Lateralization of T-lymphocyte responses in patients with stroke. Effect of sympathetic dysfunction?
OBJECTIVE
A number of clinical observations indicate that stroke affects the course of immune-mediated diseases by lateralization of the disease manifestations, such as arthritis. The purpose of this study was to assess the impact of early stroke on lateralization of immune responsiveness.


METHODS
The delayed-type hypersensitivity (DTH) reaction to purified protein derivative was used as an in vivo measure of antigen-specific T-lymphocyte reactivity. Assessment of axon reflex vasodilation was simultaneously used to test for cutaneous sympathetic activity.


RESULTS
There were no significant differences with regard to lateralization of DTH reactivity when all stroke patients were tested. However, patients with minor stroke displayed a significant (P < .001) decrease of DTH reaction on the paretic side compared with the contralateral side. In contrast, patients with major stroke showed a significant increase (P = .022) of DTH reaction on the paretic side. Patients with left hemiparesis had a significantly greater (P = .045) DTH response on the affected side than patients with a right hemiparesis. In addition, only the patients with motor deficit but not with sensory deficit or aphasia displayed side differences in DTH responses. When electrically evoked axon reflexes were studied in relation to DTH reactions, a significant correlation (r = .64; P < .001) was found between side asymmetries of DTH responses and side asymmetries of axon reflexes in an innervated skin area. No similar relation was present in skin areas where cutaneous sympathetic activity had been blocked by regional anesthesia.


CONCLUSIONS
Early stroke lateralizes T-cell-mediated cutaneous inflammation. This effect depends on (1) the localization of the brain lesion, (2) the clinical course of the disease, and (3) the presence of motor deficit and may be mediated by (4) alteration of the cutaneous sympathetic nerve traffic.
Tarkowski
E
E
Department of Clinical Immunology, University of Göteborg, Sweden.
Naver
H
H
Wallin
B G
BG
Blomstrand
C
C
Tarkowski
A
A
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001037:Aphasia / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D001369:Axons; D002561:Cerebrovascular Disorders / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D006429:Hemiplegia / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology; D006987:Hypesthesia / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D007111:Immunity, Cellular; D007428:Intradermal Tests; D008297:Male; D008875:Middle Aged; D012021:Reflex, Abnormal; D012867:Skin / Q000098:blood supply / Q000276:immunology / Q000294:innervation; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013601:T-Lymphocytes / Q000276:immunology*; D014664:Vasodilation