Managing intractable pain with an intrathecal catheter and injection port: technique and guidelines.

The objective of our study was to describe an effective technique for the management of chronic intractable pain in patients with intermediate life expectancy or as a long-term screening device prior to implantable pump therapy. In the study, an InDura intraspinal catheter is connected to a BardPort, which is accessed transdermally. We describe our surgical technique, recommended dosage calculations, cost comparison to an implantable infusion pump, and our experience with 13 cases. In our series of 13 patients, there was one seroma and one dural leak. There were no infections, and all were functioning well in the 12 cancer patients until their deaths. One case was converted to an implantable pump. There were no malfunctions or infections of the intrathecal infusion system in the 12 cancer patients. This intrathecal drug infusion system should be considered in the treatment armamentarium for chronic intractable pain and cancer pain.

Complications of epidural infusions for analgesia in postoperative and trauma patients.

Few studies compare complications of continuous and bolus epidural analgesia. Ninety-eight postoperative and trauma patients receiving epidural infusions over 15 months were retrospectively studied. Continuous epidural analgesia was used for pain management in 60 patients (61%). Bolus epidural analgesia was administered to 38 patients (39%). Sixty patients reported 98 complications. Sixty-eight per cent of complications occurred in patients receiving continuous infusions. For the continuous infusions, motor blockade (18%), nausea/vomiting, (18%), and catheter leaks (12%) were the most common complications. For bolus infusions, nausea/vomiting (25%), mental status changes (21%), and erythema at placement site (13%) were encountered. Continuous infusions were associated with an increased incidence of complications compared with bolus infusions (P < 0.05). Patients undergoing abdominal surgery had an increased incidence of complications compared with other patients (P < 0.05). Epidural catheters are safe and effective for pain management, but they are not without risk. Hemodynamic stability and pulmonary status should be considered when evaluating patients.

Inhibition of vasopressin-stimulated flank marking behavior by V1-receptor antagonists.

Flank marking, a form of olfactory communication displayed by hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. In the present study two vasopressin type-1 (V1) receptor antagonists, d(CH2)5Tyr(Me)AVP and dPTyr(Me)AVP were tested for their ability to block flank marking stimulated by the microinjection of arginine vasopressin (AVP) into the anterior hypothalamus. Dose-response curves were established for AVP and flank marking in the presence or absence of different concentrations of each antagonist. DPTyr(Me)AVP was microinjected into the anterior hypothalamus 1 h before the microinjection of AVP while d(CH2)5Tyr(Me)AVP and AVP were prepared together and delivered as a single microinjection. This procedure was necessary because dPTyr(Me)AVP, but not d(CH2)5Tyr(Me)AVP, had agonist activity when initially injected into the anterior hypothalamus in concentrations ranging from 0.90-900 microM. The ED50 values (microM) for dPTyr(Me)AVP and AVP were 17.9 and 0.90, respectively. The initial agonist activity of dPTyr(Me)AVP was always followed by blocker activity. Both V1-receptor antagonists caused a dose-dependent decrease in AVP-stimulated flank marking. Maximal inhibition of AVP-stimulated flank marking was produced with approximately 1.0 mM of either antagonist. Both antagonists blocked AVP-stimulated flank marking behavior for over 12 h following their microinjection.

A vasopressin antagonist can reverse dominant/subordinate behavior in hamsters.

Golden hamsters communicate dominance status by flank marking, a behavior that is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus-medial preoptic area (AH-MPOA). The purpose of the present study was to investigate whether arginine vasopressin (AVP) and an antagonist of AVP could alter or reverse dominant/subordinate relationships in pairs of hamsters. Microinjection of AVP into the AH-MPOA of subordinate hamsters dramatically increased their flank marking despite the presence of their dominant partners. Conversely, microinjection of the AVP antagonist into the AH-MPOA of dominant hamsters blocked flank marking in the presence of their subordinate partners. Surprisingly, the untreated subordinate hamsters significantly increased their own flank marking when tested with their dominant partners treated with the AVP antagonist, thereby reversing the pattern of flank marking normally seen in dominant/subordinate relationships. However, the effect of AVP and the AVP antagonist were limited to the day of treatment. When flank marking behavior was reversed in a pair of hamsters by treatments for three consecutive days, the pair immediately displayed the original dominant/subordinate behavior when treatment was stopped.

Microinjection of kainic acid into the hypothalamus of golden hamsters prevents vasopressin-dependent flank-marking behavior.

The purpose of this study was to define the vasopressin-sensitive area in the anterior hypothalamus-medial preoptic area (AH-MPOA) of the golden hamster that is involved in the expression of flank-marking behavior. Male hamsters implanted with guide cannulae stereotaxically aimed at various sites in the AH-MPOA were microinjected initially with 0.1 ng of arginine vasopressin (AVP) in a volume of 10 nl. Hamsters that flank-marked in response to these injections were subsequently microinjected into the same sites with kainic acid (0.2 microgram/20 nl; n = 10) or an equal volume of 1 M NaOH as a vehicle control (n = 10). Four days later hamsters were tested for odor-induced flank marking by placing them into the recently vacated home cage of other hamsters and for flank marking in response to the microinjection of AVP. Animals treated with kainic acid exhibited significantly (p less than 0.01) fewer AVP and odor-induced flank marks as compared to the number of flank marks observed prior to treatment. There was no significant reduction in the number of flank marks in hamsters microinjected with the NaOH vehicle. In another group of hamsters, microinjection of kainic acid (0.2 microgram/20 nl) into the 3rd ventricle (n = 4) and other sites of the hypothalamus (n = 4) did not significantly alter odor-induced flank marking. The locations of the microinjection sites indicate that the neurons sensitive to AVP and involved in the expression of flank-marking behavior are found in the ventromedial area of the AH-MPOA extending from the caudal border of the suprachiasmatic nucleus to the rostral limit of the supraoptic nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)