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PubMed1997

Continuous intrathecal baclofen infusion in severe spasticity after traumatic or hypoxic brain injury.

Severe spinal spasticity has been shown to be a good indication for continuous intrathecal baclofen infusion (CIBI), but there is only limited experience with this treatment in patients with supraspinal spasticity. Eighteen patients with severe spasticity from traumatic or hypoxic brain injury were treated with CIBI. In all patients spasticity could be reduced significantly. The mean Ashworth score was reduced from 4.5 to 2.33 and the mean Spasm frequency score from 2.16 to 0.94. This reduction of spasticity led to a marked pain reduction. Nursing, perineal care and mobilization became much easier. The complication rate was low. In this series we saw one infection in the pump pocket, one epileptic seizure after a bolus application of baclofen and one spinal catheter displacement. The results are similar to those reported from series of patients with spinal spasticity and correspond to the limited experience we have so far with supraspinal spasticity patients. To prevent limb contractures CIBI should be performed as soon as the patient is in a stable clinical condition after brain injury. Further prospective clinical trials will be necessary to obtain more experience with patients suffering from supraspinal spasticity.

Adult↗
PubMed1993

The effects of intrathecal administration of excitatory amino acid agonists and antagonists on the initiation of locomotion in the adult cat.

Development of pharmacological strategies for the control of locomotion in patients with spinal cord injury or disease requires an understanding of the neuroactive substances involved in the activation of the spinal cord neural systems for the control of locomotion. Studies using the in vitro preparations of the lamprey, frog embryo, and newborn rat indicate that excitatory amino acids (EAAs) are involved in the initiation of locomotion. The present study determines whether spinal EAA receptors play a role in locomotion in an in vivo, adult mammalian preparation. Experiments were performed on precollicular, postmammillary decerebrate cats, some of which were spinalized at the 13th thoracic segment. Cannulas for drug infusions were positioned intrathecally in the lumbar region of the spinal cord. A ligature around the spinal cord at the level of the 13th thoracic segment prevented rostral diffusion of the drugs. Locomotion was monitored with electromyograms in treadmill locomotion experiments and electroneurograms in fictive locomotion experiments. Intrathecal infusion of either the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid or the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione blocked hindlimb treadmill and fictive locomotion induced by electrical stimulation of the mesencephalic locomotor region (MLR) of the midbrain. Intrathecal administration of NMDA elicited hindlimb fictive locomotion in resting animals similar to that evoked by electrical stimulation of the MLR. At lower concentrations, NMDA evoked either independent bursting activity in the various nerves or loosely organized rhythmicity showing little reciprocity between antagonists. In contrast, administration of the EAA uptake blocker dihydrokainic acid (DHK) evoked intermittent periods of bursting activity characterized by a variable duration and a high degree of reciprocity between flexors and extensors. Given together at low concentrations, NMDA and DHK produced a well-coordinated locomotor pattern. Kainate and quisqualate were ineffective in producing fictive locomotion. These results are consistent with the suggestion that EAAs play a role in the initiation of mammalian locomotion. Furthermore, the results are consistent with those obtained from the neonatal rat in vitro preparations.

2-Amino-5-phosphonovalerate↗
PubMed2002

Mu-opioid receptor down-regulation and tolerance are not equally dependent upon G-protein signaling.

In the present study, the contribution of pertussis toxin (PTX)-sensitive G(i/o)-proteins to opioid tolerance and mu-opioid receptor down-regulation in the mouse were examined. Mice were injected once intracerebroventricularly and intrathecally with PTX (0.1 microg/site). Controls were treated with saline. On the 10th day following PTX treatment, continuous subcutaneous infusion of etorphine (150 or 200 microg/kg/day) or morphine (40 mg/kg/day+25 mg slow-release pellet) was begun. Control mice were implanted with inert placebo pellets. Pumps and pellets were removed 3 days later, and mice were tested for morphine analgesia or mu-opioid receptor density was determined in the whole brain, spinal cord, and midbrain. Both infusion doses of etorphine produced significant tolerance (ED50 shift=approximately 4-6-fold) and down-regulation of mu-opioid receptors (approximately 20-35%). Morphine treatment also produced significant tolerance (ED50 shift= approximately 5-8-fold), but no mu-opioid receptor down-regulation. PTX dramatically reduced the acute potency of morphine and blocked the further development of tolerance by both etorphine and morphine treatments. However, PTX had no effect on etorphine-induced mu-opioid receptor down-regulation in brain, cord, or midbrain. These results suggest that PTX-sensitive G-proteins have a minimal role in agonist-induced mu-opioid receptor density regulation in vivo, but are critical in mediating acute and chronic functional effects of opioids such as analgesia and tolerance.

Animals↗
PubMed1999

The state of implantable pain therapies in the United States: a nationwide survey of academic teaching programs.

UNLABELLED: The purpose of this questionnaire survey was to provide an overview of anesthesiology pain fellowship programs in the United States with regard to implantation of spinal cord stimulators (SCS) and opioid infusion devices. Of the 95 programs solicited, 80% responded to questions pertaining to the prevalence of use and technical considerations of implantation. Of the responding programs, 87% report implanting SCS, and 84% report implanting neuraxial infusion pumps. All programs perform a stimulation or infusion trial before implantation, although the duration varied from a trial in the operating room at the time of implantation to 25 days. Of the programs, 83% implant cylindrical leads, and 17% implant flat leads via laminectomy for their nonrevision SCS implants. Morphine, bupivacaine, hydromorphone, and baclofen are the most commonly used drugs and are used in implanted pumps by >50% of respondents. The question of industry-sponsored pain fellow education in implantable techniques is addressed. IMPLICATIONS: Of the pain teaching programs in the United States, 80% responded to a questionnaire eliciting information about the implantation of spinal cord-stimulating and opioid infusion devices. The range and diversity of responses imply a lack of agreement about implantation techniques, drugs, and protocols.

Analgesics↗
PubMed2002

Long-term infusions of p-boronophenylalanine for boron neutron capture therapy: evaluation using rat brain tumor and spinal cord models.

Rat 9L gliosarcoma cells infiltrating the normal brain have been shown previously to accumulate only approximately 30% as much boron as the intact tumor after administration of the boronated amino acid p-boronophenylalanine (BPA). Long-term i.v. infusions of BPA were shown previously to increase the boron content of these infiltrating tumor cells significantly. Experiments to determine whether this improved BPA distribution into infiltrating tumor cells after a long-term i.v. infusion improves tumor control after BNCT in this brain tumor model and whether it has any deleterious effects in the response of the rat spinal cord to BNCT are the subjects of the present report. BPA was administered in a fructose solution at a dose of 650 mg BPA/kg by single i.p. injection or by i.v. infusion for 2 h or 6 h, at 330 mg BPA/kg h(-1). At 1 h after the end of either the 2-h or the 6-h infusion, the CNS:blood (10)B partition ratio was 0.9:1. At 3 h after the single i.p. injection, the ratio was 0.6:1. After spinal cord irradiations, the ED(50) for myeloparesis was 14.7 +/- 0.4 Gy after i.p. administration of BPA and 12.9 +/- 0.3 Gy in rats irradiated after a 6-h i.v. infusion of BPA; these values were significantly different (P < 0.001). After irradiation with 100 kVp X rays, the ED(50) was 18.6 +/- 0.1 Gy. The boron compound biological effectiveness (CBE) factors calculated for the boron neutron capture dose component were 1.2 +/- 0.1 for the i.p. BPA administration protocol and 1.5 +/- 0.1 after irradiation using the 6-h i.v. BPA infusion protocol (P < 0.05). In the rat 9L gliosarcoma brain tumor model, the blood boron concentrations at 1 h after the end of the 2-h infusion (330 mg BPA/kg h(-1); n = 15) or after the 6-h infusion (190 mg BPA/kg h(-1); n = 13) were 18.9 +/- 2.2 microg 10B/g and 20.7 +/- 1.8 microg 10B/g, respectively. The irradiation times were adjusted individually, based on the preirradiation blood sample, to deliver a predicted 50% tumor control dose of 8.2 Gy ( approximately 30 photon-equivalent Gy) to all tumors. In the present study, the long-term survival was approximately 50% and was not significantly different between the 2-h and the 6-h infusion groups. The mode of BPA administration and the time between administration and irradiation influence the 10B partition ratio between the CNS and the blood, which in turn influences the measured CBE factor. These findings underline the need for clinical biodistribution studies to be carried out to establish 10B partition ratios as a key component in the evaluation of modified administration protocols involving BPA.

Animals↗
PubMed1989

Lack of effect of spinal anesthesia on drug metabolism.

The effect of spinal anesthesia on drug disposition was determined in six dogs with chronically implanted vascular catheters using propranolol as a model compound. On the first study day, 40 mg of unlabeled propranolol and 200 microCi of [3H]propranolol were injected into the portal and femoral veins respectively. Arterial blood samples were taken for 4 hr for measurement of plasma concentrations of labeled and unlabeled propranolol by high-pressure liquid chromatography (HPLC) and of [3H]propranolol by liquid scintillation counting of the HPLC eluant corresponding to each propranolol peak. Twenty-four hr later, spinal anesthesia was induced with tetracaine (mean dose 20.7 +/- 0.6 mg) with low sacral to midthoracic levels and the propranolol infusions and sampling were then repeated. Spinal anesthesia had no significant effect on either the intrinsic clearance of propranolol (2.01 +/- 0.75 L/min before and 1.9 +/- 0.7 L/min during spinal anesthesia), or on mean hepatic plasma flow (2.01 +/- 0.5 L/min before and 1.93 +/- 0.5 L/min during spinal anesthesia). The systemic clearance and elimination half-life of propranolol were also unchanged by spinal anesthesia (0.9 +/- 0.23 L/min on the first day, 0.7 +/- 0.1 L/min during spinal anesthesia; and 101 +/- 21 min on the first day, 115 +/- 16 min during spinal anesthesia, respectively). The volume of distribution (Vd) of propranolol was similarly unaffected by spinal anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Spinal↗
PubMedDate not supplied

[Evaluation of the effectiveness of anecaine in central segmental blockades in orthopedic-traumatologic interventions].

Efficacy of anecaine (A) (bupivacaine, Pliva) and marcaine (M) (bupivacaine, Astra) in central neuroaxial block combined with sedation is compared. In the group with epidural block (n = 167, ASA I-III), 102 patients were given anecaine and 65 marcaine in equivalent doses. In the group with spinal block (n = 82, ASA I-III), anecaine was administered to 52 and marcaine to 30 patients. In the epidural block group a catheter was placed at L2-3 or L3-4 with cranial direction. A test dose of bupivacaine (20 mg) was followed after 5-7 min by the main dose of 2 mg.kg-20 mg. Propofol was given for partial suppression of consciousness at a continuous infusion rate 1.6 mg.kg.hr. In spinal block group, bolus dose of bupivacaine (10-20 mg) was injected through the subarachnoidal approach at L2-3 or L3-4. Diazepam (0.1 mg.kg.hr) was used for sedation. Block onset, duration of sensor and motor block, and of effective analgesia were evaluated in all groups. Hemodynamics and respiratory function were monitored. Moderate hypotension (16-17% decline from basic values) was observed in all patients irrespective of bupivacaine brand. In a comparative non-randomized study anecaine showed a faster onset of block and longer duration of clinical effect than marcaine in epidural and spinal anesthesia for orthopedic surgery on the lower limbs.

Adolescent↗
PubMed1984

Spinal monoaminergic modulation of masculine copulatory behavior in the rat.

The sexual behavior of male rats receiving infusions of 5-HT, dopamine and noradrenaline intrathecally in the spinal cord of intracerebroventricularly (i.c.v.) in the lateral ventricle was observed. Intrathecal infusions of 5-HT and noradrenaline inhibited penile insertions and ejaculation, noradrenaline being the more potent of the amines. Dopamine was without effect. I.c.v. amine infusions impaired to various extents the masculine mating pattern, primarily by interfering with the males' tendency to approach the females. The facilitation of mating seen after intrathecal administration of the aminotetraline, 8-OH-DPAT, was more pronounced than that observed following its i.c.v. infusion.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

Effects of clonidine and yohimbine on a C-fibre-evoked blood pressure reflex in the rat.

1. The involvement of alpha 2-adrenoceptors in a capsaicin-induced depressor reflex in the rat has been investigated. 2. The reflex fall in blood pressure following an intra-arterial injection of capsaicin was partially blocked by an intrathecal infusion of clonidine (1 microgram) at the spinal cord level L4-L5, an effect which was abolished by the prior intrathecal infusion of yohimbine (5 micrograms). 3. Clonidine (1 microgram) given intracisternally blocked the depressor reflex almost completely; however, it also produced a gradual, prolonged fall in mean carotid pressure. 4. Yohimbine (20 micrograms) given intracisternally did not change mean blood pressure but had a dual effect on the depressor reflex in response to the capsaicin injection: a short period of enhanced reflex response was followed by a long lasting inhibition of the response. 5. It was concluded that alpha 2-adrenoceptors in the spinal cord inhibit the capsaicin-evoked depressor reflex and that pre- and postsynaptic alpha 2-adrenoceptors in the brain stem modulate this reflex.

Animals↗
PubMed1991

[Spinal anesthesia with bupivacaine without glucose in the elderly: effect of concentration and volume on the hemodynamic profile].

This study aimed to compare the haemodynamic effects of two different glucose-free bupivacaine solutions is thirty patients aged more than 70 years (mean age 82 years) undergoing hip surgery under spinal anaesthesia. They were randomly assigned to two groups, group A to receive 2.5 ml of a 0.5% bupivacaine solution, and group B 10 ml of a 0.125% solution in normal saline. All the patients were therefore given the same dose of bupivacaine, 12.5 mg. Lorazepam (1 mg orally) was administered to all for premedication two hours beforehand. Those patients taking antihypertensive agents were given their last dose on the eve of surgery. Lactated Ringer's solution (500 ml) was infused to all before the spinal puncture. Systolic (Pasys), mean and diastolic arterial pressures, and heart rate, were recorded every minute before volume loading, and for 30 minutes after the start of the spinal anaesthesia. Ephedrine (3 mg every two minutes if required) was given whenever Pasys decreased by more than 30% of the pre-induction value. The upper level of sensory blockade was assessed by the pin-prick test, and the quality of motor blockade with the Bromage scale. The cephalad spread of the solutions was similar, as well as the haemodynamic profile in each group. The total dose of ephedrine required in each group was not significantly different. It may therefore be concluded that, in the elderly, the upper level of, and the haemodynamic changes due to, spinal anaesthesia do not depend on the concentration or the volume of glucose-free bupivacaine solution.

Age Factors↗
PubMed2004

Roles of opiate in lower urinary tract dysfunction associated with spinal cord injury in rats.

PURPOSE: It has been reported that the opiate receptor system in the spinal cord is involved in bladder and urethral function. We determined whether U-50488 (trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide), a kappa opioid receptor agonist, could decrease detrusor-sphincter dyssynergia (DSD) and, thus, improve voiding efficiency in conscious, spinal cord injured (SCI) rats. MATERIALS AND METHODS: Experiments were done in female Sprague-Dawley rats in which the spinal cord was completely transected at the T6-8 level 4 weeks prior to performing cystometry while conscious and held in a restraining cage. Experiments were also performed in normal spinal cord rats. Saline was infused (0.1 ml per minute) via the cystostomy catheter into the bladder. Voiding efficiency was determined by measuring voided and residual volumes. After performing a control cystometrogram increasing doses of U-50488 (0.01, 0.1, 1 and 10 mg/kg) were administered intravenously at 1-hour intervals. The effects of nor-binaltorphimine dihydrochloride, a kappa opioid receptor antagonist, on U-50488 induced changes in voiding parameters were also examined. RESULTS: A high dose of U-50488 (1 to 10 mg/kg) significantly decreased contraction amplitude and bladder capacity (p <0.01 to 0.05) in normal spinal cord and SCI rats. A low dose of U-50488 (0.01 mg/kg) increased voiding efficiency by 32.7% without decreasing bladder capacity in SCI rats. Nor-binaltorphimine hydroparameters counteracted the effect of U-50488 induced changes. CONCLUSIONS: These results suggest that the kappa opioid receptor system is related to DSD caused by spinal cord injury. The kappa opioid receptor agent is believed to have therapeutic potential for treating DSD associated with SCI.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1974

The mechanism of renin release from the ischaemic kidney.

The re-establishment of blood flow to an ischaemic kidney produced an elevation of blood pressure in the rat. This response did not occur in animals with a pithed spinal cord or in rats with low blood pressure produced by haemorrhage. When the blood pressure was raised in rats with pithed spinal cords, by the intravenous infusion of noradrenaline, the response was restored. Occlusion of the subclavian arteries did not prevent the response. It is considered that the increase in blood pressure, produced by renin release, after re-establishment of the blood flow in an ischaemic kidney is a 'washout' phenomenon independent of the integrity of the nervous system.

Animals↗
PubMed1997

Auditory evoked responses under total spinal anesthesia in rats.

In order to investigate the function of the auditory pathway from the cochlea to the brain stem under total spinal anesthesia, the auditory brain stem response (ABR), compound action potential of the cochlear nerve (CAP), and cochlear microphonics (CM) were simultaneously recorded in rats. Total spinal anesthesia was induced by infusion of 2% lidocaine hydrochloride at a constant rate of 0.10 mL/min into the cerebrospinal fluid through the rats' skulls. The ABR completely disappeared within 1.5 to 4 minutes. After cessation of the injection, the ABR reappeared, starting from wave I and progressing through waves II and III to wave IV. The latency change of the CAP throughout the recording period was quite similar to that of wave I of the ABR. A reduction in amplitude of the CM was observed, but the CM did not disappear during the recording period. Disappearance of the ABR was due, not to loss of cochlear function, but to anesthetic effects on the acoustic nerve and the brain stem. Monitoring of the ABR provided information on the level of neural activity in the brain stem under total spinal anesthesia.

Action Potentials↗
PubMed1992

ATP-sensitive K+ channels are gradually recruited in the vasodepressor response to adenosine in spinally-anesthetized dogs.

Vasodepressor mechanisms of adenosine were investigated in spinally-anesthetized dogs. An i.v.-infusion of adenosine (0.1-10 mumol/kg/min) caused a slowly developing and sustained decrease in blood pressure (BP). This vasodepression was antagonized by glibenclamide, a blocker of ATP-sensitive K+ (KATP) channels. On the other hand, a transient decrease in BP caused by a single bolus i.v.-injection of adenosine was not antagonized by glibenclamide in our previous study. These results suggested that the opening of KATP channels is gradually recruited in the vasodepressor mechanisms for adenosine-induced sustained vasodepression.

Adenosine↗
PubMed2001

KT3-671, an angiotensin AT1 receptor antagonist, attenuates vascular but not cardiac responses to sympathetic nerve stimulation in pithed rats.

Effects of KT3-671 on vascular and cardiac sympathetic neurotransmission were investigated in pithed rats. The pressor response to spinal stimulation (5 Hz) of the pithed rat without the adrenals was approximately 75% of that with the adrenals. Guanethidine (8 mg/kg, i.v.) decreased by about 76% the pressor response to sympathetic stimulation in the pithed rat with intact adrenals and the guanethidine-resistant response was almost completely abolished by bilateral adrenalectomy. Therefore, the following experiments were done using the pithed rat without the adrenals. KT3-671 (1-10 mg/kg, i.v.) as well as losartan (1-10 mg/kg, i.v.) inhibited dose-dependently the pressor response to sympathetic stimulation. KT3-671 was approximately four times more potent than losartan in inhibiting the pressor response. The two angiotensin II subtype 1 receptor antagonists (10 mg/kg, i.v.) did not affect the pressor response to exogenously administered norepinephrine. Neither KT3-671 nor losartan influenced the tachycardia induced by spinal stimulation and isoprenaline. Intravenous infusion of angiotensin II (100 ng/kg/min) did not affect both pressor and tachycardic responses to sympathetic stimulation. In conclusion, KT3-671 as well as losartan inhibits vascular but not cardiac sympathetic neurotransmission of the pithed rats, which may contribute to its overall antihypertensive efficacy.

Adrenalectomy↗
PubMed2002

Chronic pain of spinal origin: the costs of intervention.

The cost of chronic benign spinal pain is large and growing. The costs of interventional treatment for spinal pain were at a minimum of $13 billion (U.S. dollars) in 1990, and the costs are growing at least 7% per year. Medical treatment of chronic pain costs $9000 to $19,000 per person per year. The costs of interventional therapy is calculated. Methods of evaluating differential treatments in terms of costs are described. Cost-minimization versus cost-effectiveness approaches are described. Spinal cord stimulation and intraspinal drug infusion systems are alternatives that can be justified on a cost basis. Cost minimization analysis suggests that epidural injections under fluoroscopy may not be justified by the current literature.

Chronic Disease↗
PubMed1991

Intrathecal baclofen for intractable axial dystonia.

Following spinal instrumentation for scoliosis, a patient developed intractable axial dystonia refractory to conservative medical management. We describe the successful treatment of this dystonia with a continuous infusion of intrathecal baclofen and the subsequent long-term management.

Adolescent↗