Blink reflex studies in focal dystonias: enhanced excitability of brainstem interneurons in cranial dystonia and spasmodic torticollis.
Identifieur interne : 005033 ( PubMed/Curation ); précédent : 005032; suivant : 005034Blink reflex studies in focal dystonias: enhanced excitability of brainstem interneurons in cranial dystonia and spasmodic torticollis.
Auteurs : E. Tolosa [Espagne] ; L. Montserrat ; A. BayesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1988.
English descriptors
- KwdEn :
- MESH :
- physiology : Interneurons.
- physiopathology : Blepharospasm, Brain Stem, Cranial Nerves, Dystonia, Torticollis.
- Blinking, Electromyography, Humans.
Abstract
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.
DOI: 10.1002/mds.870030108
PubMed: 3173365
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pubmed:3173365Le document en format XML
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<author><name sortKey="Montserrat, L" sort="Montserrat, L" uniqKey="Montserrat L" first="L" last="Montserrat">L. Montserrat</name>
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<author><name sortKey="Bayes, A" sort="Bayes, A" uniqKey="Bayes A" first="A" last="Bayes">A. Bayes</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Blepharospasm (physiopathology)</term>
<term>Blinking</term>
<term>Brain Stem (physiopathology)</term>
<term>Cranial Nerves (physiopathology)</term>
<term>Dystonia (physiopathology)</term>
<term>Electromyography</term>
<term>Humans</term>
<term>Interneurons (physiology)</term>
<term>Torticollis (physiopathology)</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Interneurons</term>
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<term>Torticollis</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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