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      Quantitative Assessment of Recovery from Motor Hemineglect in Acute Stroke Patients

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          Background and Purpose: Motor hemineglect is characterized by an underutilization of one side of the body. It is a higher-order motor disorder that resembles hemiplegia although being substantially different from it due to a preserved motor output system. Its role for poststroke recovery is still unclear. Methods: We studied 52 patients presenting with acute hemiparetic stroke over the first 7 days after symptom onset. Nineteen patients had unilateral motor hemineglect. Impairment was clinically assessed with the European Stroke Scale and a multifactorial motor score. It was further assessed quantitatively, as overall arm activity was measured continuously by Actiwatches. Lesion volumes were measured morphometrically within 24 h on perfusion- and diffusion-weighted magnetic resonance images and on average on day 9 by T<sub>2</sub>-weighted magnetic resonance imaging. Results: Patients with motor hemineglect were characterized by significantly reduced initial arm activity in comparison to patients without motor hemineglect. This was paralleled by larger brain lesions in the patients with motor hemineglect. Patients with motor neglect either recovered virtually completely (5 cases; 2/5 left hemisphere; 3/5 treated with recombinant tissue plasminogen activator, rt-PA) within 7 days or did not improve at all (14 cases; 3/14 left hemisphere; 3/14 rt-PA treated). Conclusion: Our data reveal a high incidence of motor hemineglect in patients with acute stroke. They further show that these patients are more severely compromised than those without motor hemineglect. A rapid and near complete recovery was observed in about one fourth of the motor hemineglect patients and may be related to involvement of the left hemisphere or to therapy with thrombolysis.

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          Most cited references 25

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          A cortical network for directed attention and unilateral neglect.

          Unilateral neglect reflects a disturbance in the spatial distribution of directed attention. A review of unilateral neglect syndromes in monkeys and humans suggests that four cerebral regions provide an integrated network for the modulation of directed attention within extrapersonal space. Each component region has a unique functional role that reflects its profile of anatomical connectivity, and each gives rise to a different clinical type of unilateral neglect when damaged. A posterior parietal component provides an internal sensory map and perhaps also a mechanism for modifying the extent of synaptic space devoted to specific portions of the external world; a limbic component in the cingulate gyrus regulates the spatial distribution of motivational valence; a frontal component coordinates the motor programs for exploration, scanning, reaching, and fixating; and a reticular component provides the underlying level of arousal and vigilance. This hypothetical network requires at least three complementary and interacting representations of extrapersonal space: a sensory representation in posterior parietal cortex, a schema for distributing exploratory movements in frontal cortex, and a motivational map in the cingulate cortex. Lesions in only one component of this network yield partial unilateral neglect syndromes, while those that encompass all the components result in profound deficits that transcend the mass effect of the larger lesion. This network approach to the localization of complex functions offers an alternative to more extreme approaches, some of which stress an exclusive concentration of function within individual centers in the brain and others which advocate a more uniform (equipotential or holistic) distribution. In human beings, unilateral neglect syndromes are more frequent and severe after lesions in the right hemisphere. Also, right hemisphere mechanisms appear more effective in the execution of attentional tasks. Furthermore, the attentional functions of the right hemisphere span both hemispaces, while the left hemisphere seems to contain the neural apparatus mostly for contralateral attention. This evidence indicates that the right hemisphere of dextrals has a functional specialization for the distribution of directed attention within extrapersonal space.
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            Mutations in ERCC4, encoding the DNA-repair endonuclease XPF, cause Fanconi anemia.

            Fanconi anemia (FA) is a rare genomic instability disorder characterized by progressive bone marrow failure and predisposition to cancer. FA-associated gene products are involved in the repair of DNA interstrand crosslinks (ICLs). Fifteen FA-associated genes have been identified, but the genetic basis in some individuals still remains unresolved. Here, we used whole-exome and Sanger sequencing on DNA of unclassified FA individuals and discovered biallelic germline mutations in ERCC4 (XPF), a structure-specific nuclease-encoding gene previously connected to xeroderma pigmentosum and segmental XFE progeroid syndrome. Genetic reversion and wild-type ERCC4 cDNA complemented the phenotype of the FA cell lines, providing genetic evidence that mutations in ERCC4 cause this FA subtype. Further biochemical and functional analysis demonstrated that the identified FA-causing ERCC4 mutations strongly disrupt the function of XPF in DNA ICL repair without severely compromising nucleotide excision repair. Our data show that depending on the type of ERCC4 mutation and the resulting balance between both DNA repair activities, individuals present with one of the three clinically distinct disorders, highlighting the multifunctional nature of the XPF endonuclease in genome stability and human disease. Copyright © 2013 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.
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              Role of the premotor cortex in recovery from middle cerebral artery infarction.

              To study the mechanisms underlying recovery from middle cerebral artery infarction in 7 patients with an average age of 53 years who showed marked recovery of hand function after acute severe hemiparesis caused by their first-ever stroke. Assessment of motor functions, transcranial magnetic stimulation, somatosensory evoked potentials, magnetic resonance imaging, and positron emission tomographic measurements of regional cerebral blood flow during finger movement activity. The infarctions involved the cerebral convexity along the central sulcus from the Sylvian fissure up to the hand area but spared the caudate nucleus, thalamus, middle and posterior portions of the internal capsule, and the dorsal part of the precentral gyrus in each patient. After recovery (and increase in motor function score of 57%, P<.001), the motor evoked potentials in the hand and leg muscles contralateral to the infarctions were normal, whereas the somatosensory evoked potentials from the contralateral median nerve were reduced. During fractionated finger movements of the recovered hand, regional cerebral blood flow increases occurred bilaterally in the dorsolateral and medial premotor areas but not in the sensorimotor cortex of either hemisphere. Motor recovery after cortical infarction in the middle cerebral artery territory appears to rely on activation of premotor cortical areas of both cerebral hemispheres. Thereby, short-term output from motor cortex is likely to be initiated.

                Author and article information

                Cerebrovasc Dis
                Cerebrovascular Diseases
                S. Karger AG
                May 2006
                18 May 2006
                : 21
                : 5-6
                : 307-314
                aDepartment of Neurology, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, and bBiomedical Research Centre, Heinrich Heine University Düsseldorf, Düsseldorf, Germany
                91535 Cerebrovasc Dis 2006;21:307–314
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 43, Pages: 8
                Original Paper


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