vasculitis has been pathologically con¬ firmed5·6 in two cases of intracranial hemorrhage related to amphetamine abuse. Narrowing or beading of cere¬ bral vessels has been observed angiographically in a number of amphet¬ amine abusers studied for various reasons,7 including six patients with intracranial hemorrhage.1·8·9 However, vasculitis was confirmed pathologi¬ cally in only one of these cases.6 In other cases, the radiologie appearance of arterial narrowing may have been related to arterial spasm caused by subarachnoid hemorrhage8 or by a direct action of the drug on arterial smooth muscle.4 The role of hypertension in precipi¬ tating hemorrhage from AVMs remains uncertain.10 In the present case, however, hemorrhage from an AVM occurred within minutes of an injection of methamphetamine, suggesting the possibility that hyper¬ tension induced by the noradrenergic stimulation associated with amphet¬ amine injection11 contributed to the rupture of a preexisting AVM. Radiologic evaluation of similar cases may provide further documentation of this IV association. Michael J. Aminoff, MD, provided editorial assistance. References 1. Delaney P, Estes E: Intracranial hemorrhage with amphetamine abuse. Neurology 1980; 30:1125-1128. 2. Margolis MT, Newton TH: Methamphetamine arteritis. Neuroradiology 1971;2:179-182. 3. Citron BP, Halpern M, McCarron M, et al: Necrotizing angiitis associated with drug abuse. N Engl J Med 1970;283:1003-1011. 4. Rumbaugh CL, Bergeron RT, Scanlan RL, et al: Cerebral vascular changes secondary to amphetamine abuse in the experimental animal. Radiology 1971;101:345-351. 5. Weiss SR, Raskind R, Morganstern NL, et al: Intracerebral and subarachnoid hemorrhage following the use of amphetamine. Int Surg 1970;53:123-127. 6. Kessler JT, Jortner BS, Adapan BD: Cerebral vasculitis in a drug abuser. J Clin Psychiatry 1978;39:559-564. 7. Rumbaugh CL, Bergeron RT, Fang HCH, et al: Cerebral angiographic changes in the drug abuse patient. Radiology 1971;101:335-344. 8. Cahill DW, Knipp H, Mosser J: Intracranial hemorrhage with amphetamine abuse. Neurology 1981;31:1058-1059. 9. Edwards KR: Hemorrhagic complications of cerebral arteritis. Arch Neurol 1977;34:549-552. 10. Perret G, Nishioka H: Report on the cooperative study of intracranial aneurysms and subarachnoid hemorrhage. J Neurosurg 1966; 25:467-490. 11. Goodman AG, Goodman RS, Gilman A (eds): The Pharmacologic Basis of Therapeutics. New York, Macmillan Publishing Co Inc, 1980, pp 80-81, 160-162. Focal Dystonia and Lacunar Infarction of the Basal Ganglia A Case Report Louis S. Russo, Jr, MD movement disorder first Dystonia, described Oppenheim in a by 1911,1 is most often of idiopathic origin. Although symptomatic dystonia related to specific pathologic processes does occur,2 persistent focal dystonia secondary to a vascular lesion is uncommon.3 We report a case of focal dystonia associated with a lacunar infarction in the contralateral basal ganglia. REPORT OF A CASE A 56-year-old hypertensive man had a seven-month history of involuntary movement of his left upper extremity. The condition had begun abruptly and was not associated with weakness or sensory disturbance in the affected limb. The movements were slow and caused the patient's fingers to assume unusual positions. Activity exacerbated the movements. No other part of the body was affected. Hearing loss, vertigo, tinnitus, and mild incoordination in the left upper extremity had begun abruptly two months before the onset of the movement disorder. An audiogram confirmed a sensorineural hearing loss in the left ear. Computed tomographic (CT) scan of the brain and cerebral angiogram were normal. The diagnosis was a Accepted for publication Dec 18, 1981. From the Department of Neurology, University Hospital of Jacksonville (Fla). Reprint requests to University Hospital, 655 W Eighth St, Jacksonville, FL 32209 (Dr Russo). limited brainstem infarction on the left. Symptoms gradually cleared, and he had been neurologically asymptomatic for sev¬ eral weeks before the onset of the move¬ ment disorder. Examination results were normal, except for the condition in the left upper extremity. The left hand and forearm showed involuntary movements that pro¬ duced an unusual posture, with hyperpronation and flexion at the wrist, extension of the fingers, and opposition of the thumb. There was an evident increase in tone in the affected muscle groups. There was no weakness, reflex abnormality, or sensory dysfunction. No carotid bruits were heard. A CT scan of the brain disclosed two small, low-density areas in the region of the right lenticular nucleus. These areas did not enhance with contrast (Figure). The patient was treated with haloperi¬ dol. The dosage was gradually increased to 2 mg three times a day. A substantial decrease in dystonic movements occurred. He has now been observed for an addition¬ al eight months. An attempt to discontinue the haloperidol therapy after six months produced an increase in the dystonia. He is presently well, is being maintained on 1-mg regimen three times a day, and has not experienced dystonic movements in any other body part. COMMENT The abnormal movements of this man's left hand were slow, sustained, Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/09/2015 and twisting. They produced an unusual posture in which the wrist was flexed and pronated, the fingers extended, and the thumb moderately opposed. Lacunar infarcts affecting the basal ganglia are common, but clinically evident movement disorders attributable to them are uncommon.4 However, a recent report of hemichoUnenhanced computed tomographic scan demonstrating two lacunar infarctions in right corpus striatum. rea-hemiballismus associated with a lacunar infarction has appeared,5 and the authors offered possible explana¬ tions for the rarity of an associated disorder of movements. Folstein et al6 reported a case resembling Hunting- ton's disease associated with multiple bilateral lacunar infarcts in the cor¬ pus striatum. Although the associa¬ tion is tenuous, it is tempting to ascribe the dystonia of our patient to the lesions of the contralateral basal ganglia. The literature on the association between focal dystonia and vascular lesions is limited. In 19297 Sterling described two patients. One, however, showed generalized involvement of the trunk muscles, and the second also had choreoathetotic movements of the legs. Neither was subjected to autopsy studies. Subsequent reports have described an association with an angiomatous condition in the putamen and état criblé,8 striatal ischemie necro¬ sis,9 and arteriovenous malformation of the basal ganglia.10 Zeman and Whitlock3 briefly mentioned five patients who had a restricted form of dystonia affecting the facial and lin¬ gual muscles and hands. Although they suspected cerebral arteriosclero¬ sis as the cause, no report of patholog¬ ic findings was given. The authors reviewed the literature and concluded, "We have been unable to find re¬ corded instances in which discrete focal vascular lesions of any localiza¬ tion have produced predominately dystonic manifestations." More re¬ cently, Burke et al," in a report of delayed-onset dystonia associated with static encephalopathy, described two cases presumably related to cere¬ bral infarction. In neither case was the dystonia truly focal, however. One case with dystonia affecting the face and upper extremity was associated with CT evidence of infarction in the distribution of the contralateral mid¬ dle cerebral artery. No reference was made to abnormality in the basal gan¬ glia. The second case with dystonia affecting the face, arm, and leg had no confirmatory evidence of infarction. Our case does provide clinical evi¬ dence that a focal vascular lesion of the corpus striatum may produce focal dystonia. Although this man did have a transient episode of presumed brainstem dysfunction two months before the onset of the dystonia, one can only speculate on the importance of this condition relative to the present symptoms. It is possible that the dystonia developed because of the combined effect of the basal ganglia lesion and some persistent, subclinical brainstem dysfunction. It seems more likely, however, to be related to the lesion in the contralateral corpus stri¬ atum alone. References 1. Oppenheim H: Uber eine eigenartige Drampfkrankheit des Kindlichen Alters (Dysba- sia lordotica progressiva, Dystonia musculorum deformans). Neurol Centralbl 1911;30:1090-1107. 2. Fahn S, Eldridge R: Definition of dystonia and classification of dystonic states, in Eldridge R, Fahn S (eds): Advances in Neurology. New York, Raven Press, 1976, vol 14: Dystonia, pp 1-5. 3. Zeman W, Whitlock CC: Symptomatic Dystonias, in Vinken PJ, Bruyn GW (eds): Handbook of Neurology, ed 1. New York, Elsevier North Holland Inc, 1968, vol 6: Diseases of the Basal Ganglia, pp 544-566. 4. Mohr JP, Caplan LR, Melsk JW, et al: The Harvard cooperative stroke registry: A prospective registry. Neurology 1978;28:754-762. 5. Kase CS, Maulsby GO, deJuan E, et al: Hemichorea-hemiballism and lacunar infarction in the basal ganglia. Neurology 1981;31:452-455. 6. Folstein S, Abbott M, Moser R, et al: Hereditary disorders of dystonic movement. Johns Hopkins Med J 1981;148:104-113. 7. Sterling MV: Le syndrome dystonique de la vieillesse. Rev Neurol 1929;1:937-941. 8. Foerster O: Mobile spasm of the neck muscles and its pathologic basis. J Comp Neurol 1933;58:725-735. 9. Lopez Aydillo NR, Sanz Ibanaz J: A proposito de un caso de distonia de torsion (variante miostatica o paralitica) en una diabetica glucosurica. Trab Inst Cajal Invest Biol 1956;48:81-108. 10. Markham CH, Rand RW: Physiological and anatomical influences on dystonia. Trans Am Neurol Assoc 1961;86:135-137. 11. Burke RE, Stanley F, Gold AP: Delayedonset dystonia in patients with 'static' encephalopathy. J Neurol Neurosurg Psychiatry 1980;43:789-797. Traction Injury of Peroneal Nerve Caused by Minor Athletic Trauma Electromyographic Studies Erich W. Streib, MD Adduction injuries of the knee joint with rupture of the lateral liga- ments may lead to a severe traction injury of the peroneal nerve.1,2 Less well-known injuries include minor traction or stretch injuries of the peroneal nerve, as may be caused by slipping or turning of the leg or sud- Accepted for publication April 1, 1982. From the Department of Neurology, University of Nebraska Medical Center, Omaha. Reprint requests to Department of Neurology, University of Nebraska Medical Center, 42nd Street and Dewey Avenue, Omaha, NE 68105 (Dr Streib). den stretching while serving in tennis.3 These injuries may or may not be associated with musculoskeletal traumata, such as ankle sprains or fractures. I describe a patient with such a trac- tion injury of the peroneal nerve. The electromyographic (EMG) findings shed additional light on the pathogenetic mechanisms of such injuries. REPORT OF A CASE 25-year-old During racquetball man suddenly turned on his left leg, trying a game, a Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/09/2015 to avoid the racquet of his opponent. He sustained an eye injury; while hospitalized for this injury, he noticed that he could not extend his left great toe. He denied pain in the leg, ankle, or back, or abnormal sensation. There was no early improvement, but six months after the injury, only weakness of extension of the great toe was evident. One year after the injury, strength was almost normal. EMG FINDINGS The initial study was performed six months after the injury. Results of nerve conduction studies of the right