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generalized seizures, widespread myoclonus, ataxia, and sometimes visual disturbances due to progressive chorioretinitis As the disease advances, rigidity, hyperactive re exes, Babinski signs, progressive unresponsiveness, and signs of autonomic dysfunction appear In the nal stage the child lies insensate, virtually decorticated The course is usually steadily progressive, death occurring within 1 to 3 years In about 10 percent of cases the course is more prolonged, with one or more remissions In a similar number the course is fulminant, leading to death within months of onset Exceptionally, the disease occurs in young adults In two reported cases in pregnant women, blurred vision and weakness of limbs developed before they became akinetic and mute, without a trace of myoclonus or cerebellar ataxia Nevertheless, the progressive ataxic-myoclonic chronic dementia in a child is so typical that bedside diagnosis is usually possible The EEG shows a characteristic abnormality consisting of periodic (every 5 to 8 s) bursts of 2- to 3-per-second high-voltage waves, followed by a relatively at pattern The CSF contains few or no cells, but the protein is increased, particularly the gamma globulin fraction, and agarose gel electrophoresis discloses oligoclonal bands of IgG These have been shown to represent measles virus speci c antibody (Mehta et al) Both the serum and CSF contain high concentrations of neutralizing antibody to measles (rubeola) virus, but the virus has been recovered from the brain tissue only with dif culty The MRI changes begin in the subcortical white matter and spread to the periventricular region (Anlar et al) Histologically the lesions involve the cerebral cortex and white matter of both hemispheres and the brainstem The cerebellum is usually spared Destruction of nerve cells, neuronophagia, and perivenous cuf ng by lymphocytes and mononuclear cells indicate the viral nature of the infection In the white matter there is degeneration of medullated bers (myelin and axis cylinders), accompanied by perivascular cuf ng with mononuclear cells and brous gliosis (hence the term sclerosing encephalitis) Eosinophilic inclusions, the histopathologic hallmark of the disease, are found in the cytoplasm and nuclei of neurons and glial cells Virions, thought to be measles nucleocapsids, have been observed in the inclusion-bearing cells examined electron microscopically How a ubiquitous and transient viral infection in a seemingly normal young child allows the development, many years later, of a rare encephalitis is a matter of speculation Sever believes that there is a delay in the development of immune responses during the initial infection and a later inadequate immune responses that are incapable of clearing the suppressed infection An alternative hypothesis is that certain brain cells fail to synthesize a so-called M protein, which is essential for the assembly of the viral membrane, and that this limitation of host-cell capability is related to the extent of viral seeding of the brain during the initial infection (Hall et al) The differential diagnosis includes the childhood and adolescent dementing diseases such as lipid storage diseases (Chap 37) and Schilder demyelinative disease (page 782) In presumptive clinical cases of SSPE, the ndings of periodic complexes in the EEG, elevated gamma globulin and oligoclonal bands in the CSF, and elevated measles antibody titers in the serum and CSF are suf cient to make the diagnosis No effective treatment is available The administration of amantadine and inosiplex was found by some investigators to lead to improvement and prolonged survival but others could not corroborate these effects The therapeutic value of intrathecal administration of alpha interferon is being investigated.

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Subacute Measles Encephalitis with Immunosuppression Whereas SSPE occurs in children who were previously normal, another rare type of measles encephalitis has been described, affecting both children and adults with defective cell-mediated immune responses (Wolinsky et al) In this type, measles or exposure to measles precedes the encephalitis by 1 to 6 months Seizures (often epilepsia partialis continua), focal neurologic signs, stupor, and coma are the main features of the neurologic illness and lead to death within a few days to a few weeks The CSF may be normal, and levels of measles antibodies do not increase Aicardi and colleagues have isolated measles virus from the brain of such a patient The lesions are similar to those of SSPE (eosinophilic inclusions in neurons and glia, with varying degrees of necrosis) except that in ammatory changes are lacking In a sense this subacute measles encephalitis is an opportunistic infection of the brain in an immunode cient patient The relatively short interval between exposure and onset of neurologic disease, the rapid course, and lack of antibodies distinguish this form of subacute measles encephalitis from both SSPE and postmeasles (postinfectious) encephalomyelitis (Chap 36) Progressive Rubella Panencephalitis Generally the de cits associated with congenital rubella infection are nonprogressive at least after the second or third year of life There are, however, descriptions of children with the congenital rubella syndrome in whom a progressive neurologic deterioration occurred after a stable period of 8 to 19 years (Townsend et al; Weil et al) In 1978, Wolinsky described 10 cases of this syndrome, a few of them apparently related to acquired rather than to congenital rubella Since then, this late-appearing progressive syndrome seems to have disappeared, no new cases having been reported in the past 30 years The clinical syndrome has been quite uniform On a background of the xed stigmata of congenital rubella, there occurs a deterioration in behavior and school performance, often associated with seizures, and, soon thereafter, a progressive impairment of mental function (dementia) Clumsiness of gait is an early symptom, followed by a frank ataxia of gait and then of the limbs Spasticity and other corticospinal tract signs, dysarthria, and dysphagia ensue Pallor of the optic discs, ophthalmoplegia, spastic quadriplegia, and mutism mark the nal phase of the illness The CSF shows a mild increase of lymphocytes and elevation of protein and a marked increase in the proportion of gamma globulin (35 to 52 percent of the total protein), which assumes an oligoclonal pattern on agarose gel electrophoresis The CSF and serum rubella-antibody titers are elevated Pathologic examination of the brain has shown a widespread, progressive subacute panencephalitis mainly affecting the white matter No inclusion-bearing cells were seen Thus it appears that rubella virus infection, acquired in utero or in the postnatal period, may persist in the nervous system for years before rekindling a chronic active infection Progressive Multifocal Leukoencephalopathy (PML) This disorder, rst observed clinically by Adams and colleagues in 1952, was described morphologically by Astrom and coworkers (1958) and then with a larger material by Richardson It is characterized by widespread demyelinative lesions, mainly of the cerebral hemispheres but sometimes of the brainstem and cerebellum and rarely of the spinal cord The lesions vary greatly in size and severity from microscopic foci of demyelination to massive multifocal zones of destruction of both myelin and axis cylinders involving.