Effects of lamotrigine on pain-induced chemo-somatosensory evoked potentials.

Lamotrigine, a sodium channel blocker that selectively inhibits the neuronal release of glutamate, has been shown to produce analgesia in acute and chronic pain models in rats without causing noticeable sedation. After oral administration it also reduces pain scores, as assessed by the cold pain test, in volunteers. The purpose of this study was to determine the analgesic effect of lamotrigine given by mouth to healthy volunteers as evidenced by alterations in chemo-somatosensory evoked potentials. The following factors were measured: latency to N1 and P100 peak (ms); amplitude between the N1 and P100 peak (microV); visual analogue pain intensity scores. A double-blind, randomised and crossover design was used in which 12 volunteers received either placebo or lamotrigine 300 mg on separate occasions as determined by the randomisation schedule. Volunteers were tested before and 2 h after the treatment. The plasma lamotrigine concentration was measured immediately after the end of the experimental sessions. Lamotrigine produced a significantly higher latency to P100 values at 2 h postdrug than placebo (p < 0.05) but had no significant effects on the other factors. Although plasma concentrations were similar to those observed in the cold pain test, we conclude that lamotrigine 300 mg by mouth had no analgesic effect in this acute pain model.

Patterns of self-care needs and interventions related to biologic response modifier therapy: fatigue as a model.

Many patients receiving biologic response modifier (BRM) therapy experience fatigue as a significant and, at times, dose-limiting side effect. For this reason, a multiinstitutional pilot study was designed to collect data about the needs and self-care interventions of patients who had undergone at least one prior treatment with a BRM and had experienced fatigue as a symptom. Information was also obtained on the extent to which the needs and self-care interventions identified by patients compared with those perceived by their family members and nurses. Of the 16 patients who participated in the study, seven were being treated with interleukin-2 (IL-2), eight with interferon alfa (IFN-alpha), and one with tumor necrosis factor (TNF). The study found no significant correlation between the degree or duration of fatigue and the BRM or dosage administered. Not surprisingly, patient and family member responses correlated fairly well. However, in several parameters, including the degree and duration of fatigue, nurses' perceptions did not correlate at all with those of the patient. While 46% of nurse responses matched those of the patient as to useful self-care interventions, only 17% of nurses accurately identified factors or events that patients perceived as worsening fatigue. Further, there was no correlation among patient, family member, and nurse responses on interventions that could be used by others to help the patient cope with fatigue. The overall results of this pilot study indicate that nurses need to be more attuned to assessing fatigue as a side effect of BRM therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Perforation of the gastrointestinal tract in patients receiving steroids for neurologic disease.

Between 1980 and 1984, of 107 patients receiving 16 mg/d of dexamethasone for spinal cord compression, three (2.8%) developed gastrointestinal (GI) perforation and two (1.9%) GI bleeding; of 226 being tapered from 100 mg/d of dexamethasone, perforation occurred in six (2.7%) and GI bleeding in eight (3.5%). Of 125 patients with GI perforations treated between 1979 and 1986, 41 (33%) were on steroids, 24 for neurologic disease. Median duration of steroid therapy was 24 days; 20 (91%) of the neurologic patients perforated within 30 days. The steroid group had more free peritoneal involvement (p less than 0.00001), but fewer signs and symptoms of peritonitis (p less than 0.000001) than the nonsteroid group. Seventeen patients were receiving steroids for cord compression; they had significantly more rectosigmoid perforations (p less than 0.014) and associated constipation (p less than 0.000001) than the 108 remaining patients. GI perforation is a less well-recognized complication of steroid therapy in neurologic patients than is GI bleeding though it occurs as frequently, is more difficult to diagnose, and far more serious. In steroid-treated patients, prevention of constipation might avert this serious complication, while early diagnosis will improve the outcome.