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PubMed2004

Epidural anesthesia, hypotension, and changes in intravascular volume.

BACKGROUND: The most common side effect of epidural or spinal anesthesia is hypotension with functional hypovolemia prompting fluid infusions or administration of vasopressors. Short-term studies (20 min) in patients undergoing lumbar epidural anesthesia suggest that plasma volume may increase when hypotension is present, which may have implications for the choice of treatment of hypotension. However, no long-term information or measurements of plasma volumes with or without hypotension after epidural anesthesia are available. METHODS: In 12 healthy volunteers, the authors assessed plasma (125I-albumin) and erythrocyte (51Cr-EDTA) volumes before and 90 min after administration of 10 ml bupivacaine, 0.5%, via a thoracic epidural catheter (T7-T10). After 90 min (t = 90), subjects were randomized to administration of fluid (7 ml/kg hydroxyethyl starch) or a vasopressor (0.2 mg/kg ephedrine), and 40 min later (t = 130), plasma and erythrocyte volumes were measured. At the same time points, mean corpuscular volume and hematocrit were measured. Systolic and diastolic blood pressure, heart rate, and hemoglobin were measured every 5 min throughout the study. Volume kinetic analysis was performed for the volunteers receiving hydroxyethyl starch. RESULTS: Plasma volume did not change per se after thoracic epidural anesthesia despite a decrease in blood pressure. Plasma volume increased with fluid administration but remained unchanged with vasopressors despite that both treatments had similar hemodynamic effects. Hemoglobin concentrations were not significantly altered by the epidural blockade or ephedrine administration but decreased significantly after hydroxyethyl starch administration. Volume kinetic analysis showed that the infused fluid expanded a rather small volume, approximately 1.5 l. The elimination constant was 56 ml/min. CONCLUSIONS: Thoracic epidural anesthesia per se does not lead to changes in blood volumes despite a reduction in blood pressure. When fluid is infused, there is a dilution, and the fluid initially seems to be located centrally. Because administration of hydroxyethyl starch and ephedrine has similar hemodynamic effects, the latter may be preferred in patients with cardiopulmonary diseases in which perioperative fluid overload is undesirable.

Adult↗

PubMed1991

Recombinant interferon beta: a phase I-II trial in children with recurrent brain tumors.

A multicenter phase I-II trial of intravenous (IV) human recombinant interferon beta (rIFN-beta; Betaseron; Triton Bioscience Inc, Almeda, CA) was conducted in children with recurrent or progressive primary brain and spinal cord tumors. A total of 29 patients were enrolled: high-grade astrocytoma (12), brainstem glioma (nine), and primitive neuroectadermal tumor (three), ependymoma (two), germ cell (two), and spinal cord astrocytoma (one). Betaseron was given by IV infusion over 30 minutes 3 times per week (Monday-Wednesday-Friday [MWF]). Four dose levels were studied, and at least three patients were entered at each dose level. The treatment plan began with a three-step dose escalation for each patient over 6 weeks (initiation phase). The dose-escalation schema for the four dose levels was: 50-100-200, 100-200-400, 200-300-500, and 300-400-600 x 10(6) (M) IU/m2. Patients experiencing an objective response or stable disease after 6 weeks entered the maintenance phase at the final escalated dose, ie, 200, 400, 500, or 600 mlU/m2 (MWF). Common transient effects included chills, fever, and fatigue. Dose-limiting toxicities were hematologic, hepatic, and CNS. The maintenance maximum-tolerable dose (MTD) was 500 mlU/m2, ie, dose level 3. Response was assessed at completion of the initiation phase and at 2-month intervals during the maintenance phase. Objective partial responses were seen in patients with high-grade astrocytoma (two) and brain-stem glioma (two). Thus, four of 21 (19%) assessable patients had partial responses for a median of 4 months. Eight patients had stable disease for a median of 5+ (2 to 14+) months. Antineoplastic activity has been identified in children with high-grade astrocytomas and brainstem gliomas in a dose-intensive regimen.

Brain Neoplasms↗

PubMed2005

Continuous femoral nerve blockade or epidural analgesia after total knee replacement: a prospective randomized controlled trial.

Because postoperative pain after total knee replacement (TKR) can be severe, we compared the analgesic efficacy of continuous femoral nerve blockade (CFNB) and continuous epidural analgesia (CEA) after TKR in this prospective randomized trial. Patients undergoing TKR under spinal anesthesia were randomized to receive either a femoral infusion of bupivacaine 0.2% (median infusion rate 9.3 mL/h) (n = 53) or an epidural infusion of ropivacaine 0.2% with fentanyl 4 microg/mL (median infusion rate 7.6 mL/h) (n = 55). Adjuvant analgesics were oral rofecoxib and oxycodone and IV morphine. Pain, nausea and vomiting, hypotensive episodes, motor block, range of knee movement, and rehabilitation milestones were assessed postoperatively. There were equivalent pain scores, range of movement, and rehabilitation in both groups. There was significantly less nausea and vomiting in the CFNB group (P < 0.002). The CFNB group received more rofecoxib (P < 0.04) and oxycodone (P < 0.005) than the CEA group. The operative limb displayed more motor block than the nonoperative limb in both groups at the level of the hip and knee for up to 48 h (P < 0.05, Mann-Whitney U-test), but there was no difference between groups in the nonoperative limb. CFNB is an effective regional component of a multimodal analgesic strategy after TKR.

Aged↗

PubMed2003

Neurotrophin-3 down-regulates trkA mRNA, NGF high-affinity binding sites, and associated phenotype in adult DRG neurons.

Neurotrophin-3 (NT-3) binds to multiple trks, not only its initially identified receptor trkC. Recent studies in our laboratory show that NT-3 negatively regulates nociceptive phenotype associated with the trkA subpopulation. Due to the extensive overlap in trkA and trkC expression it is uncertain whether there is a direct influence of NT-3 on trkA in adult sensory neurons. Thus, the aim of this study was to examine whether NT-3 might alter trkA and associated neuronal phenotype outside of the trkC subpopulation. The effect of a seven-day intrathecal infusion of NT-3 on intact, uninjured adult rat dorsal root ganglion neurons was investigated. Serial sections were processed for receptor radioautography or in situ hybridization to identify and colocalize neurons expressing high-affinity nerve growth factor (NGF) binding sites, substance P (SP), trkC, or trkA mRNAs and to examine the influence of NT-3 on these populations. NT-3 does not appear to alter trkC expression, but evokes a notable reduction in trkA, high-affinity NGF binding sites, and SP levels. It is unlikely that signalling by trkC greatly influences this response because the down-regulation of SP occurs most notably in trkA neurons that lack trkC. Moreover, we have shown here that message levels of two trkA isoforms are differentially modulated by NT-3; infusion results in greater down-regulation of the noninsert containing isoform. These findings suggest a clinically relevant role for NT-3 as an antagonist to NGF, but also raise the caution that not just trkC-positive neurons are influenced following exposure to the neurotrophin.

Animals↗

PubMed2000

Spinal cord bioavailability of methylprednisolone after intravenous and intrathecal administration: the role of P-glycoprotein.

BACKGROUND: High-dose intravenously administered methylprednisolone has been shown to improve outcome after spinal cord injury. The resultant glucocorticoid-induced immunosuppression, however, results in multiple complications including sepsis, pneumonia, and wound infection. These complications could be reduced by techniques that increase the spinal bioavailability of intravenously administered methylprednisolone while simultaneously decreasing plasma bioavailability. This study aimed to characterize the spinal and plasma bioavailability of methylprednisolone after intravenous and intrathecal administration and to identify barriers to the distribution of methylprednisolone from plasma into spinal cord. METHODS: The spinal and plasma pharmacokinetics of intravenous (30-mg/kg bolus dose plus 5.4 mg x kg(-1) x h(-1)) and intrathecal (1-mg/kg bolus dose plus 1 mg x kg(-1) x h(-1)) methylprednisolone infusions were compared in pigs. In addition, wild-type mice and P-glycoprotein knockout mice were used to determine the role of P-glycoprotein in limiting spinal bioavailability of methylprednisolone. RESULTS: Despite the greater intravenous dose, concentrations of methylprednisolone in pig spinal cord were far higher and plasma concentrations much lower after intrathecal administration. After intraperitoneal administration in the mouse, the concentrations of methylprednisolone in muscle were not different between mice expressing P-glycoprotein (2.39 +/- 1.79 microg/g) and those lacking P-glycoprotein (2.83 +/- 0.46 microg/g). In contrast, methylprednisolone was undetectable in spinal cords of wild-type mice, whereas concentrations in spinal cords of P-glycoprotein-deficient mice were similar to those in skeletal muscle (2.83 +/- 0.27 microg/g). CONCLUSIONS: These pig studies demonstrate that the spinal cord bioavailability of methylprednisolone is poor after intravenous administration. The studies in knockout mice suggest that this poor bioavailability results from P-glycoprotein-mediated exclusion of methylprednisolone from the spinal cord.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2003

The use of the potassium channel activator riluzole to test whether potassium channels mediate the capacity of isoflurane to produce immobility.

UNLABELLED: Inhaled anesthetics produce immobility during noxious stimulation, primarily by actions on the spinal cord. In this study, we examined whether activation of potassium channels of the KCNK subfamily alters volatile anesthetic potency. We measured the change in isoflurane minimum alveolar anesthetic concentration (MAC) during 4-h intrathecal or IV infusions of the nonspecific KCNK activator riluzole in 54 Sprague-Dawley rats. IV or intrathecal infusions of riluzole doses that did not result in permanent injury or death equally decreased isoflurane MAC. We conclude that although riluzole exhibited anesthetic effects, the similar dose response from IV or intrathecal infusion suggests systemic absorption and actions in the brain rather than the spinal cord. IMPLICATIONS: Riluzole, a drug that activates potassium channels and decreases glutamatergic neurotransmission, primarily acts on supraspinal sites to produce immobility in response to noxious stimuli. This finding does not support the hypothesis that potassium channels mediate the capacity of inhaled anesthetics to produce immobility in the face of noxious stimulation.

Anesthetics, Inhalation↗

PubMed1996

Cocaine toxicity and isoflurane anesthesia: hemodynamic, myocardial metabolic, and regional blood flow effects in swine.

OBJECTIVES: Increasing numbers of people use cocaine recreationally and may require anesthesia care, having recently abused the drug. However, no data currently exist concerning potential interactions between toxic levels of cocaine and volatile anesthetic agents. This study investigated the effects of cocaine infusion on systemic hemodynamics, myocardial metabolism, and regional organ blood flow in relation to depth of isoflurane anesthesia. DESIGN: Prospective, randomized, controlled trial. SETTING: A laboratory at a university medical center. PARTICIPANTS: Twelve miniature pigs. INTERVENTIONS: An open-chest swine model was used. Isoflurane (ISO) was the sole anesthetic, administered at 0.75 and 1.5 minimum alveolar concentration (MAC), and cocaine was infused (n = 6) at a rate of 0.5 mg/kg/min. Control animals (n = 6) received an equivalent amount of normal saline. MEASUREMENTS AND MAIN RESULTS: Systemic and pulmonary arterial pressures and thermodilution cardiac output data were collected at 0.75 MAC and 1.5 MAC ISC. Regional myocardial and blood flows to other organs were measured using radiolabeled microspheres. Arrhythmias and altered ventricular conduction were noted only in the cocaine group, along with significant elevations in diastolic arterial pressure, coronary perfusion pressure, and systemic vascular resistance. Increased subendocardial blood flow occurred during cocaine infusion (p = 0.03); subepicardial perfusion was unchanged. Cerebral (p < 0.01) and spinal cord (p < 0.05) blood flows were reduced in animals receiving cocaine. Other organ blood flows were unchanged with depth of anesthesia or cocaine administration, with the exception of splenic blood flow (p < 0.04). CONCLUSIONS: Moderately toxic cocaine levels occurring during isoflurane at 0.75 MAC and 1.5 MAC are associated with hemodynamic abnormalities, a marked increase in systemic vascular resistance, and a tendency to produce cardiac arrhythmias. A reversal of endo/epicardial myocardial perfusion ratio occurs associated with cocaine infusion during ISO anesthesia. This is probably not related to a primary redistribution of subendocardial blood flow and may be related to a combination of increased myocardial oxygen demand and epicardial coronary vasoconstriction. The reductions in cerebral and spinal cord perfusion observed may explain, in part, the neurologic sequelae of cocaine toxicity.

Anesthetics, Inhalation↗

PubMed1988

Spinal cord injury in newborns from use of umbilical artery catheters: report of two cases and a review of the literature.

Umbilical artery catheter use in sick newborns has been associated with infarction of major organs such as the intestine and kidneys; spinal cord infarction has also been reported but is rare. We report two cases of spinal cord infarction and review the six others in the literature for preventable or predisposing conditions. Infusion of blood and hypertonic solutions, shock, and high position of the catheter tip were associated with infarction of the anterior spinal cord in these infants.

Cardiac Output↗

PubMed2003

Blockade of 5-HT2A receptors may mediate or modulate part of the immobility produced by inhaled anesthetics.

UNLABELLED: Many inhaled anesthetics block the in vitro effect of the excitatory neurotransmitter serotonin on the 5-HT2A receptor, supporting the view that this receptor might mediate the capacity of inhaled anesthetics to produce immobility during noxious stimulation (i.e., would underlie MAC, the minimum alveolar concentration required to suppress movement in response to a noxious stimulus in 50% of subjects). In the present investigation in rats, we found that intrathecal administration of the 5HT-2A blocker, ketanserin, can decrease isoflurane MAC. This effect, presumably mediated by blockade of serotonin transmission in the spinal cord, reaches a maximum of 20%-25%. An additional decrease (to 60%) may be obtained by IV infusion of ketanserin, and presumably this decrease results from ketanserin's actions on supraspinal centers. The IV doses of ketanserin that decreased MAC were approximately 100 microg. kg(-1). min(-1) in rats, compared with usual clinical doses of 1.25 microg. kg(-1). min(-1) in humans. These results indicate that 5HT2A receptors are in the neural circuitry influencing isoflurane MAC. These results, together with the blocking action of isoflurane on expressed 5HT2A receptors, strengthen the case for a role for 5HT2A receptors to isoflurane-induced immobility. However, because MAC for isoflurane is predominantly determined in the spinal cord, this result is consistent at most with a minor contribution of these receptors to the immobilizing action of isoflurane. IMPLICATIONS: A subset of serotonin receptors, 5HT2A receptors, may mediate or modulate a minor portion of the immobility produced by inhaled anesthetics.

Anesthetics, Inhalation↗

PubMed1994

[Spinal anesthesia in infancy using bupivacaine 0.5%. The effect of an adrenaline addition on duration and hemodynamics].

The duration of spinal anaesthesia in infants is short compared to adult patients. When tetracaine is used, the addition of epinephrine significantly prolongs the duration. For bupivacaine, however, the influence of epinephrine on the duration is not clear. We investigated the effects of epinephrine 1:200,000 added to bupivacaine 0.5% on duration and haemodynamics. PATIENTS AND METHODS. Ten former pre-term infants with postnatal respiratory problems, scheduled for bilateral inguinal hernia repair, were enrolled in the study after informed parental consent had been obtained. The infants were fasted at least 4 h prior to surgery. If they did not receive i.v. infusions before surgery, a bolus of 10 ml/kg Ringer's acetate was injected after inserting the i.v. cannula, followed by a continuous infusion of 8 ml/kg 2/3 N NaCl with 5% dextrose. Spinal anaesthesia was performed in a sitting position with 0.6 ml bupivacaine 0.5%. Five patients received plain bupivacaine (group I) and five bupivacaine with epinephrine 1:200,000 (group II). Heart rate registered by ECG and non-invasive blood pressure were recorded prior to positioning the baby for lumbar puncture and 2, 5, 10, and 20 min after injection of bupivacaine. The duration of spinal anaesthesia was defined as the time from injection to the time when the first movements of the legs were observed after stimulation. For testing statistical differences the U test was used between the groups and the Wilcoxon and Wilcox test within the groups. RESULTS. (expressed as median and range). Additional epinephrine significantly prolonged the duration of spinal anaesthesia (group II: 95 min [60-120] vs group I: 50 min [37-85]). Haemodynamic parameters did not differ at any time between or within the groups. In group I, one infant had high spinal anaesthesia with impaired respiration but without cardiovascular effects; after 10 min of assisted ventilation by mask, sufficient respiration as judged by pulse oximetry and clinical observation had returned. The duration of spinal anaesthesia in this child was 60 min. CONCLUSIONS. Epinephrine 1:200,000 significantly prolongs the duration of spinal anaesthesia in former preterm infants. Haemodynamic parameters in this age group remain unchanged during spinal anaesthesia and are not influenced by the addition of epinephrine.

Anesthesia, Spinal↗

PubMed2001

Glucocorticoid inhibition of neuropathic hyperalgesia and spinal Fos expression.

Glucocorticoids are used to treat patients suffering from neuropathic pain and complex regional pain syndromes (CRPS). Previously we found that once-daily injections of the glucocorticoid methylprednisolone had no antihyperalgesic effect in the rat sciatic nerve transection model for CRPS, but on the basis of CRPS clinical data, we hypothesized that a continuous infusion of methylprednisolone might prove effective. We further postulated that the antihyperalgesic effects of glucocorticoids were mediated by the inhibition of spinal neuron hyperactivity and by the depletion of substance P or its NK(1) receptor. This study tested the effects of continuously infused methylprednisolone in sciatic nerve-transected rats. Continuous infusion of methylprednisolone (3 mg. kg(-1). d(-1) for 21 days), started after the development of neuropathic hyperalgesia, reversed both heat and mechanical hyperalgesia over 2 wk, and this effect persisted for at least 1 wk after discontinuing methylprednisolone. In addition, continuous methylprednisolone infusion partially reversed nerve injury-evoked Fos expression in the dorsal horns, suggesting that glucocorticoids can inhibit the spinal neuron hyperactivity induced by chronic sciatic nerve transection. Finally, no changes were observed in spinal substance P or NK(1) immunoreactivity after chronic methylprednisolone infusion, suggesting that the depletion of this neuropeptide or its receptor does not contribute to the antihyperalgesic actions of glucocorticoids.

Animals↗

PubMed1989

Paraplegia after lumbar puncture. In an infant with previously undiagnosed hemophilia A. Treatment and peri-operative considerations.

We report a 3-month-old infant who became paraplegic from an epidural hematoma caused by a diagnostic lumbar puncture for work-up of sepsis. The differential diagnosis of the cause of paraplegia was epidural hematoma formation versus spinal abscess. Hemophilia A was diagnosed when coagulation studies were discovered to be abnormal, and non-contrast CT scan revealed an epidural mass with spinal cord displacement. The coagulopathy was rapidly corrected preoperatively with an infusion of cryoprecipitate. A medially limited bilateral T8-L4 laminectomy allowed complete evacuation of the hematoma with maximum preservation of normal bone tissue, but no clinical improvement resulted. Coagulopathy should be highly suspect in an infant who becomes paraplegic after lumbar puncture. The coagulopathy may be rapidly corrected with deficient factor replacement, allowing major spinal surgery to be performed safely.

Epidural Space↗

PubMed2004

Quality of postoperative pain using an intraoperatively placed epidural catheter after major lumbar spinal surgery.

BACKGROUND: Major spinal surgery is associated with high postoperative pain scores and opioid requirement. The aim of the current prospective, randomized, placebo-controlled, double-blind study was to assess the reduction of opioid requirement and pain scores using an intraoperatively placed epidural catheter with infusion of 0.1% ropivacaine during the postoperative period. METHODS: Thirty patients undergoing major lumbar spinal surgery from a dorsal approach were included in this study. Before wound closure, the orthopedic surgeon inserted an epidural catheter. Postoperatively, patients were randomly assigned to receive an infusion of 12 ml/h ropivacaine, 0.1% (group R), or 12 ml/h saline (group N) after an initial bolus of 10 ml of the respective study solution. Additional pain relief was provided using an intravenous patient-controlled analgesia pump with the opioid piritramide. Patients were assessed with respect to pain scores (visual analog scale of 0-100), cumulative opioid requirement, side effects, and satisfaction with pain management. RESULTS: : Demographic data, duration of surgery, and type of surgery were comparable between groups. Pain scores were assessed as follows (group R vs. group N: 6 h: 24 +/-20 vs. 51 +/- 20, P = 0.002; 24 h: 33 +/- 19 vs. 53 +/- 27, P = 0.04; 48 h: 21 +/-17 vs. 40 +/- 26, P = 0.04; 72 h: 14 +/- 13 vs. 38 +/- 25, P = 0.02). The cumulative piritramide requirement after 72 h was 97 +/- 23 mg in group R and 157 +/-72 mg in group N (P = 0.03). The incidence of side effects was comparable between groups, and patient satisfaction was always higher in group R (P < 0.05). CONCLUSION: Continuous epidural infusion of 0.1% ropivacaine results in lower pain scores and opioid consumption and higher patient satisfaction when compared with placebo. Application of ropivacaine using an epidural catheter seems to be a highly effective treatment for postoperative pain after major lumbar spinal surgery.

Adult↗

PubMed1996

Use of intrathecal baclofen in the treatment of patients with dystonia.

BACKGROUND: Continuous infusion of intrathecal (IT) baclofen is a highly effective standard therapy for severe spasticity of spinal origin. By contrast, there is limited clinical experience regarding the use of IT baclofen in treating patients with dystonia, and little is known regarding the indications for treatment, efficacy, and safety of IT baclofen in this disorder. OBJECTIVE: To study retrospectively the effects of IT baclofen in treating 25 patients with severe segmental or generalized dystonia. SETTING: Neurological Institute, Columbia-Presbyterian Medical Center, New York, NY. PATIENTS: Twenty-five patients with severe segmental or generalized dystonia that was refractory to oral medications underwent IT baclofen test dosing. In addition to dystonia, 17 patients had spasticity or painful spasms. Thirteen of 25 patients responded to the test doses of IT baclofen, according to unblinded neurological assessments that included the patient's subjective report; all 13 underwent implantation of a pump for continuous IT baclofen infusion. RESULTS: In contrast to reports of patients with spasticity of spinal origin, those with dystonia in the present series had a lower response rate to bolus IT baclofen doses and a smaller degree of clinical improvement. For 10 of the 13 responders to the test doses of IT baclofen, dystonia rating scale scores of videotaped examinations by blinded observers detected no significant change (P < .07) in severity of dystonia. Retrospective data from 11 of 13 patients with implantable pumps, followed up for a mean interval of 21 months after pump insertion, showed continuing efficacy in 6 individuals (55%), based on a determination of patient satisfaction; however, only 3 patients (27%) reported a sustained improvement in functional capacity. Five (38%) of the 13 patients with implantable pumps experienced severe complications that required hospitalization. CONCLUSIONS: Despite recent reports that have described the benefit in small numbers of patients with dystonia, we concluded that the role of IT baclofen in treating severe dystonia remains uncertain. Intrathecal baclofen may be more effective when dystonia is associated with spasticity or pain. In the present series, we detected no significant difference in the response to IT baclofen in patients with or without spasticity or pain, perhaps owing to the small sample size.

Baclofen↗

PubMed2003

Glial cell line-derived neurotrophic factor normalizes neurochemical changes in injured dorsal root ganglion neurons and prevents the expression of experimental neuropathic pain.

Glial cell line-derived neurotrophic factor (GDNF) is necessary for the development of sensory neurons, and appears to be critical for the survival of dorsal root ganglion (DRG) cells that bind the lectin IB4. Intrathecal infusion of GDNF has been shown to prevent and reverse the behavioral expression of experimental neuropathic pain arising from injury to spinal nerves. This effect of GDNF has been attributed to a blockade of the expression of the voltage gated, tetrodotoxin-sensitive sodium channel subtype, Na(V)1.3, in the injured DRG. Here we report that GDNF given intrathecally via osmotic-pump to nerve-injured rats (L5/L6 spinal nerve ligation) prevented the changes in a variety of neurochemical markers in the DRG upon injury. They include a loss of binding of IB4, downregulation of the purinergic receptor P2X(3), upregulation of galanin and neuropeptide Y immunoreactivity in large diameter DRG cells, and expression of the transcription factor ATF3. GDNF infusion concomitantly prevented the development of spinal nerve ligation-induced tactile hypersensitivity and thermal hyperalgesia. These observations suggest that high dose, exogenous GDNF has a broad neuroprotective role in injured primary afferent. The receptor(s) that mediates these effects of GDNF is not known. GDNF's ability to block neuropathic pain states is not likely to be specific to Na(V)1.3 expression.

Activating Transcription Factors↗

PubMed2001

Neurotrophins BDNF and NT-3 promote axonal re-entry into the distal host spinal cord through Schwann cell-seeded mini-channels.

To promote axonal regeneration in the injured adult spinal cord, a two-phase repair strategy was employed to (i) bridge a spinal cord hemilesion cavity with a grafted Schwann cell (SC)-seeded mini-channel, and (ii) promote axonal re-entry into the distal cord by infusing two neurotrophins, BDNF and/or NT-3, directly into the distal cord parenchyma. Here we report that infusion of two neurotrophins, delivered alone or in combination, effectively promotes axonal outgrowth from SC-seeded mini-channels into the distal host spinal cord. When an anterogradely transported marker, PHA-L or BDA, was injected into the spinal cord 3 mm rostral to the graft, a large number of axons was observed to regenerate from the SC graft into the distal cord in neurotrophin-treated groups. A subpopulation of these axons was found to grow up to 6 mm within the distal spinal cord. These axons, which were confined mainly within the grey matter, arborized and formed structures which resemble terminal boutons. In channels containing no SCs, the infusion of neurotrophins did not promote axonal ingrowth from the proximal cord stump. In cases which received SC grafts but no neurotrophin infusion, axonal re-entry into the distal cord was limited. Thus, the present study demonstrates that regenerating axons not only cross a lesion site when a permissive cellular bridge is provided but also penetrate into the distal host spinal cord and elongate for a distance of several cord segments after the infusion of two neurotrophins. The latter event is prerequisite for establishment of appropriate connections between regenerating axons and target neurons and thus, functional recovery.

Animals↗

PubMed1988

Spontaneous spinal epidural hematoma causing cord compression after streptokinase and heparin therapy for acute coronary artery occlusion.

We have reported a case of spinal epidural hematoma with cord compression in a 49-year-old man treated with short-term streptokinase and continuous heparin infusion. The sudden onset of back pain with subsequent neurologic deficits in a patient treated with fibrinolytic therapy alone or in combination with an anticoagulant should prompt an evaluation for spinal epidural hematoma with associated cord compression. The risk of combined fibrinolytic and anticoagulant therapy is not clear and warrants further evaluation.

Coronary Disease↗

PubMedDate not supplied

Current methods of controlling post-operative pain.

Until recently, the clinical significance of post-surgical pain and its undertreatment were for the most part unappreciated. Recognition that inadequate analgesia adversely affects the patient's cardiovascular, pulmonary, and emotional status has spurred development of new and highly effective methods of controlling pain. With the introduction of spinal opioid and patient-controlled analgesia (PCA) came the realization that, while such forms of therapy provided superior pain relief, they were not without their own unique and occasionally serious side effects. For this reason, both techniques are more safely provided by highly trained members of a dedicated acute/post-surgical pain service. Although spinal opioid (epidural, intrathecal) techniques are invasive and require patient cooperation, they have a high degree of safety in low-risk populations (ASA 1 and 2). The major therapeutic advantage of spinal opioids is their ability to prevent pain from being perceived. PCA permits patients to titrate intravenous opioids in proportion to their particular level of pain intensity. Although PCA provides effective pain "relief," the technique is incapable of preventing pain from being appreciated. A number of studies have observed that pain scores in patients successfully employing PCA were significantly higher than those noted in individuals treated with epidural opioids. Nevertheless, the control gained by self-administration, uniformity of analgesia, and low level of adverse results associated with PCA provides higher patient satisfaction and decreased sedation when compared with traditional intramuscular dosing. The effectiveness of PCA may be improved by adjusting for patient variables, utilizing opioids having rapid onset, the addition of a basal infusion, and supplementation with non-steroidal anti-inflammatory agents. Interpleural analgesia represents an important therapeutic option in patients sensitive to opioid-induced respiratory depression. The technique is more effective when local anesthetic solutions are continually infused. Analgesic efficacy may be further enhanced by the addition of "low-dose" PCA.

Analgesia, Epidural↗