Sensory-motor deficit and recovery from thrombotic infarction of the vibrissal barrel-field cortex.
The present studies were undertaken to examine: (1) whether thrombotic infarction of the vibrissal cortical barrel-fields of the primary somatosensory cortex would produce behavioral consequences reflecting a sensory-motor deficit; and (2) whether there was any recovery of function up to two months after infarction. Specifically, in two different learning tasks requiring sensory-motor integration, rats were trained to perform a motor response consequent to the detection of vibrissal cues derived from either active exploration or from passive detection of vibrissal deflection. Once training was complete, unilateral, bilateral or sham-infarction restricted to the region of the primary somatosensory cortex was produced by a non-invasive photochemical technique, which induces platelet-activated vascular occlusion combined with blood-brain barrier changes and subsequent cell death. The results demonstrated that, regardless of the active or passive sensory characteristics of the task, unilateral and bilateral infarction resulted in a reliable performance deficit, which was not present in sham-operated control animals. Thus, the infarct disrupted the ability to integrate passively received or actively acquired vibrissal sensory information with a previously associated motor response. However, unlike the bilaterally infarcted animals, who displayed no recovery of performance level throughout the postinfarction testing sessions, the unilaterally infarcted animals exhibited a gradual improvement in performance beginning in the second or third week postinfarction and recovering to within 10-20% of preinfarction levels between postinfarction days 46-61. The similarity of the temporal pattern of behavioral recovery in the unilateral groups, despite large differences in the sensory-motor demands of the two tasks, may reflect several common underlying mechanisms of recovery. Since similar sensory-motor behavioral deficits and recovery have been described with human stroke, the present model incorporates many of the pathophysiological and behavioral properties present in the clinical situation and may be useful for future investigation of therapeutic intervention.
Hurwitz
B E
BE
Department of Psychology, University of Miami, Coral Gables, FL 33124.
Dietrich
W D
WD
McCabe
P M
PM
Watson
B D
BD
Ginsberg
M D
MD
Schneiderman
N
N
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D003216:Conditioning, Operant / Q000502:physiology*; D002542:Intracranial Embolism and Thrombosis / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013003:Somatosensory Cortex / Q000473:pathology / Q000503:physiopathology*; D014738:Vibrissae