Central post-stroke pain — a study of the mechanisms through analyses of the sensory abnormalities

Abstract

The somatosensory abnormalities in 20 men and 7 women (mean age 67 years, range 53-81) with central post-stroke pain (CPSP) have been analysed in detail with traditional neurological tests and quantitative methods. The cerebrovascular lesions were located in the lower brain-stem in 8 patients, involved the thalamus in 9 and in 6 were suprathalamic. In 4 patients the location of the CVL could not be determined. All patients had abnormal temperature and pain sensibility, with a severe deficit in most cases. All except 2 had raised thresholds to thermal pain and all except 1 had abnormal sensibility to pin-prick. Eighty-eight percent exhibited hyperpathia with combined loss and suprathreshold exaggeration of somatic sensibility. In 85% somatic stimuli evoked dysaesthesia and about half of these patients also experienced spontaneous dysaesthesia. Paraesthesias were reported by 41%, radiation of stimuli by 50%, after-sensations by 45% and allodynia by 23%. Vibration sensibility was abnormal in 41%; raised thresholds to the perception of touch were found in 52%, to 2-PD in 35%, to dermolexia in 45% and to joint movements in 37%. The results indicate that all patients with CPSP have lesions that affect the major pathways for temperature and pain sensibility, i.e., the spino-thalamo-cortical pathways. Furthermore it appears that neither the level of the lesion along the neuraxis nor concomitant injury to the medial lemniscal pathways is crucial for the development of CPSP. The results confirm the notion that CPSP is a deafferentation syndrome, but they also provide evidence against the hypothesis that CPSP is a release phenomenon caused by a lesion that removes inhibitory influences of the lemniscal pathways on neurones that evoke pain.

Analgesic Effect of Transcranial Direct Current Stimulation on Central Post-Stroke Pain

“…In 1906, Dejerine and Roussy (1906) described the clinical symptoms of unique central pain in patients with thalamic injury, which sparked interest in thalamic pain syndrome (Boivie et al 1989). However, the term was replaced with CPSP because its clinical characteristics were not precise and symptoms could be expressed in any region of the central somatic nervous system (Schott 1996).…”

“…The pain aspects of CPSP are spontaneous, continuous (Boivie et al 1989), and diverse, including burning sensations, aching pain, tingling sensations, and laceration pain. CPSP can occur in a relatively small area such as the hands, a wide area (over half of the body), and sometimes in the trunk or the face (Boivie et al 1989;Kumar et al 2009).…”

“…CPSP can occur in a relatively small area such as the hands, a wide area (over half of the body), and sometimes in the trunk or the face (Boivie et al 1989;Kumar et al 2009). Dejerine and Roussy (1906) confined the lesion that triggers CPSP to the thalamus, but owing to the development of imaging diagnostic technology, diverse central regions were found to be related.…”

“…In addition, CPSP patients undergo dysesthesia such as allodynia (triggered by weak stimuli that do not cause pain in normal people), hyperalgesia (high-intensity pain easily brought about by weak stimuli), and spontaneous pain generated without outside stimuli (Boivie et al 1989;Hansson 2004). Such changes in pain restrict motor function and physical therapy, leading to loss of motivation and negatively affecting patient quality of life.…”

Types and effectiveness of treatments used by people with chronic pain associated with spinal cord injuries: influence of pain and psychosocial characteristics

“…[18][19][20][21] Sensory changes may be quantitative (threshold changes such as hypoesthesia or hyperesthesia) or qualitative (such as allodynia, dysesthesia, or paresthesia). 22,23 Responses to sensory testing may be important for defining a specific type of pain and thus serve as a basis for prescribing pain treatment. For example, if the etiological mechanism appears to be neuropathic, the first line of treatment might be anticonvulsant medication.…”