Central post-stroke pain — neurological symptoms and pain characteristics

Abstract

The intention of the present study was to characterize patients with central post-stroke pain (CPSP) with regard to type and location of the cerebrovascular lesion (CVL), the characteristics of the pain and the neurological symptoms and signs in addition to the pain. Twenty men and 7 women with a mean age of 67 years and a mean pain duration of 44 months were examined 9–188 (mean 53) months after their stroke. The clinical symptoms and signs and the CT scans indicated that the CVL were located in the lower brain-stem in 8 patients, involved the thalamus in 9 patients and were located lateral and superior to the thalamus in 6 patients. In the remaining 4 patients the location of the CVL could not be determined with certainty. The 3 identified hematomata were all located in the thalamus. The onset of the pain was immediate in 4 patients, within the first post-stroke months in 10 patients and delayed by 1–34 months in the rest. The pain was on the left side in 18 patients. Twenty patients had hemipain. Most patients experienced more than one type of pain. The most common qualities were burning, aching, pricking and lacerating, with some differences in the frequencies according to the location of the CVL. Burning pain was most common, except among the patients with thalamic CVL, in whom lacerating pain was more common. Aching and pricking pain were also frequent. All patients considered the pain to be a great burden and most rated the pain intensity as high on a visual analogue scale. The intensity was increased by external stimuli, the most common being joint movements, cold and light touch. Five patients reported aggravation by emotional stimuli. Besides pain, the only neurological symptom common to all patients was decreased temperature sensibility, as shown by quantitative methods. It is possible that pain sensibility was also abnormal in all. Hypersensitivities to cutaneous stimuli, including evoked dysesthesias were found in 88% of the patients, while the detection thresholds for touch and vibration were abnormal in only 52% and 41%, respectively. Similarly, low figures were found for paresis and ataxia, which were present in 48% and 62%, respectively. It is concluded that only a minority of patients with central pain after stroke have thalamic lesions. The term thalamic pain is therefore inaccurate in most cases of CPSP. The symptoms and signs indicate that the crucial factor for the development of CPSP is a lesion affecting the spino-thalamo-cortical pathway important for temperature and pain sensibility. The level of the lesion along the neuroaxis is not critical for occurrence of the pain, but decides the nature of the associated neurological symptoms and appears to affect the features of the pain.