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Show 154 LETTERS TO THE EDITOR FIG. 1. MRI ( magnetic resonance image) revealing dolichoectatic vertebrobasilar artery compressing facial nerve at root entry zone ( arrow). asymmetry in the facial spasm. Bilateral hemifacial spasm is characterized by the temporally separate onset of asynchronous, asymmetric spasms. It is important to be aware that bilateral hemifacial spasm can exist, and to distinguish it from essential blepharospasm and other facial dystonias in order to offer appropriate evaluation and treatment options to the patient. MRl or CT scan is not routinely indicated in the evaluation of blepharospasm, but the posterior fossa should be evaluated with one of these studies in cases of hemifacial spasm. While rare, bilateral hemifacial spasm must be included in the differential diagnosis of a bilateral facial squeezing disorder. John B. Holds, M. D. Richard L. Anderson, M. D. Department of Ophthalmology University of Utah School of Medicine Salt Lake City, Utah David R. Jordan, M. D. Department of Ophthalmology University of Ottawa Ottawa, Ontario, Canada James R. Patrinely, M. D. Cullen Eye Institute Baylor College of Medicine Houston, Texas REFERENCES 1. Digre KB, Corbett n, Smoker WRK, McKusker S. CT and hemifacial spasm. Neurology 1988; 38: 1111- 3. 2. Janetta PJ. Microvascular decompression for hemifacial spasm. In: May M, ed. The facial nerve. New York: Thieme Inc, 1986: 499- 508. 3. Ehni G, Woltman HW. Hemifacial spasm: review of one hundred and six cases. Arch Neurol Psychiatry 1945; 53: 205- 11. 4. Eckman PB, Kramer RA, Altrocchi PH. Hemifacial spasm. Arch NeuroI1971; 25: 81- 7. Angiography for IIIrd Nerve Palsy in Children To the Editor: Dr. Allan J. Fox recently published an interesting paper concerning angiography for IIIrd nerve palsy in children ( 1). Dr. Fox asked for reader responses, so here is mine. I have included three pictures illustrating the case of a six- year- old girl presenting ophthalmoplegia in upward gaze and on adduction of her right eye, without lid ptosis or pupillary involvement Fig. 1. Patient in primary gaze- note that there is no ptosis of her right eye. The pupil was also not involved, although difficult to see with a- dark iris in this picture. 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 |
