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exion-supination of the arm and between exion and extension of the ngers, the exed and adducted thumb being trapped by the exed ngers as the hand closes Other characteristic movements are eversion-inversion of the foot, retraction and pursing of the lips, twisting of the neck and torso, and alternate wrinkling and relaxation of the forehead or forceful opening and closing of the eyelids The movements appear to be slower than those of chorea, but all gradations between the two are seen; in some cases, it is impossible to distinguish between them, hence the term choreoathetosis Discrete voluntary movements of the hand are executed more slowly than normal, and attempts to perform them may result in a cocontraction of antagonistic muscles and a spread (over ow) of contraction to muscles not normally required in the movement (intention spasm) The over ow appears related to a failure of the striatum to suppress the activity of unwanted muscle groups Like polymyoclonus (see Chap 6), some forms of athetosis occur only during the performance of projected movement (intention or action athetosis) In other forms, the spasms appear to occur spontaneously, ie, they are involuntary and, if persistent, give rise to more or less xed dystonic postures, as described by Yanagisawa and Goto Athetosis may affect all four limbs or may be unilateral, especially in children who have suffered a hemiplegia at some previous date (posthemiplegic athetosis) Many athetotic patients exhibit variable degrees of rigidity and motor de cit due to associated corticospinal tract disease; these may account for the slower quality of athetosis compared to chorea In other patients with generalized choreoathetosis, as pointed out above, the limbs may be intermittently hypotonic The combination of athetosis and chorea of all four limbs is a cardinal feature of Huntington disease and of a state known as double athetosis, which begins in childhood Athetosis appearing in the rst years of life is usually the result of a congenital or postnatal condition such as hypoxia or rarely kernicterus Postmortem examinations in some of the cases have disclosed a peculiar pathologic change of probable hypoxic etiology, a status marmoratus, in the striatum (Chap 38); in other cases, of probable kernicteric (hyperbilirubinemic) etiology, there has been a loss of nerve cells and myelinated bers a status dysmyelinatus in the same regions In adults, athetosis may occur as an episodic or persistent disorder in hepatic encephalopathy, as a manifestation of chronic intoxication with phenothiazines or haloperidol, and as a feature of certain degenerative diseases, most notably Huntington chorea but also Wilson disease, Hallervorden-Spatz disease, Leigh disease, and other mitochondrial disease variants; less frequently, athetosis may be seen with Niemann-Pick (type C) disease, Kufs disease, neuroacanthocytosis, and ataxia telangiectasia It may also occur as an effect of excessive L-dopa in the treatment of Parkinson disease, in which case it appears to be due to a decrease in the activity of the subthalamic nucleus and the medial segment of the globus pallidus (Mitchell et al) Athetosis, usually in combination with chorea, may occur rarely in patients with AIDS and in those taking anticonvulsants Localized forms of athetosis may occasionally follow vascular lesions of the lenticular nucleus or thalamus, as in the cases described by Dooling and Adams Ballismus This term designates an uncontrollable, poorly patterned inging movement of an entire limb As remarked earlier, it is closely related to chorea and athetosis, indicated by the frequent coexistence of these movement abnormalities and the tendency for ballismus to blend into a less obtrusive choreoathetosis.

always important to keep in mind the possibility of neoplasia, HIV, tuberculosis, cryptococcosis, sarcoidosis, syphilis, borreliosis, and inadequately treated bacterial meningitis each of which may simulate aseptic meningitis and each of which presents an urgent diagnostic problem By contrast, the various viral forms of aseptic meningitis are usually self-limited and benign; establishing a speci c etiologic diagnosis is usually not necessary

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From the foregoing discussion it is evident that the separation of the clinical syndromes of aseptic meningitis and encephalitis is not always easy In some patients with aseptic meningitis, mild drowsiness or confusion may be present, suggesting cerebral involvement Conversely, in some patients with encephalitis, the cerebral symptoms may be mild or inapparent, and meningeal symptoms and CSF abnormalities predominate These facts make it dif cult to place complete reliance on statistical data from various virus laboratories about the relative incidence of meningitis and encephalitis The common practice is to assume that viral meningitis causes only fever, headache, stiff neck, and photophobia; if any other CNS symptoms are added, the condition is generally called meningoencephalitis As has been emphasized, it appears that the same spectrum of viruses gives rise to both meningitis and encephalitis It is our impression that many cases of enteroviral and practically all cases of mumps and LCM encephalopathy are little more than examples of intense meningitis Rarely have they caused death with postmortem demonstration of cerebral lesions, and surviving patients seldom have residual neurologic signs Conversely, several agents, notably the arboviruses, may cause encephalitic lesions with only mild meningeal symptoms The core of the encephalitis syndrome consists of an acute febrile illness with evidence of meningeal involvement (sometimes only headache), added to which are various combinations of the following symptoms and signs: convulsions, delirium, confusion, stupor, or coma; aphasia; hemiparesis with asymmetry of tendon re exes and Babinski signs; involuntary movements, ataxia, and myoclonic jerks; nystagmus, ocular palsies, and facial weakness The spinal uid invariably shows a cellular reaction and the protein is slightly elevated Imaging studies of the brain are most often normal but may show diffuse edema or enhancement of the cortex and, in certain infections, subcortical and deep nuclear involvement as well as, in the special case of HSV encephalitis, selective damage of the inferomedial temporal and frontal lobes One or another of these ndings predominates in certain types of encephalitis, but the clinical diagnosis of encephalitis in the setting of a febrile aseptic meningitis always rests on the demonstration of derangement of the function of the cerebrum, brainstem, or cerebellum Differentiation of Viral from Postinfectious Encephalitis The acute encephalitis syndrome described above may take two forms: the more common direct invasion of brain and meninges (true viral encephalitis) and a postinfectious encephalomyelitis that is based on an auto-immune reaction to the systemic viral infection but in which virus is not present in neural tissue The distinction between postinfectious encephalomyelitis (page 790) and infectious encephalitis may be dif cult, especially in younger patients who have a proclivity to develop the postinfectious variety The latter, termed acute disseminated encephalomyelitis (ADEM), occurs after a latency of several days, as the infectious illness is subsiding It is expressed by a low-grade fever and cerebral symptoms such as.