Assessment of post-stroke pain
Robert D Helme
The commonest cause of central neuropathic pain is from stroke disease. Patients with stroke who develop pain are most likely to have a lesion affecting the nociceptive conducting pathways, which are also associated with thermal sensitivity. These neurons mostly project through the spinothalamic tract (STT). Patients with STT lesions have a combination of diminished pin-prick, cool and/or warm sensitivity with preserved light touch and vibration. Typical clinical correlates with Central post-stroke pain (CPSP) are also said to include allodynia and hyperpathia. This study was designed as part of a continuing series to investigate methods for measuring spontaneous and evoked pain after stroke. It is anticipated that such studies will lead to answers to such questions as the precise combination of clinical findings that might predict which patients will develop pain after stroke and when that might happen, what features characterise these patients as opposed to other patients with neuropathic pain, and which therapeutic approaches may be most appropriate for individual patients with pain after stroke. In this study we compared two groups of patients; those with pain after stroke, and those with comparable clinical and imaging findings but without pain.
Patients with stroke likely to result in pain were sourced from the files of the stroke service at Western Hospital, Melbourne, Australia. Ten patients with pain and seven without pain but with sensory deficits typical of those who develop pain were recruited into the study. All patients underwent baseline testing for mood disturbance and their pain scores were recorded using the McGill Pain Questionnaire (MPQ), the Gracely Pain and Unpleasantness Scales, and the Leeds Assessment of Neuropathic Signs and Symptoms (LANSS).
Sensory testing was performed using semi-quantifiable tests of warm, cold and vibration thresholds (Physitemp) as well as tactile sensibility with calibrated Von Frey monofilaments. Repetitive stimulation of the affected body area was performed using a toothpick at a frequency of 1 Hz for up to 60 seconds to evoke hyperpathia, and the presence of allodynia was assessed by brushing foam lightly over the skin. Results were analysed using SPSS v14.0 and Chi2 testing as appropriate.
Using the Gracely Scales a significant group interaction effect was found whereby pain intensity was higher in the pain group as expected, but the two groups had comparable unpleasantness ratings. The LANSS scores between the two groups were significantly different, with a higher mean score in the pain group compared to the control group. There were no group differences in the number of words chosen on the MPQ. Tactile and vibration acuity was uniformly expressed across all patients, and thermal discrimination was affected regardless of the manifestation of CPSP. However, it was found that heat and cold pain thresholds were more severely affected in the pain group as was the mean side-to-side differences of tactile sensibility. Further correlations indicated that hyperpathia generally coexisted with allodynia and was exclusive to the pain group.
These results provide a baseline for the exploration of new methods to predict, assess and treat central neuropathic pain from stroke. We are currently exploring more precise measures of these clinical features, with a particular emphasis on the characteristics of hyperpathia induced using repetitive thermal stimulation.
Time of Presentation
1530
