Quantitative Assessment of Recovery from Motor Hemineglect in Acute Stroke Patients

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

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.

Related collections

Most cited references 25

Record: found
Abstract: found
Article: not found

A cortical network for directed attention and unilateral neglect.

M M Mesulam (1981)

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.

0 comments Cited 283 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Mutations in ERCC4, encoding the DNA-repair endonuclease XPF, cause Fanconi anemia.

Nicolaas Jaspers, Orlando D. Schärer, Aldana M. Ramirez … (2013)

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.

0 comments Cited 123 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Role of the premotor cortex in recovery from middle cerebral artery infarction.

P Höflich, L Tellmann, Michael H. Herzog … (1998)

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.

0 comments Cited 57 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (publisher-id): CED

Journal ID (nlm-ta): Cerebrovasc Dis

Journal ID (doi): 10.1159/issn.1015-9770

Title: Cerebrovascular Diseases

Publisher: S. Karger AG

ISSN (Print): 1015-9770

ISSN (Electronic): 1421-9786

Publication date Subscription-year: 2006

Publication date (Print): May 2006

Publication date (Electronic): 18 May 2006

Volume: 21

Issue: 5-6

Pages: 307-314

Affiliations

^aDepartment of Neurology, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, and ^bBiomedical Research Centre, Heinrich Heine University Düsseldorf, Düsseldorf, Germany

Article

Publisher ID: 91535 Other ID: Cerebrovasc Dis 2006;21:307–314

DOI: 10.1159/000091535

PubMed ID: 16490939

SO-VID: 1be81de4-0707-4ed2-bb01-800651b2159b

License:

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 02 May 2005

Date accepted : 24 October 2005

Page count

Figures: 5, Tables: 1, References: 43, Pages: 8

Comments

Comment on this article

scite_

Cited by 11

See all cited by

Most referenced authors 278

See all reference authors

- Version 1

Call for Papers: Sex and Gender in Neurodegenerative Diseases

Submit here before September 30, 2024

Quantitative Assessment of Recovery from Motor Hemineglect in Acute Stroke Patients

Read this article at

Abstract

Related collections

Karger: Neurology and Neuroscience

Most cited references 25

A cortical network for directed attention and unilateral neglect.

Mutations in ERCC4, encoding the DNA-repair endonuclease XPF, cause Fanconi anemia.

Role of the premotor cortex in recovery from middle cerebral artery infarction.

Author and article information

Journal

Affiliations

Article

History

Page count

Categories

Comments

Comment on this article

Similar content 218

Cited by 11

Most referenced authors 278