Pain is more common in multiple sclerosis (MS) than has previously been recognised. In the present study we have investigated the occurrence of central pain (CP) in MS and defined its characteristics. Questionnaires were sent to all 429 patients with definite MS in the patient register at our neurology department. All admitting to pain were interviewed and offered an extended interview and examination. Three hundred and sixty four patients responded (86%), of whom 57.5% reported pain during the course of their disease (21% nociceptive, 2% peripheral neuropathic and 1% related to spasticity). One hundred patients (27.5%) had CP, including 18 patients (4.9%) with trigeminal neuralgia. The non-trigeminal CP was, in 87%, located in the lower and in 31% in the upper extremities. It was mostly bilateral (76%) and constant, with 88% experiencing daily pain. Only 2% had paroxysmal attacks. Aching, burning, pricking were the commonest qualities. The pain was intense with small to moderate spontaneous variation. In 5.5% of all patients (20% of the patients with CP), pain was a presenting symptom, alone or in combination with other symptoms. The most common neurological symptoms/signs besides CP were sensory abnormalities (98%, dominated by abnormal sensibility to painful stimulus and temperature). Trigeminal neuralgia in MS started later in life and after longer disease duration than non-trigeminal pain. Both types of CP existed either chronically or as a feature of relapse. Central pain is thus an important symptom in MS (around 30%) and causes much suffering.

Many patients with multiple sclerosis (MS) develop central neuropathic pain (CP). In the present study somatosensory abnormalities have been analysed in detail in 62 patients with MS and CP (42 women, 20 men; mean age 52 years) and in a control group of 10 women and 6 men (mean age 47 years) with MS and sensory symptoms, but without pain. Assessment included clinical testing and quantitative methods (QST) for the measurement of perception thresholds for touch, vibration, and temperatures. All CP patients except two (97%) had abnormal thresholds for innoxious and/or noxious temperatures, compared to 81% in the control group (p<0.05). There was a tendency towards the opposite regarding sensibility to touch, which was decreased in 66% vs. 87% (n.s.), vibration (55% vs. 81%; n.s.) and to joint movement (32% vs. 62%; p<0.04). Comparisons between painful and non-painful regions showed both the absolute threshold values and the index values to be significantly more abnormal, in the CP regions, for warmth (p<0.001), cold (p<0.05), difference limen (innoxious warmth and cold, p<0.01), cold pain (p<0.01) and heat pain/cold pain combined (p<0.001). Also the comparisons between regions with central pain and regions with sensory symptoms in the controls showed significantly more abnormal thresholds in the CP patients for warmth (p<0.05), cold (p<0.01), difference limen (innoxious warmth and cold, p<0.01) and heat pain/cold pain combined (p<0.001). The results support the general hypothesis that only patients who have lesions affecting the spinothalamo-cortical pathways run the risk of developing central pain.

The relevance of the increased mean value of plasma tHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. We can not, however, exclude the possibility of a genetically induced dysfunction of the homocysteine metabolism relevant for the development of neuroinflammation/degeneration. Our findings indicate that, regardless of a significant increase in plasma tHcy in MS patients, the MS disease is not generally associated with vitamin B12 deficiency since we did not find any other factors indicating vitamin B12 deficiency. Analysis of CSF MMA and CSF tHcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. We conclude that B12 deficiency, in general, is not associated with MS.

The prevalence of pain in 211 HIV-infected patients with and without intravenous drug use was assessed and the prognostic information inherent in pain reporting was evaluated, using a questionnaire on pain and HIV-related symptoms combined with data on disease classification, route of HIV transmission, CD4+ lymphocyte counts in blood (CD4) and mortality rates at 15 months after completing the questionnaire. The pain prevalence was significantly higher among intravenous drug users (IDUs) compared with non-IDUs [76/89 (85%) vs 87/122 (71%);p<0.05], especially among the patients classified as asymptomatic [43/53 (81%) vs 35/59 (59%);p = 0.01]. No significant difference was found among AIDS patients. In non-IDUs, a strong correlation was found between HIV disease stages according to the Centers for Disease Control classification (CDC) and pain prevalence (CDC A: 59%vs B: 74%vs C: 96%, p<0.001), and between the number of concurrent pain sites and both the CD4 levels (no pains: CD4 0.26 x 10(9)/l vs 1-2 pain sites: CD4 0.22 vs>2 pain sites: CD4 0.09;r = 0.35, p<0.001), and the mortality rate [no pains: 2/35 (6%) vs 1-2 pain sites: 8/45 (18%) vs> 2 pain sites: 12/42 (29%), p<0.01]. In IDUs, no such correlations were found. Our data demonstrates differences in the development, prevalence and prognostic value of pain among HIV-infected patients, with and without intravenous drug use, clearly indicating the need to differentiate risk groups in pain related studies. Copyright 1999 European Federation of Chapters of the International Association for the Study of Pain.

Pain in multiple sclerosis (MS) is more common than has previously been believed. About 28% of all MS patients suffer from central pain (CP), a pain that is difficult to treat. In the present study we have investigated the responsiveness of this pain to morphine. Fourteen opioid-free patients (eight woman and six men) with constant, non-fluctuating, long-lasting CP caused by MS were investigated. Placebo (normal saline), morphine and naloxone were given intravenously in a standardized manner. The study design was non-randomized, single blind and placebo controlled. Ten patients experienced less than 50% pain reduction by placebo and less than 50% pain reduction by morphine. Four patients were opioid responders, i.e. had minimal or no effect on pain by placebo, >50% pain reduction after morphine and >25% pain increase after naloxone, given intravenously following morphine. However, this response was obtained after high doses of morphine (43 mg, 47 mg, 50 mg and 25 mg; mean 41 mg). Thus, compared with nociceptive pain, only a minority of the patients with CP due to MS responded to morphine and only at high doses. The present results are in accord with experimental studies indicating that neuropathic pain is poorly responsive but not totally unresponsive to opioids. The results do not support the routine use of strong opioids in MS patients with CP.