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Blink reflex in patients with hemispheric cerebrovascular accident (CVA). Blink reflex in CVA
Insights
Abnormal blink reflexes (R1 and R2) are common after stroke, with R2 suppression suggesting widespread internuncial excitability loss. This reflex testing may help localize brain lesions.
Area of Science:
- Neuroscience
- Neurology
- Clinical Neurophysiology
Background:
- The blink reflex, comprising early (R1) and late (R2) components, is a valuable clinical neurophysiological test.
- Acute hemispheric cerebrovascular accidents (strokes) can significantly alter blink reflex pathways.
Purpose of the Study:
- To investigate the characteristics and clinical correlations of blink reflex abnormalities in patients during the acute phase of hemispheric stroke.
- To explore the neurophysiological basis of blink reflex alterations and their potential for lesion localization.
Main Methods:
- Assessed R1 and R2 components of the blink reflex in 66 patients with acute hemispheric stroke using electrophysiological techniques.
- Correlated blink reflex abnormalities with clinical neurological examination and CT scan findings.
- Utilized paired stimuli to differentiate between R1 and R2 pathway involvement.
Main Results:
- R1 and R2 were abnormal in 30 and 50 patients, respectively. R2 was profoundly suppressed, often unresponsive to paired stimuli.
- Abnormalities in R2 suggested diffuse loss of internuncial excitability contralateral to the lesion.
- CT scans showed lesion overlap in the inferior Rolandic area for abnormal blink reflexes, contrasting with sparing in normal cases.
Conclusions:
- The blink reflex, particularly the R2 component, is frequently impaired in acute hemispheric stroke, indicating disrupted central processing.
- Abnormalities suggest significant disfacilitation at the interneuronal level and potential crossed cortical facilitation.
- Blink reflex testing, combined with neuroimaging, may aid in understanding stroke pathophysiology and lesion localization, especially involving the sensory cortex.
Abstract:
A blink reflex consists of an early unilateral component, R1, and a late bilateral component, R2. During an acute phase of hemispheric cerebrovascular accident, R1 and R2 were abnormal in 30 and 50 of 66 patients, respectively. Paired stimuli usually corrected R1 but not R2, which was profoundly suppressed. The discrepancy between polysynaptic R2 and oligosynaptic R1 indicates a greater disfacilitation at the level of interneurons than at the motoneuron, which serves as the final common path. Abnormality of R2 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 R2 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 R2 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 post-central 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.