Brain, Vol. 117, No. 6, 1457-1474, 1994
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Abnormal eye movements in blepharospasm and involuntary levator palpebrae inhibition
Clinical and pathophysiological considerations
1The Graduate School of Neurosciences, AZUA, Department of NeurologyAcademic Medical Centre Amsterdam, The Netherlands 2The Graduate School of Neurosciences, AZUA, Division of Clinical Neurophysiology Academic Medical Centre Amsterdam, The Netherlands
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Correspondence to: Dr M. Aramideh, Department of Neurology/Clinical Neurophysiology (H2-214), Academic Medical Centre, Meibergdreef 9, NL-1105 AZ, Amsterdam, The Netherlands
We report on four patients with involuntary eyelid closure and eye movement disorders. Three were healthy until the onset of their illness and one had a mild generalized choreoathetosis and dystonia due to kernicterus. Electromyographic recording revealed solely blepharospasm in two patients and blepharospasm in combination with involuntary levator palpebrae inhibition in the other two. The eye movement abnormalities were clinically characterized by inability to fix gaze and short or prolonged episodes of uncontrollable eye deviations accompanied, in two patients, by diplopia in horizontal or vertical directions. These episodes occurred independently of a disorder of eyelid movement. Eye movement recordings with a double magnetic induction technique showed saccadic intrusions in horizontal directions. They consisted of highly frequent square wave jerks in three and sporadic macro-square wave jerks in two patients. There were also episodes of extraocular muscle dystonia, commonly known as oculogyric crises, resulting in involuntary upward eye deviation in all patients and lateral deviation in three patients. In one patient, nasal-ward deviations were sometimes restricted to one eye. We conclude that these abnormal eye movements do not necessarily point to a symptomatic form of dystonia and that they may limit the beneficial effect of botulinum toxin or surgical intervention in the therapeutic management of involuntary eyelid closure. We suggest that either basal ganglia, especially substantia nigra pars reticularis and the brainstem structures, especially the paramedian pontine reticular formation, or both, may be involved in the pathogenesis of these abnormal movements.
blepharospasm; levator palpebrae inhibition; extraocular muscle dystonia; saccadic intrusions; oculogyric crises
Received March 11, 1994. Revised May 17, 1994. Accepted June 13, 1994.
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