cpsp - central post-stroke pain

I didn't have this but some people I know did
Some research;
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0K-4864XWP-6R&_user=10&_coverDate=01%2F31%2F1989&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_searchStrId=1716204310&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=361c1f1cf672fdf23d67e993befa2779&searchtype=a

Abstract

A double-blind, 3-phase, cross-over, placebo-controlled trial of the pain-relieving effect of amitriptyline and carbamazepine was carried out in 15 patients with central post-stroke pain (CPSP) but without signs of depression. Treatment was given, in randomized order, for periods of 4 weeks, separated by 1 week wash-out. The final doses were 75 and 800 mg/day, respectively, for amitriptyline and carbamazepine. The treatment effects were assessed by daily ratings of pain intensity on a 10-step verbal scale and at the end of each treatment period by a global rating of the analgesic effect on a 5-step verbal scale. For the assessment of depression the Comprehensive Psychopathological Rating Scale (CPRS) was used.
Amitriptyline produced a statistically significant reduction of pain when compared to placebo. According to the global rating, 10 of the 15 patients were responders to this drug. The effect could already be noticed during the second treatment week and it appeared to be correlated to the plasma concentration, since the median total ami- and nortriptyline concentrations were 497 and 247 nmol/1, respectively, for responders and non-responders. The early onset, together with the fact that the patients were not depressed, nor did they obtain reduced scores on ratings of depressive symptoms and signs, provides strong support for the conclusion that the pain relief was not caused by an antidepressive effect.
Five of the 14 patients treated with carbamazepine reported some pain relief, but the effect did not reach statistical significance when compared to placebo. No correlation was found between effect and plasma concentration.
In general, the patients tolerated the planned final dose of amitriptyline well. No final dose reduction was necessary. Carbamazepine caused more side effects and the final dose had to be reduced in 4 patients. However, only 1 patient had to be taken off medication, on day 25, due to drug interaction.

Keywords: Central post-stroke pain; Controlled trial; Amitriptyline; Carbamazepine; Placebo

Or:

http://thejns.org/doi/abs/10.3171/jns.1998.89.4.0585

Object. The goal of this study was to identify the neurological characteristics of patients with poststroke pain who show a favorable response to motor cortex (MC) stimulation used to control their pain.

Methods. The neurological characteristics of 31 patients treated by MC stimulation were analyzed. In 15 patients (48%), excellent or good pain control (pain reduction > 60%) was achieved for follow-up periods of more than 2 years by using MC stimulation at intensities below the threshold for muscle contraction. Satisfactory pain control was achieved in 13 (73%) of 18 patients in whom motor weakness in the painful area was virtually absent or mild, but in only two (15%) of the 13 patients who demonstrated moderate or severe weakness in the painful area (p < 0.01). Muscle contraction was inducible in the painful area in 20 patients when stimulated at a higher intensity. No such muscle response was inducible in the remaining 11 patients, no matter how extensively the authors attempted to determine appropriate stimulation sites. Satisfactory pain control was achieved in 14 (70%) of the 20 patients in whom muscle contraction was inducible, but in only one (9%) of the 11 patients in whom muscle contraction was not inducible (p < 0.01). No significant relationship was observed between pain control and various sensory symptoms, including the presence of hypesthesia, spontaneous dysesthesia, hyperpathia, and allodynia, or the disappearance of the N20 component of the median nerve—evoked somatosensory scalp potential. No significant relationship existed between the effect of MC stimulation on the pain and stimulation-induced phenomena, including paresthesia, improvement in motor performance, and attenuation of involuntary movements.

Conclusions. These findings suggest that the pain control afforded by MC stimulation requires neuronal circuits that are maintained by the presence of intact corticospinal tract neurons originating from the MC. Preoperative evaluation of motor weakness of the painful area appears to be useful for predicting a favorable response to MC stimulation in the control of poststroke pain.

Key Words • central pain • motor cortex • pain • brain stimulation • stroke • thalamic pain

This site has lots of good information:
http://www.painclinic.org/nervepain-centralpoststrokepain.htm