Movement of an affected hand after stroke is associated with increased activation of ipsilateral motor cortical areas, suggesting that these motor areas in the undamaged hemisphere may adaptively compensate for damaged or disconnected regions. However, this adaptive compensation has not yet been demonstrated directly. Here we used transcranial magnetic stimulation (TMS) to interfere transiently with processing in the ipsilateral primary motor or dorsal premotor cortex (PMd) during finger movements. TMS had a greater effect on patients than controls in a manner that depended on the site, hemisphere, and time of stimulation. In patients with right hemiparesis (but not in healthy controls), TMS applied to PMd early (100 ms) after the cue to move slowed simple reaction-time finger movements by 12% compared with controls. The relative slowing of movements with ipsilateral PMd stimulation in patients correlated with the degree of motor impairment, suggesting that functional recruitment of ipsilateral motor areas was greatest in the more impaired patients. We also used functional magnetic resonance imaging to monitor brain activity in these subjects as they performed the same movements. Slowing of reaction time after premotor cortex TMS in the patients correlated inversely with the relative hemispheric lateralization of functional magnetic resonance imaging activation in PMd. This inverse correlation suggests that the increased activation in ipsilateral cortical motor areas during movements of a paretic hand, shown in this and previous functional imaging studies, represents a functionally relevant, adaptive response to the associated brain injury.

This paper makes an outline case for the need for a low-cost, easy to administer method for detecting dementia within the growing at risk population. It proposes two methods for electroencephalogram (EEG) analysis for detecting dementia that could fulfil such a need. The paper describes a fractal dimension-based method for analyzing the EEG waveforms of subjects with dementia and reports on an assessment which demonstrates that an appropriate fractal dimension measure could achieve 67% sensitivity to probable Alzheimer's disease (as suggested by clinical psychometric testing and EEG findings) with a specificity of 99.9%. An alternative method based on the probability density function of the zero-crossing intervals is shown to achieve 78% sensitivity to probable Alzheimer's disease and an estimated sensitivity to probable Vascular (or mixed) dementia of 35% (as suggested by clinical psychometric testing and EEG findings) with a specificity of 99.9%. This compares well with other studies, reported by the American Academy of Neurology, which typically provide a sensitivity of 81% and specificity of 70%. The EEG recordings used to assess these methods included artefacts and had no a priori selection of elements "suitable for analysis." This approach gives a good prediction of the usefulness of the methods, as they would be used in practice. A total of 39 patients (30 probable Alzheimer's Disease, six Vascular Dementia and three mixed dementia) and 42 healthy volunteers were involved in the study. However, although results from the preliminary evaluation of the methods are promising, there is a need for a more extensive study to validate the methods using EEGs from a larger and more varied patient cohorts with neuroimaging results, to exclude other causes and cognitive scores to correlate results with severity of cognitive status.

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Proximal myopathy presents as symmetrical weakness of proximal upper and/or lower limbs. There is a broad range of underlying causes including drugs, alcohol, thyroid disease, osteomalacia, idiopathic inflammatory myopathies (IIM), hereditary myopathies, malignancy, infections and sarcoidosis. Clinical assessment should aim to distinguish proximal myopathy from other conditions that can present similarly, identify patients who need prompt attention, like those with cardiac, respiratory or pharyngeal muscle involvement, and determine underlying cause of myopathy. Initial evaluation should include simple tests, like creatine kinase, thyroid function and (25)OH vitamin D levels, but further evaluation including neurophysiological studies, muscle imaging and muscle biopsy should be considered for patients in whom no toxic, metabolic or endocrine cause is found, and in those with clinical features suggestive of inflammatory or hereditary myopathy. Additionally, screening for malignancy and testing for anti-Jo1 antibody is indicated for selected patients with IIM. Management depends on underlying cause, and includes measures, such as removal of offending agent, correction of endocrine or metabolic problem, corticosteroids and immunosuppressive therapy for IIM, and physical therapy, rehabilitation and genetic counselling for muscular dystrophies.