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PubMed1988

Blink reflex studies in focal dystonias: enhanced excitability of brainstem interneurons in cranial dystonia and spasmodic torticollis.

We have studied the orbicularis oculi reflex to paired stimuli in patients with various forms of focal dystonia and in normal controls. In normals, the conditioning stimulus (CS) facilitated the test stimulus (TS) early response (R1), but markedly inhibited the TS polysynaptic late response (R2). In all types of dystonias studied the CS facilitated the TSR1 as in normals. However, in patients with blepharospasm (alone or associated with oromandibular dystonia), spasmodic torticollis, or spasmodic dysphonia, it inhibited the TSR2 significantly less than that of the controls, with marked enhancement of the recovery curve of the late response. The TSR2 recovery curve of patients with focal arm dystonia was normal. These results are indicative of increased brainstem interneuron excitability in the various dystonias mediated by the cranial nerves, but not in focal arm dystonias such as dystonic writer's cramp. This abnormality might be caused by an abnormal input possibly from the basal ganglia upon these brainstem cells. Our results also suggest that a similar pathophysiology underlies the various focal dystonias of the head and neck.

Blepharospasm↗
PubMed1988

Physiologic and anatomic basis for contralateral R1 in blink reflex.

We studied the rate of appearance and mechanism of contralateral R1 responses in normal subjects. Contralateral R1 could be produced by facilitating maneuvers such as a gentle contraction of the orbicularis oculi and conditioning stimulus of the median nerve. In addition, changing the position of the stimulating anode to the midline evoked these responses that were abolished by blocking the contralateral supraorbital nerve, confirming its peripheral origin. We conclude that crossed trigeminofacial pathways probably exist in normal subjects, but in some instances contralateral peripheral trigeminal ophthalmic sensory fibers may be stimulated, giving rise to a contralateral R1 response.

Blinking↗