Ocular flutter, an exceptional complication of amphetamine misuse

We present the first case of ocular flutter related with amphetamine intoxication and discuss the physiopathology of this interesting syndrome and the biochemical differences between OF and OC. A-15-years-old Caucasian male with not previous medical history experienced a rapid onset of dizziness. On neurological admission the patient was nervous, there were no cognitive deficit. Clinical eye movements examination revealed frequent horizon tal and symmetric involuntary burst of large to-and fro. There was a bilateral pupil mydriasis but no motor or sensory deficit, no tremor and no limb ataxia and deep tendon reflexes were all presents. Blood pressure was 145/90 mm Hg and pulse 105 beats/min CT performed on admission was normal. CSF contained 0 lymphocytes/ mm3, 45 mg/dl and normal glucose levels. Urine drugs analysis was positive for amphetamine. All symptoms progressively resolved within 6 hours. An MRI performed was normal. On follow up the patient remained asymptomatic six months later. Amphetamine produces a delayed and sustained increase in glutamate levels (6, 7). The amphetamine increase will induce an stimulation in common oculomotor integrator and in IPBN, and secondary to the IPBN and OP cells inhibition. The result of these neurotransmitters changes is a burst of involuntary saccadic movement. The horizontal predominance of burst movement could be explained because horizontal IPBN neuron seems to be gycergic and vertical-IPBN neurons gabaergic. Although al lesion of OPN could produce OF, a dysfunction in other neuron of the saccadic system could explain this syndrome. Amphetamine intoxication should be consider in the differential diagnosis of OF.