Anamnestic recall of stroke-related deficits: an animal model.
OBJECTIVE
Anamnestic recall of stroke-related deficits is a common clinical observation, especially during periods of systemic infection. The pathophysiology of this transient re-emergence of neurological dysfunction is unknown.


METHODS
Male Lewis rats underwent 3 hours middle cerebral artery occlusion and were treated with lipopolysaccharide or saline at the time of reperfusion. The delayed-type hypersensitivity (DTH) response to myelin basic protein was examined 28 days after middle cerebral artery occlusion. Changes in behavioral outcomes were assessed after DTH testing and repeat administration of lipopolysaccharide or saline at 34 days. At the time of euthanasia (36 days), the immunologic response of splenocytes to myelin basic protein, neuron-specific enolase, and proteolipid protein was determined by enzyme-linked immunospot assay and the number of lymphocytes in the brain determined by immunocytochemistry.


RESULTS
Animals treated with lipopolysaccharide at middle cerebral artery occlusion had a greater DTH response to myelin basic protein than animals treated with saline. Among those animals that had fully recovered on a given behavioral test before DTH testing, those treated with lipopolysaccharide at middle cerebral artery occlusion displayed more neurological deterioration after DTH testing and had more CD8(+) lymphocytes within the ischemic core of the brain. Furthermore, the Th1 immune response to brain antigens in the spleen was more robust among those animals that deteriorated after DTH testing and there were more CD4(+) lymphocytes in the penumbral region of animals with a Th1 response to myelin basic protein.


CONCLUSIONS
Our data suggest that an immune response to the brain contributes to the phenomenon of anamnestic recall of stroke-related deficits after an infection. The contribution of the immune response to this phenomenon deserves further investigation.
Zierath
Dannielle
D
Department of Neurology, University of Washington School of Medicine, Harborview Medical Center, Seattle, WA, USA.
Hadwin
Jessica
J
Savos
Anna
A
Carter
Kelly T
KT
Kunze
Allison
A
Becker
Kyra J
KJ
D000647:Amnesia / Q000276:immunology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000139:chemically induced / Q000276:immunology; D007107:Immune System / Q000503:physiopathology*; D020244:Infarction, Middle Cerebral Artery / Q000276:immunology*; D008070:Lipopolysaccharides / Q000009:adverse effects / Q000494:pharmacology; D008297:Male; D023421:Models, Animal; D004676:Myelin Basic Protein / Q000009:adverse effects; D009422:Nervous System Diseases / Q000276:immunology*; D051381:Rats; D011917:Rats, Inbred Lew; D020521:Stroke / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D013997:Time Factors
D008070:Lipopolysaccharides; D004676:Myelin Basic Protein