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these disorders will re ect differences in the patterns of expression of the affected proteins; ie, each is expressed in different subpopulations of neurons and at different stages in development This raises the possibility that the cascade of events that triggers neuronal degeneration is similar in each of the diseases with a CAG expansion and that a therapy might be discovered that is effective in all of them Table 39-5 summarizes the chromosomal loci, genetic terminology, related neural abnormalities, and clinical features of the CAG-dependent (and other) cerebellar atrophies The main types are summarized again here with some clinical comments: SCA 1: 6p; ophthalmoparesis, pyramidal and extrapyramidal signs; included in this group are most of the olivopontocerebellar atrophies SCA 2: 12q; slowed eye movements and saccades (Wadia type) Dentatorubropallidoluysian atrophy (DRPLA): 12p SCA 3:14q; the Machado-Joseph phenotype with several allelic variants SCA 4: 16q; sensory neuropathy and pyramidal signs SCA 7: 3p; retinal degeneration SCA 6: 19p; related to the alpha subunit of a voltage-dependent calcium channel; a different mutation at the same locus causes the acetazolamide-responsive episodic ataxia (EA-2) EA-1: (episodic ataxia) 12p; potassium channelopathy EA-2: (acetazolamide-responsive episodic ataxia) 19p; calcium channelopathy Differential Diagnosis of the Degenerative Ataxias (See Table 51, Page 78) Sporadic forms of cerebellar ataxia in adults are in some instances traceable to strokes involving cerebellar pathways (Safe et al) These are, of course, of acute onset Some cases of ataxia are alcoholic-nutritional in origin, and a few are related to abuse of drugs, especially anticonvulsants, which may in a few cases cause a slowly progressive and permanent ataxia; rarely, organic mercury induces subacute cerebellar degeneration, and adulterated heroin causes a more abrupt and severe ataxic syndrome The paraneoplastic variety of cerebellar degeneration often enters into the differential diagnosis; as a rule it occurs mostly in women with breast or ovarian cancers and evolves much more rapidly than any of the heredodegenerative forms The more rapid onset of ataxia and the presence of anti-Purkinje cell antibodies (anti-Yo; page 583) are central to identifying the nature of this disease From time to time one observes a similar idiopathic variety of subacute cerebellar degeneration, particularly in women who have no neoplasm and lack the speci c antibodies of the paraneoplastic disease (Ropper) Rare cases of ataxia have been associated with celiac disease and Whipple disease, as noted in Chap 5 Ataxia may also be an early and prominent manifestation of Creuutzfeldt-Jakob disease caused by a transmissible prion (see Chap 33) or of an inherited metabolic disease (Chap 37) Of the latter, late-onset GM2 gangliosidosis may simulate a cerebellar degeneration in adults (page 826) Rare cases of aminoacidopathy manifesting for the rst time in adult life have also provoked a cerebellar syndrome Treatment This has been unsatisfactory and is limited largely to supportive measures such as the prevention of falling Amantadine 200 mg daily for several months has shown limited bene t in some studies (Boetz et al) Whether thalamic electrical stimulators, or the type used for the treatment of Parkinson disease, have a role in suppressing the cerebellar tremor is not known
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The syndrome of quick, arrhythmic, involuntary single or repetitive twitches of a muscle or group of muscles was described in Chap 6, where it was pointed out that the condition has many causes Those due to hereditary metabolic diseases are presented in Chap 37 Familial forms are known, one of which, associated with cerebellar ataxia, was discussed earlier (dyssynergia cerebellaris myoclonica of Ramsay Hunt) But there is another disease, known as hereditary essential benign myoclonus, that occurs in relatively pure form unaccompanied by ataxia (page 87) In the latter condition, it may at times be dif cult to evaluate coordination because willed movement is interrupted by the myoclonus and may be mistaken for intention tremor Only by slowing the voluntary movement can the myoclonus be reduced or eliminated This myoclonic disease is inherited as an autosomal dominant trait It becomes manifest early in life; once established, it persists with little or no change in severity throughout life, often with rather little disability It can, by its natural course, be differentiated from some of the hereditary metabolic diseases such as the Unverricht and Lafora types of myoclonic epilepsy, the lipidoses, tuberous sclerosis, and myoclonic disorders that follow certain viral infections and anoxic encephalopathy Of interest is the response of this form of movement disorder, as in the case of acquired postanoxic myoclonus (page 89), to certain pharmacologic agents, notably clonazepam, valproic acid, and 5-hydroxytryptophan, the amino acid precursor of serotonin, particularly when these agents are used in combination The main clinical distinctions to be made are from Creutzfeldt-Jakob subacute spongiform encephalopathy; drug-induced myoclonus, particularly lithium; renal failure and other acquired metabolic disorders; asterixis; and from the startle responses (page 90) Myoclonus as one component of a more complex movement disorder in corticobasal-ganglionic degeneration has already been mentioned
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