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Sensory abnormalities in consecutive, unselected patients with central post-stroke pain
Karsten Vestergaard1, Jesper Nielsen, Grethe Andersen
1Department of Neurology, Aalborg Hospital, DK-9100 Aalborg, Denmark Department of Medical Informatics, Aalborg University Center, Aarhus University Hospital, Aarhus, Denmark Department of Radiology, Aalborg Hospital, DK-9100 Aalborg, Denmark Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.
Pain
|May 1, 1995
Summary
Central post-stroke pain (CPSP) involves sensory abnormalities, particularly altered temperature detection and cold allodynia. These findings support damage to the spino-thalamo-cortical pathway as a cause of CPSP.
Area of Science:
- Neuroscience
- Neurology
- Pain Research
Background:
- Central post-stroke pain (CPSP) is a debilitating condition following ischemic or hemorrhagic stroke.
- Sensory abnormalities are common in CPSP patients, but their precise nature requires further investigation.
Purpose of the Study:
- To investigate the sensory abnormalities in patients with central post-stroke pain (CPSP) more than 1 year after stroke.
- To correlate sensory deficits with lesion location and pain characteristics.
Main Methods:
- Quantitative sensory examination including detection and pain thresholds for thermal stimuli, von Frey hairs, and argon laser testing in 11 CPSP patients.
- Stimulus-response function determination in the 10-45°C range.
- Clinical examination, MRI for lesion verification, McGill Pain Questionnaire, and Visual Analog Scale (VAS) for pain assessment.
Main Results:
- All patients exhibited sensory abnormalities in the painful area, with elevated warm detection thresholds in all and increased cold detection thresholds in most.
- Cold allodynia was present in 56% of patients within the 10-45°C range.
- Damage to the spino-thalamo-cortical pathway, including thalamic and brainstem/cerebellar lesions, was observed in all patients.
Conclusions:
- The findings support the hypothesis that damage to the spino-thalamo-cortical pathway is essential for CPSP development.
- Spontaneous pain in CPSP may result from hyperexcitability or spontaneous discharges in thalamic or cortical neurons with disrupted input.