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In the diagnosis of disorders characterized by generalized cerebellar ataxia (affecting limbs, gait, and speech), the mode of onset

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Intoxication with alcohol, lithium, barbiturate, phenytoin or other anticonvulsants (associated with dysarthria, nystagmus, and sometimes confusion; Chaps 42, 43) Diamox-responsive episodic ataxia (Chap 37) Childhood hyperammonemias (Chap 37) Postinfectious, with mild in ammatory changes in CSF (Chap 36) Viral cerebellar encephalitis (Chap 33) Hyperthermia with coma at onset (Chap 17) Intoxication with mercury compounds or toluene (glue snif ng; spray painting; Chap 43) Postanoxic with intention myoclonus Brain tumors such as medulloblastoma, astrocytoma, hemangioblastoma (usually with headache and papilledema; Chap 31) Alcoholic-nutritional (Chaps 41 and 42) Paraneoplastic, often with opsoclonus and speci c anticerebellar antibodies (particularly with breast and ovarian carcinoma; Chap 31) Creutzfeldt Jakob disease (Chap 33) Cerebellar abscess (Chap 32) Whipple disease (often with myoclonus and oculomasticatory movements) Sprue (gluten enteropathy) Multiple sclerosis Friedreich ataxia and other spinocerebellar degenerations; other hereditary cerebellar degenerations [olivopontocerebellar degenerations; cerebellar cortical degenerations (Chap 39)] Adult form of fragile-X syndrome Hereditary metabolic diseases, often with myoclonus (Chap 37) Childhood ataxias, including ataxia telangiectasia, cerebellar agenesis, and dyssynergia cerebellaris myoclonica of Ramsay Hunt (Chap 39)

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caused by infarction or tumor in the ipsilateral cerebellar hemisphere or by demyelinating disease affecting cerebellar connections in the brainstem The ataxia of severe sensory neuropathy and of posterior column disease of the spinal ( sensory ataxia ) cord may simulate cerebellar ataxia; presumably this is due to involvement of the large peripheral spinocerebellar afferent bers However, there should seldom be dif culty in separating the two if one takes note of the loss of distal joint position sense, absence of associated cerebellar signs such as dysarthria or nystagmus, loss of tendon re exes, and the corrective effects of vision on sensory ataxia In peripheral neuropathy of this nature and in spinal cord disease, the Romberg sign is invariably present, re ecting a parallel dysfunction of large afferent bers in the posterior columns; this sign is not found in lesions of the cerebellar hemispheres except that the patient may initially sway with eyes open and a bit more with eyes closed This type of tremor reaches an extreme form in the large- ber polyneuropathy related to antibodies against myelin-associated glycoprotein (MAG) but the features are closer to an exaggerated essential tremor, as discussed in the next chapter and in Chap 46 In the Miller Fisher syndrome, which is considered to be a variant of Guillain-Barre neuropathy, sensation is intact or affected only slightly and the severe ataxia and intention tremor are presumably

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due to a highly selective peripheral disorder of spinocerebellar nerve bers Affection of these same bers in the spinocerebellar tracts of the cord may produce the same effects; subacute compressive lesions such as thoracic meningioma or demyelinating lesions are the usual causes Again, there is a prominent Romberg sign Occassionally, a cerebellar-like tremor in one limb results from a lesion in the dorsolateral cord that interrupts afferent bers, presumably those directed to the spinocerebellar tracts Vertiginous ataxia is primarily an ataxia of gait and is distinguished by the obvious complaint of vertigo and listing to one side, past-pointing, and rotary nystagmus (Chap 15) The nonvertiginous ataxia of gait due to vestibular paresis (eg, streptomycin toxicity) has special qualities described in Chap 7 Vertigo and cerebellar ataxia may be concurrent, as in some patients with a paraneoplastic disease and in those with infarction of the lateral medulla and inferior cerebellum An unusual and transient ataxia of the contralateral limbs occurs acutely after infarction or hemorrhage in the anterior thalamus (thalamic ataxia); in addition to neighborhood signs, there is often an accompanying unilateral asterixis Also, a lesion of the superior parietal lobule (areas 5 and 7 of Brodmann) may rarely result in a similar ataxia of the contralateral limbs