Background and Purpose-There is currently no consensus on (1) the percentage of patients who develop spasticity after ischemic stroke, (2) the relation between spasticity and initial clinical findings after acute stroke, and (3) the impact of spasticity on activities of daily living and health-related quality of life. Methods-In a prospective cohort study, 301 consecutive patients with clinical signs of central paresis due to a first-ever ischemic stroke were examined in the acute stage and 6 months later. At both times, the degree and pattern of paresis and muscle tone, the Barthel Index, and the EQ-5D score, a standardized instrument of health-related quality of life, were evaluated. Spasticity was assessed on the Modified Ashworth Scale and defined as Modified Ashworth Scale Ͼ1 in any of the examined joints. Results-Two hundred eleven patients (70.1%) were reassessed after 6 months. Of these, 42.6% (nϭ90) had developed spasticity. A more severe degree of spasticity (Modified Ashworth Scale Ն3) was observed in 15.6% of all patients. The prevalence of spasticity did not differ between upper and lower limbs, but in the upper limb muscles, higher degrees of spasticity (Modified Ashworth Scale Ն3) were more frequently (18.9%) observed than in the lower limbs (5.5%).Regression analysis used to test the differences between upper and lower limbs showed that patients with more severe paresis in the proximal and distal limb muscles had a higher risk for developing spasticity (PՅ0.001). Spasticity of the upper and lower limb was more frequent in patients with hemihypesthesia than in patients without sensory deficits (PՅ0.001). Patients with spasticity showed a lower Barthel Index and EQ-5D score compared with the group without spasticity. Conclusions-Spasticity was present in 42.6% of patients with initial central paresis. However, severe spasticity was relatively rare. Predictors for the development of spasticity were a severe degree of paresis and hemihypesthesia at stroke onset. (Stroke. 2010;41:2016-2020.)

No abstract

Imaging techniques have been used to elucidate the neural correlates that underlie deception. The scientifically best understood paradigm for the detection of deception, however, the guilty knowledge test (GKT), was rarely used in imaging studies. By transferring a GKT-paradigm to a functional magnetic resonance imaging (fMRI) study, while additionally quantifying reaction times and skin conductance responses (SCRs), this study aimed at identifying the neural correlates of the behavioral and electrodermal response pattern typically found in GKT examinations. Prior to MR scanning, subjects viewed two specific items (probes) and were instructed to hide their knowledge of these. Two other specific items were designated as targets and required a different behavioral response during the experiment and eight items served as irrelevant stimuli. Reaction times and SCR amplitudes differed significantly between all three item types. The neuroimaging data revealed that right inferior frontal and mid-cingulate regions were more active for probe and target trials compared to irrelevants. Moreover, the differential activation in the right inferior frontal region was modulated by stimulus conflicts. These results were interpreted as an increased top-down influence on the stimulus-response-mapping for concealed and task-relevant items. Additionally, the influence of working memory and retrieval processes on this activation pattern is discussed. Using parametric analyses, reaction times and SCR amplitudes were found to be linearly related to activity in the cerebellum, the right inferior frontal cortex, and the supplementary motor area. This result provides a first link between behavioral measures, sympathetic arousal, and neural activation patterns during a GKT examination.

Bilateral vestibular failure (BVF) is a rare disorder of the labyrinth or the eighth cranial nerve which has various aetiologies. BVF patients suffer from unsteadiness of gait combined with blurred vision due to oscillopsia. Functional MRI (fMRI) in healthy subjects has shown that stimulation of the visual system induces an activation of the visual cortex and ocular motor areas bilaterally as well as simultaneous deactivations of multisensory vestibular cortex areas. Our question was whether the chronic absence of bilateral vestibular input (BVF) causes a plastic cortical reorganization of the above-described visual-vestibular interaction. We used fMRI to measure the differential effects of horizontal visual optokinetic stimulation (OKN) on activations and deactivations in 10 patients with BVF and compared their data directly to those of pairwise age- and sex-matched controls. We found that bilateral activation of the primary visual cortex (inferior and middle occipital gyri, Brodmann area BA 17, 18, 19), the motion-sensitive areas V5 in the middle and inferior temporal gyri (BA 37), and the frontal eye field (BA 8), the right paracentral and superior parietal lobule and the right fusiform and parahippocampal gyri was significantly stronger and the activation clusters were larger than that of the age-matched healthy controls. Small areas of BOLD signal decreases (deactivations), located primarily in the right posterior insula containing the parieto-insular vestibular cortex, were similar to those in the healthy controls. No other sensory brain areas showed unexpected activations or deactivations, e.g. the somatosensory or auditory cortex areas. Our finding of enhanced activations within the visual and ocular motor systems of BVF patients suggests that they might be correlated with an upregulation of visual sensitivity during tracking of visual motion patterns. Functionally, these enhanced activations are independent of optokinetic performance, since the mean slow-phase velocity of OKN in the BVF patients did not differ from that in normals. Although psychophysical and neurophysiological tests have provided various examples of how sensory loss in one modality leads to a substitutional increase of functional sensitivity in other modalities, this study presents the first evidence of visual substitution for vestibular loss by functional imaging.