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From the Department of Neurology, Faculty of Medicine, and Institute of
Neurological Sciences and Psychiatry, Hacettepe University (H.B., T.D.),
Ankara, Turkey.
Correspondence to Turgay Dalkara, MD, PhD, Department of Neurology, Hacettepe University Hospitals, Ankara 06100, Turkey. E-mail dalkara{at}tr-net.net.tr
Background 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.
Department
of Pathology (Neuropathology),
Henry Ford Hospital,
Detroit, Michigan
© 1998 American Heart Association, Inc.
Original Contributions
Mechanisms of Motor Dysfunction After Transient MCA Occlusion: Persistent Transmission Failure in Cortical Synapses Is a Major Determinant
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