J. Nielsen

NMDA receptor blockade in chronic neuropathic pain: a comparison of ketamine and magnesium chloride

&NA; Ten patients (4 female, 6 male) aged 34–67 years suffering from peripheral neuropathic pain participated in a double‐blind placebo‐controlled study where ketamine or magnesium chloride were administered by a 10 min bolus infusion (ketamine: 0.84 &mgr;mol/kg = 0.2 mg/kg, magnesium: 0.16 mmol/kg) followed by a continuous infusion (ketamine: 1.3 &mgr;mol/kg/h = 0.3 mg/kg/h, magnesium: 0.16 mmol/kg/h). Ongoing pain determined by VAS score, area of touch‐evoked allodynia, detection and pain thresholds to mechanical and thermal stimuli were measured before and during drug infusion. Ketamine produced a significant reduction of spontaneous pain (57%) and of the area of allodynia (33%). Magnesium chloride reduced pain (29%) and area of allodynia (18%) insignificantly. following ketamine there was a significant correlation between the reduction in ongoing pain and reduction in area of touch‐evoked allodynia. Detection and pain thresholds to mechanical and thermal stimuli were not significantly changed by the drugs. These findings suggest that both ongoing pain and touch‐evoked pain (allodynia) in neuropathic pain are inter‐related phenomena, which may be mediated by the same mechanism and involving a N‐methyl‐D‐aspartate receptor.

Pain Produced by Electric Stimulation of the Rectum in Patients with Irritable Bowel Syndrome: Further Evidence of Visceral Hyperalgesia

BACKGROUNDnVisceral hyperalgesia is most likely a phenomenon of substantial clinical importance and may also play a role in the pathophysiology of the irritable bowel syndrome (IBS). We investigated the manifestation of visceral hyperalgesia in IBS patients by nociceptive electric stimulation of the rectosigmoid junction and rectum.nnnMETHODSnTwelve IBS patients fulfilling the Rome criteria and 9 healthy controls were studied. Visceral single and repeated electric burst stimuli were applied with a bipolar electric stimulator inserted through the sigmoidoscope. The sensation (ST) and pain detection (PDT) thresholds were determined in response to single and repeated stimuli at the rectosigmoid junction, and PDT to repeated stimuli at four different positions in the rectum. Cutaneous single and repeated electric stimuli were applied to the lateral aspect of the foot, determining ST and PDT.nnnRESULTSnCutaneous stimulation showed no significant differences for ST and PDT between patients and controls. The rectosigmoid junction showed significantly lower ST for single stimuli (P<0.01) and a significantly lower PDT for single and for repeated stimuli (P<0.05 and P<0.02) in IBS patients. In the rectum the IBS patients had a significantly lower PDT than controls (P<0.001).nnnCONCLUSIONSnFor cutaneous electric stimulation no differences in the pain thresholds between the two groups were found, showing that there is no generalized hyperalgesia in IBS patients. The IBS patients had a specific decrease of the pain thresholds in the rectum and rectosigmoid junction, indicating visceral hyperalgesia. These results point to central visceral hyperexcitability as an important factor in the pathophysiology of IBS.

An experimental pain model based on electric stimulations of the colon mucosa

BACKGROUNDnPain intensity and distribution related to diseases of the gut are important diagnostic indicators in gastroenterology. Experimental pain models provide a unique possibility for standardized activation of the nociceptive system, but only few human models exist.nnnMETHODSnAn experimental pain model based on electric stimuli in the human colon was developed and applied. Eleven patients who were referred for surveillance colonoscopy due to earlier polyps in the colon were included. None had any abdominal pain complaints. The following areas were stimulated with single, repeated, or continuous electric current: the cecum, the hepatic and splenic flexures, and the rectosigmoid junction.nnnRESULTSnAll subjects felt deep, diffuse pain during the stimulation, with referral to localized somatic structures. The pain detection thresholds after repeated stimuli were similar in the four areas. The threshold for single stimulation was higher than the threshold for repeated stimulation. Most reported pain in the lower and left site of the abdominal wall during stimuli at the splenic flexure and rectosigmoid junction. Stimuli at the right colon, however, resulted mostly in pain at the contralateral site of the abdomen.nnnCONCLUSIONSnThe presented model was robust and suitable for eliciting pain in different regions of the large intestine. The importance of temporal summation in visceral pain was shown. Mapping of the referred pain areas mimics clinical observations and has ontogenetic and anatomic consistency. The model may therefore improve the evaluation of pain in patients with diseases of the colon.

Exteroceptive suppression of masseter muscle : assessment of two methods for quantitating suppression periods

Objectives– The late exteroceptive suppression period (ES2) of the masseter muscle is conventionally quantified by a combination of measures of duration, amplitude, or mean activity. The combination of measures makes it difficult to compare ES2s obtained from different set‐ups. An unbiased method for quantitating ES2 is introduced allowing ranking of ES2s. The introduced method is utilized to evaluate stimulus and recording conditions under which ES2 is maximal. Material and methods– Fifteen male volunteers participated in 3 experiments designed to determine the effect of level of teeth clenching, stimulus intensity, and perceived pain intensity on the ES2. Results– Coefficients of variance (1 h/1 month) were: duration: 11%/43%, latency: 9%/12%, and magnitude of suppression: 11%/12%. A level of teeth clenching of 66% of maximal voluntary bite force, and a stimulus intensity below pain detection threshold was associated with maximal magnitude of suppression of ES2. Conclusion– The introduced method is reproducible and allows ranking and stimulus‐response estimations of ES2. It is suggested that ES2 does not reflect activity along the nociceptive pathways in the trigeminal region.