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movement, to the point where the arm may strike the face This is due to a delay in contraction of the triceps muscle, which ordinarily would arrest over exion of the arm This abnormality, incorrectly referred to as Holmes s rebound phenomenon, is more appropriately designated as an impairment of the check re ex Stewart and Holmes, who rst described this test, made the point that when resistance to exion is suddenly removed, the normal limb moves only a short distance in exion and then recoils or rebounds in the opposite direction In this sense, rebound of the limb is actually de cient in cerebellar disease but is exaggerated in spastic states Patients with these various abnormalities of tone may show little or no impairment of motor power, indicating that the maintenance of posture involves more than the voluntary contraction of muscles It is noteworthy that most of the additional signs of cerebellar hypotonia are absent in the accid muscles of peripheral nerve disease indicating that the cerebellum exerts a unique modulating effect at spinal segmental levels Other Symptoms of Cerebellar Disease A slight loss of muscular power and excessive fatigability of muscle may occur with acute cerebellar lesions Also, in unilateral cerebellar disease, the ipsilateral arm may not swing normally in walking Insofar as these symptoms cannot be explained by other disturbances of motor function, they may be regarded as primary manifestations of cerebellar disease, but they are never severe or persistent and are of little clinical importance; anything approaching a hemiparesis in distribution or severity should not be attributed to cerebellar disease Myoclonic movements ie, brief (50- to 100-ms), random contractions of muscles or groups of muscles are, in some disease processes, combined with cerebellar ataxia When multiple jerks mar a volitional movement, they may be mistaken for an ataxic tremor (The same error may be caused by asterixis) Ramsey Hunt described myoclonus in connection with a rare heredodegenerative disease (see page 937), but it has also been observed in neuronal storage diseases of various kinds Action myoclonus may be the principal residual sign of hypoxic encephalopathy, as described on page 89, and it has been proposed that these conditions have a cerebellar origin Myoclonus is described more fully in Chap 6 More abstruse than the role of the cerebellum in motor control is the proposed participation of this structure in all manner of cognitive function and behavior (see the reviews by Leiner et al and by Schmahmann and Sherman) These authors and others have described a wide range of de cits of memory and cognition, language function, and behavior in patients with disease apparently limited to the cerebellum (as determined by computed tomography and magnetic resonance imaging) It is true that cerebellar lesions interfere with the establishment of conditioned re exes and perhaps some deterioration in certain learning tasks as detected by specialized tests To date, however, a uniform clinical pathologic syndrome in which a distinctive cognitive-behavioral de cit or group of de cits is related to a particular cerebellar lesion has not emerged, and the mechanisms by which discrete cerebellar lesions might in uence cognitive function remain uncertain.

(rate of development) and degree of permanence of the ataxia are of particular importance, as summarized in Table 5-1 Each of the major causes is discussed in an appropriate chapter In adults, paraneoplastic and demyelinating cases account for the largest proportion of cases of subacute onset, and hereditary forms are the usual cause of very slowly progressive and chronic ones, particularly if gait alone is affected The latter now constitute a large and heterogeneous group for which the genetic basis has been established in most cases; they are reviewed extensively in Chap 39 Unilateral ataxia without accompanying signs is most often Table 5-1 Diagnosis of generalized cerebellar ataxia

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HEISS WD: Flow thresholds of functional and morphological damage of brain tissue Stroke 14:329, 1983 HENNERICI M, TROCKEL U, RAUTENBERG W, et al: Spontaneous progression and regression of carotid atheroma Lancet 1:1415, 1985 HEYMAN A, WILKINSON WE, HEYDEN S, et al: Risk of stroke in asymptomatic persons with cervical arterial bruits N Engl J Med 302:838, 1980 HEYMAN A, WILKINSON WE, HURWITZ BJ, et al: Risk of ischemic heart disease in patients with TIA Neurology 34:626, 1984 HIJDRA A, VANGIJN, STEFANKO S, et al: Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: Clinicoanatomic correlations Neurology 36:329, 1986 HOMAN RW, DEVOUS MD, STOKELY EM, BONTE FJ: Quanti cation of intracerebral steal in patients with arteriovenous malformation Arch Neurol 43:779, 1986 HOSSMAN K-A: Pathophysiology of cerebral infarction, in Vinken PJ, Bruyn GW, Klawans HL (eds): Handbook of Clinical Neurology: Vol 53 Vascular Diseases Part I Amsterdam, Elsevier, 1988, pp 27 46 HOUSER OW, BAKER HL JR, SANDOK BA, HOLLEY KE: Fibromuscular dysplasia of the cephalic arterial system, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology: Vol 11 Vascular Disease of the Nervous System Part 1 Amsterdam, North-Holland, 1972, pp 366 385 HUPPERTS RMM, LODDER J, MEUTS-VAN RAAK EPM, et al: Infarcts in the anterior choroidal artery territory: Anatomical distribution, clinical syndromes, presumed pathogensis, and early outcome Brain 117:825, 1994 INGALL TJ, HOMER D, BAKER HL JR, et al: Predictors of intracranial carotid artery atherosclerosis: Duration of cigarette smoking and hypertension are more powerful than serum lipid levels Arch Neurol 48:687, 1991 INTERNATIONAL STUDY OF UNRUPTURED INTRACRANIAL ANEURYSMS INVESTIGATORS: Unruptured intracranial aneurysms: Natural history, clinical outcome, and risks of surgical and endovascular treatment Lancet 362:103, 2003 INTERNATIONAL SUBARACHNOID ANEURYSM TRIAL (ISAT) COLLABORATIVE GROUP: International Subarachnoid Aneurysm Trial of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: A randomised trial Lancet 360:1267, 2002 INZITARI D, ELIASZIW, M, GATES P, et al: The causes and risks of stroke in patients with asymptomatic internal-carotid-artery stenosis N Engl J Med 342:1693, 2000 IREY NS, MCALLISTER HA, HENRY JM: Oral contraceptives and stroke in young women: A clinicopathologic correlation Neurology 28:1216, 1978 ISHIKAWA K, UYAMA M, ASAYAMA K: Occlusive thromboaortopathy (Takayasu s disease): Cervical arterial stenoses, retinal arterial pressure, retinal microaneurysms and prognosis Stroke 14:730, 1983 ITOH T, MATSUMOTO M, HANDA N, et al: Paradoxical embolism as a cause of ischemic stroke of uncertain etiology: A transcranial Doppler sonographic study Stroke 25:771, 1994 JACOBS K, MOULIN T, BOGOUSSLAVSKY J, et al: The stroke syndrome of cortical vein thrombosis Neurology 47:376, 1996 JOHNSON RT, RICHARDSON EP: The neurological manifestations of systemic lupus erythematosus Medicine 47:337, 1968 JONES HR, NAGGAR CZ, SELJAN MP, DOWNING LL: Mitral valve prolapse and cerebral ischemic events: A comparison between a neurology population with stroke and a cardiology population with mitral valve prolapse observed for ve years Stroke 13:451, 1982 JOUTEL A, VAHEDI K, CORPECHOT C, et al: Strong clustering and stereotyped nature of Notch 3 mutations in CADASIL patients Lancet 350: 1511, 1997 JUNG HH, BASSETTI C, TOURIER-LASSERVE E: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: A clinicopathologic and genetic study of a Swiss family J Neurol Neurosurg Psychiatry 59:138, 1995.

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