and teratoma) paralysis of upward gaze and pupils fixed to light (Parinaud syndrome) Colloid (paraphysial) Signs of intermittent or persistent increased cyst of third ventricle ICP (headache) and hydrocephalus Craniopharyngioma In children and adolescents, delayed sexual maturation and growth, diabetes insipidus combined with visual loss from chiasmatic–optic nerve lesions; in adults, visual loss, signs of hydrocephalus, mild corticospinal and hypothalamic signs 4777 Victor Ch 30 p268-276 6/11/01 3:04 PM Page 274 TABLE 30-4 Distinctive Tumor Syndromes: Local Signs Predominate and General Cerebral Deficits and Increased ICP Are Late or Absent Acoustic neuroma Usually solitary; may be part of (schwannoma) neurofibromatosis, either solitary (type I) or bilateral (type II, autosomal dominant); unilateral neurosensory deafness, loss of balance, facial weakness and loss of sensation, later ataxia of ipsilateral limbs and gait and raised intracranial pressure Carotid body tumor Painless mass at bifurcation of common carotid, below angle of jaw; grows slowly; compresses cranial nerves IX to XII and sympathetics; rarely familial and bilateral Pituitary adenomas (with enlarged sella, rule out empty-sella syndrome by CT-MRI). See also page 239. Prolactinomas Increased incidence with age; headache, (usually achromatic bitemporal hemianopia, or mixed chromophobe, chiasmatic–optic nerve changes; sella sometimes acidophilic turcica expands; hypothyroidism, adenoma) hypoadrenalism; in females, amenorrhea, galactorrhea, serum prolactin increased (Ͼ100 ng/mL); in males, impotence Acromegaly-gigantism Oversecretion of growth hormone (GH); (eosinophilic before closure of the epiphyses, gigantism; adenoma) after closure, acromegaly Cushing disease Oversecretion of ACTH; sella not enlarged; (basophil or truncal obesity, striae, hirsutism; nonbasophil adenoma) hypertension; glycosuria; amenorrhea; osteoporosis; proximal muscle weakness; mental changes Meningioma of Mainly in women, average age 50 years; sphenoid ridge unilateral exophthalmos, slight temporal bulge, anosmia, ocular palsies, Tolosa-Hunt syndrome, monocular blindness Meningioma of Older adults; anosmia and frontal lobe olfactory groove signs; high CSF protein Meningioma of Older adults, mainly women; bitemporal tuberculum sellae hemianopia with normal-sized sella Glioma of brainstem Onset mainly in childhood; progressive cranial nerve and long tract signs; increased ICP late; prognosis varies with degree of anaplasia Glioma of optic Mainly in children and adolescents, nerve and chiasm sometimes with neurofibromatosis; progressive loss of vision with optic atrophy or chiasmal field defect (continued) CHAPTER 30 / INTRACRANIAL NEOPLASMS 275 4777 Victor Ch 30 p268-276 6/11/01 3:04 PM Page 275 5. Limbic and brainstem encephalitis (see the Principles, pp 687–688) 6. Progressive multifocal leukoencephalopathy (Chap. 32) 7. Necrotizing myelopathy (Chaps. 35 and 43) 8. Retinopathy For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 642–694. ADDITIONAL READING Dawson DM: Antineoplastic drugs, in Asbury AK, McKhann GM, McDonald WI (eds): Diseases of the Nervous System, 2nd ed. Philadelphia, Saunders, 1992, pp 1121–1129. DeAngelis LM: Current management of primary central nervous system lym- phoma. Oncology 9:63, 1995. Glantz MJ, Rottenberg DA: Harmful effects of radiation on the nervous system, in Asbury AK, McKhann GM, McDonald WI (eds): Diseases of the Nervous System, 2nd ed. Philadelphia, Saunders, 1992, pp 1130–1143. Henson RA, Urich H: Cancer and the Nervous System. Oxford, Blackwell, 1982. Klibanski A, Zervas NT: Diagnosis and management of hormone-secreting pitu- itary adenomas. New Engl J Med 324:822, 1991. Levine AJ, Schmidek HH (eds): Molecular Genetics of Nervous System Tumors. New York, Wiley-Liss, 1993, pp 357–369. Posner JP: Neurologic Complications of Cancer. Philadelphia, FA Davis, 1995. Russell DS, Rubinstein LJ: Pathology of Tumors of the Nervous System. 5th ed. Baltimore, Williams & Wilkins, 1989. 276 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE TABLE 30-4 Distinctive Tumor Syndromes: Local Signs Predominate and General Cerebral Deficits and Increased ICP Are Late or Absent (cont.) Chordoma Common sites are clivus and sacrococcygeal region; cauda equina syndrome or successive multiple cranial nerve signs, with conduction deafness, facial pain, and ataxia Nasopharyngeal or Multiple upper cranial nerve abnormalities; sinus tumors nasopharyngeal mass; erosion base of skull Tumors of Pain in occiput and posterior neck; foramen magnum combination of lower cranial nerve, cervical cord, and cerebellar signs 4777 Victor Ch 30 p268-276 6/11/01 3:04 PM Page 276 31 Nonviral Infections of the Nervous System (Bacterial, Spirochetal, Fungal, Parasitic) and Sarcoidosis BACTERIAL INFECTIONS The most important members of this group in decreasing order of their frequency are meningitis, brain abscess, subdural empyema, dural sinus thrombophlebitis, and focal bacterial encephalitis. In all of these and other conditions, bacteria reach the brain in one of several ways: by hematogenous spread (i.e., septicemia or infected emboli), by extension from infected cranial structures (ears, sinuses, osteomyelitic foci), by penetrating cranial injuries, or by surgical invasion. Bacterial Meningitis Definition This consists essentially of a bacterial infection of the pia and arachnoid and the cerebrospinal fluid that they enclose. Since the subarachnoid space is continuous around the brain, spinal cord, and optic nerves, an infective agent (or blood or tumor cells) gaining entry to any part of the space spreads to all of it. Thus meningitis is always cerebrospinal. Infection also reaches the ventricles and their ependymal lining by reflux from the subarachnoid space. All structures bathed by the CSF—ependyma, choroid plexuses, intra-arachnoidal portions of the cranial and spinal nerves, cerebral and cerebellar cortices, and sur- face veins and arteries—are exposed to the meningeal infection. Epidemiology Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, and Listeria monocytogenes—the most com- mon bacteria causing meningitis—have a worldwide distribution and a more or less even incidence throughout the year. Meningococcal meningitis tends to occur in epidemics, in roughly 10-year cycles. This form of meningitis is most frequent in children and adolescents but occurs throughout adult life. H. influenzae meningitis affects mainly children between the ages of 2 months and 5 years but is now being reported in adults over 50 years of age. Pneumococcal meningitis pre- dominates in the very young and old and has a predilection for patients with sickle-cell anemia and those who have had a skull fracture or splenectomy. Escherichia coli, Staphylococcus aureus, group A strep- tococci, Klebsiella, Proteus, and Listeria monocytogenes are associated 277 4777 Victor Ch 31 p277-289 6/11/01 2:10 PM Page 277 Copyright 1998 The McGraw-Hill Companies, Inc. Click Here for Terms of Use. with immunodeficiency states, trauma, and neurosurgical procedures, including ventricular shunts. Pathogenesis and pathology The usual routes by which bacteria reach the meninges have been indicated above. Once bacteria enter the CSF, they excite an acute inflammatory reac- tion, mainly in the vascular pia. Hyperemia, exudation of blood pro- teins, and migration of neutrophils occur within hours. This exudate continues to accumulate for the next few days. Thereafter, lymphocytes and then plasma cells begin to appear in the pia as part of an immune response. Veins in the pia may thrombose and cause brain infarction. As the meningeal exudate blocks the subarachnoid space around the brainstem and the foramina of Luschka and Magendie, tension hydro- cephalus develops. There is also an ependymitis at an aqueductal level which may contribute to the obstruction of CSF flow. Cranial nerve roots, as they pass through purulent exudate in the subarachnoid space, may be involved. Although the brain is not invaded by bacteria, their endotoxins diffuse through the pia and along the Virchow-Robin spaces and excite a subpial edema and even a superficial focal necrosis. The thin arachnoid, especially in infants, may be transgressed, with devel- opment of a subdural inflammatory reaction and a hygroma. If the meningitis is not treated successfully, arteritis and thrombosis, cerebral infarction, and hydrocephalus may result. Clinical features Fever, severe headache, generalized convulsions, various degrees of drowsiness and confusion, and even coma are the usual manifestations in adults and older children. Generalized seizures occur more often in infants and young children. Signs of meningeal irri- tation—stiffness of the neck on forward flexion, with flexion of the knees and hips (Brudzinski sign) and inability to completely extend the legs (Kernig sign)—become evident. In infants and newborns, in whom meningitis is often lethal, the infection expresses itself by fever and bulging of the fontanels, vomiting, drowsiness, and, in some instances, convulsions; stiff neck may not be evident. Certain clinical clues may betray the type of meningitis: 1. Petechial and purpuric rash and circulatory collapse—meningococ- cal meningitis with Waterhouse-Friderichsen syndrome (a similar rash may be seen with certain enteroviral infections) 2. Ventriculoatrial or peritoneal shunt, cranial trauma, or neurosurgical procedure—coagulase-negative Staphylococcus, other nosocomial organisms 3. Upper respiratory and ear infections in children—H. influenzae 4. Immunocompromised host—Strep. pneumoniae, L. monocytogenes, E. coli 5. Infection of ears, sinuses, lung, heart valves—Strep. pneumoniae or mixed infections, including anaerobic organisms 278 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE 4777 Victor Ch 31 p277-289 6/11/01 2:10 PM Page 278 Ancillary examinations The one indispensable laboratory procedure is lumbar puncture and examination of the spinal fluid. The CSF is usu- ally under increased pressure (200 to 400 mmH 2 O), is cloudy owing to the presence of cells, mainly polymorphonuclear, (a few hundred, or even less, to 10,000 mm 3 ), and contains bacteria seen on Gram stain, increased protein (100 to 500 mg/dL), and decreased glucose (Ͻ40 mg/dL or Ͻ40 percent of the blood glucose, which should be measured simultaneously). The fluid needs to be cultured. The CSF latex agglutination test and now the polymerase chain reaction (PCR) for detection of bacterial antigens are especially useful in cases of par- tially treated meningitis. Also, throat and blood cultures should be obtained. The peripheral white blood cells are increased with a shift to the left. After treatment is underway, films of sinuses and chest are indicated. Similarly, CT scanning and MRI can be performed to exclude brain abscess and subdural empyema. Actually, brain abscess rarely compli- cates meningitis. In infants and children, ultrasound examination is pre- ferred because anesthesia is not required. Treatment Bacterial meningitis is a medical emergency. Every hour of delay in starting antibacterial therapy increases the risk of complica- tions and permanent neurologic residua. Treatment with broad-spec- trum antibiotics should be started immediately after the LP, while identification of the organism is awaited. In Tables 31-1 and 31-2 are listed the recommended antibiotics at each age and the dosages for dif- ferent types of meningitis. LP pressure above 400 mmH 2 O warns of cerebellar herniation and requires treatment with mannitol. The ad- ministration of dexamethasone to children with meningitis reduces the incidence of deafness. Treatment should continue for 10 to 14 days. Persistent and recurrent subdural hygromas usually respond to repeated aspiration or shunting. Preventive measures should not be neglected. All household contacts of patients with meningitis, particularly children, should receive rifampin, 10 mg/kg q 12h by mouth daily for 2 days. Immunization against Neisseria meningitidis is effective and should be given during epidemics. Children after 2 months of age should be vaccinated against H. influenzae with a new protein-conjugate vaccine. Bacterial Encephalitis In acute and subacute bacterial endocarditis (SBE), the brain is seeded with bacteria-laden emboli; in subacute endocarditis the bacteria are characteristically of low virulence and do not produce brain abscesses. Sterile meningeal reactions and small infarcts, some with blood in the CSF, are the usual complications; mycotic aneurysms may form but are rare. The emboli of acute bacterial endocarditis do give rise to miliary CHAPTER 31 / NONVIRAL INFECTIONS OF THE NERVOUS SYSTEM 279 4777 Victor Ch 31 p277-289 6/11/01 2:10 PM Page 279 abscesses, infarcts, small hemorrhages, and bacterial meningitis; large abscesses are rare. Treatment in both types is directed to the endocardi- tis and septicemia. Legionnaire’s disease, Mycoplasma pneumoniae, and L. monocyto- genes may cause a direct infection of the brain—strictly speaking, a picture of bacterial encephalitis. The clinical picture may be one of a confusional state, seizures, brain swelling, cerebellar ataxia, or, in the case of Listeria, lower cranial nerve palsies coupled with meningitis (rhomboencephalitis). Lyme disease probably belongs in this category as well (see p. 286). Subdural Empyema This is a purulent infection of the subdural space, stemming usually from disease of the frontal or ethmoid sinuses or middle ears and mas- toid cells. Pus accumulates over one cerebral hemisphere (occasionally interhemispheric). The arachnoid prevents organisms from entering the subarachnoid space in sufficient numbers to induce a bacterial menin- gitis. There is, however, a polymorphonuclear pleocytosis (50 to 1000 per mm 3 ) and an elevated CSF protein; the glucose is normal. Meningeal veins that underlie the empyema become thrombosed and give rise to cortical infarction, which is the cause of the cerebral symp- toms. 280 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE TABLE 31-1 Empiric Therapy of Bacterial Meningitis Age of patient Antimicrobial therapy* 0–4 weeks Cefotaxime plus ampicillin 4–12 weeks Third-generation cephalosporin † plus ampicillin 3 months–18 years Third-generation cephalosporin † (Ϯ ampicillin); or ampicillin plus chloramphenicol 18–50 years Third-generation cephalosporin* (Ϯ ampicillin) Ͼ50 years Third-generation cephalosporin † plus ampicillin Immunocompromised state Vancomycin plus ampicillin and ceftazidime Basilar skull fracture Third-generation cephalosporin † Head trauma; neurosurgery Vancomycin plus ceftazidime CSF shunt Vancomycin plus ceftazidime * In communities where highly penicillin resistant pneumococcus is reported, vancomycin should be added. † Cefotaxime and ceftriaxone are currently used. 4777 Victor Ch 31 p277-289 6/11/01 2:10 PM Page 280 Diagnosis is based on the presence of a known sinus or ear infection, generalized headache and fever, rapid accession of focal seizures, hemiparesis, hemisensory loss and aphasia, and a sterile CSF under increased pressure. CT scanning and MRI disclose the extracerebral accumulation of pus. Treatment consists of surgical drainage and administration of large doses of broad-spectrum antibiotics (20 to 24 million units penicillin per day plus a third generation cephalosporin and metronidazole, mod- ified according to bacteriologic findings). Cranial Extradural Abscess This is usually associated with osteomyelitis of a cranial bone. Local pain and tenderness, purulent discharge from an ear or sinus, palsies of cranial nerves V and VI (Gradenigo syndrome), and a normal CSF (except for a few cells) are the usual manifestations. Staph. aureus is the most common agent. An intensive course of antibiotics and, later, surgical removal of the infected bone are the recommended therapeutic measures. Spinal epidural abscess is considered in Chap. 43. CHAPTER 31 / NONVIRAL INFECTIONS OF THE NERVOUS SYSTEM 281 TABLE 31-2 Recommended Dosages of Antimicrobial Agents for Bacterial Meningitis in Adults with Normal Renal and Hepatic Function* Antimicrobial Total daily Dosing interval, agent dose hours Amikacin † 15 mg/kg 8 Ampicillin 12 g 4 Cefotaxime 8–12 g 4–6 Ceftazidime 6 g 8 Ceftriaxone 4 g 12–24 Chloramphenicol ‡ 4–6 g 6 Gentamicin † 3–5 mg/kg 8 Nafcillin 9–12 g 4 Oxacillin 9–12 g 4 Penicillin G 24 million units 4 Rifampin § 600 mg 24 Tobramycin † 3–5 mg/kg 8 Trimethoprim- sulfamethoxazole¶ 20 mg/kg 6–12 Vancomycin †Ƚ 2–3 g 8–12 *Unless indicated, therapy is administered intravenously. † Peak and trough serum concentrations must be monitored. ‡ Higher dose recommended for pneumococcal meningitis. §Oral administration. ¶ Dosage based on trimethoprim component. Ƚ CSF concentrations may have to be monitored in severely ill patients. 4777 Victor Ch 31 p277-289 6/11/01 2:10 PM Page 281 Intracranial Thrombophlebitis The lateral sinus may become thrombosed in the course of an ear infec- tion and block cerebral venous drainage sufficiently to cause a rise in CSF pressure. Facial and nasal infections may lead to thrombosis of the anterior part of the cavernous sinus on one or both sides, manifested by orbital edema and involvement of cranial nerves III, IV, and VI and ophthalmic division of V and sometimes, inexplicably, blindness. Thrombosis of the superior longitudinal (sagittal) sinus and its drain- ing veins gives rise to headache, seizures, and unilateral or bilateral paralysis, mainly of the legs. In sagittal and lateral sinus thromboses, the CSF pressure is greatly elevated and there may be papilledema. The occurrence of these conditions should always be suspected in the pres- ence of some other form of intracranial suppuration—meningitis, sinus or ear infection, subdural empyema, extradural or brain abscess. Thrombosis of major venous sinuses can often be detected by MRI, which may also demonstrate an area of hemorrhagic infarction adjacent to the occluded sinus. The diagnosis can be corroborated by failure of the superior sagittal or lateral sinuses to fill during the late phase of carotid arteriography. Treatment of intracranial thrombophlebitis consists of large doses of antibiotics, after which surgery of the affected ear or sinus may be nec- essary. The role of anticoagulation, shown to be of value in aseptic venous occlusion, is still uncertain. Brain Abscess The brain is resistant to abscess formation, but this will occur under conditions that cause necrosis of tissue with simultaneous bacterial infection. The disease states that are conducive to the formation of brain abscess are chronic pulmonary infections (pneumonitis, bronchiectasis, lung abscess); chronic and recurrent sinusitis, otitis, or mastoiditis; con- genital heart disease or pulmonary vascular malformation; distant infection of skin, bone, and kidney; and, rarely, acute bacterial endo- carditis. In a considerable proportion of cases, the source of the abscesses cannot be determined. The abscess, as it forms over a period of several weeks, passes through several stages—from localized suppurative encephalitis to complete encapsulation. There may be a solitary abscess or several abscesses, depending on the cause. Those secondary to ear and sinus infection are single, with one or more daughter abscesses, and are local- ized in the part of the brain nearest the source. Thus, with frontal-eth- moidal sinusitis, the abscess tends to form in the frontal lobe; with sphenoid sinusitis, in the frontal or anterior temporal lobe; with otitis media, in the middle or posterior temporal lobe; and with mastoiditis, in the cerebellum. 282 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE 4777 Victor Ch 31 p277-289 6/11/01 2:10 PM Page 282 [...]... syphilis, the clinical characteristics of the neurologic syndrome, and the laboratory testing for reagin and treponemal antibodies (VDRL and FTA-ABS) 4777 Victor Ch 31 p27 7-2 89 2 86 6/11/01 2:10 PM Page 2 86 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE FIG 3 1-1 Diagram of the evolution of neurosyphillis in the immunecompetent host The CSF is abnormal in all cases of active neurosyphilis (increase... screening tests are now available, all of them based on an enzyme-linked immunoassay (ELISA) While highly sen- 4777 Victor Ch 32 p29 0-3 01 298 6/ 11/01 2:11 PM Page 298 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE TABLE 3 2-2 Neurologic Complications in HIV-1–Infected Patients Brain Predominantly nonfocal AIDS dementia complex (subacute-chronic HIV encephalitis) Acute HIV-related encephalitis Cytomegalovirus... Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 742–7 76 ADDITIONAL READING Antel JP, Rasmussen T: Rasmussen’s encephalitis and the new hat Neurology 46: 9, 19 96 4777 Victor Ch 32 p29 0-3 01 6/ 11/01 2:11 PM Page 301 CHAPTER 32 / VIRAL INFECTIONS OF THE NERVOUS SYSTEM 301 Berger JR, Levy RM (eds): AIDS and the Nervous System, 2nd ed Hagerstown, MD, Lippincott-Raven, 1997 Brew B, Sidtis J, Petito... Creutzfeldt-Jakob disease by two-dimensional gel electrophoresis of cerebrospinal fluid Lancet 348:8 46, 19 96 4777 Victor Ch 33 p30 2-3 26 33 6/ 11/01 2:11 PM Page 302 Cerebrovascular Diseases Next to heart disease and cancer, cerebrovascular disease is the most frequent cause of death in the western world And at least one-half of all neurologic patients in general hospitals have some type of cerebrovascular disease... Treatment consists of IV administration of amphotericin B After a test dose of 5 mg, the drug is given in a dosage of 1.0 mg/kg daily or every second day to a total of 2 to 3 g The addition of flucytosine (150 mg/kg per day) results in fewer failures and decreased nephrotoxicity, but the mortality is still 4777 Victor Ch 31 p27 7-2 89 288 6/ 11/01 2:10 PM Page 288 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC... (see the Principles) For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 69 5–741 ADDITIONAL READING Coonrod JD, Dans PE: Subdural empyema Am J Med 53:85, 1972 Feigin RD, McCracken GH Jr, Klein JO: Diagnosis and management of meningitis Pediatr Infect Dis J 11:785, 1992 Garcia-Monco JC, Benach JL: Lyme neuroborreliosis Ann Neurol 37 :69 1, 1995... Companies, Inc Click Here for Terms of Use 4777 Victor Ch 32 p29 0-3 01 6/ 11/01 2:11 PM Page 291 CHAPTER 32 / VIRAL INFECTIONS OF THE NERVOUS SYSTEM 2 3 4 5 6 291 These viruses account for 80 percent of cases of established viral origin Mumps: Highest incidence is in late winter and spring Male-tofemale ratio is 3:1 Herpes simplex, type 2, genital (rarely type 1), Epstein-Barr virus (EBV), and rarely cytomegalovirus... 4777 Victor Ch 33 p30 2-3 26 6/11/01 2:11 PM Page 305 CHAPTER 33 / CEREBROVASCULAR DISEASES 305 FIG 3 3-1 Middle Cerebral Artery Diagram of the left cerebral hemisphere, lateral aspect, showing the branches and distribution of the middle cerebral artery and the principal regions of cerebral localization Following is a list of the clinical manifestations of infarction in the territory of this artery and the... parietal anosognosia, hemiasomatognosia, lobe unilateral neglect, agnosia for the left half of external space, “dressing apraxia,” “constructional apraxia,” loss of topographic memory (continued) 4777 Victor Ch 33 p30 2-3 26 3 06 6/11/01 2:11 PM Page 3 06 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE FIG 3 3-1 Middle Cerebral Artery (continued) Signs and symptoms Inaccurate localization in the half... Victor Ch 33 p30 2-3 26 6/11/01 2:11 PM Page 307 CHAPTER 33 / CEREBROVASCULAR DISEASES 307 FIG 3 3-2 Anterior Cerebral Artery Diagram of a cerebral hemisphere, medial aspect, showing the branches and distribution and the principal regions of cerebral localization Following is a list of the clinical manifestations of infarction in the territory of this artery and the corresponding regions of cerebral damage . INTRACRANIAL NEOPLASMS 275 4777 Victor Ch 30 p 26 8-2 76 6/11/01 3:04 PM Page 275 5. Limbic and brainstem encephalitis (see the Principles, pp 68 7 68 8) 6. Progressive multifocal leukoencephalopathy. irritation of the meninges by blood, by contents of a cra- niopharyngioma, or by substances injected intrathecally. 6. Recurrent and chronic inflammatory meningitides of obscure ori- gin—Vogt-Koyanagi-Harada. and 43) 8. Retinopathy For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 64 2 69 4. ADDITIONAL READING Dawson DM: Antineoplastic drugs,