Idiopathic peripheral neuropathy responsive to sympathetic nerve blockade and oral clonidine.

A 52-year-old female presented with idiopathic stocking-glove neuropathy. She underwent a series of right and left stellate ganglion blocks with ropivacaine and clonidine, followed by lumbar sympathetic blocks. This resulted in complete symptom relief for two weeks. These procedures were repeated after a two-month interval; at that time she was still experiencing partial relief from the first series. She again remained completely pain free for several weeks following the injections. As the pain partially returned, daily oral clonidine was initiated and resulted in almost complete cessation of her symptoms, which persisted at a three-month follow-up examination.

Gabapentin inhibits catecholamine release from adrenal chromaffin cells.

BACKGROUND: Gabapentin is most commonly prescribed for chronic pain, but acute perioperative effects, including preemptive analgesia and hemodynamic stabilization, have been reported. Adrenal chromaffin cells are a widely used model to investigate neurosecretion, and adrenal catecholamines play important physiologic roles and contribute to the acute stress response. However, the effects of gabapentin on adrenal catecholamine release have never been tested. METHODS: Primary cultures of bovine adrenal chromaffin cells were treated with gabapentin or vehicle for 18-24 h. The authors quantified catecholamine secretion from dishes of cells using high-performance liquid chromatography and resolved exocytosis of individual secretory vesicles from single cells using carbon fiber amperometry. Voltage-gated calcium channel currents were recorded using patch clamp electrophysiology and intracellular [Ca2+] using fluorescent imaging. RESULTS: Gabapentin produced statistically significant reductions in catecholamine secretion evoked by cholinergic agonists (24 ± 3%, n = 12) or KCl (16 ± 4%, n = 8) (mean ± SEM) but did not inhibit Ca2+ entry or calcium channel currents. Amperometry (n = 51 cells) revealed that gabapentin inhibited the number of vesicles released upon stimulation, with no change in quantal size or kinetics of these unitary events. CONCLUSIONS: The authors show Ca2+ entry was not inhibited by gabapentin but was less effective at triggering vesicle fusion. The work also demonstrates that chromaffin cells are a useful model for additional investigation of the cellular mechanism(s) by which gabapentin controls neurosecretion. In addition, it identifies altered adrenal catecholamine release as a potential contributor to some of the beneficial perioperative effects of gabapentin.

Rebleeding and survival after acute lower gastrointestinal bleeding.

BACKGROUND: Previous studies of acute lower gastrointestinal bleeding (LGIB) have focused on evaluation and therapy. Measurement of long-term outcome has been rare. The purpose of this study was to document rebleeding and survival rates in patients with acute LGIB. METHODS: A retrospective review of all patients undergoing technetium-labeled red blood cell scans for LGIB from January of 1997 to December of 2002 was performed. Rebleeding was defined as identification of enteric bleeding requiring a transfusion 2 or more weeks after the initial bleeding episode. RESULTS: A total of 119 patients met inclusion criteria. Rebleeding was documented in 14 of 102 patients surviving for more than 2 weeks. The actuarial rebleeding rate was 15% at 2 years. No factors were identified that portended a higher likelihood of rebleeding. The 30-day mortality was 18% and the median survival was 60 months for the entire cohort. Of the 36 patients in whom cause of death was documented, 4 died of surgical complications and a single patient died as a direct result of hemorrhage. CONCLUSIONS: Rebleeding after an initial episode of LGIB occurs in a small percentage of individuals. Although survival is poor for patients with LGIB, few patients die as a direct consequence of hemorrhage.