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PubMed2004

Intrathecal anesthesia and recovery from radical prostatectomy: a prospective, randomized, controlled trial.

BACKGROUND: Previous studies suggest that intraoperative anesthetic care may influence postoperative pain and recovery from surgery. The authors tested the hypothesis that the addition of intrathecal analgesia to general anesthesia would improve long-term functional status and decrease pain in patients undergoing radical retropubic prostatectomy. METHODS: One hundred patients received either general anesthesia supplemented with intravenous fentanyl or general anesthesia preceded by intrathecal administration of bupivacaine (15 mg), clonidine (75 microg), and morphine (0.2 mg). Patients and providers were masked to treatment assignment. All patients received multimodal pain management postoperatively. Primary outcomes included pain and functional status over the first 12 postoperative weeks. RESULTS: Patients receiving intrathecal analgesia required more intravenous fluids and vasopressors intraoperatively. Pain was well controlled throughout the study (mean numerical pain scores < 3 in both groups at all times studied). Intrathecal analgesia decreased pain and supplemental intravenous morphine use over the first postoperative day but increased the frequency of pruritus. Pain and functional status after discharge from the hospital did not differ between groups. Intrathecal analgesia significantly decreased the duration of hospital stay (from 2.8 +/- 2.0 to 2.1 +/- 0.5 days; P < 0.01) as a result of five patients in the control group who stayed in the hospital more than 3 days. CONCLUSIONS: The benefits of improved immediate analgesia and decreased morphine requirements resulting from intrathecal analgesia must be weighed against factors such as pruritus, increased intraoperative requirement for fluids and vasopressors, and resources needed to implement this modality. Further studies are needed to determine the significance of the decrease in duration of hospital stay.

Adult↗
PubMed1993

N-methyl-D-aspartate (NMDA)-mediated muscle relaxant action of dextromethorphan in rats.

The present study examined whether the antitussive agent dextromethorphan, which is an antagonist at the N-methyl-D-aspartate (NMDA) receptor, depresses spinal reflexes in rats. Injection of both the specific NMDA antagonist (-)-2-amino-7-phosphonoheptanoate and of dextromethorphan dose-dependently reduced the magnitude of the polysynaptic flexor reflex without affecting the monosynaptic H-reflex. In contrast, the non-NMDA antagonist 6,7-dinitroquinoxaline-2,3-dione depressed the H-reflex in a dose-dependent manner without affecting the flexor reflex. The depressant effect of dextromethorphan on the flexor reflex was prevented by co-administration with NMDA but not with the non-NMDA agonist alpha-amino-3-hydroxy-5-terthyl-4-isoxazole-propionic acid. These data suggest that dextromethorphan exerts a muscle relaxant action via the NMDA receptor.

2-Amino-5-phosphonovalerate↗
PubMed1998

Intrathecal pethidine: pharmacology and clinical applications.

Pethidine is the only member of the opioid family that has clinically important local anaesthetic activity in the dose range normally used for analgesia. Pethidine is unique as the only opioid in current use that is effective as the sole agent for spinal anaesthesia. In lower doses, intrathecal pethidine is also an effective analgesic for treating pain in labour. This paper reviews the pharmacology of intrathecal pethidine and clinical experience reported to date. Articles reviewed include those identified by a Medline search using keywords "intrathecal" or "spinal anaesthesia/ anesthesia" and "pethidine" or "meperidine". Reference lists from identified papers were scrutinized to identify further relevant articles.

Adjuvants, Anesthesia↗
PubMed1984

Pain.

Explore the source record for details and available documents.

Afferent Pathways↗
PubMed2005

Neural precursor cells can be delivered into the injured cervical spinal cord by intrathecal injection at the lumbar cord.

Neural precursor cells (NPCs) are promising grafts for treatment of traumatic CNS injury and neurodegenerative disorders because of their potential to differentiate into neurons and glial cells. When designing clinical protocols for NPC transplantation, it is important to develop alternatives to direct parenchymal injection, particularly at the injury site. We reasoned that since it is minimally invasive, intrathecal delivery of NPCs at lumbar spinal cord (lumbar puncture) represents an important and clinically applicable strategy. We tested this proposition by examining whether NPCs can be delivered to the injured cervical spinal cord via lumbar puncture using a mixed population of neuronal-restricted precursors (NRPs) and glial-restricted precursors (GRPs). For reliable tracking, the NPCs were derived from the embryonic spinal cord of transgenic donor rats that express the marker gene, human placental alkaline phosphatase, under the control of the ubiquitous Rosa 26 promoter. We found that mixed NRP/GRP grafts can be efficiently delivered to a cervical hemisection injury site by intrathecal delivery at the lumbar cord. Similar to direct parenchymal injections, transplanted NRP/GRP cells survive at the injury cavity for at least 5 weeks post-engraftment, migrate into intact spinal cord along white matter tracts and differentiate into all three mature CNS cell types, neurons, astrocytes, and oligodendrocytes. Furthermore, very few graft-derived cells localize to areas outside the injury site, including intact spinal cord and brain. These results demonstrate the potential of delivering lineage-restricted NPCs using the minimally invasive lumbar puncture method for the treatment of spinal cord injury.

Alkaline Phosphatase↗
PubMed1983

Uptake and elimination of methylprednisolone from contused cat spinal cord following intravenous injection of the sodium succinate ester.

The uptake and elimination of methylprednisolone by the injured cat lumbar spinal cord were examined following a single 30-mg/kg intravenous bolus injection of the sodium succinate ester. The findings were considerably different from those previously reported for normal lumbar cord. When the glucocorticoid was administered 30 minutes after a 400 gm-cm contusion injury, peak tissue concentrations in both injured and uninjured segments of traumatized spinal cord were not achieved until 30 minutes following drug administration. The elimination of methylprednisolone from injured spinal cord tissue was biphasic in nature, with a rapid elimination phase occurring between 1 and 2 hours after drug administration. This rapid elimination phase was followed by a slower phase which paralleled the constant elimination rate from uninjured tissue of traumatized cord (approximate half-time = 6 hours). Significantly more methylprednisolone accumulated in the injured segment of traumatized spinal cord than in an uninjured segment adjacent to the injury site. This was only true, however, if the drug was administered at times up to 1 hour after injury. If injected after 1 hour, uptake by the injured segment decreased significantly with time after trauma and was no different from that observed for the uninjured segment in the same animal, which showed no significant variation with time after trauma. The probable basis for these differences and the possible clinical implications of these pharmacokinetic characteristics are discussed.

Animals↗