7-aminobutyric acid levels.10 The dra¬ matic results that we have seen in our patient justify a trial of valproic acid in patients with DCM who are dis¬ abled by myoclonus. References 1. Hunt JR: Dyssynergia cerebellaris myoclonica: Primary atrophy of the dentate system: A contribution to the pathology and symptomatology of the cerebellum. Brain 1921;44:490-538. 2. Roger J, Soulayrol R, Hassoun J: La dyssynergie cerebelleuse myoclonique (syndrome de Ramsay Hunt). Rev Neurol 1968;119:85-106. 3. Guilleminault C, Tharp B, Cousin D: HVA and 5HIAA CSF measurements and 5 HTP trials in some patients with involuntary movements. J Neurol Sci 1973;18:435-441. 4. Chadwick D, Hallett M, Harris R, et al: Clinical, biochemical and physiological features distinguishing myoclonus responsive to 5\x=req-\ hydroxytryptophan, tryptophan with a monoamine oxidase inhibitor and clonazepam. Brain 1977;100:455-487. 5. Thal L, Sharpless N, Wolfson L, et al: Clinical and metabolic observations on the treatment of myoclonus with L-5-HTP and carbidopa. Trans Am Neurol Assoc 1976;101:48-52. 6. Lance JW, Anthony M: The anticonvulsant action of sodium valproate (Epilim) in 100 patients with various forms of epilepsy. Med J Aust 1977;1:911-915. 7. Lance JW, Adams RD: The syndrome of intention or action myoclonus as a sequel to hypoxic encephalopathy. Brain 1963;86:111-136. 8. Fahn S: Post-anoxic action myoclonus: Improvement with valproic acid. N Engl J Med 1978;299:313-314. 9. Lhermitte F, Peterflavie M, Marteau R, et al: Analyse pharmacologigue d'un cas de myoclonies d'intention et d'action post-anoxiques. Rev Neurol 1971;124:21-31. 10. Godin Y, Heiner L, Mark J, et al: Effects of di-n-propylacetate, an anticonvulsive compound, on GABA metabolism. JNeurochem 1969;16:869\x=req-\ 873. Capsular Ataxic Hemiparesis Vicente J. Iragui, MD, PhD, Charlotte B. McCutchen, MD \s=b\ Left hemiparesis and left-sided ataxia developed in a 67-year-old man. Computed tomography (CT) showed an area of decreased attenuation in the anterior part of the rostral posterior limb of the right internal capsule that enhanced with contrast. As the patient's condition improved, the contrast enhancement resolved. The clinical course combined with the changes in CT scans indicates that the responsible lesion was an infarct. This report suggests that ataxic hemiparesis can result from an infarct of the posterior limb of the internal capsule. (Arch Neurol 1982;39:528-529) and Cole1 described "pMsher brovascular syndrome in which a cere¬ cerebellar ataxia and pyramidal signs involved the limbs of the same side, affecting the leg more than the arm, for which the designation of "ataxic hemiparesis" has been suggested.2 Frequently preceded by transient ischemie attacks and characterized by a stuttering onset, this syndrome occurs most often in hypertensive patients and is believed to be the result of cerebrovascular disease. Since recovery usually occurs, satis¬ factory clinicopathologic correlation is rare; therefore, localization of the responsible lesion is still controver¬ sial. Fisher and Cole1 tentatively located the lesion in the posterior limb of the internal capsule and coro¬ na radiata contralateral to the symp¬ tomatic side, on the basis of findings from postmortem examination of one Accepted for publication July 19, 1981. From the Department of Neurosciences, University of California at San Diego and the Veterans Administration Medical Center, San Diego. Reprint requests to Department of Neurosciences (M-008), University of California at San Diego, La Jolla, CA 92093 (Dr Iragui). However, their specimen showed several other infarcts in addition to the one in the internal capsule, and the authors pointed out that the clinicopathologic correlation was not con¬ clusive. Subsequently, Fisher2 exam¬ ined the brains of three persons with the syndrome and found, in each, a small infarct located in the upper basis pontis contralateral to the involved limbs. Perman and Racy3 described a patient with this syn¬ drome whose computed tomographic (CT) scan demonstrated a lesion in the posterior limb of the internal capsule and thalamus that was believed to be an infarct. We describe a patient with ataxic hemiparesis of the left extremities that resulted from a lesion in the posterior limb of the right internal capsule, with characteristic CT scan changes of infarction. case. REPORT OF A CASE A 67-year-old hypertensive, right- handed man experienced the sudden loss of control of his left leg four days before hospitalization. There was swinging out and slapping down of his left foot in walk¬ ing and a tendency to fall to the left. There was clumsiness of his left hand as well, but no other symptoms. At admission, examination (Sept 10, 1977) showed moderate obesity and a BP of 150/112 mm Hg. There were left carotid and bilateral femoral bruits, with absent posterior tibial and pedal pulses. He was alert and had normal mental status and speech. Visual acuity and fields were nor¬ mal. The optic fundi showed narrowing of arterioles. The pupils were normal in appearance and reaction. The extraocular movements were full, and no nystagmus was present. Facial sensation and corneal reflexes were intact. Facial and mandibu¬ lar movements were normal, as was the jaw reflex. There was mild bilateral hear¬ ing loss. Results of Weber's and Rinne's tests were normal. The palate moved sym¬ metrically, the gag reflex was normal, and there was no dysphagia. The tongue pro¬ truded in the midline. Strength was nor¬ mal in the neck and shoulders but was reduced to 4/5 in the extensor muscles of the left upper extremity and flexors of the left lower extremity, except for the perone¬ al muscles, which showed a strength of 3/5. Tone was mildly decreased in the left, leg more than arm, as were the muscle stretch reflexes. The superficial abdominal re¬ flexes were reduced on the left, and Babinski's sign was present on the left. The snout reflex was obtained, but palmomental, glabellar, and grasp reflexes were not present. Sensory function was normal for touch, pain, temperature, vibration, posi¬ tion, graphesthesia, two-point discrimina¬ tion, and double simultaneous stimulation. There was dysmetria of the left extremi¬ ties that was mild in the arm and severe in the leg. Rapid alternating movements were slow and clumsy on the left side with abnormal rebound phenomena. Although station was normal, the gait was unsteady, and the patient tended to fall to the left, particularly during tandem testing. Walk¬ ing movements of the left leg and associ¬ ated movements of the left were decreased. Weakness and ataxia progressed in a stepwise fashion for the next three days. Examination on the sixth day showed a strength of 3/5 in the extensor muscles of the left upper extremity and flexor mus¬ cles of the left lower extremity, except for the peroneal muscles, which showed a strength of 2/5. The left Babinski's sign, hypotonia, and hyporeflexia persisted, and the left superficial abdominal reflexes were absent. The ataxia in the left limbs had worsened, with the condition more pronounced in the leg than in the arm. The patient was then unable to walk alone and would fall to the left. The fasting blood glucose level was 224 mg/dL. Cerebrospi¬ nal fluid and an EEG were normal. A complete CT scan obtained on the sixth day Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/23/2015 of illness showed a small area of decreased attenuation in the anterior portion of the posterior limb of the right internal capsule at the most rostral level. This area dis¬ played a peripheral rim of enhancement after contrast injection (Fig 1). No other abnormalities were present. At the end of the third week of illness, the weakness and ataxia of the left arm were no longer detectable, and only mild weakness and moderate ataxia of the left lower extremity remained. Eleven months after the onset of illness, there was no weakness, the left arm functioned normal¬ ly, and there was only minimal ataxia of the left leg. A CT scan at that time (Aug 2, 1978) again showed an area of decreased attenuation in the anterior portion of the posterior limb of the right internal cap¬ sule, similar to that in the first CT scan, but there was no enhancement (Fig 2). COMMENT The clinical features of this case were weakness and ataxia of the left extremities. There were no mental changes, signs of cranial nerve involvement, brainstem dysfunction, or sensory deficits. The weakness alone was not sufficient to explain the incoordination, which was indistin¬ guishable from that seen with cere¬ bellar lesions. The weakness and changes in cutaneous reflexes were typical for an upper motor neuron lesion. The lesion seen on the CT scan was in the anterior half of the posterior limb of the internal capsule, adjacent to the ventral lateral nuclear group of the thalamus. The first CT scan was performed six days after the onset of the symptoms, and the lesion con¬ sisted of an area of decreased attenu¬ ation that enhanced with contrast. A second CT scan obtained 11 months later showed a similar area of decreased attenuation but no en¬ hancement after the contrast infu¬ sion. This evolution of findings in the CT scans, the stuttering onset of symptoms, and the favorable clinical course in a patient with a history of peripheral vascular disease, hyperten¬ sion, and diabetes all suggest that the lesion was the result of an ischem¬ ie cerebrovascular event. The CT changes also suggest that the lesion observed in our patient six days after the beginning of symptoms was a recent one45 and most likely was responsible for the initial symptoms. Several investigators have held the view that the ataxia resulting from supratentorial lesions is caused by interruption of corticopontine fibers that project to the ipsilateral pontine nuclei.1·6 The corticopontine projection originates from all four lobes of the cerebrum.7 The temporopontine, pari- Fig 1.—Scan after contrast injection on sixth day of illness. Note lucent area, periphery of which enhances with contrast (arrow). Fig 2.—Scan after contrast injection 11 months after onset of symptoms. Arrow points to lucent area that does not etopontine, and occipitopontine fibers, which together form Türck's bundle, course in the retrolenticular and sublenticular portions of the internal capsule and were spared in our patient. The frontopontine tract (Arnold's bundle) arises from the prefrontal cortex (areas 10, 9, 8, 45, and 46) and from the precentrai region (areas 4 and 6). The prefrontal fibers occupy the anterior limb of the inter¬ nal capsule and were also spared in our case. The corticopontine fibers from the precentrai cortex, however, descend in the posterior limb of the internal capsule, where the lesion was located in our patient. The corticospinal tract also resides in the posterior limb of the internal capsule and occu¬ pies its anterior half at a rostral level.8 It seems, therefore, reasonable to postulate that the lesion in the posterior limb of the internal capsule, involving both corticospinal and Therefore, frontopontine fibers, was responsible for the symptoms of contralateral weakness and ataxia. Involvement of a cerebellar outflow via the dentatorubro-thalamo-cortical pathway may also have contributed to the ataxia in our patient. Fisher2 has shown that a lesion in the basis pontis may be responsible for pyramidal and cerebellar signs contralateral to the lesion. Our obser¬ vation indicates that a lesion in the internal capsule may also result in a similar combination of symptoms as has been previously suggested.1·3 Our patient had no signs of brainstem dysfunction, whereas two of the three patients with lesions in the basis pon¬ tis studied by Fisher2 had horizontal and vertical nystagmus, and the third patient had vertical nystagmus. enhance. our case more closely resembles that reported by Fisher and Cole1 and that reported by Perman and Racy,3 neither of which included nystagmus. Thus, such cases may rep¬ resent an entity different from that resulting from pontine lesions and perhaps could be designated "capsular ataxic hemiparesis." To date, ataxic hemiparesis has been reported in a patient with a midbrain lesion9 and in another patient with a lesion in the basis pontis.10 In both patients, the lesion was demonstrated by CT scan. Marlene Brindell assisted in the preparation of the manuscript. References 1. Fisher CM, Cole M: Homolateral ataxia and crural paresis: A vascular syndrome. J Neurol Neurosurg Psychiatry 1965;28:48-55. 2. Fisher CM: Ataxic hemiparesis. Arch Neurol 1979;35:126-128. 3. Perman GP, Racy A: Homolateral ataxic and crural paresis: Case report. Neurology 1980;30:1013-1015. 4. Yock DH Jr, Marshall WH Jr: Recent is- chemic brain infarcts and computed tomography: Appearances pre and postcontrast infusion. Radiology 1975;117:599-608. 5. Weisberg LA: Computerized tomographic enhancement patterns in cerebral infarction. Arch Neurol 1980;37:21-24. 6. Garcin R: The ataxias, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology. New York, Elsevier North Holland Inc, 1969, vol 1: Disturbances of Nervous Function, pp 309-355. 7. Carpenter MB: Human Neuroanatomy, ed 7. Baltimore, Williams & Wilkins Co, 1976, pp 586\x=req-\ 587. 8. Ross ED: Localization of the pyramidal tract in the internal capsule by whole brain dissection. Neurology 1980;30:59-64. 9. Bendheim PE, Berg BO: Ataxic hemiparesis from a midbrain mass. Ann Neurol 1981;9:405\x=req-\ 407. 10. Sakai T, Murakami S, Ito K: Ataxic hemiparesis with trigeminal weakness. Neurology 1981;31:635-636. Downloaded From: http://archneur.jamanetwork.com/ by a Penn State Milton S Hershey Med Ctr User on 05/23/2015