Beum-Saeng Kim

Contralateral Hyperhidrosis After Cerebral Infarction Clinicoanatomic Correlations in Five Cases

BACKGROUND Excessive sweating from cerebral infarction has been reported rarely in the available stroke literature, and its pathophysiological mechanisms and clinical significance have remained obscure. In addition, there have been no reports that medullary infarction results in only contralateral hemihyperhidrosis without ipsilateral Horners syndrome. In the hope of increasing recognition of this phenomenon, we describe five patients with hyperhidrosis, including two patients with medullary infarction, and discuss the clinicoanatomic correlations. CASE DESCRIPTIONS Contralateral hyperhidrosis occurred in two patients with large strokes involving both superficial cortical and deep subcortical structures of the middle cerebral artery territory and in two patients with medullary infarctions. Bilateral hyperhidrosis of the face was noted in one patient with basilar artery thrombosis and bilateral cerebellar and pontine infarctions. The hyperhidrosis typically involved the face and arm and was transient, lasting from 2 days to 2 months. No associated Horners syndrome, hypothalamic dysfunction, or other autonomic dysfunction was observed. CONCLUSIONS The phenomenon of hyperhidrosis might be attributed to a lesion of a putative sympathoinhibitory pathway that controls sweating. This pathway might originate in the cortex, possibly in the operculum, and make terminal connections with the contralateral thoracic spinal cord. Our observations suggest that the fibers of this putative pathway may be very close to the corticospinal tract.

IC-P-003

Background: Mild cognitive impairment (MCI) refers to a transitional state between normal aging and dementia, and it is clinically heterogeneous. Although most imaging studies of MCI have focused on gray matter alterations, many MCI patients have subcortical vascular disease on magnetic resonance imaging (MRI) scan. However it is not known whether these findings are associated with the cognitive dysfunction. Diffusion tensor imaging (DTI) detects the microstructural alterations in white matter by measuring the directionality of molecular diffusion. Objective: We investigated the alterations of white matter as well as hippocampus in MCI patients according to the presence or the absence of subcortical vascular disease by using DTI, and compared the differences between two groups. Methods: Forty consecutive patients with memory complaints, at least one neuropsychological memory test below 1.5 standard deviation of the normal for age and education, and maintained activities of daily living, were included. 21 patients with MCI had no ischemic lesions and 19 patients were found to have subcortical vascular changes, by the Erkinjuntti’s imaging criteria. For 21 non-vascular MCI (nvMVI), 19 vascular MCI (vMCI) and 17 controls, mean diffusivity (MD) and fractional anisotropy (FA) were measured in the bilateral temporal, frontal, parietal and occipital white matter regions as well as in the bilateral hippocampi, sentrum semiovale and the corpus callosum (genu and splenum), and the differences were compared by analysis of variance and multiple comparison. Results: All patients with MCI, both vascular and non-vascular, showed that decreased FA and increased MD values in the other regions except occipital white matter, compared to the controls. For the FA, both types of MCI patients had decreased FA values in the corpus callosum, frontal and temporal regions, compared to the controls. In the parietal areas and centrum semiovale, vMCI patients had more decreased FA values than nvMCI patients and the controls. In the hippocampus, FA values were lowest in the nvMCI patients. FA values of vMCI patients were also significantly lower than the controls. The findings of region-specific MD increases were similar to those of FA. Conclusions: The DTI can be a useful tool to quantify MCI pathology in vivo, and to evaluate the alterations of intracerebral microstructure.