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PubMed2003

Dissemination and proliferation of neural stem cells on the spinal cord by injection into the fourth ventricle of the rat: a method for cell transplantation.

We examined the distribution of hippocampus-derived neural stem cells on the spinal cord surface for up to 3 weeks following injection through the fourth ventricle. The injected cells were disseminated as tiny spots on the pia mater of the spinal cord and proliferated into large cell-clusters. On both the dorsal and ventral side, cell clusters increased in number rapidly up to 5 days after injection and thereafter decreased gradually due to the coalition of neighbouring clusters. Concomitantly, individual cell clusters continuously increased in size, occupying almost 50% of the spinal cord surface. Cell attachment was usually found around blood vessels, along which cells invaded into the spinal cord. In the injured site, cells migrated into the lesion and were integrated into the spinal cord tissue, some of which had differentiated into astrocytes 1-2 weeks after injection. BrdU-uptake experiments demonstrated that the transplanted cells proliferated within the host cerebrospinal fluid. These results indicate that application of neural stem cells through the ventricle is an effective method to disseminate cells all over the spinal cord and that they can migrate and be integrated into the injured spinal cord.

Animals↗
PubMed1998

Cervical epidural steroid injection with intrinsic spinal cord damage. Two case reports.

STUDY DESIGN: Intrinsic cervical spinal cord damage represents the serious and permanent complications that can occur if cervical epidural steroid injections are administered while the patient is sedated. Two case reports are presented. OBJECTIVES: To draw attention to the dangerous consequences that can arise from sedating a patient before administering a cervical epidural steroid injection. SUMMARY OF BACKGROUND DATA: Reported complications of cervical epidural steroid injections have been minor and infrequent. No reports of intrinsic cervical cord damage could be found in a comprehensive English language literature search. METHODS: Two case reports of permanent intrinsic cervical cord damage in patients who had been administered cervical epidural steroid injections while under intravenous sedation are presented. Magnetic resonance imaging was performed before and after the administration of cervical epidural steroid injections. Each patient had herniated nucleus pulposus before they received cervical epidural steroid injections and intrinsic cord damage on postinjection magnetic resonance images. RESULTS: Both patients developed increased pain and neurologic symptoms within 24 hours of injection. To date, these symptoms appear to be permanent. However, Patient 1 had pain relief in her right arm and shoulder after undergoing a microdiscectomy, but pain was still persistent in her left leg, and she has developed a positive Lhermitte's sign. CONCLUSION: These case reports indicate fluoroscopic guidance will not insure or prevent intrathecal perforation or spinal cord penetration during the administration of cervical epidural steroid injections. In addition, although intravenous sedations during cervical epidural steroid injections have been used numerous times without reported complications, it appears intravenous sedation in these two cases resulted in the inability of the patient to experience the expected pain and paresthesias at the time of spinal cord irritation. Therefore, the authors conclude that the patient should be fully awake during the administration of cervical epidural steroid injections, with only local anesthetic in the skin used for analgesia.

Adult↗
PubMed1996

Tachycardia after glutamate injection in rat spinal cord is not blocked by kynurenate or mimicked by metabotropic agonists.

1. We have used microinjections of glutamate, an ionotropic excitatory amino acid receptor antagonist (kynurenate) and selective ionotropic (NMDA and kainate) and metabotropic (1S-3R-ACPD, trans-ACPD and L-AP4) receptor agonists in the thoracic IML of the rat to define the receptors mediating the tachycardia produced by excitatory amino acid antagonists. 2. Injection of glutamate (delta heart rate = 76 +/- 8 beats/min n = 16), NMDA (delta heart rate = 116.5 +/- 5 beats/min n = 6) or kainate (delta heart rate = 92 +/- 22 beats/min n =6 evokes a tachycardia when injected into the thoracic intermediolateral column. Kynurenate blocked the response to NMDA (-2% of initial response) and markedly attenuated the response to kainate (14% of initial response) but did not alter the response to glutamate (106% of initial response). 3. IS-3R-ACPD did not elicit a tachycardia when injected into the thoracic intermediolateral column and neither trans-ACPD nor L-AP4 induced a tachycardia after kynurenate injection into the thoracic intermediolateral column. 4. Thus stimulation of either NMDA or AMPA/kainate receptors elicits tachycardia in rat thoracic spinal cord but glutamate also activates another receptor type to elicit a tachycardia. The lack of a tachycardia when trans-ACPD, 1S-3R-ACPD or L-AP4 were injected into the thoracic spinal cord suggests that the kynurenate resistant tachycardia elicited by glutamate is not mediated by metabotropic receptors. The kynurenate resistant tachycardia elicited by glutamate is not mediated by any of the known excitatory amino acid receptor types.

Aminobutyrates↗
PubMed1995

Transneuronal labeling of neurons in the adult rat brainstem and spinal cord after injection of pseudorabies virus into the urethra.

Transneuronal tracing techniques were used to identify sites in the central nervous system involved in the neural control of urethral function. The distribution of virus-infected neurons was examined in the spinal cord and brainstem at various intervals (56-96 hours) following pseudorabies virus (PRV) injection into the urethra. In the lumbosacral (L6-S1) spinal cord at 56 hours, neurons containing PRV immunoreactivity (PRV-IR) were located in the region of the sacral parasympathetic nucleus (SPN), around the central canal, and in the dorsal commissure. Some animals also exhibited PRV-IR in cells in the L6 dorsolateral motor nucleus. At longer survival times (72-96 hours), PRV-IR cells were observed in the superficial and deeper laminae of the dorsal horn, and increased numbers of PRV-IR cells were consistently detected in the region of the SPN, around the central canal, and in the dorsal commissure. PRV-IR fiber-like staining also occurred along the lateral edge of the dorsal horn extending from Lissauer's tract to the region of the SPN. In rostral lumbar segments (L1-L2), PRV-IR cells were located in the region of the dorsal commissure and the intermediolateral cell nucleus (IML), around the central canal, and in the dorsal horn. After 72-84 hours, PRV-IR cells were also noted at more rostral levels of the neuraxis including the medulla, pons, midbrain, and diencephalon. At 72 hours, PRV-IR cells were consistently observed in Barrington's nucleus (pontine micturition center), nucleus raphe magnus (RMg), parapyramidal reticular formation, and the A5 and A7 regions. At 78-84 hours, additional regions exhibited PRV-IR cells, including the periaqueductal gray, locus coeruleus, the dorsal and ventral subcoeruleus alpha, and the red nucleus. A few cells were also located in the lateral hypothalamic area. This distribution of PRV-labeled cells in the spinal cord and brainstem is similar in many respects to the distribution of cells labeled in previous studies by PRV injection into the urinary bladder. This overlap of urethra and bladder neurons is consistent with the results of physiological experiments indicating a close coordination between the central nervous control of bladder and urethral activity.

Animals↗
PubMed2002

Epidural morphine injection after combined spinal and epidural anaesthesia.

BACKGROUND AND OBJECTIVE: Although combined spinal and epidural anaesthesia is efficient and easy to perform, the technique can be a double-edged sword having the potential risk that an increased flux of drugs across the meninges through the hole made in it may lead to severe adverse effects. The aim was to compare the incidence of adverse events when an epidural injection of morphine was given after combined spinal and epidural anaesthesia or after epidural anaesthesia. METHODS: Fifteen patients had an epidural catheter inserted at the L2-3 interspace, and then a spinal block administered via the L3-4 interspace. Another 15 patients only had an epidural catheter inserted. After the onset of spinal or epidural anaesthesia had been confirmed, morphine 2 mg was injected into the epidural space, and a continuous epidural infusion of morphine was started. At the end of the operation and at 4, 8 and 12 h after the administration of epidural morphine and on the next day, the following variables were examined: blood pressure, heart rate, respiratory rate, arterial blood-gas analysis, visual analogue scale pain scores, nausea/vomiting scores, and pruritus scores. RESULTS: In the study population, the epidural injection of morphine was not associated with a significantly higher incidence of adverse events when given after spinal anaesthesia than after epidural anaesthesia. CONCLUSIONS: The adverse effects associated with epidural morphine given after spinal anaesthesia did not increase significantly when a 27-G Whitacre needle was used. Thus, the morphine flux through the meningeal hole into the cerebrospinal fluid was trivial.

Aged↗
PubMed1978

Longitudinal spread of intraneurally injected local anesthetics. An experimental study of the initial neural distribution following intraneural injections.

Unexpected spinal anesthesia, occurring after peripheral nerve blocks close to the spine, may be caused by a centripetal spread of the local anesthetic along the injected nerve to the spinal cord. In order to analyze the pathway of such a spread, a radioactive local anesthetic mixed with a fluorescent dye was injected into difrerent compartments of the rabbit sciatic nerve, and the early distribution of these tracers was studied by scintillation counting and fluorescence microscopy. Epineurial (extrafascicular) injections were of low injection pressure (25-60 mmHg) (3.3-7.9 kPa) and limited spread, while endoneurial (intrafascicular) injections reached higher pressures (300-750 mmHg) (39.9-99.7 kPa) and caused a rapid spread over long distances within the fascicle. The sacral plexus seemed difficult to pass. However, 20% of endoneurial injections reached the spinal cord, where the injectate primarily spread in the thin subpial space. Our experimental findings suggest that intraneural injections of local anesthetics are responsible for the reported cases of unexpected spinal anesthesia due to inadvertent intrafascicular spread. Although intrafascicular injections are rarely made, we recommend that intraneural injections of local anesthetics or other solutions close to the spine should be avoided, as they may cause unexpected spinal anesthesia or lesion of the cord.

Anesthesia, Spinal↗
PubMed2004

Spinal manipulation, epidural injections, and self-care for sciatica: a pilot study for a randomized clinical trial.

OBJECTIVE: To assess the feasibility of recruiting sciatica patients and to evaluate their compliance in preparation for a full-scale randomized clinical trial. We also aimed to determine the responsiveness of key outcome measures. METHODS: Thirty-two subjects were randomly assigned to spinal manipulation (n=11), epidural steroid injections (n=11), or self-care education (n=10). No between-group comparisons were planned because of the small sample size. RESULTS: At week 12 (the end of the treatment phase), the outcome measures indicating the most improvement/change were the Oswestry disability score (mean, 22.9; SD, 19.9; effect size [ES], 1.8), leg pain severity (mean, 2.9; SD, 1.7; ES, 1.7), and if the symptoms were bothersome (mean, 25.2; SD, 16.0; ES, 1.6). Twenty-four patients were either "very satisfied" or "completely satisfied," and 22 of 32 patients reported 75% or 100% improvement. After 52 weeks, the outcome measure showing the most improvement/change was leg pain severity (mean, 2.3; SD, 2.6; ES, 1.35), followed by the Oswestry disability score (mean, 15.6; SD, 20; ES, 1.2) and if symptoms were bothersome (mean, 18.1; SD, 22.6; ES, 1.1). Eighteen patients were either "very satisfied" or "completely satisfied," and 15 of 32 patients reported 75% or 100% improvement. CONCLUSIONS: The results of this pilot study suggest that it is feasible to recruit subacute and chronic sciatica patients and to obtain their compliance for a full-scale randomized clinical.

Adult↗
PubMed1998

Naltrexone, but not atropine or yohimbine, antagonizes suppression of formalin-induced spinal sensitization by intrathecal nociceptin.

We investigated the effects of spinal nociceptin on formalin-induced spinal sensitization and examined the role of the opioidergic, alpha 2-adrenergic and muscarinic cholinergic receptors in the nociceptin-produced suppression of spinal sensitization. The results demonstrated that spinal nociceptin suppressed the formalin-induced spinal sensitization in a dose-dependent manner (1, 5 and 10 nmol). The inhibitory effect of 10 nmol of nociceptin on spinal sensitization, was readily antagonized by naltrexone, but not by atropine or yohimbine. Each of the antagonists, naltrexone, atropine or yohimbine, alone had no effect on the formalin-induced spinal sensitization. Our results show that spinal nociceptin elicits dose-dependent, naltrexone-reversible suppression of spinal sensitization evoked by injection of formalin.

Animals↗
PubMed1994

An N-terminal fragment of substance P, substance P(1-7), down-regulates neurokinin-1 binding in the mouse spinal cord.

Injected intrathecally, substance P (SP) down-regulates neurokinin-1 (NK-1) binding in the spinal cord and desensitizes rats to the behavioral effect of SP. N-terminal fragments of SP, such as SP(1-7), induce antinociception and play a role in desensitization to SP in mice. The goal of this study was to assess the abilities of N- and C-terminal fragments of SP to down-regulate NK-1 binding. Binding of [3H]SP to mouse spinal cord membranes was inhibited by SP, CP-96,345, and to a lesser extent by SP(5-11), but not SP(1-7), consistent with these binding sites being NK-1 receptors. Injection of SP(5-11) intrathecally did not affect the affinity (Kd) or concentration (Bmax) of [3H]SP binding. However, injection of 1 nmol of SP(1-7) decreased the Bmax of [3H]SP binding in the spinal cord at 6 h after its injection just as this dose of SP decreased the Bmax at 24 h. These data suggest that the N-terminus of SP is responsible for down-regulation of NK-1 binding. As SP(5-11) did not down-regulate NK-1 binding, activation of NK-1 sites does not appear necessary or sufficient for down-regulation of SP binding. In contrast, SP(1-7), in spite of its inability to interact with NK-1 sites, did down-regulate SP binding, suggesting an indirect mechanism dissociated from NK-1 receptors.

Animals↗