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PubMed2005

Spinal cord infarction following cervical transforaminal epidural injection: a case report.

STUDY DESIGN: Case report. OBJECTIVE: A review of the literature about spinal cord infarction with epidural steroid injections and report of one case. SUMMARY OF BACKGROUND DATA: A 53-year-old man with a history of chronic cervical pain and multilevel degenerative disc disease with multiple posterior disc protrusions on cervical imaging. The patient received a left C6 tranforaminal injection for therapeutic pain relief, with fluoroscopic confirmation of left C6 nerve root sheath spread of injectable contrast. Approximately 10 to 15 minutes post-procedure, he noted weakness in his left arm and bilateral lower limbs. Initial cervical magnetic resonance imaging revealed no cord signal change, but a follow-up study 24 hours later demonstrated patchy increased T2 and short tau inversion recovery signal in the cervical cord from the odontoid to C4-C5 vertebral levels. This was consistent with a diffuse vascular infarct to the cervical cord, resulting in motor-incomplete tetraplegia. RESULTS: This is one of a few reported cases of spinal cord infarction after cervical epidural injections. No direct cord trauma occurred. Previously reported risk factors of spinal infarction, such as hypotension and large injectate volumes, were noncontributory in this case. CONCLUSIONS: Cervical epidural injections, despite careful localization, carry a risk of vascular infarction to the spinal cord, even in the absence of direct cord trauma. The etiology of these infarctions and identifying those patients at risk remain uncertain.

Anti-Inflammatory Agents↗
PubMed1995

Hypobaric spinal anaesthesia with bupivacaine (0.1%) gives selective sensory block for ano-rectal surgery.

Twenty adult male patients undergoing anorectal surgery in the jackknife position under spinal anaesthesia were studied for the anaesthetic properties of 5 ml hypobaric 0.1% bupivacaine. The patients were positioned in the prone, jack-knife position with a pillow under the hips and with an operating table break angulation of 30 degrees with head down tilt of 20 degrees. In this position a 25-gauge Quincke spinal needle was inserted intrathecally through L3-4 and 5 ml solution, prepared by mixing 1 ml bupivacaine 0.5% with 4 ml of distilled water with a specific gravity of 1.001 at 20 degrees C, was given over 15-20 sec. Onset time, progression and upper level of sensory blockade evaluated by pin prick, and the extent of motor block (1 = full motor movement at ankle and knee joint, 2 = restricted motor movements, 3 = full motor block, no movements) were measured at one minute intervals for the first five minutes, then every five minutes for 30 min. The number of dermatomes blocked was also noted. The median level of cephalad sensory blockage was of L1, with a range from T10-L3. On average, nine dermatomes were blocked (range 7-12). Motor blockade was not observed in any patient. Changes in heart rate and blood pressure were minimal. The average duration of postoperative analgesia was 339.5 +/- 182.9 min. Post-spinal headache was not observed in any patients. In conclusion, 5 ml intrathecal hypobaric bupivacaine, 0.1%, provided excellent perioperative analgesia without motor blockade and haemodynamic stability in patients undergoing anorectal surgery in jackknife position.

Adolescent↗
PubMed2004

Addition of epinephrine to intrathecal tetracaine augments depression of the bispectral index during intraoperative propofol sedation.

PURPOSE: Epinephrine added to local anesthetic agents for spinal anesthesia is frequently used to prolong the duration of anesthesia. Epinephrine stimulates the alpha-adrenoceptor, and it is known that the alpha2-adrenoceptor agonists have a central inhibitory effect. We investigated the effect of intrathecal epinephrine during propofol sedation with spinal anesthesia, using a bispectral index (BIS) monitor. METHODS: Twenty adult patients, scheduled for spinal anesthesia, were allocated to the control group ( n = 10) or epinephrine group ( n = 10). Patients in the control group received 14 mg of tetracaine, whereas the epinephrine group received 14 mg of tetracaine and 0.2 mg of epinephrine. Immediately after the pinprick test, propofol was administered at 0.5 mg x kg(-1) by infusion for the initial dose, then continuously at 2 mg x kg(-1) x h(-1) in both groups. BIS scores were recorded before subarachnoid block, and then every 5 min for 90 min after subarachnoid block. RESULTS: There were significant differences in the BIS score between the two groups at 45-55 min and at 60-70 min after subarachnoid block. CONCLUSION: Intrathecal epinephrine augments the sedative effect of propofol during spinal anesthesia.

Adult↗
PubMed1982

Lumbar intrathecal naloxone blocks analgesia produced by microstimulation of the ventromedial medulla in the rat.

In lightly barbiturate-anesthetized rats. low threshold (less than 10 micro A) electrical stimulation within the rostral ventromedial medulla inhibited the tail-flick response to noxious heat. Naloxone applied intrathecally at the lumbar level reversed this inhibition, but the same dose of naloxone applied to the cervical intrathecal space had no effect. Doses of naloxone 1- to 4-fold greater than the intrathecal dose did not antagonize tail-flick suppression when given systemically. Because neither systemic nor intrathecal naloxone had any effect on base-line tail-flick latencies, we conclude that the inhibition of the tail-flick response resulting from microstimulation in the ventromedial medulla is mediated by a spinal opioid synapse.

Animals↗
PubMed1990

Spinal cord substance P mediates carbachol-induced cardiovascular responses from the rostral ventrolateral medulla.

Intrathecal (i.t.) infusion of substance P (SP) antagonist, (D-Pro2, D-Trp7,9)-substance P (20 micrograms), lowered blood pressure profoundly without any significant change of heart rate. The hypertensive and tachycardic responses elicited by microinjection of carbachol (25 ng/site) into the bilateral rostral ventrolateral medulla (rVLM) were blocked by i.t. infusion of SP antagonist. These data provided evidence that an excitatory cardiovascular effect induced by cholinergic system in rVLM may be mediated mainly by the SP receptors in spinal cord.

Animals↗
PubMed1980

The potentiation of spinal analgesia by leucine enkephalin.

In two strains of rats, intrathecal administration of morphine and met-enkephalin was found to produce a dose-dependent analgesic effect as measured by the tail-flick assay. Prior administration of leu-enkelphalin at a dose which had no analgesic effect was found to reduce significantly the analgesic ED50 of both morphine and met-enkephalin. Met-enkephalin pretreatment, at a similar sub-analgesic dose, was without effect. Thus, a differential interaction of the enkephalins with morphine is evident at spinal structures.

Anesthesia, Spinal↗
PubMed1985

The effect of local and systemic application of dopaminergic agents on tail flick latency in the rat.

Dopamine (DA) is thought to have a neurotransmitter role in the spinal cord of the rat. Intrathecal administration of the DA receptor agonist apomorphine has previously been shown to reduce nocifensive responses. The present experiments investigated the site of action of apomorphine, and the mechanisms by which DA agonists apparently produce antinociception. Small doses of apomorphine (40-80 micrograms/kg) increased the tail flick latency (TFL) in lightly anaesthetised rats when given intrathecally and intravenously but not intracerebroventricularly. This effect is probably mediated via D2 receptors since the D2 agonist LY171555 had a similar effect whereas the D1 agonist SK&F 38393 was inactive. Furthermore the D2 antagonist sulpiride blocked the effects of apomorphine and LY171555. The spinal monosynaptic reflex was not modified by 150 micrograms/kg apomorphine suggesting that sensory rather than motor processes are being influenced. Pretreatment with the serotonin receptor antagonist methysergide prevented the apomorphine induced increase in TFL. It is concluded that exogenously applied DA agonist can result in antinociception in the spinal cord and that this effect may be dependent upon activity in the spinal 5-hydroxytryptaminergic and noradrenergic systems.

Analgesics↗
PubMed1993

Increase of nitric oxide by L-arginine potentiates beta-endorphin- but not mu-, delta- or kappa-opioid agonist-induced antinociception in the mouse.

L-Arginine pretreated i.c.v. produced a time- and dose-dependent potentiation of beta-endorphin-induced inhibition of the tail-flick response in ICR mice. However, the inhibition of the tail-flick response induced by morphine, DAMGO ([D-Ala2,NMePhe4,Gly5-ol]enkephalin), DPDPE ([D-Pen2,D-Pen5]enkephalin or U50,488H given i.c.v. was not potentiated by i.c.v. pretreated L-arginine. The results indicate that L-arginine selectively potentiates antinociception induced by epsilon-opioid receptor agonist, but not mu-, delta- or kappa-opioid receptor agonist. L-Arginine pretreated i.t. did not potentiate i.c.v. administered beta-endorphin-induced inhibition of the tail-flick response, indicating that the potentiating effect of L-arginine on beta-endorphin-induced antinociception is located at the supraspinal sites but not at the spinal sites.

Analgesics↗
PubMed1995

Intrathecal alpha-trinositol facilitates the flexor reflex but does not block the depressive effect of neuropeptide Y.

We have studied the effects of alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate, PP56), a putative antagonist of neuropeptide Y receptors, on the nociceptive flexor reflex in decerebrate, spinalized rats after intrathecal and intravenous administration. Intrathecal alpha-trinositol caused strong and prolonged facilitation of the flexor reflex, which was usually associated with an increase in spontaneous motoneuron activity. The reflex depressive effect of intrathecal neuropeptide Y was neither blocked nor reversed by alpha-trinositol. Intravenous alpha-trinositol at low doses had no effect on the flexor reflex and at high dose, reflex facilitation was sometimes observed. It is concluded that alpha-trinositol acts as a spinal excitant and is not an antagonist of the neuropeptide Y receptor in the rat spinal cord.

Animals↗
PubMed1994

Inhibition of clonic seizure-like excitatory effects induced by intrathecal morphine using two NMDA receptor antagonists: MK-801 and ACEA-1011.

Microinjection of high doses of morphine into the spinal lumbar intrathecal (i.t.) space of mice produces dose-dependent clonic seizure-like excitatory effects. Naloxone, an opioid antagonist (10 mg/kg, i.p.), injected 5 min prior to i.t. morphine, did not reverse the seizure-like motor effects, suggesting that these effects of morphine are not mediated through opioid receptors. Systemic administration of MK-801, a non-competitive NMDA receptor antagonist (0.01-0.10 mg/kg, i.p.), or ACEA-1011, a novel NMDA receptor/glycine site antagonist (0.5-20.0 mg/kg, i.p.), attenuated the clonic seizure-like excitatory effects induced by i.t. morphine in a dose-dependent manner. Sensorimotor performance of the mice was evaluated using the rotarod test. Although both compounds (MK-801 and ACEA-1011) impaired the sensorimotor performance of mice in a dose-dependent fashion, there was no impairment of motor performance at doses employed to block the excitatory effects induced by i.t. morphine. These data suggest that NMDA receptors play a pivotal role in the clonic seizure-like behaviors induced by i.t. morphine.

Analgesics↗
PubMed1996

Intrathecal pituitary adenylate cyclase activating polypeptide facilitates the spinal nociceptive flexor reflex in the rat.

We have examined the effects of intrathecal (i.t.) pituitary adenylate cyclase activating polypeptide on the spinal nociceptive flexor reflex in decerebrate, spinalized, unanaesthetized rats. The flexor reflex was elicited by electrical stimulation applied subcutaneously to the sural nerve innervation area and recorded as electromyogram activity from ipsilateral hamstring muscles. Pituitary adenylate cyclase activating polypeptide(l-27) was administered over a wide dose range (10 ng to 10 mu g) and elicited a dose-dependent facilitation of the flexor reflex and did not depress the reflex at any dose. Furthermore, pituitary adenylate cyclase activating polypeptide did not inhibit the facilitation of the flexor reflex induced by repetitive stimulation of C-fibres. It is concluded that pituitary adenylate cyclase activating polypeptide had an excitatory effect on spinal cord function which may indicate a role for this peptide in nociceptive transmission and modulation. Moreover, in contrast to previous studies, we found no evidence suggesting that pituitary adenylate cyclase activating polypeptide exerts antinociceptive action at spinal level.

Animals↗
PubMed2004

Intrathecal neuropeptide Y inhibits behavioral and cardiovascular responses to noxious inflammatory stimuli in awake rats.

To test the hypothesis that administration of neuropeptide Y (NPY) to the spinal cord reduces inflammatory pain, we evaluated the effects of intrathecal NPY on behavioral and cardiovascular markers of the nociception associated with intraplantar formalin injection in rats. Before the administration of formalin, NPY dose dependently increased blood pressure, an effect that could be prevented with the coadministration of the Y2 antagonist, BIIE0246. This effect lasted only 20 min, and thus was over before initiation of the formalin test. NPY dose dependently inhibited the flinching, licking, pressor, and tachycardia responses associated with formalin injection. The Y1 receptor antagonist BIBO 3304 partially reversed the antinociceptive effect of NPY at a dose that did not by itself have an effect (3 microg). We conclude that intrathecal NPY acts in part via Y1 receptors to inhibit ongoing inflammatory nociception.

Animals↗
PubMed2001

Activation of spinal serotonin(2A/2C) receptors augments nociceptive responses in the rat.

The role of spinal 5-HT(2A/2C) receptors in the regulation of spinal nociceptive transmission was studied. The 5-HT(2A/2C) agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and the antagonist ketanserin tartrate were administered intrathecally immediately before the formalin test. Activation of spinal 5-HT(2A/2C) receptors increased the pain-like behavioural response in both the early and late phases. The findings support the hypothesis that spinal 5-HT(2A/2C) receptors augment the spinal afferent nociceptive impulses induced by peripheral inflammation.

Amphetamines↗
PubMed1997

Capsaicin-induced bladder overactivity and nociceptive behaviour in conscious rats: involvement of spinal nitric oxide.

To investigate the role of nitric oxide (NO) in spinal regulation of lower urinary tract function and bladder nociceptive behaviour, cystometry was performed in conscious rats. The effects of intra-arterial and intrathecal administration of the NO synthase (NOS)-inhibitor, L-NG-nitroarginine methyl ester (L-NAME), were studied on volume- and capsaicin-induced micturitions. The incidence of nociceptive behaviour after intravesical capsaicin was investigated in the absence and presence of L-NAME. Intrathecal L-NAME (0.5 mg) had no effect on the normal, volume-induced micturition. Intravesical capsaicin (30 microM) increased the micturition pressure (p < 0.01), the basal pressure (p < 0.01) and decreased the bladder capacity (p < 0.01) and the micturition volume (p < 0.01). Administration of L-NAME intrathecally (0.5 mg) or intra-arterially (25 mg/kg) had no effects on the capsaicin-induced bladder activity. During capsaicin-infusion, the rats showed signs of distress such as licking and head-turning directed toward the abdomen. This nociceptive behaviour was shown during 31 +/- 3% (n = 6) of the observation period. The capsaicin-induced nociceptive behaviour was markedly reduced by intrathecal and to a less extent by intra-arterial, administration of L-NAME. The percentage time spent licking and head-turning was reduced to 11 +/- 2%, n = 6 (p < 0.001) and 18 +/- 3%, n = 6 (p < 0.05) in rats treated with intrathecal and intra-arterial L-NAME, respectively. The results suggest that NO is not involved in the spinal regulation of the volume- or capsaicin-induced micturition. In contrast, the nociceptive behaviour evoked by intravesical capsaicin seems to involve spinal NO.

Administration, Intravesical↗
PubMed2002

Blockade of the antinociceptive effect of spinally administered kyotorphin by naltrindole in mice.

We investigated the role of spinal opioid receptors in the antinociceptive effect of kyotorphin (Tyr-Arg, KTP) by using an in vivo mice tail-pinch test and an in vitro opioid receptor binding assays. Intrathecal administration of KTP produced a dose-dependent antinociceptive effect with an ED(50) value of 24 microg/mouse. This antinociception, which was reversed by the KTP antagonist Leu-Arg, was completely blocked by naltrindole but not by naloxonazine, beta-funaltrexamine, or nor-binaltorphimine. The results from the binding study in vitro indicated that KTP bound to spinal KTP receptors but not to any opioid receptors in the mouse spinal cord. These results suggest that KTP-induced antinociception is mediated by binding to KTP receptors followed by an indirect activation of the delta-opioid receptors in the spinal cord.

Analgesics↗
PubMed2000

Antihyperalgesic effects of intrathecally administered magnesium sulfate in rats.

Intrathecal administration of MgSO(4) is reported to cause paralysis. However, the characteristic sensory disturbances have not been thoroughly investigated. We examined the effect of intrathecally administered MgSO(4) on the nociceptive threshold, using three different nociceptive measures, formalin test, hot plate test and paw pressure test in rats. The dose of MgSO(4) was 30, 100 or 300 microg. In acute nociceptive tests, intrathecal MgSO(4) did not cause any significant changes in the pain threshold. However, phase 2 of the formalin test was suppressed dose-dependently. It is known that spinal NMDA receptors are involved in the changes seen during the second (tonic) phase of the formalin test and in vitro studies showed that Mg(2+) can cause voltage-dependent blockade of NMDA receptor channel in the neurons of spinal dorsal horn. Thus, the suppressive effect of intrathecally administered MgSO(4) on the tonic inflammation-evoked behavior is mediated by the spinal NMDA receptors. Our results suggest that intrathecal administration of MgSO(4) may be therapeutically beneficial for patients with tonic pain involving the spinal NMDA receptors.

Animals↗