Steroid-induced rapid recovery from respiratory dysfunction in a patient with myasthenia gravis after spinal anesthesia.

We report an 83-year-old man with myasthenia gravis (MG) who developed respiratory depression after spinal anesthesia for transurethral laser enucleation of the prostate. He became less responsive after complained of dyspnea, with a decrease of SpO2 to 83% approximately 13 min after intrathecal administration of 0.5% isobaric bupivacaine 3 ml. With a diagnosis of exacerbation of MG, hydrocortisone 100 mg was administered, following which both consciousness and spontaneous respiration rapidly improved. Cold sense was observed below the C4 dermatome. We provided general anesthesia without using muscle relaxants until disappearance of the effect of spinal anesthesia. Surgery completed uneventfully and confirmed wearing off the local anesthetics effect. He was discharged without respiratory problems on postoperative 3 day.

Correction to: Awake fiberoptic intubation with an epidural catheter in a morbidly obese patient.

In the original publication of the article, the acknowledgment section was not included and provided in this correction.

Awake fiberoptic intubation with an epidural catheter in a morbidly obese patient.

We report successful awake intubation in a morbidly obese patient (body mass index of 61.2) using an epidural catheter inserted through the external forceps channel of the fiberscope for delivery of local anesthetic. Direct application of local anesthetic to the pharyngolaryngeal area and proximal tracheal, through the use of a relatively firm epidural catheter. We conclude that awake intubation can be achieved by this method which spares the subsequent use of any sedative drugs.

[Anesthetic Management of Laparoscopic Cholecystectomy in a Patient with Mitochondrial Encephalomyopathy].

We report the anesthetic management during the laparoscopic cholecystectomy in a 60-year-old woman (height 150 cm, 'Weight 46 kg) with mitochondrial encephalopathy (chronic progressive external ophthal- moplegia, or CPEO). CPEO causes a disorder of aero- bic energy metabolism in various organs due to mito- chondrial dysfunction. It is thus very important in anesthetic management to maintain energy balance of demand and supply in organs and to protect the patient's respiratory muscles. Our patient had devel- oped CPEO 46 years earlier, and at her presentation she was bedridden and receiving both respiratory assistance via tracheostomy and tube feeding. Her hearing and understanding were intact, but she was blind due to lagophthalmos. We performed intravenous anesthesia with propofol (TCI) and remifentanil com- bined with epidural anesthesia. Rocuronium was injected under a train-of-four (TOF) monitoring. The operative time for the laparoscopic cholecystectomy was 4 hours. A total of 50 mg of rocuronium and 2,050 ml of bicarbonic ringer was injected during the opera- tion. The patient's blood lactate and glucose remained at normal levels throughout the operation. Because of severe adhesion, the laparoscopic procedure was changed to a laparotomy. However, during the peri-and post-operative periods, epidural anesthesia was valuable for analgesia during the management of the patient's respiratory care with a decreasing amount of narcotic medication. Post-operatively, the patient was monitored in an intensive care unit with the spontaneous respira- tory rate of 15 · min⁻¹ under oxygen 1l without any analgesics. The day after the operation she was returned to the ward, as her general condition was satisfactory.

[Anesthesia for Patients with Obstructive Sleep Apnea Syndrome Associated with Severe Obesity].

A 41-year-old woman with concomitant severe obesity, obstructive sleep apnea syndrome, and asthma was scheduled for endoscopic cholecystectomy. She was 165.8 cm tall and weighed 141.2 kg, with BMI of 51.4. We were concerned with difficulty in ventilation and intubation at the time of anesthesia induction and intra- and post-operative ventilatory failure. After sedation with fentanyl and droperidol together with intraoral local anesthesia with lidocaine (Xylocaine Viscous), the intubating laryngeal mask (ILMA) was inserted while awake, and after the confirmation of adequate ventilation, the bronchoscope was inserted into the guide. Although she received no nerve block, she did not choke at the time of intubation. Because of airway pressure elevation during surgery, volume-controlled ventilation was changed to pressure-controlled ventilation, and, because of a worsening P/F ratio, the recruitment procedure was performed during surgery, with a consequent improvement in the ratio. Although the use of the reservoir and NPPV equipment after extubation was considered, her respiratory status was stable, and she returned to her room with oxygen mask.

[Anesthetic management of posterior lumbar spinal fusion in a patient suspected of having acute exacerbation of chronic interstitial pneumonia].

A patient complicated with interstitial pneumonia required emergency posterior lumbar spinal fusion. The blood gas analysis showed relatively benign values (PaO2 81 torr, PaCO2 44 torr, under room air), but the honeycombing lungs were noted in the bilateral lung fields on CT, and the KL-6 level was high (1,000 U x ml(-1)), for which the acute exacerbation of interstitial pneumonia was suspected. Sivelestat sodium administration was initiated during the surgery and continued postoperatively. During surgery, setting the FIO2 at 0.34, the P/F ratio and intra-airway pressure could be maintained at 500 and 25 mmHg, respectively. To reduce postoperative respiratory complication, anesthesia was maintained with desflurane, which is dissipated easily, and 0.5% ropivacaine 15 ml was subcutaneously injected to the surgical field at the time of wound closure to reduce the total doses of intraoperative fentanyl and postoperative analgesics. After the completion of surgery, the endotracheal tube was removed with head elevated position, and the patient was transported back to the ward. No acute exacerbation occurred thereafter, and the patient was discharged 67 days after surgery. The prediction of acute exacerbation of interstitial pneumonia is difficult. Moreover, there is no established preventive method, although the mortality is high. Therefore, physicians should be thoroughly informed about the currently available evidence, including developmental factors.

[A case of malignant hyperthermia with evident symptoms in the postoperative period].

A 36-year-old man (185 cm tall, weighing 85 kg) was scheduled for fixation of a right carpal bone fracture. He had no operative history, and his preoperative laboratory data were normal. A laryngeal mask was inserted after intravenous propofol and fentanyl administration without a muscle relaxant. Anesthesia was maintained by sevoflurane in a mixture of air and oxygen. A tourniquet was placed on the right upper arm. One hour after the operation, his heart rate increased to 90-100 beats x min(-1) from 70-80 beats x min(-1) at the start of the operation, and tachycardic continued, even after release of the tourniquet. Although end-tidal CO2 was 50-60 mmHg, his body temperature remained 37.6 degrees C, and neither muscle stiffness nor brown urine was observed. The duration of the operation and the duration of anesthesia were 2 hours 40 min and 4 hours, respectively. The patient went back to the ward without myalgia after removal of the laryngeal mask. On the postoperative day one, the patient had brown urine. On the postoperative day 2, he experienced myalgia of the upper and lower extremities and masseter muscle. On the postoperative day 3, myoglobinuria was detected. As in this case, although evident symptoms of malignant hyperthermia are not always observed during operations, some cases show obvious symptoms during the postoperative period. Thus, it is important to be aware of the symptoms of malignant hyperthermia postoperatively for early diagnosis and treatment.

Intrathecally administered ropivacaine is less neurotoxic than procaine, bupivacaine, and levobupivacaine in a rat spinal model.

PURPOSE: The aim of this study was to compare the neurotoxicity of intrathecal procaine, bupivacaine, levobupivacaine, and ropivacaine in an animal model. METHODS: The study comprised two experiments. In the concentration experiment, rats (n = 78) were administered 0.12 µL·g(-1) body weight (BW) of 2% or 20% procaine, 0.5% or 5% bupivacaine, 0.5% or 5% levobupivacaine, or 0.5% or 5% ropivacaine. Based on the findings, the doses were increased by volume in the subsequent volume experiment using 0.12, 0.24, or 0.48 µL·g(-1) BW of 6% procaine, 6% levobupivacaine, or 6% ropivacaine (n = 79). Walking behaviour and sensory threshold were analyzed, and a histological examination of the spinal cord, posterior and anterior roots, and cauda equina was performed. RESULTS: The concentration experiment showed abnormalities only in the 5% bupivacaine group, and these abnormal findings were in the posterior root (PR) and posterior column (PC). The volume experiment revealed that procaine 0.24 µL·g(-1) was neurotoxic, mainly affecting the PR. At 0.48 µL·g(-1), severe injury was observed in the PR and PC in all six procaine rats and four of six levobupivacaine rats, while milder injury was limited to the PR in one of six ropivacaine rats, which differed significantly from the former two groups (P = 0.006 and P = 0.014, respectively). Electron microscopy showed axonal degeneration. CONCLUSION: All four local anesthetics seemed to cause identical neurotoxic lesions commencing in the PR and extending to the PC by axonal degeneration. Bupivacaine appeared to be the most neurotoxic of the four drugs, and the neurotoxicity at higher doses increased by volume with procaine > levobupivacaine > ropivacaine.

Neurotoxicity of intrathecally administered fentanyl in a rat spinal model.

OBJECTIVE: Intrathecally administered fentanyl rarely causes drug tolerance or formation of inflammatory masses and might therefore be a suitable treatment option for chronic pain. However, the neurotoxicity of intrathecally administered fentanyl remains to be clarified. We examined the histological changes, neurodysfunction, and side effects of intrathecal fentanyl in rats. DESIGN: The rats received fentanyl at 0.12 µL/g body weight (0, 50, 1000, 2000, and 5000 µg/mL in saline) via an intrathecal catheter. Seven days after the injection, the spinal cord with both roots were removed for histological examination. The neurological function was evaluated by monitoring walking behavior and latencies to radiant heat. Side effects were also recorded. RESULTS: No histological abnormalities were observed in the spinal cord, anterior and posterior roots, cauda equina nerves, or arachnoid membrane. Formation of white neomembrane was noted around the catheter in some animals, but there was no significant difference in the incidence among the groups. The sensory threshold was significantly higher at 1 and 2 hours after injection in the 50 and 5000 µg/mL groups, respectively. However, there was no significant difference in the sensory threshold among the five groups at 7 days postinjection. All of the rats walked normally within 4 hours even after injection of 5000 µg/mL fentanyl. The incidence of apnea, muscular rigidity, and bradycardia increased significantly at ≥ 1000 µg/mL dose. CONCLUSION: The side effects of intrathecally administered fentanyl were concentration-dependent, although no neuronal tissue damage, inflammation, or irreversible neurodysfunction were observed even at 5000 µg/mL.

[Case of anesthesia for laparoscopic cholecystectomy in a patient with a history of frequent anaphylaxis].

Idiopathic anaphylaxis is a rare disease that induces anaphylactic shock without extrinsic incentive. We had a patient with such frequent episodes undergoing laparoscopic cholecystectomy. Steroid was administered both at preoperative and intraoperative periods. Epidural anesthesia and general anesthesia by inhalation anesthesia, which are low risk for anaphylaxis, were used to reduce perioperative stress and restricted usage of drugs even in postoperative period. Consequently, we can safety manage anesthesia without episode of anaphylactic shock. To prepare for anaphylaxis we prepared usual therapeutic drugs for shock and measured serum tryptase, which has longer half-life than that of histamine.

[Increased dose of remifentanil caused difficult ventilation at emergence from general anesthesia].

Remifentanil induces a higher incidence of respiratory rigidity than other opioids, especially when it is given at bolus injection for anesthetic induction. A 71-year-old man underwent pharyngo-laryngeal surgery under general anesthesia with remifentanil and sevoflurane. At the end of surgery, the ventilation through a tracheal tube became difficult due to muscle rigidity simultaneously with the increased dose of remifentanil and the decreased sevoflurane concentration. It should be kept in mind that increased doses of remifentanil during as well as at the end of surgery cause difficult ventilation associated with muscle rigidity.

Vesicle disruption, plasma membrane bleb formation, and acute cell death caused by illumination with blue light in acridine orange-loaded malignant melanoma cells.

Acridine orange (AO), a weakly basic fluorescent dye, is permeable to plasma and vesicle membranes and preferentially remains in intracellular acidic regions. Using fluorescence microscopy, we observed dynamic changes in AO-loaded cultured malignant melanoma cells during illumination with blue light. Immediately after the start of the illumination, the successive disruption of vesicles was observed as a flash of fluorescence, and shortly after that, blebs were formed on the plasma membrane. These cells died within 5 min. Vesicle disruption was completely inhibited when cells were treated with the vacuolar H(+)-ATPase inhibitor bafilomycin A1 followed by loading with AO, but not when bafilomycin A1 was treated after AO loading. Thus, the filling of AO in the vesicle, which is driven by vacuolar H(+)-ATPase, is initially required for vesicle disruption. In contrast, bafilomycin A1 did not prevent plasma membrane blebbing, indicating that the blebs are formed independently of the vesicle disruption. Acute cell death was inhibited by treatment with bafilomycin A1 before but not after AO loading. Thus, AO- and blue light-induced acute cell death is associated with vesicle disruption rather than bleb formation. Both the vesicle disruption and the formation of plasma membrane blebs were inhibited by removal of oxygen from the cell environment and by singlet oxygen scavengers, sodium azide, ascorbic acid, and L-histidine, but not inhibited by the hydroxyl radical scavenger dimethyl thiourea. Acute cell death was also prevented by singlet oxygen scavengers but not by dimethyl thiourea. Thus, these phenomena are likely caused at least in part by the generation of singlet oxygen. The photosensitive features of plasma and vesicle membranes observed in the present study may be based on the use of the photodynamic effect, such as cancer therapy.

Neurotoxicity of intrathecally administered bupivacaine involves the posterior roots/posterior white matter and is milder than lidocaine in rats.

BACKGROUND AND OBJECTIVES: Clinical and laboratory studies suggest that lidocaine is more neurotoxic than bupivacaine. However, histological evidence of their comparative neurotoxicity is sparse. We thus pathologically and functionally compared the intrathecal neurotoxicity of these agents. METHODS: Rats received 0.12 microL/g body weight lidocaine (0%, 2%, 10%, or 20%) or bupivacaine (0%, 0.5%, 2.5%, or 5%) in distilled water via an intrathecal catheter. The influence of high osmolarity was also examined using 5% bupivacaine in 20% glucose solution (5% BG) and a control 25% glucose solution. The L3 spinal cord, the posterior and anterior roots, and the cauda equina were examined by light and electron microscopy. Walking behavior and sensory threshold were investigated as neurofunctional tests. RESULTS: The posterior root and posterior white matter showed axonal degeneration in rats treated with 10% and 20% lidocaine and 5% bupivacaine in distilled water (5% BDW) and in 5% BG, but not in rats treated with 2% lidocaine, 0.5% and 2.5% bupivacaine, distilled water, or 25% glucose solution. The histological damages were more severe in 20% lidocaine-treated rats than in 5% bupivacaine-treated rats. The damage of posterior white matter was observed only when the posterior root was severely injured. No significant difference of histological findings was observed between 5% BDW and 5% BG. Functional abnormalities were found only in rats treated with 20% lidocaine. CONCLUSIONS: The neurotoxic lesions caused by bupivacaine and lidocaine were indistinguishable in the primary site and the extending pattern, such as axonal degeneration originating from the posterior roots and extending to the posterior white matter. The intrathecal neurotoxicity is greater in lidocaine than in bupivacaine.

Effects of sodium bisulfite with or without procaine derivatives on axons of cultured mouse dorsal root ganglion neurons.

BACKGROUND AND OBJECTIVES: Sodium bisulfite (NaHSO3) was clinically used as a preservative agent for local anesthetics but was later suspected to be neurotoxic. However, recent studies reported that NaHSO3 reduces the neurotoxicity of local anesthetics. The purpose of this study was to examine the effects of NaHSO3 with and without procaine on axonal transport in cultured mouse dorsal root ganglion (DRG) neurons. METHODS: Experiment 1 served to determine the dose-dependent effects of NaHSO3 on axonal transport (DRG neurons were treated with 0.01, 0.1, 1, 10, or 20 mM of NaHSO3), whereas experiment 2 investigated the effect of 0.1 mM NaHSO3 on the action of local anesthetics on axonal transport (DRG neurons were treated with 1 mM procaine alone, or with 0.1 mM NaHSO3 plus 1 mM procaine). As an additional experiment, DRG neurons were also treated with 1 mM chloroprocaine alone, or with 0.1 mM NaHSO3 plus 1 mM chloroprocaine. In these experiments, we analyzed the percent change in the number of anterogradely and retrogradely transported organelles and recorded changes in neurite morphology using video-enhanced microscopy. RESULTS: In experiment 1, NaHSO3 at more than 1 mM caused cell membrane damage and complete inhibition of axonal transport, whereas 0.1 mM NaHSO3 maintained axonal transport at 40% to 60% of control with intact cell membrane. In experiment 2, 1 mM procaine alone maintained axonal transport at 90% to 100%. However, application of 1 mM procaine-0.1 mM NaHSO3 solution resulted in deformation of neurites and with complete cessation of axonal transport. Likewise, although 1 mM chloroprocaine maintain axonal transport at 80% to 100%, 1 mM chloroprocaine-0.1 mM NaHSO3 arrested axonal transport. CONCLUSIONS: NaHSO3 resulted in a dose-dependent damage to the cell membrane and axonal transport, especially when used in combination with procaine or chloroprocaine.

Safety and Efficacy of Continuous Epidural Anesthesia Following Scoliosis Surgery in Respiratory-Impaired Neuromuscular Children: A Pilot Study.

STUDY DESIGN: Retrospective comparative study. OBJECTIVE: To identify the usefulness of epidural anesthesia for postoperative pain without opioid in respiratory-impaired children with neuromuscular scoliosis. SUMMARY OF BACKGROUND DATA: Safety and adequate postoperative pain control is the most important concern in respiratory-impaired children. In general, after a massively invasive operation analgesia is performed with continuous intravenous infusion of opioid. However, the opioid side effect of respiratory depression could be critical for these patients. METHODS: The authors compared a group of 5 patients with continuous epidural anesthesia (Epi[+]) and a group of 5 patients without epidural anesthesia (Epi[-]). Spinal correction was performed under general anesthesia. At the end of surgery, for patients in the Epi[+] group, an epidural catheter was inserted by a surgeon. Nonsteroidal anti-inflammatory medication was prescribed regularly for postoperative pain; additional medications were permitted following the same protocol in both groups. Via the epidural catheter, 0.2% ropivacaine was continuously infused at 4 to 6ml/hour for 3 days. The researchers compared the numeric rating scale, the frequency of use of an additional painkiller, the day patients were able to leave the bed, and the duration of the hospital stay. RESULTS: The numeric rating scale in the Epi[+] group was significantly lower than in the Epi[-] group each day; the frequency of using an additional painkiller was also lower in the Epi[+] group than the Epi[-] group. In addition, the researchers could find no complications including respiratory depression related to epidural anesthesia. CONCLUSIONS: Continuous epidural anesthesia could be effective and safe in children with neuromuscular scoliosis. It could control postoperative pain from scoliosis surgery without opioids, which may cause pulmonary depression. This pilot study indicates the need for further investigations to confirm the potential benefits of this method.

Intrathecal mepivacaine and prilocaine are less neurotoxic than lidocaine in a rat intrathecal model.

BACKGROUND AND OBJECTIVES: Histologic evidence of the comparative neurotoxicity of lidocaine, mepivacaine, and prilocaine is incomplete. We compared the intrathecal neurotoxicity in rats among these 3 drugs based on morphologic and neurofunctional findings. METHODS: Rats (n=169) randomly received 0.12 microL/g of 0%, 2%, 5%, 7.5%, 10%, or 20% lidocaine, mepivacaine, or prilocaine or 25% glucose dissolved in distilled water via a chronically implanted intrathecal catheter. The effect of the agents on neurofunction was evaluated by movement of the hind limb (behavior test) and by sensory threshold (paw-stimulation test). The L1 spinal cord, the posterior and anterior roots, and the cauda equina were removed en bloc 5 days later and examined by light and electron microscopy. RESULTS: A significant decrease in sensory threshold or irreversible hind-limb limitation was observed only in rats receiving 20% lidocaine. Morphologic abnormalities characterized by axonal degeneration were observed in rats receiving > or =7.5% lidocaine, 20% mepivacaine, and 20% prilocaine, at the posterior white matter and the proximal portion of the posterior root just at the entrance into the spinal cord. The incidence of lesions was significantly higher in rats receiving lidocaine than mepivacaine and prilocaine. CONCLUSION: It is suggested that intrathecal mepivacaine and prilocaine are less neurotoxic than highly concentrated lidocaine in a rat intrathecal model.

Intrathecal lidocaine causes posterior root axonal degeneration near entry into the spinal cord in rats.

BACKGROUND AND OBJECTIVES: The neurotoxicity of lidocaine is not fully understood, and the primary lesion of lidocaine-induced spinal neurotoxicity has not been defined. Here we examine the effects of various concentrations of intrathecally administered lidocaine. METHODS: Forty-seven Wistar rats received 20%, 10%, 7.5%, 5%, 3%, or 0% lidocaine dissolved in distilled water, or 25% glucose solution via a chronically implanted intrathecal catheter. The spinal cord at L1, posterior and anterior roots, and cauda equina were dissected out 5 days later, sectioned, and prepared for light and electron microscopy. The effect of the agent on function was evaluated by movement of the hind limb (behavior test) and by sensory threshold (paw stimulation test). Another 7 rats were used to establish the precise locus of lesion within the posterior root after intrathecal 20% lidocaine injection. RESULTS: Rats treated with 10% or 20% lidocaine developed lesions both in the posterior roots and posterior columns, characterized by axonal degeneration. Rats injected with 7.5% lidocaine developed degenerative lesions limited to the posterior roots. Lesions in the posterior roots were localized to the proximal portion of the roots. Injections of 5% or less lidocaine did not cause any pathological changes. One of 5 rats receiving 20% lidocaine showed hind-limb paralysis for 4 days, but the remaining 4 rats recovered within 4 days after drug injection. Rats injected with < or = 10% lidocaine were completely recovered within 4 hours. The threshold for paw stimulation was significantly decreased in rats injected with 20% lidocaine. CONCLUSION: Our results suggest that spinal lidocaine neurotoxicity after supra-clinical concentrations of lidocaine is limited initially to the posterior roots at their entry to the spinal cord, and the extent and severity of the lesions are closely associated with lidocaine concentration. Unlike severe lesions in rats injected with 20% lidocaine, mild lesions caused by lower concentrations may not manifest neurofunctional deficits.

[Serum and urinary inorganic fluoride concentrations with renal and hepatic functions after repeated sevoflurane anesthesia].

The purpose of this study is to examine changes in serum and urinary inorganic fluoride (F) concentrations with their effects on renal and hepatic functions after repeated sevoflurane anesthesia with relatively short time interval. Eight patients received sevoflurane anesthesia twice within 7 days for gynecological surgery. Serum and urine F levels before induction, 0.5 and 1 hour after induction, and 0.5 hour after anesthesia were compared between first and second anesthesia. There were no significant differences in serum and urine F concentrations at the same point between first and second anesthesia. Two obese patients exhibited peak concentrations greater than 50 mumol.l-1 of F. Laboratory findings of renal function remained stable throughout 2 operations, whereas hepatic function deteriorated in the two obese patients after the first anesthesia, and resolved within 14 days after the second anesthesia. In conclusion, it is suggested that the second exposure to sevoflurane within 7 day interval does not alter the sevoflurane metabolism. However, obesity may contribute to a rise in serum inorganic fluoride after repeated sevoflurane anesthesia.

Neurotropin inhibits axonal transport in cultured mouse dorsal root ganglion neurons.

Axonal transport is a basic neuronal cell function and important for the supply of materials that maintain neuronal cells, and any increase or decrease in axonal transport expresses the state of neurons. Neurotropin is an analgesic agent commonly used for the treatment of chronic pain, but its mechanism of action remains not fully understood. The effects of neurotropin have been investigated in various animal models of nerve injury and chronic pain. In the present study, we dissected the effects of neurotropin on sensory neurons with a special focus on axonal transport using cultured mouse dorsal root ganglion (DRG) neurons. Movement of organelles in neurites was recorded by real-time video-enhanced microscopy. Neurotropin significantly reduced bidirectional axonal transport in time- and concentration-dependent manners without affecting the diameter of these neurites. This is the first report to show the inhibitory effect of neurotropin on axonal transport, and suggest that this action may mediate, at least in part, the analgesic effects of this agent.

Epinephrine administered with lidocaine solution does not worsen intrathecal lidocaine neurotoxicity in rats.

BACKGROUND: Epinephrine can potentially worsen the neurotoxic effects of local anesthetics when used for spinal or epidural anesthesia. The vasoconstrictive property of epinephrine reduces dural blood flow, which in turn reduces the clearance of local anesthetics from the subarachnoid space. This study examined the histological and neurofunctional effects of intrathecally administered lidocaine combined with epinephrine in rats. METHODS: Sixty-two rats were divided into 9 treatment groups: 5% or 7.5% lidocaine in 10% glucose solution with or without 0.1 or 0.5 mg/mL epinephrine, or epinephrine alone at 0.1 or 0.5 mg/mL in 10% glucose, or 10% glucose alone. Hind-limb motor function was evaluated immediately after drug injection by walking behavior. Sensory function was assessed by the response to radiant heat stimulation at just before and 1 week after the injection. Seven days after the injection, L3 spinal cord with anterior and posterior roots, the dorsal ganglion, and cauda equina were harvested and examined histologically. RESULTS: Histological lesions were limited to the posterior root just at entry into the spinal cord in rats injected with 7.5% lidocaine, with and without epinephrine. No histological abnormalities were noted in other areas or other groups. There was no significant change in sensory threshold in all groups. Significantly, prolongation of gait recovery time was noted in 5% and 7.5% lidocaine with epinephrine groups compared with 5% or 7.5% lidocaine alone. CONCLUSIONS: Intrathecal epinephrine prolonged the action of intrathecal lidocaine but did not worsen lidocaine-induced histological damage and functional impairment.