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Long latency responses in pure sensory stroke due to thalamic infarction
Author(s) -
Chen C. C.,
Chen J. T.,
Wu Z. A.,
Kao K. P.,
Liao K. K.
Publication year - 1998
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1998.tb07376.x
Subject(s) - thalamus , somatosensory evoked potential , somatosensory system , medicine , median nerve , stroke (engine) , sensory system , cerebral infarction , infarction , physical medicine and rehabilitation , thumb , stimulation , wrist , anesthesia , neuroscience , cardiology , psychology , surgery , ischemia , physics , myocardial infarction , thermodynamics
Objectives – Our study was designed to clarify the role of the thalamus in the generation of the electrically elicited long‐latency reflexes (LLR) in voluntarily activated hand muscles. Materials and methods – EMG responses of the thenar muscles were evoked by electrical stimulation of the median nerve at the wrist at motor threshold intensity in 10 patients with acute pure sensory stroke due to thalamic infarction. Concomitant recording of somatosensory evoked potentials (SEPs) was performed. The subjects were asked to steadily abduct the thumb at 20–30% of maximal force against a force transducer. Rectified and averaged EMG activities were recorded. Results – The LLR II was missing completely or significantly attenuated in the majority of the patients (9 of 10), of whom 3 also had delayed latency. Abnormal SEPs were documented in 7 patients (7 of 10). In the follow‐up, 5 patients had partial reversal of LLR II. LLR II was still pathological in 1 fully recovered patient. Conclusion – Our results further confirm the transcortical generation of LLR II and imply that a thalamic relay is present in the afferent limb of the LLR.