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Arboviral Encephalitis
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The common arthropod-borne viruses (arboviruses) that cause encephalitis in the United States and their geographic range have been listed earlier There are alternating cycles of viral infection in mosquitoes and vertebrate hosts; the mosquito becomes infected by taking a blood meal from a viremic host (horse or bird) and injects virus into the host, including humans The seasonal incidence of these infections is practically limited to the summer and early fall, when mosquitoes are biting In the equine encephalitides, regional deaths in horses usually precede human epidemics In St Louis encephalitis, the urban bird or animal or possibly the human becomes the intermediate host West Nile outbreaks are preceded by illness in common birds such as crows and jays St Louis, California and La Crosse agents are endemic in the United States because of the cycle of infection in small rodents The clinical manifestations of the various arbovirus infections are almost indistinguishable from one another, although they do vary with the age of the patient The incubation period after mosquito bite transmission is 5 to 15 days There may be a brief prodromal fever with arthralgias or rash (eg, West Nile fever) In infants, there may be only an abrupt onset of fever and convulsions In older children, the onset is usually less abrupt, with complaints of headache, listlessness, nausea or vomiting, drowsiness, and fever for several days before medical attention is sought; convulsions, confusion, stupor, and stiff neck then become prominent Photophobia, diffuse myalgia, and tremor (of either action or intention type) may be observed in this age group and in adults Asymmetry of tendon re exes, hemiparesis, extensor plantar signs, myoclonus, chorea, and sucking and grasping re exes may also occur McJunkin and colleagues have described the clinical features of 127 patients with La Crosse infection seen at their medical center over a decade, and their data are representative of other arboviral infections In addition to the typical features of viral encephalitis, they emphasize, in a proportion of patients, hyponatremia, raised intracranial pressure with cerebral swelling, and, most notable to us, signal changes in the MRI that simulate herpes encephalitis It affects children mainly, causing fever, seizures, and focal neurologic signs, but is otherwise benign in most instances, with full recovery A special syndrome of febrile, accid, paralytic poliomyelitis resulting from West Nile virus infection has also been described It evolves over several days and in a few cases is accompanied by facial paralysis (see Jeha et al) A few cases have begun with an extrapyramidal syndrome; these syndromes occur also with the other aviviruses (Japanese encephalitis, Murray valley, St Louis)
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MAJOR CATEGORIES OF NEUROLOGIC DISEASE
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The CSF ndings are much the same as in aseptic meningitis (lymphocytic pleocytosis, mild protein elevation, normal glucose values) Recovery of virus from blood or CSF is usually not possible and PCR testing has not been routinely applied However, antiviral IgM is present within the rst days of symptomatic disease and can be detected and quanti ed by means of ELISA Some patients have not developed antibodies by the time of admission to the hospital and the test may have to be repeated The MRI may be normal or show signal changes and edema in the cortex, basal ganglia, or thalamus (the latter is described in the Japanese virus group) The fever and neurologic signs subside after 4 to 14 days unless death supervenes or destructive CNS changes have occurred No antiviral agents are known to be effective in the treatment of arboviral encephalitis; one must rely entirely on supportive measures; on occasion, brain swelling reaches a degree that requires speci c therapy, as outlined on pages 317 and 766 The pathologic changes consist of widespread degeneration of single nerve cells, with neuronophagia as well as scattered foci of in ammatory necrosis involving both the gray and white matter The brainstem is relatively spared In some cases of eastern equine encephalitis, the destructive lesions may be massive, involving the major part of a lobe or hemisphere and are readily displayed by MRI, but in the other arbovirus infections the foci are microscopic in size (see Deresiewicz et al) West Nile virus may also produce a regional pattern of neuronal damage that affects the anterior horn cells of the spinal cord, as mentioned above A pathologic description of this process has been provided by our colleagues and by others (see Asnis et al) Perivascular cuf ng by lymphocytes and other mononuclear leukocytes and plasma cells as well as a patchy in ltration of the meninges with similar cells are the usual histopathologic hallmarks of viral encephalitis Of the arbovirus infections in the United States, eastern equine encephalitis is among the most serious, since a large proportion of those infected develop encephalitis; about one-third die and a similar number, more often children, are left with disabling abnormalities mental retardation, emotional disorders, recurrent seizures, blindness, deafness, hemiplegia, extrapyramidal motor abnormalities, and speech disorders While only a small proportion of those exposed become infected, the poliomyelitis and parkinsonian syndromes of the aviviruses may be permanent residua as mentioned earlier (see Solomon) The mortality rate in other arbovirus infections varies from 2 to 12 percent in different outbreaks, and the incidence of serious sequelae is about the same
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Clinical Features The symptoms, which evolve over several days, are in most cases like those of any other acute encephalitis namely, fever, headache, seizures, confusion, stupor, and coma In some patients these manifestations are preceded by symptoms and ndings that betray the predilection of this disease for the inferomedial portions of the frontal and temporal lobes They include olfactory or gustatory hallucinations, anosmia, temporal lobe seizures, personality change, bizarre or psychotic behavior or delirium, aphasia, and hemiparesis Although several seizures at the onset of illness are not an uncommon presentation, status epilepticus is rare An affection of memory can often be recognized, but usually this becomes evident only later, in the convalescent stage, as the patient awakens from stupor or coma Swelling and herniation of one or both temporal lobes through the tentorium may occur, leading to deep coma and respiratory arrest during the rst few days of the illness The CSF is typically under increased pressure and almost invariably shows a pleocytosis (range, 10 to 200 cells per cubic millimeter, infrequently more than 500) The cells are mostly lymphocytes, but there may be a signi cant number of neutrophils early on In a few cases, 3 to 5 percent in some large series, the spinal uid has been normal in the rst days of the illness, only to become abnormal when re-examined Also, in only a minority of cases, red cells, sometimes numbering in the thousands, and xanthochromia are found, re ecting the hemorrhagic nature of the brain lesions; but it should be emphasized that more often red cells are few in number or absent The protein content is increased in most cases Rarely, the CSF glucose levels may be reduced to slightly less than 40 mg/dL, creating confusion with tuberculous and fungal meningitides Pathology The lesions take the form of an intense hemorrhagic necrosis of the inferior and medial temporal lobes and the medioorbital parts of the frontal lobes The region of necrosis may extend upward along the cingulate gyri and sometimes to the insula or the lateral parts of the temporal lobes or caudally into the midbrain but always contiguous with areas of mediotemporal lobe necrosis The temporal lobe lesions are usually bilateral but not symmetrical This distribution of lesions is so characteristic that the diagnosis can be made by gross inspection or by their location and appearance on imaging studies Cases described in past years as acute necrotizing encephalitis and inclusion body encephalitis were likely to have been instances of HSV encephalitis In the acute stages of the disease, intranuclear eosinophilic inclusions are found in neurons and glial cells, in addition to the usual microscopic abnormalities of acute encephalitis and hemorrhagic necrosis The unique localization of the lesions in this disease could possibly be explained by the virus s route of entry into the CNS Two such routes have been suggested (Davis and Johnson) The virus is thought to be latent in the trigeminal ganglia and, with reactivation, to infect the nose and then the olfactory tract Alternatively, with reactivation in the trigeminal ganglia, the infection may spread along nerve bers that innervate the leptomeninges of the anterior and middle fossae The lack of lesions in the olfactory bulbs in as many as 40 percent of fatal cases (Esiri) is a point in favor of the second pathway Diagnosis Acute herpes simplex encephalitis must be distinguished from other types of viral encephalitis, from acute hemorrhagic leukoencephalitis of Weston Hurst (page 792), and from subdural empyema, cerebral abscess, cerebral venous thrombosis, and septic embolism (Chap 32) When aphasia is the initial man-
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