Linked Life Data

10962222

Source:http://linkedlifedata.com/resource/pubmed/id/10962222

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-10-11
pubmed:abstractText
Catatonia is a psychomotor syndrome with an inability to execute and terminate movements completely, leading consecutively to akinesia and posturing, which both respond almost immediately to benzodiazepines, i.e. gaba-potentiators like lorazepam. However, pathophysiological mechanisms of cortical motor and gaba-ergic dysfunction remain unclear. We therefore investigated movement-related cortical potentials (MRPs) and movement kinematics during a motor task before and after lorazepam. Ten akinetic catatonic patients were compared with 10 psychiatric (similar age, sex, medication, and underlying psychiatric disease but without catatonic syndrome) and 20 healthy controls. MRPs from frontal (F), central (C), and parietal (P) sites were recorded to obtain measures of early and late readiness potential and movement potential. Kinematic measures included parameters for amplitude of movements, peak velocity, average duration of movements, elevation angle, and angle velocity. The motor task consisted in self-initiated extension of the right index finger. All catatonic and psychiatric control patients received intravenous lorazepam (1mg), whereas healthy controls were subjected to a placebo-controlled (10 received lorazepam, 10 received placebo) double-blind study design.Catatonics showed a significantly delayed onset of late readiness and movement potential in central electrodes (Cz, C3) compared with psychiatric and healthy controls. This delayed onset correlated significantly with catatonic motor symptoms and movement duration. Lorazepam led to significantly stronger delays in onset of late readiness potential in left fronto-parietal (F3, C3, P3) electrodes in catatonic patients than in psychiatric and healthy controls. It is concluded that delayed latencies in late MRP components in catatonic patients may reflect their inability to execute and terminate movements completely. Differential and stronger response to lorazepam in catatonia suggests dysfunction in inhibitory control of cortical motor function with increased gaba-ergic sensitivity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0920-9964
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
193-211
pubmed:dateRevised
2010-9-2
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Delayed onset of late movement-related cortical potentials and abnormal response to lorazepam in catatonia.
pubmed:affiliation
Department of Psychiatry of Otto-von Guericke, University Magdeburg, Leipziger Strasse 44, 39120, Magdeburg, Germany. georg.northoff@medizin.uni-magdeburg.de
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't