OBJECTIVE: To study acute autonomic dysfunction (AD) on the hemibody contralateral to the lesion in the acute phase of stroke.
BACKGROUND: Acute AD on the hemibody involved by the deficit is sometimes mentioned in acute stroke. It is reported mainly as hand edema or discoloration of skin with hypersudation and sometimes painful syndromes, but it has not been studied prospectively.
DESIGN/METHODS: 100 consecutive patients (median age ±IQR: 74 y ±21, range 19-93 y, 51 women 80 y±17 and 49 men 70 y ±17) were studied prospectively in the acute phase of stroke for acute AD. Changes in cutaneous temperature, aspect or coloration, diaphoresis, pain or edema were noted in the first three days post stroke. Associatons of AD with topography (cortical pre- and/or post-central, corona radiata, basal ganglia, internal capsule, thalamus, brainstem), age, gender, ischemic or hemorrhagic etiology and presence of sensorimotor deficits or ataxia was performed using chi-square statistic and logistic regression analysis.
RESULTS: AD was significantly associated with the presence of a lesion in the following localizations: postcentral cortex (p=0.034), internal capsule (p=0.003) or the basal ganglia (p=0.001) and negatively with the presence of a lesion in the brainstem (p=0.001). Logistic regression analysis including all studied topographic variables show that brainstem strokes were significantly associated with a decreased risk to develop AD (OR = .095, 95 %CI 0.011-0.801, p=0.031) whereas internal capsule lesions had a risk for more severe dysautonomia (OR =3.3, 95% CI 1.04-10.1, p=0.04). More severe AD dysfunction with edema of the hand was observed in association with internal capsule (p=0.001) or basal ganglia (p=0.003) lesions, while a negative association was seen when lesions were located in the brainstem (p=0.007). AD was not associated with the ischemic or hemorrhagic nature of the lesion, side of lesion, age, gender, hyper-or hypo-tonic paresis, hyper- or hyporeflexia. AD was significantly found in association with sensory deficits (p=0.0001) and ipsilateral hyperkinesia (p=0.004).
CONCLUSIONS: acute AD on the side of the deficit is more prone to be seen in hemispheric lesions involving sensory pathways from cortex to internal capsule. AD is significantly absent with isolated thalamus and brainstem lesions.