Motor cortex excitability after thalamic infarction.
OBJECTIVE
We examined 8 patients with hemihypesthesia due to an ischemic thalamic lesion to explore the effects of a central sensory dysfunction on motor cortex excitability.


METHODS
Motor excitability was assessed using transcranial magnetic stimulation techniques and electrical peripheral nerve stimulation. Motor function was evaluated by the Nine-Hole-Peg Test and measurement of hand grip strength. The affected side was compared with the non-lesioned side and with an age-matched control group.


RESULTS
Patients had a loss of inhibition and an increase of facilitation in the motor cortex of the affected side. The silent period was prolonged and motor function was impaired on the affected side.


CONCLUSIONS
A thalamic lesion can modulate motor cortical excitability.


CONCLUSIONS
This study suggests that, under normal conditions, somatosensory afferents influence inhibitory and excitatory properties in the motor cortex.
Liepert
J
J
Department of Neurology, University Hospital Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany. liepert@uke-hamburg.de
Restemeyer
C
C
Münchau
A
A
Weiller
C
C
D000328:Adult; D000344:Afferent Pathways / Q000503:physiopathology; D000368:Aged; D020520:Brain Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D004558:Electric Stimulation; D019054:Evoked Potentials, Motor / Q000502:physiology; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D005260:Female; D018737:Hand Strength / Q000502:physiology; D006801:Humans; D008280:Magnetics; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000503:physiopathology*; D009069:Movement Disorders / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D018908:Muscle Weakness / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D009431:Neural Conduction / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D010291:Paresis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D011930:Reaction Time / Q000502:physiology; D012678:Sensation Disorders / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D013003:Somatosensory Cortex / Q000503:physiopathology; D013786:Thalamic Diseases / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D020651:Ventral Thalamic Nuclei / Q000473:pathology / Q000503:physiopathology