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Show Journal of Clinical Neuro- ophlhalnrology 11( 4): 297- 299, 1991. © 1991 Raven Press, Ltd., New York Bilateral Internuclear Ophthalmoplegia After Smoking " Crack" Cocaine Enrique Diaz- Calderon, M. D., Oscar H. Del Brutto, M. D., Rafael Aguirre, M. D., and Tomas A. Alarcon, M. D. A previously healthy 35- year- old man developed sudden diplopia after smoking " crack" cocaine. Neuroophthalmologic examination revealed findings consistent with a tegmental mesencephalic lesion which correlated closely with the computed tomographic documentation of a small midbrain hemorrhage. Cocaine abuse is a recognized cause of intracranial hemorrhage. In most patients, however, the bleeding is localized in the subarachnoid space or the subcortical white matter. To our knowledge, this is the first case of isolated midbrain hemorrhage secondary to cocaine abuse. Key Words: Cocaine-" Crack" cocaine- Brain stemMidbrain- Hemorrhage- Diplopia- Internuclear ophthalmoplegia. From the Neurologic Service, Hospital Regional del Instituto Ecuatoriano de Seguridad Social, Guayaquil, Ecuador. Address correspondence and reprint requests to Dr. Oscar H. Del Brutto at P. O. Box ( 09- 01) 3734, Guayaquil, Ecuador. 297 The use of cocaine as a recreational drug has increased over recent years, Associated with this increase has been an increased recognition of neurologic complications related to cocaine abuse ( 1,2). Cerebrovascular disease, either ischemic or hemorrhagic, ranks first among such complications ( 3), and cocaine abuse is now considered a major risk factor for stroke in young adults ( 4). Moreover, the recent increase in popularity of " crack," a highly purified free- base form of cocaine, has created concern because " crack" is associated with a greater incidence of cerebrovascular disease ( 5,6). Proposed mechanisms of stroke induced by cocaine include acute elevation of blood pressure, cerebral vasospasm, increased thrombotic activity, rupture of an occult aneurysm or arteriovenous malformation, immuno- allergic vasculitis, and cardiogenic emboli ( 7- 10). Cocaine- related strokes are most often hemorrhagic rather than ischemic ( 3). Hemorrhages are usually located in the subarachnoid space or the subcortical white matter ( 11- 13). In addition, a few patients with deep thalamic hemorrhages have been reported ( 3,14,15). We describe a patient with an isolated midbrain hemorrhage who presented with prominent neuro- ophthalmologic signs after smoking " crack" cocaine. CASE REPORT A 35- year- old right- handed man was evaluated because of the sudden onset of diplopia, vertigo, and incoordination of his right limbs. A few hours before admission, he had been at a party and had smoked several vials of " crack" cocaine. There was no history of arterial hypertension or any medical illness, but he admitted to the sporadic use of cocaine for the previous 3 years. In the emergency room the blood pressure was 110/ 80 mm Hg, and 298 E. DfAZ- CALDER6N ET AL. the general physical examination was unremarkable. Neurologic examination showed an alert and oriented patient with normal speech and comprenhension. Visual acuity was 20/ 20 in each eye and the appearance of the fundi was normal. Visual fields were normal. Pupils were 4 mm in diameter and showed no response to direct or consensual light, but accomodation was spared ( light- near dissociation). There was bilateral ptosis. Upward movements of the eyes were limited to 30° and induced convergence- retraction nystagmus. Abduction of the right eye was full, but adduction was absent. Abduction of the left eye was restricted to 30° and adduction was absent. Convergence was absent. In addition to the neuroophthalmologic findings, the patient had a discrete right hemiparesis and truncal ataxia. The rest of the examination was normal. Complete blood and platelet counts, prothrombin and partial thromboplastin times, serum glucose and cholesterol levels/ liver and renal function tests, and urinalysis were all normal. Rheumatoid factor and VORL were negative. Electrocardiogram and chest roentgenogram were normal. Computed tomography showed a small hemorrhage confined to the midbrain tegmentum ( Fig. 1). The patient's hospital course was uneventful and he was discharged with diplopia on vertical gaze and lateral veering to the right. Two months later, the unsteadiness of gait had resolved and the only deficit remaining FIG. 1. Plain compult d lomo9ra,. ohic llr. Rn showino a small hemorrhage in the midbrain tegmentum. JClin Neuro- op/ ltilJUmol. \/ 0;. J;. ;'[". · 1. 1991 was limitation of upward gaze. Computed tomography done at this time showed complete resolution of the hematoma. DISCUSSION Isolated midbrain hemorrhages are rare and account for 1% of all intracranial hemorrhages ( 16). The clinical picture of this condition is usually dominated by neuro- ophthalmologic findings. At least 5 clinical syndromes, which have correlated closely with the location of bleeding, have been recognized. Peduncular hemorrhages are characterized by partial or complete fascicular third nerve lesions ( 17,18) that mayor may not be associated with crossed motor signs ( Weber's syndrome) ( 19,20). Tegmental hemorrhages also produce third nerve lesions associated with cerebellar signs ( Claude's syndrome) and corticospinal tract signs ( syndrome of Benedikt) ( 21,22). Tectal hemorrhages at the level of the inferior colliculus produce trochlear nerve lesions, contralateral sensory deficit, or both ( 23,24). More rostral tectal hemorrhages cause vertical gaze paresis, pupillary abnormalities, internuclear ophthalmoplegia, and convergence- retraction nystagmus ( 20,25). In addition, mixed clinical syndromes may be observed when the bleeding trespasses these anatomic boundaries, when the perilesional edema compresses neighboring structures, or when supratentorial hydrocephalus ensues as the result of aqueductal obstruction ( 26- 29). Neuro- ophthalmologic findings in our patient resembled those described in the anterior type of bilateral internuclear ophthalmoplegia, in which paresis of ocular adduction upon attempted lateral gaze is associated with loss of convergence ( 30). Such findings, together with bilateral ptosis, pupillary abnormalities showing light- near dissociation, and convergence- retraction nystagmus on attempted upward gaze, suggested a tegmental periaqueductal mesencephalic lesion ( 31). This clinical assumption was confirmed by CT findings of a small midbrain hemorrhage ( Fig. 1), stressing the value of neuroophthalmologic examination in patients with suspected brainstem lesions. Unlike patients with pontine, thalamic, or putaminal hemorrhages, most patients with midbrain hemorrhages have been normotensive middle- aged adults in whom a through neuroradiological investigation has failed to detect the primary cause of bleeding ( 17/ 20,22,23/ 25). On the other hand, data from patients in whom the hematoma has been surgically removed suggest that the most likely etiology of midbrain hemorrhage is a cryptic OPHTHALMOPLEGIA AND " CRACK" COCAINE 299 vascular malformation ( 27,28,32). Such lesions are usually destroyed after the bleeding episode and escape angiographic detection ( 22). Widespread use of magnetic resonance imaging will permit preoperative recognition of these angiographically occult vascular malformations by showing the characteristic hemosiderin deposits from recurrent bleeding ( 33) and will increase our knowledge of the etiology of midbrain hemorrhage. Our patient, a previously healthy man, developed a midbrain hemorrhage after smoking " crack" cocaine. We believe that this event was caused by the rupture of a cryptic arteriovenous malformation in the midbrain. As previously noted, cocaine enhances sympathetic activity, causing acute elevation of blood pressure which, in tum, causes rupture of an occult aneurysm or arteriovenous malformation ( 1,3,7). This report reinforces our knowledge on the hazards of cocaine abuse and describes, for the first time, an isolated midbrain hemorrhage after smoking " crack" cocaine. REFERENCES 1. Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl I Med 1986; 315: 1495-- 500. 2. 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