Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-5-25
pubmed:abstractText
The disinhibition hypothesis of post-stroke central pain (CPSP) suggests that 'the excessive response (dysesthesia/hyperalgesia/allodynia) is accompanied by a em leader loss of sensation' resulting from a lesion of a 'lateral nucleus' of thalamus or of 'cortico-thalamic paths' [Brain 34 (1911) 102]. One recent elaboration of this hypothesis proposes a submodality specific relationship, such that injury to a cool-signaling lateral thalamic pathway disinhibits a nociceptive medial thalamic pathway, thereby producing both burning, cold, ongoing pain and cold allodynia. The current study quantitatively evaluated the sensory loss and sensory abnormalities to discern submodality relationships between these sensory features of CPSP. The present results were statistically tested within individuals so that sensory loss and sensory abnormality are directly related by occurrence in the same individual. The results demonstrate that individuals with CPSP and normal tactile detection thresholds experience tactile allodynia significantly more often than those with tactile hypoesthesia. Most patients (11/13) exhibited hypoesthesia for the perception of cool stimuli, but few of these (2/11) showed cold allodynia. The most dramatic case of cold allodynia occurred in a patient who had a normal detection threshold for cold. Individuals with cold hypoesthesia, strictly contralateral to the cerebro-vascular accident (CVA or stroke), were often characterized by the presence of burning, cold, ongoing pain, and by the absence, not the presence, of cold allodynia. Overall, these results in CPSP suggest that tactile allodynia occurs in disturbances of thermal/pain pathways that spare the tactile-signaling pathways, and that cold hypoesthesia is neither necessary nor sufficient for cold allodynia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0304-3959
pubmed:author
pubmed:issnType
Print
pubmed:volume
109
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
357-66
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15157697-Adult, pubmed-meshheading:15157697-Afferent Pathways, pubmed-meshheading:15157697-Aged, pubmed-meshheading:15157697-Data Interpretation, Statistical, pubmed-meshheading:15157697-Female, pubmed-meshheading:15157697-Gyrus Cinguli, pubmed-meshheading:15157697-Humans, pubmed-meshheading:15157697-Hyperalgesia, pubmed-meshheading:15157697-Male, pubmed-meshheading:15157697-Middle Aged, pubmed-meshheading:15157697-Models, Neurological, pubmed-meshheading:15157697-Neural Inhibition, pubmed-meshheading:15157697-Neurologic Examination, pubmed-meshheading:15157697-Pain, Intractable, pubmed-meshheading:15157697-Physical Stimulation, pubmed-meshheading:15157697-Sensation Disorders, pubmed-meshheading:15157697-Stroke, pubmed-meshheading:15157697-Syndrome, pubmed-meshheading:15157697-Thalamus, pubmed-meshheading:15157697-Thermosensing, pubmed-meshheading:15157697-Touch, pubmed-meshheading:15157697-Ventral Thalamic Nuclei
pubmed:year
2004
pubmed:articleTitle
Allodynia in patients with post-stroke central pain (CPSP) studied by statistical quantitative sensory testing within individuals.
pubmed:affiliation
Department of Biomedical Sciences, University of Maryland Dental School, and University of Maryland Program in Neuroscience, Baltimore, MD 21201, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.