Journal article
Blink reflex in patients with hemispheric cerebrovascular accident (CVA): Blink reflex in CVA
Journal of the neurological sciences, Vol.67(1), pp.15-28
1985
DOI: 10.1016/0022-510X(85)90018-8
PMID: 3981210
Abstract
A blink reflex consists of an early unilateral component, R
1, and a late bilateral component, R
2. During an acute phase of hemispheric cerebrovascular accident, R
1 and R
2 were abnormal in 30 and 50 of 66 patients, respectively. Paired stimuli usually corrected R
1 but not R
2, which was profoundly suppressed. The discrepancy between polysynaptic R
2 and oligosynaptic R
1 indicates a greater disfacilitation at the level of interneurons than at the motoneuron, which serves as the final common path.
Abnormality of R
2 occurred bilaterally with stimulation on the affected side of face and contralaterally after stimulation on the normal side in 31 patients. This finding suggests a diffuse loss of internuncial excitability, contralateral to the hemispheric lesion. Changes of R
2 implicated the brainstem pathways forming the afferent and efferent arc of the reflex in 7 and 8 patients, respectively. The remaining 4 comatose patients had no R
2 irrespective of stimulus sites.
Clinical localization of the hemispheric lesion showed no consistent correlation with the type of blink reflex abnormalities. The CT scans revealed widely scattered changes in 29 patients with abnormal blink reflex but with a tendency to overlap in the inferior Rolandic area. This contrasted with conspicuous sparing of the inferior postcentral region in 10 patients with normal blink reflex. These findings suggest the presence of crossed facilitation to this reflex from wide areas of the cortex but most prominently from the sensory representation of the face.
Details
- Title: Subtitle
- Blink reflex in patients with hemispheric cerebrovascular accident (CVA): Blink reflex in CVA
- Creators
- Jun Kimura - Division of Clinical Electrophysiology, Stroke Unit, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 U.S.AJ.Terry Wilkinson - Division of Clinical Electrophysiology, Stroke Unit, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 U.S.AHanna Damasio - Division of Clinical Electrophysiology, Stroke Unit, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 U.S.AHarold R Adams - Division of Clinical Electrophysiology, Stroke Unit, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 U.S.AEssatollah Shivapour - Division of Clinical Electrophysiology, Stroke Unit, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 U.S.AThoru Yamada - Division of Clinical Electrophysiology, Stroke Unit, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 U.S.A
- Resource Type
- Journal article
- Publication Details
- Journal of the neurological sciences, Vol.67(1), pp.15-28
- Publisher
- Elsevier B.V
- DOI
- 10.1016/0022-510X(85)90018-8
- PMID
- 3981210
- ISSN
- 0022-510X
- eISSN
- 1878-5883
- Language
- English
- Date published
- 1985
- Academic Unit
- Neurology; Iowa Neuroscience Institute
- Record Identifier
- 9984020631802771
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