Abstract TP328: Hand motor deficits ipsilateral to acute stroke

BACKGROUND: Hand motor deficits are known to occur ipsilateral to stroke, but their cause and impact remain uncertain. Here we examined these issues by exploring associations with acute hand motor deficits ipsilateral to stroke, including genetic and neuroanatomical factors. We hypothesized that severity of hand motor deficits ipsilateral to stroke in the acute setting would [1] reflect interhemispheric interactions and so correlate with extent of injury to corpus callosum, but not corticospinal tract (CST) or primary motor cortex (M1); [2] persist but improve over time; and [3] be related more strongly to motor rather than cognitive deficits. METHODS: A total of 763 patients with a new stroke were studied longitudinally over 1 year across 28 US sites. Genetic data were collected in each, and neuroimaging data were available in 448. Acutely, grip strength was measured in the hand ipsilateral to stroke, and NIHSS was scored. At the 3-mo visit, grip strength testing was repeated. RESULTS: Acutely, deficits in grip strength ipsilateral to stroke were common: patients on average were 0.39 SD below normative values that accounted for age, gender, and body side; in 16.3% of patients, values were >1 SD below normal. Extent of these deficits was associated with acute NIHSS total score (r=-.11, p=0.002) and affected arm motor score (r=-0.07, p<0.05), but not with extent of aphasia or neglect; with extent of injury to the splenium (r=-0.17, p=0.0002) and body (r=-0.1, p=0.04) of the corpus callosum, but not extent of injury to CST or to M1; were more severe with ischemic stroke than intracerebral hemorrhage (p=0.01); and were unrelated to the BDNF val66met and ApoE e4 polymorphisms. At 3-mo, patients on average were 0.34 SD below normative values, and 11.4% were >1 SD below normal; gains over time were significant (p<0.002). CONCLUSIONS: Deficits in grip strength ipsilateral to stroke measured acutely are associated with stroke severity and with contralateral arm weakness. These ipsilateral deficits improve but persist over time, and correlated with motor but not language or hemineglect symptoms. Common genetic polymorphisms were unrelated. Imaging results favor a model based on interhemispheric interactions in the pathogenesis of hand motor deficits ipsilateral to acute stroke.