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Show LETTERS TO THE EDITOR 155 Fig. 2. Note limitation of elevation of patients right eye on up gaze. Right eye also had limited adduction and this is also evidenced by slight abduction noted in up gaze. ( Figs. 1 and 2). A computed tomography scan showed a posterior communicating artery aneurysm ( Fig. 3), later confirmed by angiography and surgically removed. I conclude that this six- year- old girl who was without ptosis or pupillary involvement, still had an aneurysm. Whenever we are worried because of a IIIrd nerve palsy, angiographic studies of the intracranial carotid arteries are indicated. The more you consider the possibility of aneurysms, the less you will miss them. Dr. Roberto Ebner Neuro- ophthalrnology Unit British Hospital of Buenos Aires Buenos Aires, Argentina 1. Fox AJ. Angiography for IIIrd nerve palsy in children. JClin Neuro- aphtha/ mo/ 1989; 9: 37- 38.0( O): 000-- 00O Ocular Flutter To The Editor: I recently encountered a young depressed patient who twice had ocular flutter movements when treated with a combination of imipramine ( Tofranil) and phenelzine ( Nardil). Since this combination of drugs is rarely used nowadays, any practical importance the observation may have as a warning of oncoming toxicity is probably small. The combination, however, may provide the means of experimentally investigating ocular instability. Fig. 3. Computed tomography shows right posterior communicating artery aneurysm in this patient. This was confirmed also by arteriography and surgery. This 27- year- old chronically depressed woman treated for 2V2 years with tricyclic agents, lithium, fluoxetine, and monoamine oxidase inhibitors, failed to respond favorably. She declined electrotherapy. Under these circumstances, a trial of combined therapy with imipramine and phenelzine was instituted. Imipramine by itself in a dose of 300 mg daily in divided amounts and phenelzine by itself in a dose of 45 mg daily in divided amounts were each tolerated without affecting eye movements. The combination was begun at a dose of imipramine, 100 mg, and phenelzine, 15 mg, daily and was increased to 200 mg of imipramine and 30 mg of phenelzine, over 6 days, at which time, a flutter- flutter- like movement of the eyes was present of which the patient was unaware. On examination, the ocular excursions were full in all directions. On forward gaze, the eyes oscillated horizontally about the point of fixation at about 6 Hz with an amplitude of about 2 mm. The motion was constant and conjugate. It was regular in rate and amplitude, and there was no vertical component. It was superimposed on horizontalpursuit saccades, and on up and down excursions produced a saw- tooth configuration. There was no nystagmus or dysmetria. According to one observer, the motion ceased during reading, but this finding was not further investigated. The pupils were 8 mm in diameter and reacted slightly to a bright light. Visual acuity was 16/ 20 in the right eye and 16/ 15 in the left eye. The remainder of the neurological examination including cerebellar function and balance was normal. There was no tremor of the limbs. Medication was discontinued and 46 h later, the I Clin Neuro- ophthalmol. Vol. 10, No. 2, 1990 156 LETTERS TO THE EDITOR adventitious movements had disappeared. Another trial was begun and 1 week later, with a daily dose of 250 mg of imipramine and 45 mg of phenelzine, the movements were again present. The same dose was continued, but 5 days later the patient reported she had increased the medication to 300 mg of imipramine and 60 mg of phenelzine daily. The oscillating movements were still present. The pupils were 8 mm in diameter and scarcely reacted to light. The patient was sweating heavily over her scalp. She was unusually talkative but said her depression was unimproved. The neurological examination was normal. The medication was discontinued and 4 days later, the eyes were steady. On each occasion, the only prescribed medicines taken by the patient were imipramine and phenelzine. She was not taking alcoholic drinks and in the past when she did, there had been no nystagmus. A toxic screen of the blood should have been obtained at the time of the abnormal eye movements, but one 4 days later was negative for nine common drugs. The ocular oscillations might have been " voluntary," but the patient did not have oscillopsia, the movements were constant, she seemed to be making no effort, and the lids were quiet. Eye movements were normal both before and afterwards. With these reservations, it was concluded that the imipramine and phenelzine combination was responsible. It was not feasible to undertake a third trial or try each drug again individually. The only other sign of toxicity was pupillary di-lation with a reduced light reflex that probably represented an anticholinergic effect rather than an adrenergic action. The blood pressure was not elevated although the patient did not carefully observe the dietary restrictions required with phenelzine therapy. The mechanism of the ocular flutter can only be surmised. The abnormal activity disappeared within 48 h, suggesting an easily reversible quantitative chemical reaction. Imipramine is hypothesized to act by blocking uptake of norepinephrine at adrenergic synapses, while phenelzine is a monoamine oxidase inhibitor with the potential for widespread changes in the eNS. On each occasion ocular flutter was observed, the pupils were widely dilated, suggesting both abnormalities shared a common mechanism in whole or in part. If this type of ocular flutter could be produced in experimental animals, it might be possible to investigate the hypothesis that a small delay in the eye position feedback loop with preserved coordination of the burst neurons of the two sides of the pons accounts for the oscillations ( 1,2). C. Miller Fisher, M. D. Massachusetts General Hospital Boston, MA REFERENCES 1. Zee OS, Robinson OA. A hypothetical explanation of saccadic oscillations. Ann NeuroI1979; 5: 405- 14. 2. Leigh RJ, Zee OS. The neurology of eye movement. Philadelphia: FA Oavis Company, 1983: Ch. 3. |
