BACKGROUND: Local anesthetics can reduece excitotoxic neuronal injury from ischemia. We investigated neuroprotective effects of intrathecally administered bupivacaine and hypothermia in rat model of transient spinal cord ischemia. METHODS: A PE-10 intrathecal catheter was implanted into thirty six male Sprague-Dawley rats through L4-5 interlaminar space. Animals of normothermia (N) and hypothermia (H) groups were administered 15microliter of normal saline, and 15microliter of 0.5% bupivacaine for bupivacaine (B) and bupivacaine-hypothermia (BH) groups. Transient spinal cord ischemia was induced by inflation of a 2 F Fogarty catheter placed into aortic arch for 12 minutes. During ischemia, rectal temperature was maintained to 37.0+/-0.5 degrees C for N and B groups, 34.5 +/- 0.5degrees C for H and BH groups. Motor and sensory deficit score were assessed 2 and 24 hour after reperfusion. Lumbar spinal cords were harvested for histopathology, and for immunoreactivity of heat shock protein 70 (HSP70). RESULTS: The motor and sensory deficit score of N and B group was significantly higher than H group (P < 0.05) and BH group (P < 0.05). There were also significant difference in the motor and sensory deficit score between H and BH group at 24 hr (P < 0.05). Neuronal cell death and immunoreactivity of HSP70 was frequently observed in the N and B groups, but not in the H and BH groups. CONCLUSIONS: These results suggest that intrathecal bupivacaine did not provide neuroprotection during normothermic transient spinal cord ischemia in rats, but it can enhance neuroprotective effects of hypothermia.
Anesthetics, Local ; Animals ; Aorta, Thoracic ; Bupivacaine* ; Catheters ; Cell Death ; HSP70 Heat-Shock Proteins ; Humans ; Hypothermia* ; Inflation, Economic ; Ischemia ; Male ; Models, Animal ; Neurons* ; Neuroprotective Agents ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Spinal Cord Ischemia* ; Spinal Cord*

OBJECTIVE: Excitatory amino acids play important roles in the development of secondary pathology following spinal cord injury (SCI). This study was designed to evaluate morphological changes in the dorsal horn of the spinal cord and assess profiles of pain behaviors following intraspinal injection of N-methyl-D-aspartate (NMDA) or quisqualate (QUIS) in rats. METHODS: Forty male Sprague-Dawley rats were randomized into three groups : a sham, and two experimental groups receiving injections of 125 mM NMDA or QUIS into their spinal dorsal horn. Following injection, hypersensitivity to cold and mechanical stimuli, and excessive grooming behaviors were assessed serially for four weeks. At the end of survival periods, morphological changes in the spinal cord were evaluated. RESULTS: Cold allodynia was developed in both the NMDA and QUIS groups, which was significantly higher in the QUIS group than in the NMDA group. The mechanical threshold for the ipsilateral hind paw in both QUIS and NMDA groups was significantly lower than that in the control group. The number of groomers was significantly higher in the NMDA group than in the QUIS group. The size of the neck region of the spinal dorsal horn, but not the superficial layer, was significantly smaller in the NMDA and QUIS groups than in the control group. CONCLUSION: Intraspinal injection of NMDA or QUIS can be used as an excitotoxic model of SCI for further research on spinal neuropathic pain.
Animals ; Cold Temperature ; Excitatory Amino Acids ; Grooming ; Horns ; Humans ; Hyperalgesia ; Hypersensitivity ; Injections, Spinal ; Male ; N-Methylaspartate ; Neck ; Neuralgia ; Quisqualic Acid ; Rats ; Rats, Sprague-Dawley ; Salicylamides ; Spinal Cord ; Spinal Cord Injuries

Lumbar spinal stenosis is a commonly treated with epidural injections of local anesthetics and corticosteroids, however, these therapies may relieve leg pain for weeks to months but do not influence functional status. Furthermore, the majority of patients report no substantial symptom change over the repeated treatment. Utilizing balloon catheters, we successfully treated with three patients who complained persistent symptoms despite repeated conventional steroid injections. Our results suggest that transforaminal decompression using a balloon catheter may have potential in the nonsurgical treatment of spinal stenosis by modifying the underlying pathophysiology.
Adrenal Cortex Hormones ; Anesthetics, Local ; Catheters ; Decompression ; Humans ; Injections, Epidural ; Leg ; Spinal Stenosis

BACKGROUND: Spinal nerve ligation (SNL) injury in rats produces a pain syndrome that includes mechanical and thermal allodynia. Previous studies have indicated that proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) play an important role in peripheral mediation of neuropathic pain, and that altered dorsal root ganglion (DRG) function and degree of DRG neuronal apoptosis are associated with spinal nerve injury. The present study was conducted to evaluate the expression of TNF-alpha and the extent of apoptosis in the dorsal root ganglion after SNL in rats. METHODS: Sprague-Dawley rats were subjected to SNL of the left L5 and L6 spinal nerves distal to the DRG and proximal to the formation of the sciatic nerve. At postoperative day 8, TNF-alpha protein levels in the L5-6 DRG were compared between SNL and naive groups using ELISA. In addition, we compared the percentage of neurons injured in the DRG using immunostaining for apoptosis and localization of activated caspase-3. RESULTS: SNL injury produced significant mechanical and cold allodynia throughout the 7-day experimental period. TNF-alpha protein levels were increased in the DRG in rats that had undergone SNL (12.7 +/- 3.2 pg/100 microg, P < 0.001) when compared with naive rats (4.1 +/- 1.4 pg/100 microg). The percentage of neurons or satellite cells co-localized with activated caspase-3 were also significantly higher in rats with SNL than in naive rats (P < 0.001, P < 0.05, respectively). CONCLUSIONS: SNL injury produces mechanical and cold allodynia, as well as TNF-alpha elevation and apoptosis in the DRG.
Animals ; Apoptosis ; Caspase 3 ; Cold Temperature ; Cytokines ; Diagnosis-Related Groups ; Enzyme-Linked Immunosorbent Assay ; Ganglia, Spinal ; Hyperalgesia ; Ligation ; Negotiating ; Neuralgia ; Neurons ; Rats ; Rats, Sprague-Dawley ; Sciatic Nerve ; Spinal Nerves ; Tumor Necrosis Factor-alpha

BACKGROUND: Discharge after day-surgery can be delayed for postoperative pain in a video-assisted thoracic sympathicotomy (VATS). However, there seems to be no research about postoperative pain after a VATS. We examined the characteristics of patients and operative factors, and compared the severity of postoperative pain according to different anesthetics. METHODS: We examined the age, sex, obesity index, and pain tolerance in 194 VATS patients of ASA physical status 1 or 2. The patients were randomly divided into two groups each with 97 patients. Group P was anesthetized with propofol, and group E with enflurane. We measured the visual analog scale (VAS) score at 5 minute, 2 hours, and 6 hours after arrival at the recovery room. RESULTS: There was no difference in the VAS score according to age, sex, obesity index, or pain tolerance. The VAS score at coughing was significantly higher than at rest. The VAS score in group P was higher than group E, but there was no significant difference. The patients who had a complication of a pneumothorax had a significantly higher VAS score. CONCLUSIONS: Postoperative pain seems to be aggravated by remaining air within the thorax after VATS.
Anesthetics ; Cough ; Enflurane ; Humans ; Obesity ; Pain, Postoperative ; Pneumothorax ; Propofol ; Recovery Room ; Thoracic Surgery, Video-Assisted ; Thorax ; Visual Analog Scale

BACKGROUND: Neuropathic pain resulting from diverse causes is a chronic condition for which effective treatment is lacking. The goal of this study was to test whether dexamethasone exerts a preemptive analgesic effect with bupivacaine when injected perineurally in the spared nerve injury model. METHODS: Fifty rats were randomly divided into five groups. Group 1 (control) was ligated but received no drugs. Group 2 was perineurally infiltrated (tibial and common peroneal nerves) with 0.4% bupivacaine (0.2 ml) and dexamethasone (0.8 mg) 10 minutes before surgery. Group 3 was infiltrated with 0.4% bupivacaine (0.2 ml) and dexamethasone (0.8 mg) after surgery. Group 4 was infiltrated with normal saline (0.2 ml) and dexamethasone (0.8 mg) 10 minutes before surgery. Group 5 was infiltrated with only 0.4% bupivacaine (0.2 ml) before surgery. Rat paw withdrawal thresholds were measured using the von Frey hair test before surgery as a baseline measurement and on postoperative days 3, 6, 9, 12, 15, 18 and 21. RESULTS: In the group injected preoperatively with dexamethasone and bupivacaine, mechanical allodynia did not develop and mechanical threshold forces were significantly different compared with other groups, especially between postoperative days 3 and 9 (P < 0.05). CONCLUSIONS: In conclusion, preoperative infiltration of both dexamethasone and bupivacaine showed a significantly better analgesic effect than did infiltration of bupivacaine or dexamethasone alone in the spared nerve injury model, especially early on after surgery.
Animals ; Bupivacaine ; Dexamethasone ; Hair ; Hyperalgesia ; Neuralgia ; Rats

BACKGROUND: Nefopam is a centrally acting non-opioid analgesic agent. Its analgesic properties may be related to the inhibitions of monoamine reuptake and the N-methyl-D-aspartate (NMDA) receptor. The antinociceptive effect of nefopam has been shown in animal models of acute and chronic pain and in humans. However, the effect of nefopam on diabetic neuropathic pain is unclear. Therefore, we investigated the preventive effect of nefopam on diabetic neuropathic pain induced by streptozotocin (STZ) in rats. METHODS: Pretreatment with nefopam (30 mg/kg) was performed intraperitoneally 30 min prior to an intraperitoneal injection of STZ (60 mg/kg). Mechanical and cold allodynia were tested before, and 1 to 4 weeks after drug administration. Thermal hyperalgesia was also investigated. In addition, the transient receptor potential ankyrin 1 (TRPA1) and TRP melastatin 8 (TRPM8) expression levels in the dorsal root ganglion (DRG) were evaluated. RESULTS: Pretreatment with nefopam significantly inhibited STZ-induced mechanical and cold allodynia, but not thermal hyperalgesia. The STZ injection increased TRPM8, but not TRPA1, expression levels in DRG neurons. Pretreatment with nefopam decreased STZ-induced TRPM8 expression levels in the DRG. CONCLUSIONS: These results demonstrate that a nefopam pretreatment has strong antiallodynic effects on STZ-induced diabetic rats, which may be associated with TRPM8 located in the DRG.
Animals ; Ankyrins ; Chronic Pain ; Diabetic Neuropathies ; Diagnosis-Related Groups ; Ganglia, Spinal ; Humans ; Hyperalgesia ; Injections, Intraperitoneal ; Models, Animal ; N-Methylaspartate ; Nefopam* ; Neuralgia* ; Neurons ; Rats* ; Streptozocin

Conventional thoracoscopic sympathectomy is an effective method in treating palmar-axillary hyperhidrosis. However, this may result in a postoperatively compensatory hyperhidrosis. Conservative treatments of compensatory hyperhidrosis consist of aluminum chloride, anticholinergics, iontrophoresis, and botulinum toxin A injections. Surgical treatments in compensatory hyperhidrosis include excision of axillary tissue, liposuction, and thoracoscopic sympathectomy. Intradermal injection of botulinum toxin A has used to treat focal axillary or palmar hyperhidrosis. Botulinum toxin A bestows significant benefits with few side-effects and is well-tolerated, with beneficial results lasting from 4-16 months. We report a case illustrating the beneficial use of botulinum toxin A in a 25-year-old healthy male patient with compensatory sweating of the flank after thoracoscopic sympathectomy. Modified Minor's starch iodine test was used to allow accurate assess the impact of hyperhidrosis on the patient. In conclusion, Botulinum toxin type A is a valuable therapy for compensatory sweating after endoscopic thoracic sympathectomy.
Adult ; Aluminum ; Aluminum Compounds ; Botulinum Toxins ; Botulinum Toxins, Type A ; Chlorides ; Cholinergic Antagonists ; Humans ; Hyperhidrosis ; Injections, Intradermal ; Iodine ; Lipectomy ; Male ; Starch ; Sweat ; Sweating ; Sympathectomy

BACKGROUND: The injury by a nerve ligation produces a mechanical allodynia. The antiallodynic effect resulted from intrathecal administration of the adenosine analogues has been well known. ATP-sensitive potassium channel blockers have been known to reverse the effect of some antinociceptive drugs in animal and human studies. Therefore, the present study is to assess the relationship between antiallodynic effect of N6-(R)-phenylisopropyl adenosine (R-PIA) and mitochondrial ATP-sensitive potassium (mKATP) channel in a neuropathic pain model. METHODS: Allodynia was induced in male Sprague Dawley rats by the tight ligation of the left lumbar 5th and 6th spinal nerves. We tested the mechanical allodynia by pricking von Frey filaments to the left hind paw and assessed withdrawal thresholds of paw with up-down method. For the estimation of the antiallodynic effect of R-PIA, R-PIA (0.5, 1 and 2microgram) or saline were administered intrathecally.To investigate the reversal effect on antiallodynic effect of R-PIA, variable amounts of 5-hydroxydecanoate (5-HD, 20, 30 and 40 mg), mKATP channel blocker were administered intraperitoneally at 5 min prior to the intrathecal injection of 2microgram of R-PIA, and the degree of allodynia was assessed. RESULTS: The paw withdrawal threshold was gradually increased with increased dose of R-PIA and reached the maximum level with 2microgram R-PIA (P < 0.05). The increase of paw withdrawal threshold with 2microgram R-PIA was significantly reversed dose-dependently by intraperitoneal pretreatment of 20, 30 and 40 mg/kg 5-HD (P < 0.05). CONCLUSIONS: In our results, intraperitoneal injection of 5-HD before intrathecal injection of R-PIA had reversed the antiallodynic effect of R-PIA. This results suggest that the mechanism of mechanical antiallodynia induced by intrathecal injection of R-PIA may relate with the mK(ATP) channel in a rat model of nerve ligation injury.
Adenosine ; Animals ; Decanoic Acids ; Humans ; Hydroxy Acids ; Hyperalgesia ; Injections, Intraperitoneal ; Injections, Spinal ; Ligation ; Male ; Neuralgia ; Polymethacrylic Acids ; Potassium ; Potassium Channel Blockers ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P1 ; Spinal Nerves

BACKGROUND: Nefopam is a centrally acting non-opioid analgesic agent. Its analgesic properties may be related to the inhibitions of monoamine reuptake and the N-methyl-D-aspartate (NMDA) receptor. The antinociceptive effect of nefopam has been shown in animal models of acute and chronic pain and in humans. However, the effect of nefopam on diabetic neuropathic pain is unclear. Therefore, we investigated the preventive effect of nefopam on diabetic neuropathic pain induced by streptozotocin (STZ) in rats. METHODS: Pretreatment with nefopam (30 mg/kg) was performed intraperitoneally 30 min prior to an intraperitoneal injection of STZ (60 mg/kg). Mechanical and cold allodynia were tested before, and 1 to 4 weeks after drug administration. Thermal hyperalgesia was also investigated. In addition, the transient receptor potential ankyrin 1 (TRPA1) and TRP melastatin 8 (TRPM8) expression levels in the dorsal root ganglion (DRG) were evaluated. RESULTS: Pretreatment with nefopam significantly inhibited STZ-induced mechanical and cold allodynia, but not thermal hyperalgesia. The STZ injection increased TRPM8, but not TRPA1, expression levels in DRG neurons. Pretreatment with nefopam decreased STZ-induced TRPM8 expression levels in the DRG. CONCLUSIONS: These results demonstrate that a nefopam pretreatment has strong antiallodynic effects on STZ-induced diabetic rats, which may be associated with TRPM8 located in the DRG.
Animals ; Ankyrins ; Chronic Pain ; Diabetic Neuropathies ; Diagnosis-Related Groups ; Ganglia, Spinal ; Humans ; Hyperalgesia ; Injections, Intraperitoneal ; Models, Animal ; N-Methylaspartate ; Nefopam ; Neuralgia ; Neurons ; Rats ; Streptozocin