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Journal of the Korean Neurological Association ; : 682-685, 2005.
Article in Korean | WPRIM | ID: wpr-199757

ABSTRACT

Apraxia of lid opening (ALO) has been suggested to be a dysfunction of the supranuclear control of the levator palpebrae superioris caused mainly by basal ganglial lesion. The hypometabolism of the medial frontal lobe may be a pathophysiologic mechanism in ALO. We report two ALO patients who developed these symptoms as a delayed complication after traumatic brain injury (TBI). Their MRI showed encephalomalacia in the Rt. medial frontal cortex, which was not shown in initial brain CT scans. Delayed pathologic changes after TBI may contribute to the development of ALO in these cases.


Subject(s)
Humans , Apraxias , Brain , Brain Injuries , Encephalomalacia , Frontal Lobe , Magnetic Resonance Imaging , Tomography, X-Ray Computed
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