CHEMICAL RHIZOTOMY FOR RELIEF OF SPASTICITY IN AMBULANT PATIENTS.
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Electromyography↗
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Effects of midazolam in the spinal nerve ligation model of neuropathic pain in rats.
Potential changes in the spinal GABAergic activity after nerve injury were studied by comparing the effects of systemic administration of the benzodiazepine midazolam on the noxious evoked responses of dorsal horn in rats with spinal nerve ligation of neuropathy and control animals. The tight ligation of the L(5) and L6 spinal nerves was performed in adult male Sprague-Dawley rats and resulting mechanical and cold allodynia were assessed with von Frey hairs and the acetone drop test. Single unit extracellular recordings of dorsal horn neurones were performed 15-18 days after the surgery under halothane anaesthesia using transcutaneous electrical stimulation of the receptive field at three times the C-fibre threshold. The rats in the spinal nerve ligation group, but not in the sham-operated control group developed mechanical and cold allodynia. Subcutaneous administration of midazolam 0.1-3.0 mg/kg reduced the Adelta-fibre evoked activity in a dose-related manner in all study groups, but the C-fibre evoked activity was significantly reduced only in the spinal nerve ligation group. The inhibitory effects of s.c. midazolam were significantly reversed by i.t. administration of flumazenil, suggesting a spinal site of action. Midazolam reduced C-fibre evoked firing significantly more in the spinal nerve ligation model than in the non-operated or sham controls. These results indicate changes in the spinal GABAergic system in the neuropathic animals and could be of importance in the development of new treatments for neuropathic pain.
Animals↗
Lateral C1-2 puncture for cervical myelography. Part II: Recognition of improper injection of contrast material.
The interpretation of cervical metrizamide myelography requires specific anatomic considerations, particularly when the lateral C1-2 puncture technique is employed. Fresh unfixed cervical spine specimens were injected with a mixture of metrizamide and methylene blue. Radiologic examinations of these specimens were compared with a retrospective analysis of 100 consecutive unselected cervical myelograms obtained by lateral C1-2 puncture during the years 1979-1980. Epidural, subdural, subpial, dentate ligament, and spinal cord injections may be encountered when the lateral C1-2 puncture for myelography is employed; possible artifacts from such injection are discussed.
Humans↗
Enhanced analgesic effect of morphine-nimodipine combination after intraspinal administration as compared to systemic administration in mice.
Calcium plays an important role in the pathophysiology of pain. A number of studies have investigated the effect of L-type calcium channel blockers on the analgesic response of morphine. However, the results are conflicting. In the present study, the antinociceptive effect of morphine (2.5 microg) and nimodipine (1 microg) co-administered intraspinally in mice was observed using the tail flick test. It was compared to the analgesic effect of these drugs (morphine - 250 microg subcutaneously; nimodipine - 100 microg intraperitoneally) after systemic administration. Nimodipine is highly lipophilic and readily crosses the blood brain barrier. Addition of nimodipine to morphine potentiated the analgesic response of the latter when administered through the intraspinal route but not when administered through systemic route. It may be due to direct inhibitory effect of morphine and nimodipine on neurons of superficial laminae of the spinal cord after binding to mu -opioid receptors and L-type calcium channels respectively.
Analgesics, Opioid↗
Timing and positioning of occlusion of the spinal neurocele in the chick embryo.
The timing and positioning of occlusion of the spinal neurocele were studied in living and serially sectioned chick embryos at stages 8-14. Occlusion occurs in three phases: preocclusion, incipient occlusion, and definitive occlusion. Preocclusion occurs at stage 8. At this time, the neural groove of the spinal cord has not yet closed to form a neural tube. Incipient occlusion begins as early as stage 9 and lasts until stage 11. The neural groove of the cranial spinal cord closes during these stages and incipient occlusion occurs concomitantly with this closure. Seventy-eight percent of the embryos exhibit incipient occlusion. Incipient occlusion extends along the mid-somitic region of the neuroaxis, occupying about one-half the length of the spinal cord. Injection of the brains of living embryos with dyes often reopens incipient occluded areas. Definitive occlusion occurs at stages 11-14 and is present in 89% of the embryos. Definitive occlusion is restricted to mid-somitic regions, as was incipient occlusion, but it extends approximately two-thirds the length of the spinal cord. Injection of the brains of living embryos with dyes rarely reopens definitive occluded areas, even when injection pressures are maximal. Six morphological types of definitive occlusion can be identified on the basis of the relative proportions and locations of total and partial occlusion. Closure of the cranial neuropore and roof plate of the hindbrian occurs near the end of the incipient occlusion phase, whereas closure of the caudal neuropore occurs well after definitive occlusion is initiated.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
Glyceryl nonivamide, a nonpungent analogue of capsaicin, enhances substance P release and renal function in rats.
Effects of glyceryl nonivamide (GLNVA), a nonpungent analogue of capsaicin, on spinal substance P release, blood pressure and renal function were investigated in rats. GLNVA was administered intrathecally or intracerebroventricularly, and renal clearance function was measured. The addition of GLNVA at concentrations of 2, 20 and 200 mumol/l during in vivo spinal superfusion resulted in concentration-dependent increases in the release of substance P. Capsaicin pretreatment (50 mg/kg/day, s.c. for 2 weeks) blunted the GLNVA-induced substance P release, suggesting a stimulation of GLNVA on the spinal terminals of capsaicin-sensitive primary afferent nerves to release substance P. Intracerebroventricular administration of GLNVA at concentrations of 20, 40 and 80 nmol/l evoked a concentration-dependent depressor response. Despite the hypotensive effect, GLNVA caused significant increases in glomerular filtration rate, urine flow, absolute and fractional excretion of sodium and potassium, osmolar clearance and free water reabsorption rate. These data suggest that central administration of GLNVA stimulates spinal substance P release, reduces blood pressure but enhances renal excretion of water and electrolytes due to an increased filtered load and a decreased tubular reabsorption.
Absorption↗
A low-dose radioisotope procedure for assessment of subcutaneous drug delivery systems used for slow intrathecal infusion of antispasmodic agents.
STUDY DESIGN: Retrospective single centre study. OBJECTIVES: To evaluate a low-dose radioisotope imaging procedure for assessment of implanted intrathecal drug delivery and to compare the radiation dose and diagnostic value of these studies with other reported studies using higher administered radiation dose. SETTING: National Spinal Injuries Centre, Stoke Mandeville Hospital, UK. METHOD: A total of 11 spinally injured patients with subcutaneous drug delivery systems and uncontrolled spasm were investigated for catheter failure using a low-dose radioisotope procedure with an administered dose of radioactivity of 40 MBq Technetium-99m. RESULTS: Loss of catheter patency was demonstrated in six patients, enabling identification of the site of blockage. Catheter patency and subsequent perfusion of CSF (ie normal result) was demonstrated in five patients. Radiation effective dose was estimated at 1.3 mSv per patient study, with a low associated risk of deleterious effect of one in 13,000. CONCLUSION: Radioisotope investigation using a reduced administered dose of 40 MBq Technetium-99m DTPA, formulated according to a strict radiopharmaceutical protocol, provides a safe test for assessment of intrathecal drug delivery systems.
Drug Delivery Systems↗
Neurologic deficits and neuronal injury in rats resulting from nonopioid actions of the delta opioid receptor antagonist ICI 174864.
The delta opioid receptor antagonist ICI 174864 produces postural abnormalities and barrel rolling after i.c.v. injection and hindlimb and tail flaccidity after spinal subarachnoid injection in rats. These effects appear to result from nonopioid characteristics of ICI 174864 because they are neither shared nor blocked by other opioid antagonists (naloxone, ICI 154129 and WIN 44,441-3) and are produced by two compounds (ICI 174644 and ICI 178173) that are structurally related to ICI 174864 but lack its delta antagonist properties. Barrel rolling and hindlimb paralysis are also produced by dynorphin A-related peptides; however, rats failed to demonstrate tolerance or cross-tolerance to the hindlimb paralytic actions of ICI 174864 or dynorphin A (1-13) after 7 days of continuous spinal intrathecal infusion of either of these compounds. Whereas hindlimb responses to low doses of ICI 174864 (1.6-6.2 nmol intrathecally) were usually transient, higher doses (6.2-25 nmol intrathecally) produced persistent hindlimb motor dysfunction, altered nociception, priapism, hindlimb edema, bladder infarction and atony and urinary incontinence. Neuronal and axonal changes in the lumbosacral spinal cords of rats with persistent and transient neurologic deficits provided direct evidence of the neuropathologic actions of ICI 174864 (3.1 and 6.2 nmol) and ICI 174644 (25 nmol). These results indicate that 1) use of ICI 174864 as a selective delta opioid receptor antagonist is potentially compromised by its nonopioid neuropathologic actions and 2) ICI 174864 and dynorphin A-related peptides are unique among opioid agonists and antagonists in sharing barrel rolling and hindlimb paralytic effects. A similar mechanism of action may underlie the shared nonopioid actions of these peptides.
Animals↗
Anti-nociceptive effect of tricyclic anti-depressants following intrathecal administration.
The anti-nociceptive effects of three tricyclic anti-depressants (desipramine, protriptyline, fluoxetine) were evaluated in mice following intrathecal administration. Nociceptive behavior was produced by intrathecal administration of Substance P and measured for 60 seconds following subcutaneous and intrathecal administration of vehicle and increasing doses of the drugs being tested. Systemically administered protriptyline produced dose related antinociception in this paradigm. A similar effect was seen following systemic desipramine; while fluoxetine was inactive systemically. Both protriptyline and desipramine given intrathecally were antinociceptive while fluoxetine had a biphasic effect, being analgesic only at low doses. These results indicate that tricyclic antidepressants may produce analgesia at the spinal level in rodents. This action may be related to the therapeutic success of tricyclic antidepressants in chronic pain syndromes.
Analgesics↗
Isoflurane and nociception: spinal alpha2A adrenoceptors mediate antinociception while supraspinal alpha1 adrenoceptors mediate pronociception.
BACKGROUND: The authors recently established that the analgesic actions of the inhalation anesthetic nitrous oxide were mediated by noradrenergic bulbospinal neurons and spinal alpha2B adrenoceptors. They now determined whether noradrenergic brainstem nuclei and descending spinal pathways are responsible for the antinociceptive actions of the inhalation anesthetic isoflurane, and which alpha adrenoceptors mediate this effect. METHODS: After selective lesioning of noradrenergic nuclei by intracerebroventricular application of the mitochondrial toxin saporin coupled to the antibody directed against dopamine beta hydroxylase (DbetaH-saporin), the antinociceptive action of isoflurane was determined. Antagonists for the alpha1 and alpha2 adrenoceptors were injected at spinal and supraspinal sites in intact and spinally transected rats to identify the noradrenergic pathways mediating isoflurane antinociception. Null mice for each of the three alpha2-adrenoceptor subtypes (alpha2A, alpha2B, and alpha2C) and their wild-type cohorts were tested for their antinociceptive response to isoflurane. RESULTS: Both DbetaH-saporin treatment and chronic spinal transection enhanced the antinociceptive effects of isoflurane. The alpha1-adrenoceptor antagonist prazosin also enhanced isoflurane antinociception at a supraspinal site of action. The alpha2-adrenoceptor antagonist yohimbine inhibited isoflurane antinociception, and this effect was mediated by spinal alpha2 adrenoceptors. Null mice for the alpha2A-adrenoceptor subtype showed a reduced antinociceptive response to isoflurane. CONCLUSIONS: The authors suggest that, at clinically effective concentrations, isoflurane can modulate nociception via three different mechanisms: (1) a pronociceptive effect requiring descending spinal pathways, brainstem noradrenergic nuclei, and supraspinal alpha1 adrenoceptors; (2) an antinociceptive effect requiring descending noradrenergic neurons and spinal alpha2A adrenoceptors; and (3) an antinociceptive effect mediated within the spinal cord for which no role for adrenergic mechanism has been found.
Adrenergic alpha-Antagonists↗
Effects of intrathecally administerd NaV1. 8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion.
Neuropathic pain has been hypothesized to be the result of aberrant expression and function of sodium channels at the site of injury. To investigate the effects of NaV1. 8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion (DRG) neurons in chronic neuropathic pain. 24 Sprague-Dawley rats weighing 200-260 g were anesthetized with the intraperitoneal injection of 300 mg x kg(-1) choral hydrate. The CCI model was made by loose ligation of sciatic nerve trunk by 4-0 chromic gut. The mechanical and thermal pain threshold were measured before operation and 1, 3, 5, 7, 9, 11, 13 days after operation. A PE-10 catheter was implanted in subarachnoid space at lumbar region. On the 7th postoperative day the animals were randomly divided into 4 groups. The drugs were injected intrathecally twice a day for 5 consecutive days in group 2-4. The animals were decapitated 14 days after the surgery. The L4-L6 DRG of the operated side was removed and crushed, and total RNA was extracted with Trizol reagent. The contralateral side was used as control. The change of NaV1. 8 sodium channel transcripts was determined by RT-PCR. Pain threshold was significantly lowered after CCI as compared with that in control group and was elevated 3 days after antisense oligonucleotide injection. Sensory neuron specific TTX-R sodium channel NaV1. 8 transcript was down-regulated after antisense oligonucleotide injection at the dosage of 45 microg as compared with that in CCI group (P < 0.01), and it was even greater at the dosage of 90 microg. The intrathecally injected NaV1. 8 antisense oligonucleotide can reduce the mechanical allodynia and thermal hyperalgesia partially by downregulating the SNS transcript expression.
Animals↗
(+/-) Epibatidine increases acetylcholine release partly through an action on muscarinic receptors.
Epibatidine has been used in a wide dose range and was found to produce both nociceptive and antinociceptive effects. The different effects were partly explained by an action on multiple nicotinic receptor systems. The present study investigated the possibility that part of the action of intraspinally or subcutaneously administered (+/-) epibatidine, is mediated through an action on muscarinic receptors. Radioligand receptor assays were performed using homogenates of rat spinal cord and muscarinic M1-M5 receptors expressed in Sf9 cells. The intraspinal acetylcholine releasing effect of intraspinally and subcutaneously administered (+/-) epibatidine was studied with and without with atropine pretreatment. (+/-) Epibatidine has affinity for muscarinic receptors both in spinal cord tissue and expressed in Sf9 cells. The intraspinal administration of 160 microM (+/-) epibatidine produced an increase in acetylcholine release that was reduced by pretreatment with 100 microM atropine. Subcutaneous administration of 30 microg/kg (+/-) epibatidine produced an increase in intraspinal acetylcholine release that was not inhibited by 5 mg/kg subcutaneous atropine pretreatment. We conclude that (+/-) epibatidine, in microM concentrations, is a partial muscarinic receptor agonist that may interact with spinal muscarinic receptors to increase acetylcholine release. Epibatidine induced spinal acetylcholine release observed after subcutaneous administration appears not to be mediated via muscarinic receptor. The dual action on both nicotinic receptors and muscarinic receptors may explain the potent analgesic effect observed after epibatidine administration.
Acetylcholine↗
Organization of anterogradely labeled spinocervical tract terminations in the lateral cervical nucleus of the cat.
The anterograde transport of horseradish peroxidase following injections into the cervical, thoracic, or lumbosacral spinal cord was used to examine the organization of spinocervical tract terminations in the lateral cervical nucleus (LCN) of the cat. A somatotopic organization of the labeling originating from different spinal levels was observed in the mediolateral dimension. Cervical labeling generally occurred in the ventromedial portion and lumbosacral labeling in the dorsolateral portion of the LCN. Thoracic labeling occurred both in the middle and the most lateral edge of the nucleus. In all cases, labeling was distributed over most of the rostrocaudal extent of the LCN. In addition, distinct patches of labeling were present in the medialmost portion of the nucleus, regardless of the spinal level injected. These observations corroborate the topographical organization of the LCN described previously on the basis of physiological and retrograde labeling data, and support the identification of the medialmost part of the LCN as a distinct portion of the nucleus. Terminal labeling in the LCN always occurred in multiple, longitudinally distributed fields. The afferent input to each terminal field coursed in separate, loose bundles of fibers that descended from the superficial dorsolateral funiculus. Large injections resulted in more extensive, overlapping terminal fields. These observations indicate that collateral projections result in several discrete representations of a given portion of the skin over the longitudinal extent of the LCN, but that topographical relationships are longitudinally maintained. It is suggested that these multiple terminal fields are the anatomical correlate of the functionally selective convergence of spinocervical tract terminations, that has previously been postulated on physiological grounds to explain the generation of LCN receptive fields with homogenous receptor input within a somatotopic framework.
Animals↗
Increased expression of gamma-aminobutyric acid transporters GAT-1 and GAT-3 in the spinal trigeminal nucleus after facial carrageenan injections.
The present study aimed to elucidate the distribution of gamma-aminobutyric acid (GABA) transporters in the spinal trigeminal nucleus after carrageenan injections. Dense GAT-1 and GAT-3 but very little GAT-2 immunoreactivity was observed in the normal rat spinal trigeminal nucleus. The GAT-1-positive glial cells in the normal rat spinal trigeminal nucleus contained dense bundles of glial filaments and had features of astrocytes. Some GAT-3-positive cells contained dense bundles of glial filaments and had features of astrocytes, whilst others lacked glial filaments, and contained dense marginated heterochromatin, and had features of oligodendrocyte precursor cells. An increase in immunoreactivity to both transporters was observed on the injected but not the contralateral side 3 days after facial carrageenan injections. In rats given three further weekly injections of carrageenan and killed 3 days after the fourth injection, further increases in GAT-1 and GAT-3 immunoreactivities were observed. Electron microscopy showed that transporter immunoreactivity in the spinal trigeminal nucleus of carrageenan-injected rats was predominantly present in glial processes, showing that the increase in the number of processes observed at light microscopy was due to increased immunoreactivity in glial processes. An increased expression of GABA transporters in the carrageenan-injected spinal trigeminal nucleus could therefore result in a faster removal of GABA from the synaptic cleft of GABAergic axon terminals compared to normal rats. This could result in reduced inhibition/increased activity of the trigeminothalamic neurons in the spinal trigeminal nucleus, and could contribute to hyperalgesia after carrageenan injections.
Animals↗
Enhancement of spontaneous and heat-evoked activity in spinal nociceptive neurons by the endovanilloid/endocannabinoid N-arachidonoyldopamine (NADA).
N-arachidonoyldopamine (NADA) is an endogenous molecule found in the nervous system that is capable of acting as a vanilloid agonist via the TRPV1 receptor and as a cannabinoid agonist via the CB1 receptor. Using anesthetized rats, we investigated the neural correlates of behavioral thermal hyperalgesia produced by NADA. Extracellular single cell electrophysiology was conducted to assess the effects of peripheral administration of NADA (i.pl.) on nociceptive neurons in the dorsal horn of the spinal cord. Injection of NADA in the hindpaw caused increased spontaneous discharge of spinal nociceptive neurons compared with injection of vehicle. The neurons also displayed magnified responses to application of thermal stimuli ranging from 34 to 52 degrees C. NADA-induced neural hypersensitivity was dose dependent (EC50 = 1.55 microg) and TRPV1 dependent, as the effect was abolished by co-administration of the TRPV1 antagonist 5'-iodoresiniferatoxin (I-RTX). In contrast, co-administration of the CB1 antagonist SR 141716A did not attenuate this effect. These results suggest that the enhanced responses of spinal nociceptive neurons likely underlie the behavioral thermal hyperalgesia and implicate a possible pain-sensitizing role of endogenous NADA mediated by TRPV1 in the periphery.
Action Potentials↗
Central oxytocinergic and dopaminergic mechanisms regulating penile erection in conscious rats.
A series of in vivo studies in a conscious rat model was conducted to investigate the role of oxytocinergic and dopaminergic neurotransmission in the central regulation of penile erection. Oxytocin, when administrated either intracerebroventricularly (i.c.v.) or intrathecally (i.t.) at the spinal levels of L4-L6, produced dose-related erectogenic effects with a maximum at 0.1 microg/rat i.c.v. or 0.03 microg/rat i.t. Oxytocin-evoked penile activity was attenuated by the inhibitory effect of the selective oxytocin antagonist vasotocin analog [Pmp-Tyr(Me)-Ile-Thr-Asn-Cys]-Pro-Orn-Tyr-NH2 (0.1-1 microg, i.c.v. or i.t.). Penile erection induced by oxytocin was blocked by the dopaminergic receptor antagonist clozapine (1-10 micromol/kg i.p.) in a dose-dependent manner. Conversely, oxytocin antagonist microinjected locally (i.c.v. or i.t.) significantly attenuated the pro-erectile effects of systemic (s.c.) apomorphine, a centrally acting erectogenic agent through dopaminergic receptors. Together, these data indicate a possible concomitant role between dopamine and oxytocin in mediating penile erection at both the spinal and supraspinal sites.
Animals↗
Buprenorphine alleviates neuropathic pain-like behaviors in rats after spinal cord and peripheral nerve injury.
We have studied and compared the antinociceptive and anti-hyperalgesic effect of the partial opioid receptor agonist buprenorphine in normal and neuropathic rats. In normal rats, systemic buprenorphine produced dose-dependent antinociception on the hot plate test. In rats with peripheral nerve or spinal cord injury, buprenorphine markedly alleviated neuropathic pain-related behaviors, including mechanical and cold allodynia/hyperalgesia at doses comparable to that producing antinociception. The results suggest that buprenorphine may be a useful analgesic for treating neuropathic pain and thus is an atypical opioid since morphine tends to be less potent after nerve injury.
Analgesics, Opioid↗
Cyclooxygenase-2 inhibition potentiates morphine antinociception at the spinal level in a postoperative pain model.
BACKGROUND AND OBJECTIVES: After peripheral inflammatory stimuli, spinal cord cyclooyxgenase-2 (COX-2) mRNA and protein levels increase, whereas COX-1 is unchanged. In animal models of inflammatory pain, intrathecal COX-2 selective inhibitors suppress hyperalgesia. However, the role of spinal COX-2 inhibition in postoperative pain is not well elucidated. This study investigates whether a water-soluble COX-2 selective inhibitor, L-745337, can modify allodynic responses in a rat model of postoperative pain. METHODS: Allodynia was induced in the left plantar hindpaw by surgical incision. Animals then received intrathecal (0-80 micro g) or subcutaneous (0-30 mg/kg) L-745337 coadministered with intrathecal morphine (0-2 nmol). Reduction of mechanical allodynia (increased withdrawal threshold) was quantified with calibrated von Frey hairs. RESULTS: L-745337 alone, whether intrathecal or systemic, had no effect on withdrawal threshold. When intrathecal L-745337 at doses of 40 to 80 micro g was combined with a subthreshold dose (0.5 nmol) of morphine, withdrawal thresholds were increased in a dose-dependent manner. Adding 80 micro g L-745337 to 1 nmol morphine produced an antiallodynic effect greater than that of morphine at twice the dose. Subcutaneous L-745337, up to 30 mg/kg combined with intrathecal morphine resulted in the same antiallodynic response as morphine alone. CONCLUSION: These results suggest a spinal interaction of COX-2 inhibition with opiate analgesia may allow a reduction of postoperative pain with lower doses of opiate.
Analgesics, Opioid↗