a 15-year old boy attempted suicide by taking a high dose of disulfiram ( 20 mg ) . upon arrival at the hospital , he was alert and vital signs were stable .
one month after , he suddenly developed an acute insult consisted of anxiety attack and subsequent retrocollis and forceful upward deviation of the eyes . during the attack , he could not close his eyes and speak , making only grunting noises .
he could not move his eyes voluntarily at all , but horizontal oculocephalic reflexes could be elicited .
the frequency , duration and intensity of the attacks increased gradually over a period of eight years , occurring more than 10 times a day and lasted up to 2 hours .
he had no motor weakness or sensory deficits , but he needed a help to walk due to foot dystonia .
t2-weighted brain mri studies showed high signal intensity lesions at the bilateral globus pallidus and left substantia nigra ( figure 1 ) .
levodopa treatment was not effective , but the frequency of the attacks decreased markedly after trihexyphenidyl hydrochloride ( 2.5 mg tid ) treatment . also , the foot dystonia improved partially and the patient could walk a short distance without assistance .
disulfiram is metabolized to cyanide disulfide ( cs2 ) and produce lesions at the globus pallidus and substantia nigra pars reticulata in monkeys.7 in huans , pallidal or lenticular lesions after disulfiram intoxication have been reported.6,7 however , to our knowledge , lesion at the substantia nigra after disulfiram intoxication is rarely documented on brain mri studies .
ogc occurs frequently in association with neuroleptic treatment , postencephalitic parkinsonism , and focal brain lesions at the putamen or globus pallidus.1,2,4,5 these findings suggest that ogc can be caused by basal ganglia dysfunction , particularly of the dopaminergic system . in our patient ,
neuronal discharges from pathologically reorganized basal ganglia circuit to the midbrain ocular motor center might lead to tonic deviation of the eyes .
we reported a patient who developed disulfiram induced parkinsonism , dystonia , and ogc , responding markedly to the anticholinergics treatment .
 we report a man who developed oculogyric crisis one month after disulfiram intoxication . 
 brain mri showed lesions involving bilateral globus pallidus and left substantia nigra . in our patient 
 , neuronal discharges from pathologically reorganized basal ganglia circuit to the mid - brain ocular motor center might lead to tonic deviation of the eyes . 