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PubMed1991

[An epidural spinal abscess with caudal symptoms as a complication of Crohn's disease].

Progressive symptoms of caudal compression (flaccid paraparesis, sensory disorders), accompanied by severe pain and fever, developed over a few days in a 26-year-old man with Crohn's disease for 11 years. Spinal computed tomography, performed under the diagnosis of herniated disc, revealed intraspinal soft tissue, as well as gas in the spinal canal (L2-S3) and the paravertebral muscles. This led to the diagnosis of acute epidural abscess and a laminectomy was performed (at L4-S2). Intraspinally there was thickened, bluish fatty tissue; thick pus exuded between dura and the sacral roots. Suction-irrigation of the spinal canal was undertaken via an epidural drain. Postoperative contrast infusion into the colon demonstrated a fistula directed towards the sacrum. The postoperative course was complicated by severe respiratory impairment of which the patient died.--Epidural abscess is a rare complication of Crohn's disease. Because of its poor prognosis early diagnosis with magnetic resonance imaging or computed tomography should be undertaken in every patient with Crohn's disease who has back pain, fever or, particularly, symptoms of spinal compression.

Abscess↗
PubMed1995

Intravenous midazolam suppresses noxiously evoked activity of spinal wide dynamic range neurons in cats.

The effects of intravenously (i.v.) administered midazolam on noxiously evoked activity of spinal wide dynamic range (WDR) neurons were investigated in decerebrate, spinal-cord-transected cats. Extracellular, single-unit recordings were measured during stimulation by pinching the receptive field on the hind paw and the effect of midazolam at doses of 0.25, 0.5, 1, 2, and 4 mg/kg were measured. Two series of experiments were performed to characterize the analgesic effects of midazolam. In the first, dose-response experiments (n = 59) demonstrated a dose-dependent suppression of the noxiously evoked activity of spinal WDR neurons after midazolam administration. This effect of midazolam was maximal at a dose of 1 mg/kg i.v.. The second series of experiments (n = 14) demonstrated that a benzodiazepine antagonist, flumazenil (n = 8), promptly reversed the effect of midazolam, while an opioid antagonist, naloxone (n = 6), had no effect on the effect of midazolam. The present study demonstrates that i.v. administered midazolam suppresses noxiously evoked activity of spinal WDR neurons that is reversible by a benzodiazepine antagonist. This is consistent with an analgesic action of midazolam.

Animals↗
PubMed2002

Propofol reduces spinal motor neuron excitability in humans.

IMPLICATIONS: We investigated in humans whether changes in spinal motor neuron excitability correlate with the predicted propofol concentration (Cpt) achieved by a target-controlled infusion system. Propofol suppressed F-wave persistence in a Cpt-dependent manner, indicating that propofol depresses spinal motor neuron excitability at clinically relevant concentrations.

Adult↗
PubMed1997

Treatment of hypotension after hyperbaric tetracaine spinal anesthesia. A randomized, double-blind, cross-over comparison of phenylephrine and epinephrine.

BACKGROUND: Despite many advantages, spinal anesthesia often is followed by undesirable decreases in blood pressure, for which the ideal treatment remains controversial. Because spinal anesthesia-induced sympathectomy and management with a pure alpha-adrenergic agonist can separately lead to bradycardia, the authors hypothesized that epinephrine, a mixed alpha- and beta-adrenergic agonist, would more effectively restore arterial blood pressure and cardiac output after spinal anesthesia than phenylephrine, a pure alpha-adrenergic agonist. METHODS: Using a prospective, double-blind, randomized, cross-over study design, 13 patients received sequential infusions of epinephrine and phenylephrine to manage hypotension after hyperbaric tetracaine (10 mg) spinal anesthesia. Blood pressure, heart rate, and stroke volume (measured by Doppler echocardiography using the transmitral time-velocity integral) were recorded at baseline, 5 min after injection of tetracaine, and before and after management of hypotension with epinephrine and phenylephrine. Cardiac output was calculated by multiplying stroke volume x heart rate. RESULTS: Five min after placement of a hyperbaric tetracaine spinal anesthesia, significant decrease in systolic (from 143 +/- 6 mmHg to 125 +/- 5 mmHg; P < 0.001), diastolic (from 81 +/- 3 to 71 +/- 3; P < 0.001), and mean (from 102 +/- 4 to 89 +/- 3; P < 0.001) arterial pressures occurred. Heart rate (75 +/- 4 beats/min to 76 +/- 4 beat/min; P = 0.9), stroke volume (115 +/- 17 to 113 +/- 13; P = 0.9), and cardiac output (8.0 +/- 1 l/m to 8.0 +/- 1l/m; P = 0.8) did not change significantly after spinal anesthesia. Phenylephrine was effective at restoring systolic blood pressure after spinal anesthesia (120 +/- 6 mmHg to 144 +/- 5 mmHg; P < 0.001) but was associated with a decrease in heart rate from 80 +/- 5 beats/min to 60 +/- 4 beats/min (P < 0.001) and in cardiac output from 8.6 +/- 0.7 l/m to 6.2 +/- 0.7 l/m (P < 0.003). Epinephrine was effective at restoring systolic blood pressure after spinal anesthesia (119 +/- 5 mmHg to 139 +/- 6 mmHg; P < 0.001) and was associated with an increase in stroke volume from 114 +/- 12 ml to 142 +/- 17 (P < 0.001) and cardiac output from 7.8 +/- 0.6 l/m to 10.8 +/- 1.1 l/m (P < 0.001). CONCLUSIONS: Epinephrine management of tetracaine spinal-induced hypotension increases heart rate and cardiac output and restores systolic arterial pressure but does not restore mean and diastolic blood pressure. Phenylephrine management of tetracaine spinal-induced hypotension decreases heart rate and cardiac output while restoring systolic, mean, and diastolic blood pressure.

Adrenergic Agonists↗
PubMed1996

Chronic intrathecal infusion of phosphorothioate or phosphodiester antisense oligonucleotides against cytokine responsive gene-2/IP-10 in experimental allergic encephalomyelitis of lewis rat.

The role of CRG-2 protein (murine IP-10) in experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis, was tested by blocking crg-2 mRNA synthesis using chronic infusion of antisense oligonucleotides into lumbar subarachnoid space by osmotic minipumps. After injection with myelin basic protein, rats developed hind limb paralysis and their spinal cords showed crg-2 mRNA expression and the presence of inflammation. When antisense phosphorothioate oligonucleotides to crg-2 (AS-PScrg2) or nonspecific oligonucleotides (AS-PSscram) were infused at rates from 0.18 to 5.4 nmol/hr, they caused hind limb paralysis that was clinically different from EAE and tissue necrosis of the spinal cord. Natural phosphodiester (AS-PO) oligonucleotides that were infused at rates from 1.8 to 5.4 nmol/hr had no toxic effects. AS-POcrg2 reduced the initial appearance of crg-2 mRNA and this may be responsible for the significant reduction in the EAE scores at the height of clinical disease. The antisense treatment did not alter inflammation of the spinal cord. While AS-PS oligonucleotides were unsuitable for intrathecal administration, AS-POcrg2 were not toxic and reduced paralysis due to EAE.

Animals↗
PubMed1999

Continuous intrathecal baclofen infusions. An introduction and overview.

Continuous intrathecal baclofen infusion (CIBI) is a relatively new treatment modality for severe spasticity of spinal cord origin. Literature review suggests relief of severe spasms and rigidity is proven with CIBI, in patients with spinal cord injury and multiple sclerosis, while ongoing research exists for patients with acquired brain injury and cerebral palsy. Criteria for patient selection, the screening trial process, an outline of the surgical procedure, and generalities of maintenance therapies, will be reviewed broadly as per literature, as well as specifically to the Vancouver experience with adults. Additionally, reported patient outcomes and implications for nursing will be shared.

Adult↗
PubMed1996

Effects of intrathecal baclofen on chronic spinal cord injury pain.

The pain of 16 patients with spasticity secondary to spinal cord injury was assessed prior to intrathecal baclofen pump implantation and again 6 and 12 months postoperatively. Chronic pain was delineated into neurogenic and musculoskeletal components, noting changes in nature, quality, and severity of pain (visual analogue scale) and use of analgesic medications. Twelve of 16 patients had chronic pain preoperatively and were included in the study. Six patients had neurogenic pain, three had musculoskeletal pain, and three had both pain components. Postoperatively, at both 6- and 12-month intervals, seven patients with neurogenic pain (78%) demonstrated no significant change in pain severity, while in five patients (83%) musculoskeletal pain decreased significantly. Two patients with neurogenic pain (22%) demonstrated an increase in pain severity at both 6- and 12-month intervals. This study suggests that intrathecal baclofen reduces chronic musculoskeletal pain associated with spasticity but does not decrease chronic neurogenic spinal cord injury pain.

Adult↗
PubMed1991

[Demand-controlled continuous spinal-cerebral morphine administration via an implanted programmable pump].

The significance of the demand-controlled spinal and cerebral administration of morphine has increased with the improvements in the variable techniques (including programmable implanted pumps). Continuous low-dose infusion enables sustained pain-free state with minimal risks and side effects, so that this method is also feasible for treatment of very severe therapy-resistant pain in benign conditions. Neurostimulation of the lemniscal system (dorsal columns of the spinal cord, specific thalamus, etc., especially in deafferentation pain) and surgical interruption of pain pathways and centers (especially in nociceptive pain) as a last resort continue to be indispensable. In our view, the assumption that spinal and cerebral application of morphine is not appropriate in deafferentation pain is not justified on the basis of the most recent discussions and our own observations. Merely higher doses are probably required for this type of pain.

Adult↗
PubMed1998

Distribution, tolerability and tissue compatibility of intrathecal tizanidine in the sheep.

BACKGROUND: Tizanidine (TZD) is an alpha-2-adrenergic drug with potential spinal analgesic action and could be a substitute or additive for intrathecal (i.t.) opiates in chronic pain treatment. However, long-term tolerability and tissue compatibility are not yet established. METHODS: Three sheep were infused intrathecally with TZD up to 4000 micrograms/d over a time period of up to 440 d using implantable drug administration devices; one control animal was infused with vehicle only; standard values were collected from untreated sheep. CSF samples and blood samples were analyzed to determine pharmacokinetics and systemic redistribution. Behavioral effects were studied. The spinal cord tissue was investigated using standard laboratory histology. RESULTS: Bolus kinetics after i.t. injection of TZD are best described by a two-phase model. Elimination half-lives of TZD in CSF were 15 min and 152 min, respectively. Clearance of TZD from lumbar CSF was 0.48 ml/min. Doses higher than 500 microgram i.t. caused dose-dependent motor inactivity and sleepiness. Continuous i.t. TZD up to 4 micrograms/d was well tolerated regarding behavioral, physical activity, heart rate, muscle counts and total protein were detected both in saline and TZD-treated animals, presumably due to local irritation by the catheter and repeated sampling procedures. Histological evaluation of the spinal cord and adjacent tissues showed no abnormalities. CONCLUSION: The long-term intrathecal infusion of TZD is well tolerated and non-toxic in the sheep. The data favor clinical trials in patients with chronic pain.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Autoregulation of spinal cord blood flow: is the cord a microcosm of the brain?

The autoregulatory capability of regional areas of the brain and spinal cord was demonstrated in 18 rats anesthetized with a continuous infusion of intravenous pentothal. Blood flow was measured by the injection of radioactive microspheres (Co57, Sn113, Ru103, Sc46). Blood flow measurements were made at varying levels of mean arterial pressure (MAP) which was altered by neosynephrine to raise MAP or trimethaphan to lower MAP. Autoregulation of the spinal cord mirrored that of the brain, with an autoregulatory range of 60 to 120 mm Hg for both tissues. Within this range, cerebral blood flow (CBF) was 59.2 +/- 3.2 ml/100 g/min (SEM) and spinal cord blood flow (SCBF) was 61.1 +/- 3.6. There was no significant difference in CBF and SCBF in the autoregulatory range. Autoregulation was also demonstrated regionally in the left cortex, right cortex, brainstem, thalamus, cerebellum, hippocampus and cervical, thoracic and lumbar cord. This data provides a coherent reference point in establishing autoregulatory curves under barbiturate anesthesia. Further investigation of the effects of other anesthetic agents on autoregulation of the spinal cord is needed. It is possible that intraspinal cord compliance, like intracranial compliance, might be adversely affected by the effects of anesthetics on autoregulation.

Anesthesia, Intravenous↗
PubMed1987

Effect of naloxone in experimental acute spinal cord injury.

Naloxone, an opiate antagonist, has been reported to improve spinal cord blood flow and restore the neurological function of spinal cord in experimental animals. The present study investigated the short term effect of naloxone infusions in acute preparations. An impact of a 20-g weight dropped from 6 cm high was used to traumatize the thoracolumbar spinal cord in cats. Treatment was started immediately after trauma. The naloxone-treated cats received intrathecal (2 mg in 0.5 ml) as well as systemic (2-mg/kg bolus, 2 mg/kg/hour for 4 hours) doses of naloxone. In the control group, equal volumes of saline were administered. The physiological integrity of the spinal cord as measured by averaged spinal evoked potentials (SEPs) ceased immediately after trauma in both groups. No recovery of the SEP in response to sciatic nerve stimulation occurred in either group during the 4 hours of treatment and monitoring in this study.

Animals↗
PubMed1998

Bronchial arterial angio-CT: evaluation of intradural and oesophageal enhancement before bronchial arterial infusion.

Ultrafast CT combined with bronchial angiography (BA angio-CT) demonstrated a supply from the bronchial arteries to the oesophagus and spinal cord which is not identified on conventional bronchial arteriography using a digital subtraction technique. 20 patients with bronchial carcinoma and one with lung metastasis were examined using BA angio-CT, before bronchial artery infusion. 20 ml of non-ionic iodinated contrast medium (300 mgI ml-1) was injected into the bronchial artery, and ultrafast CT of the whole mediastinum was commenced when 10 ml had been injected. The 6 mm single slice mode was used and 40 images were obtained. Intradural and oesophageal enhancement was evaluated on BA angio-CT, and compared with the findings on digital subtraction angiography (DSA) of the bronchial arteries. BA angio-CT clearly showed intradural enhancement in eight patients. Marked spinal cord enhancement was demonstrated in three, and a coaxial catheter technique was used to avoid infusing the intercostal branch of the intercostobronchial trunk. Oesophageal enhancement was demonstrated in 18 patients on BA angio-CT. In contrast, no enhancement of these structures was seen on bronchial arterial DSA. In conclusion, BA angio-CT enabled precise evaluation of intradural and oesophageal enhancement.

Adult↗
PubMed1993

Effects of adenosine triphosphate (ATP) on somatosensory evoked potentials in humans anesthetized with isoflurane and nitrous oxide.

In order to examine the usefulness of adenosine triphosphate (ATP) as an adjuvant to anesthesia for surgery requiring intraoperative somatosensory evoked potential (SSEP) monitoring, we have studied the effects of ATP on SSEPs in patients anesthetized with isoflurane and nitrous oxide (N2O). A control recording of SSEP was performed while anesthesia was maintained with 0.5% end-tidal concentration of isoflurane in 60% N2O. The recordings were repeated after an ATP infusion had been added to this basal anesthesia at the rates of 100 micrograms.kg bw-1.min-1 and 200 micrograms.kg bw-1.min-1. SSEP was also studied when end-tidal isoflurane concentration was increased to 1.5% after cessation of ATP infusion. An infusion of ATP combined with 0.5% isoflurane and 60% N2O effectively inhibited an increase in blood pressure during surgery. The amplitude of the cortical component of SSEP was lowered by 1.5% isoflurane, which also increased both cortical and spinal latencies as well as central conduction time (CCT). In contrast ATP infusions at both rates induced no significant changes in latencies, amplitude and CCT. The results indicate that ATP infusion combined with 0.5% isoflurane in 60% N2O can be a useful anesthetic technique for intraoperative SSEP monitoring because adequate anesthetic depth can be maintained by a low concentration of anesthetics without further suppression of SSEPs.

Adenosine Triphosphate↗
PubMed1980

Severe hypertension in patients with high spinal cord lesions undergoing electro-ejaculation--management with prostaglandin E2.

Intra-arterial blood pressure (BP) and heart rate (HR) were continuously recorded in five patients with spinal cord injuries at different levels who were undergoing electro-ejaculation. In three patients with lesions at C7, C5 and T4 insertion of the electrode and electrical stimulation caused severe hypertension and bradycardia. In a patient with a T7/8 lesion and in another with a T10 lesion there were either moderate or minimal cardiovascular changes. Severe hypertension during electro-ejaculation is a serious problem in patients with high lesions and is probably part of the syndrome of autonomic dysreflexia. In the three patients with high spinal cord lesions the procedures were repeated during an intravenous infusion of Prostaglandin E2. Resting BP was lowered and resting HR raised. The level of BP recorded during electrical stimulation was substantially reduced. This enabled larger stimuli to be used for a longer period and resulted in successful ejaculation in two patients.

Adult↗
PubMed2004

[Combined spinal and epidural anesthesia for cesarean section: a retrospective study with 0.5% hyperbaric bupivacaine].

BACKGROUND: We investigated retrospectively the relationship between the intrathecal dose of 0.5% hyperbaric bupivacaine and the use of 2% mepivacaine through an epidural catheter. METHODS: Forty-nine patients undergoing cesarean section with combined spinal and epidural anesthesia (CSEA) were analyzed. They were divided into two groups; with (CSEA group) and without additional epidural injection group (spinal group). RESULTS: In the CSEA group (24 patients received 1.2 +/- 0.4 ml of 0.5% hyperbaric bupivacaine), 5-10 ml of 2% mepivacaine were required to achieve the adequate surgical anesthesia. In the spinal group (25 patients received 1.6 +/- 0.3 ml of 0.5% hyperbaric bupivacaine), cesarean section was performed without additional mepivacaine before delivery. The analgesic level and the amount of fluid infusion were similar in the two groups. However, 20% of patients in the spinal group showed hypotension (systolic blood pressure below 80 mmHg), although no patients in the CSEA group developed hypotension. The amount of ephedrine used before delivery was significantly larger in the spinal group (8.9 +/- 7.7 mg) than in the CSEA group (3.9 +/- 4.3 mg). CONCLUSIONS: Spinal anesthesia induced by 1.2 ml of 0.5% hyperbaric bupivacaine with sequential epidural block induced by 5-10 ml of 2% mepivacaine caused no hypotension during cesarean section.

Adult↗
PubMed2000

The surgical treatment of spasticity.

Many neurosurgical procedures have been designed for or applied to the treatment of spasticity arising from different disorders, including cerebral palsy; traumatic, ischemic, or hypoxic brain injury, multiple sclerosis, and spinal cord injury. Neurosurgical procedures are primarily aimed at reducing spasticity by interrupting the stretch reflex at various sites along the spinal reflex arc or attempting to increase the centrally mediated inhibitory influence on the pool of motor neurons in the anterior horn. Surgical interventions for spasticity can be classified into peripheral ablative procedures, such as rhizotomy or peripheral neurectomy, and central ablative procedures, such as cordectomy, myelotomy, or stereotactic procedures. Non-ablative procedures include peripheral nerve or motor point blocks, the implantation of cerebellar or spinal stimulators, and the implantation of subdural catheters for infusion of pharmacologic agents to increase inhibitory activity. Several proposed mechanisms for spasticity are reviewed so that the rationale for the various surgical interventions for spasticity described may be better understood.

Efferent Pathways↗
PubMed1997

Intra-aneurysmal GDC embolization followed by intrathecal tPA administration for poor-grade basilar tip aneurysm.

BACKGROUND: This 42-year-old male presented with subarachnoid hemorrhage of Hunt and Kosnik Grade IV, complicated by neurogenic pulmonary edema, prolongation of the electrocardiographic Q-Q interval, and acute renal failure. METHODS: Surgical clipping was not indicated, so intra-aneurysmal embolization using Guglielmi detachable coils (GDCs) was performed followed by intrathecal infusion of tissue-type plasminogen activator (tPA) via spinal drainage. RESULTS: The patient made a complete recovery 2 1/2 months later except for partial third cranial nerve palsy. CONCLUSIONS: Intra-aneurysmal GDC embolization followed by intrathecal tPA via spinal drainage is an excellent method for treating aneurysms that are difficult to treat surgically.

Adult↗
PubMed2004

Small dose of clonidine mixed with low-dose ropivacaine and fentanyl for epidural analgesia after total knee arthroplasty.

BACKGROUND: We studied whether a small dose of clonidine added to a ropivacaine-fentanyl mixture improves epidural analgesia without provoking side effects typically related to larger amounts of epidural clonidine. METHODS: In this randomized, double-blinded study, patients (< or =85 yr, ASA I-III) underwent total knee arthroplasty (TKA) performed under spinal anaesthesia. After the operation, patients received an epidural infusion consisting of ropivacaine 2 mg ml(-1) and fentanyl 5 microg ml(-1) either without (Group RF, n=33) or with clonidine 2 microg ml(-1) (Group RFC, n=36). The infusion rate was adjusted within the range 3-7 ml h(-1). RESULTS: Average rate of infusion was slightly smaller in Group RFC than in Group RF (mean (sd) 4.7 (0.72) vs 5.2 (0.8) ml h(-1), P=0.004). Compared with the RF group, patients in the RFC group required significantly less rescue pain medication, that is i.m. oxycodone (median (25th, 75th percentile) 0 (0, 7) vs 7 (0, 12) mg, P=0.027). Arterial pressure and heart rate were slightly lower in Group RFC throughout the study period (mean difference between the groups 5 mm Hg (P<0.002) and 3 min(-1) (P=0.12), respectively). The groups did not differ statistically with respect to nausea, motor block, and sedation. CONCLUSIONS: The small amount of clonidine added to the low-dose ropivacaine-fentanyl mixture reduced the need for opioid rescue pain medication after TKA. Clonidine slightly decreased arterial pressure and heart rate without jeopardizing haemodynamics. Otherwise, the side effect profiles were comparable in both groups.

Adult↗