Central pain in the face and head.

All kinds of lesions in the central nervous system can induce central neuropathic pain (e.g., stroke, multiple sclerosis, spinal cord injury, syringobulbia, syringomyelia). The location is the most important feature of the lesion. In stroke, the onset of pain is often delayed. It is mostly constant, but it may be intermittent or paroxysmal. In stroke patients the pain is frequently a hemipain (75%), whereas in the 28% of all multiple sclerosis patients who develop central pain it dominates in the legs (87%) and 5% have trigeminal neuralgia caused by lesions in the brainstem. There is a large variation in the quality of central pain. Central pain is associated with abnormalities in sensitivity to temperature and pain. It is hypothesized that central pain is caused by lesions of the spinothalamic pathways, including their thalamocortical projections, but some other (unknown) factors appear to be crucial for the development of the pain because many patients with such lesions do not develop central pain. Central pain usually responds poorly to analgesics. The first-line treatments are tricyclic antidepressants and antiepileptic drugs.

Gabapentin in traumatic nerve injury pain: a randomized, double-blind, placebo-controlled, cross-over, multi-center study.

A double-blind, randomized, placebo-controlled cross-over multi-center study was conducted to evaluate the efficacy and safety of gabapentin in the treatment of neuropathic pain caused by traumatic or postsurgical peripheral nerve injury, using doses up to 2400 mg/day. The study comprised a run-in period of two weeks, two treatment periods of five weeks separated by a three weeks' washout period. The primary efficacy variable was the change in the mean pain intensity score from baseline to the last week of treatment. Other variables included pain relief, health related quality of life (SF-36), interference of sleep by pain, Clinician and Patient Global Impression of Change, and adverse effects. Nine centers randomized a total of 120 patients, 22 of whom withdrew. There was no statistically significant difference between the treatments for the primary outcome efficacy variable. However, gabapentin provided significantly better pain relief (p=0.015) compared with placebo. More patients had at least a 30% pain reduction with gabapentin compared with placebo (p=0.040) and pain interfered significantly less with sleep during gabapentin treatment compared with placebo (p=0.0016). Both the Patient (p=0.023) and Clinician (p=0.037) Global Impression of Change indicated a better response with gabapentin compared with placebo. Gabapentin was well tolerated. The most common adverse effects were dizziness and tiredness.

Morphine responsiveness in a group of well-defined multiple sclerosis patients: a study with i.v. morphine.

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.

Painful polyneuropathy in patients with and without diabetes: clinical, neurophysiologic, and quantitative sensory characteristics.

OBJECTIVES: To study pain characteristics and peripheral nerve involvement in patients with painful diabetic and nondiabetic polyneuropathy in comparison with patients with non-painful polyneuropathy. PATIENTS AND METHODS: Fifty-five patients with polyneuropathy (37 with painful polyneuropathy, of whom 19 had diabetes and 18 had no diabetes; and 18 with painless polyneuropathy of different etiologies) were examined clinically using quantitative sensory tests and neurophysiology. Pain intensity and characteristics were analyzed by daily ratings on a 10-step verbal scale and by a questionnaire. RESULTS: Most patients experienced pain of more than one character. There was no clear difference in character or duration of pain between patients with and without diabetes. The mean value of the daily rating of pain intensity showed that pain was more severe in the evenings than in the mornings and that diabetic patients reported worse pain than nondiabetic patients. Thirty-two of the 37 patients with pain had paresthesias and/or dysesthesias, whereas only 7 of 18 patients without pain had paresthesias. Pain was always located in the feet, and, in most patients, also in the lower part of the legs. Some patients also experienced pain in the hands. Tactile sensibility, measured by quantitative tests, was more affected in both diabetic and nondiabetic patients with painful polyneuropathy compared with patients without pain (p = 0.02). Temperature, pain, and vibratory sensibility were equally affected in all patient groups. Nerve conduction velocity, amplitudes, and distal latency were equally affected in the pain group as compared with the control group, indicating that both thin and thick nerve afferents are affected in patients with painful as well as non-painful polyneuropathy and that etiology has no clear impact on nerve involvement. CONCLUSIONS: Neuropathy pain was always located in the feet and more severe in diabetic patients compared with patients with neuropathy pain of other etiologies. The authors also found evidence for a greater tactile sensibility involvement in patients with neuropathy pain, irrespective of etiology, whereas other quantitative sensibility and neurography parameters were equally affected in all patient groups.

A correlative anatomical and clinical study of pain suppression by deep brain stimulation.

The clinical results of electrical stimulation in medial thalamic regions for cancer pain have been correlated with the exact location of the stimulation sites. Five brains were examined by post-mortem histology. Chronic implantation of enamel coated platinum-iridium electrodes for up to 17 months caused relatively mild glial and neuronal reactions and no significant haemorrhage or infarction. The anatomical verifications showed that the electrodes were close to, but not exactly in, the regions defined by the stereotactic coordinates. From the clinico-anatomical correlations it appears that good pain relief can be obtained by electrical stimulation in the periventricular gray region of the posterior thalamus.