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SCHOLD SC, CHO E-S, SOMASUNDARAM M, POSNER JB: Subacute motor neuronopathy: A remote effect of lymphoma Ann Neurol 5:271, 1979 SCHRELL UM, RITTIG NG, ANDERS M, et al: Hydroxyurea for treatment of unresectable and recurrent meningiomas II Decrease in the size of meningiomas in patients treated with hydroxyurea J Neurosurg 86:840, 1997 SEIZINGER BR, ROULEAN GA, OZELIUS LJ, et al: Von Hippel Lindau disease maps to the region of chromosome 3 associated with renal carcinoma Nature 332:268, 1988 SHAPIRO WR: Therapy of adult malignant brain tumors: What have the clinical trials taught us Semin Oncol 13:38, 1986 SHAW EG, DAUMAS-DUPORT C, SCHEITHAUER BS, et al: Radiation therapy in the management of low-grade supratentorial astrocytomas J Neurosurg 70:853, 1989 SHEIBANI K, BATTIFORA H, WINBERG CD, et al: Further evidence that malignant angioendotheliomatosis is an angiotropic large-cell lymphoma N Engl J Med 314:943, 1986 SMITT PS, KINOSHITA A, LEEUW B, et al: Paraneoplastic cerebellar ataxia due to autoantibodies against a glutamate receptor N Engl J Med 342: 21, 2000 SORENSON SC, EAGAN RT, SCOTT M: Meningeal carcinomatosis in patients with primary breast or lung cancer Mayo Clin Proc 59:91, 1984 SPARLING HJ, ADAMS RD, PARKER F: Involvement of the nervous system by malignant lymphoma Medicine 26:285, 1947 TOMLINSON BE, PERRY RH, STEWART-WYNNE EG: In uence of site of origin of lung carcinomas on clinical presentation and central nervous system metastases J Neurol Neurosurg Psychiatry 42:82, 1979 VERMA A, BERGER JR, SNODGRASS S, PETITO C: Motor neuron disease: A paraneoplastic process associated with anti-Hu antibody and smallcell lung carcinoma Ann Neurol 40:112, 1996 VINCENT A, BUCKLEY C, SCHOTT JM, et al: Potassium channel antibodyassociated encephalopathy: A potentially immunotherapy-responsive form of limbic encephalitis Brain 127:701, 2004 VOLTZ R, GULTEKIN SH, ROSENFELD MR, et al: A serologic marker of paraneoplastic limbic and brain-stem encephalitis in patients with testicular cancer N Engl J Med 340:1788, 1999 WAGA S, MORIKAWA A, SAKAKURA M: Craniopharyngioma with midbrain involvement Arch Neurol 36:319, 1979 WASSERSTROM WR, GLASS JP, POSNER JB: Diagnosis and treatment of leptomeningeal metastases from solid tumors: Experience with 90 patients Cancer 49:759, 1982 WEISS HD, RICHARDSON EP: Solitary brainstem metastasis Neurology 28:562, 1978 YU Z, KRYZER TJ, GRIESMANN GE, et al: CRMP-5 neuronal antibody: Marker of lung cancer and thymoma-related autoimmunity Ann Neurol 49:164, 2001 YUNG WA, HORTEN BC, SHAPIRO WR: Meningeal gliomatosis: A review of 12 cases Ann Neurol 8:605, 1980 ZENTNER J, WOLF HK, OSTERTUN B, et al: Gangliogliomas: Clinical, radiological, and histopathological ndings in 51 patients J Neurol Neurosurg Psychiatry 57:1497, 1994 ZIMMERMAN HM: Brain tumors: Their incidence and classi cation in man and their experimental production Ann NY Acad Sci 159:337, 1969 ZULCH KJ: Brain Tumors, Their Biology and Pathology, 3rd ed New York, Springer-Verlag, 1986.

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This chapter is concerned mainly with the pyogenic or bacterial infections of the central nervous system (CNS), ie, bacterial meningitis, septic thrombophlebitis, brain abscess, epidural abscess, and subdural empyema The granulomatous infections of the CNS notably tuberculosis, syphilis and other spirochetal infections, and certain fungal infections are also discussed in some detail In addition, consideration is given to sarcoid, a granulomatous disease of uncertain etiology, and to the CNS infections and infestations caused by certain rickettsias, protozoa, worms, and ticks A number of other infectious diseases of the nervous system are more appropriately discussed elsewhere in this book Diseases due to bacterial exotoxins diphtheria, tetanus, botulism are considered with other toxins that affect the nervous system (Chap 43) Leprosy, which is essentially a disease of the peripheral nerves, is described in Chap 46, and trichinosis, mainly a disease of muscle, in Chap 48 Viral infections of the nervous system, because of their frequency and importance, are allotted a chapter of their own (Chap 33)

Pyogenic infections reach the intracranial structures by one of two pathways, either by hematogenous spread (emboli of bacteria or infected thrombi) or by extension from cranial structures (ears, paranasal sinuses, osteomyelitic foci in the skull, penetrating cranial injuries, or congenital sinus tracts) In a number of cases, infection is iatrogenic, being introduced in the course of cerebral or spinal surgery, the placement of a ventriculoperitoneal shunt, or rarely by a lumbar puncture needle Increasingly, infection is nosocomial, ie, acquired in-hospital; in urban hospitals, nosocomial meningitis is now as frequent as the non-hospital-acquired variety (Durand et al) Surprisingly little is known about the mechanisms of hematogenous spread, for human autopsy material seldom provides information on this point, and animal experiments involving the injection of virulent bacteria into the bloodstream have yielded somewhat contradictory results In most instances of bacteremia or septicemia, the nervous system seems not to be infected; yet sometimes a bacteremia due to pneumonia or endocarditis is the only apparent predecessor to meningitis With respect to the formation of brain abscess, the resistance of cerebral tissue to infection is notable Direct injection of virulent bacteria into the brain of an animal seldom results in abscess formation In fact, this condition has been produced consistently only by injecting culture medium along with the bacteria or by causing necrosis of the tissue at the time bacteria are inoculated In humans, infarction of brain tissue 592

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due to arterial occlusion (thrombosis or embolism) or venous occlusion (thrombophlebitis) appears to be a common and perhaps necessary antecedent The mechanism of meningitis and brain abscess from infection of the middle ear and paranasal sinuses is easier to understand The cranial epidural and subdural spaces are practically never the sites of blood-borne infections, in contrast to the spinal epidural space, where such infections are almost always introduced by the hematogenous route Furthermore, the cranial bones and the dura mater (which essentially constitutes the inner periosteum of the skull) protect the cranial cavity against the ingress of bacteria This protective mechanism may fail if suppuration occurs in the middle ear, mastoid cells, or frontal, ethmoid, and sphenoid sinuses Two pathways from these sources have been demonstrated: (1) infected thrombi may form in diploic veins and spread along these vessels into the dural sinuses (into which the diploic veins ow), and from there, in retrograde fashion, along the meningeal veins into the brain, and (2) an osteomyelitic focus may form, with erosion of the inner table of bone and invasion of the dura, subdural space, piaarachnoid, and even brain Each of these pathways has been observed by the authors in some fatal cases of epidural abscess, subdural empyema, meningitis, cranial venous sinusitis and meningeal thrombophlebitis, and brain abscess However, in many cases coming to autopsy, the pathway of infection cannot be determined With a hematogenous infection in the course of a bacteremia, usually a single type of virulent organism gains entry to the cranial cavity In the adult the most common pathogenic organisms are pneumococcus (Streptococcus pneumoniae), meningococcus (Neisseria meningitides), Haemophilus in uenzae, Listeria monocytogenes, and staphylococcus; in the neonate, Escherichia coli and group B streptococcus; in the infant and child, H in uenzae By contrast, when septic material embolizes from infected lungs, pulmonary arteriovenous stulas, or congenital heart lesions or extends directly from ears or sinuses, more than one type of bacterial ora common to these sources may be transmitted Such mixed infections pose dif cult problems in therapy Occasionally in these latter conditions, the demonstration of the causative organisms may be unsuccessful, even from the pus of an abscess (mainly because of inadequate culturing techniques for anaerobic organisms and the prior use of antibiotics) Infections that follow neurosurgery or the insertion of a cranial appliance are usually staphylococcal; a small number are due to mixed ora, including anaerobic ones, or the enteric organisms In determining the most likely invading organism, the age of the patient, the clinical setting of the infection (community-acquired, postsurgical, or nosocomial), the immune status of the patient, and evidence of systemic and local cranial disease all must be taken into account.

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