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myoclonus, nystagmus, and a highly characteristic oculomasticatory movement described as myorhythmia (which looks more to us like rhythmic myoclonus) have been noted less often than the dementing syndrome The rhythmic myoclonus or spasm occurs in synchronous bursts involving several adjacent regions, mainly the eyes, jaw, and face Almost always the myorhythmias are accompanied by a supranuclear vertical gaze paresis that sometimes affects horizontal eye movements as well Presumably, the neurologic complications are the result of in ltration of the brain by the organism, but this has not been satisfactorily established Approximately half of the patients have a mild pleocytosis and some of these have PAS-positive material in the CSF A variety of brain imaging abnormalities have been recorded, none characteristic, but either enhancing focal lesions or a normal scan may be found The diagnosis is made mainly from PAS staining of an intestinal (jejunal) biopsy, as already mentioned, supplemented by PCR testing of the bowel tissue or biopsy material from brain or lymph node In cases of subacute progressive limb and gait ataxia occurring in middle-aged or older men in whom no cause is uncovered by less invasive means, it is justi able to perform these tests (see Chap 5) Rarely, the neurologic symptoms may occur in the absence of gastrointestinal disease (Adams et al) In the extensive review of 84 cases by Louis and colleagues, 71 percent had cognitive changes, half with psychiatric features; 31 percent had myoclonus; 18 percent, ataxia; and 20 percent had the oculomasticatory and skeletal myorhythmias that are virtually pathognomonic of Whipple disease (Schwartz et al) Treatment A course of penicillin and streptomycin followed by trimethoprim-sulfamethoxazole or ceftriaxone and continued for 1 year is one of the currently recommended treatment regimens An alternative approach is 2 weeks of ceftriaxone followed by treatment with trimethoprim-sulfamethoxazole or a tetracycline for a year Antibiotic-resistant cases and instances of relapse after antibiotic treatment are known The review by Anderson may be consulted for details Acute Toxic Encephalopathy Lyon and colleagues described acute encephalopathy of obscure origin in children, a febrile and sometimes fatal illness that could not be ascribed to direct infection of the nervous system During the height of a systemic bacterial or sometimes viral infection, the child sinks into coma, seizures are infrequent, the neck is supple, and the spinal uid shows no changes or only a few cells This is undoubtedly an illness of diverse causes, among them uid overload and electrolyte imbalance, Reye syndrome (page 969), and, possibly most common, postinfectious encephalitis Nonetheless, cases continue to be reported, such as those of Thi and colleagues, which can only be classi ed as a noninfectious bacterial encephalopathy or encephalitis A relationship to the septic encephalopathy of adults, which has been emphasized by the group from London, Ontario, is possible but unproved The term acute toxic encephalopathy still has some utility in these cases, but a careful search for better-characterized causes of febrile coma must be undertaken.

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Subdural empyema is an intracranial (rarely intraspinal) suppurative process between the inner surface of the dura and the outer surface of the arachnoid The term subdural abscess, among others, has been applied to this condition, but the proper name is empyema, indicating suppuration in a preformed space Contrary to prevailing

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opinion, subdural empyema is not a rarity (although it is only about one- fth as frequent as cerebral abscess) It is distinctly more common in males, a feature for which there is no explanation The infection usually originates in the frontal or ethmoid or, less often, the sphenoid sinuses and in the middle ear and mastoid cells As with bacterial meningitis, there have been in the last decade an increasing number of cases that follow surgery of the sinuses and other cranial structures In infants and children and infrequently in adults, there may be spread from a leptomeningitis Infection gains entry to the subdural space by direct extension through bone and dura or by spread from septic thrombosis of the venous sinuses, particularly the superior longitudinal sinus Rarely, the subdural infection is metastatic, from infected lungs; hardly ever is it secondary to bacteremia or septicemia Occasionally it extends from a brain abscess It is again of interest that cases of sinus origin predominate in adolescent and young adult men (Kaufman et al) In such cases, streptococci (nonhemolytic and viridans) are the most common organisms, followed by anaerobic streptococci (often Strep milleri) or Bacteroides Less often Staph aureus, E coli, Proteus, and Pseudomonas are causative In about half the cases unrelated to surgery, no organisms can be cultured or seen on Gram s stain The factors that lead to a subdural empyema rather than to a cerebral abscess are not fully understood Pathology A collection of subdural pus, in quantities ranging from a few milliliters to 100 to 200 mL, lies over the cerebral hemisphere Pus may spread into the interhemispheric ssure or be con ned there; occasionally it is found in the posterior fossa, covering the cerebellum The arachnoid, when cleared of exudate, is cloudy, and thrombosis of meningeal veins may be seen The underlying cerebral hemisphere is depressed, and in fatal cases there is often an ipsilateral temporal lobe herniation Microscopic examination discloses various degrees of organization of the exudate on the inner surface of the dura and in ltration of the underlying arachnoid with small numbers of neutrophilic leukocytes, lymphocytes, and mononuclear cells The thrombi in cerebral veins seem to begin on the sides of the veins nearest the subdural exudate The super cial layers of the cerebral cortex undergo ischemic necrosis, which probably accounts for the unilateral seizures and other signs of disordered cerebral function (Kubik and Adams) Symptomatology and Laboratory Findings Usually the history includes reference to chronic sinusitis or mastoiditis with a recent are-up causing local pain and increase in purulent nasal or aural discharge In sinus cases, the pain is over the brow or between the eyes; it is associated with tenderness on pressure over these parts and sometimes with orbital swelling General malaise, fever, and headache at rst localized, then severe and generalized and associated with vomiting are the rst indications of intracranial spread They are followed in a few days by drowsiness and increasing stupor, rapidly progressing to coma At about the same time, focal neurologic signs appear, the most important of which are unilateral motor seizures, hemiplegia, hemianesthesia, aphasia, and paralysis of lateral conjugate gaze Fever and leukocytosis are always present and the neck is stiff Cases that follow surgery may be more indolent The usual CSF ndings are an increased pressure, pleocytosis in the range of 50 to 1000 per cubic millimeter, a predominance of polymorphonuclear cells, elevated protein content (75 to 300 mg/ dL), and normal glucose values The uid is often sterile, but on.