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dc.contributor.authorBolay, H
dc.contributor.authorDalkara, T
dc.date.accessioned2019-12-10T11:25:19Z
dc.date.available2019-12-10T11:25:19Z
dc.date.issued1998
dc.identifier.issn0039-2499
dc.identifier.urihttps://doi.org/10.1161/01.STR.29.9.1988
dc.identifier.urihttp://hdl.handle.net/11655/15704
dc.description.abstractBackground and Purpose-Failure of prompt motor recovery after spontaneous recirculation or thrombolytic therapy may be due to an unsatisfactory restoration of synaptic activity within cortex and/or blockade of electrical impulses at the severely ischemic subcortical region. Methods-Afferent, efferent, and synaptic activities were focally examined within the rat sensorimotor cortex by recording the somatosensory-evoked potential (SEP) and motor area response evoked by stimulation of premotor afferents (PmEP) intracortically and the motor-evoked potential (MEP) generated by stimulation of the forelimb area from the brain stem. The effect of ischemia on electrical activity in the cortex and on axonal conduction in the subcortical region was studied differentially by proximal or distal occlusion of the MCA. Results-MEP consisted of direct and indirect waves generated by direct activation of pyramidal axons and indirect excitation of pyramidal neurons via cortical synapses, respectively. MEP, PmEP, and SEP disappeared on proximal occlusion. Following reperfusion after 1 to 3 hours of ischemia, the direct wave of MEP readily recovered but the indirect wave showed no improvement, suggesting a restored axonal conduction but impaired cortical synaptic transmission. The synaptic defect, which also caused a poor recovery in PmEP and SEP and on electrocorticogram, was persistent and detected 24 hours after 1 hour of proximal occlusion. Conclusions-Our data suggest that motor dysfunction is caused by loss of cortical excitability and blockade of motor action potentials at the subcortical level during ischemia. After brief transient ischemia, axonal conduction readily recovers; however, a persistent transmission failure at cortical synapses leads to motor dysfunction.
dc.language.isoen
dc.publisherLippincott Williams & Wilkins
dc.relation.isversionof10.1161/01.STR.29.9.1988
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNeurosciences & Neurology
dc.subjectCardiovascular System & Cardiology
dc.titleMechanisms Of Motor Dysfunction After Transient Mca Occlusion - Persistent Transmission Failure In Cortical Synapses Is A Major Determinant
dc.typeinfo:eu-repo/semantics/article
dc.relation.journalStroke
dc.contributor.departmentNöroloji
dc.identifier.volume29
dc.identifier.issue9
dc.identifier.startpage1988
dc.identifier.endpage1993
dc.description.indexWoS


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