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Treatment of cancer pain is generally based on the three-step World Health Organization (WHO) pain relief ladder, which utilizes a sequential approach with drugs of increasing potency. Goals of pain management include optimization of analgesia, optimization of activities of daily living, minimization of adverse effects, and avoidance of aberrant drug taking. In addition, it is recommended that analgesic regimens are individualized and simplified to help ensure patient compliance and should provide the least invasive, easiest, and safest route of opioid administration to ensure adequate analgesia. Buprenorphine and fentanyl are two opioids available for the relief of moderate-to-severe cancer pain. Available clinical data regarding the transdermal (TD) formulations of these opioids and the extent to which they fulfill the recommendations mentioned earlier are systematically reviewed, with the aim of providing additional information for oncologists and pain specialists regarding their comparative use. Due to lack of studies directly comparing TD buprenorphine with TD fentanyl, data comparing these with other step-3 opioids are also evaluated in a network fashion., Video abstract

Except for neurotrophin, no drug had an indication for postherpetic neuralgia (PHN) in Japan prior to pregabalin approval. This approval might have changed PHN treatment patterns. This study aimed to compare PHN treatment patterns and medical costs between patients who started treatment before and after pregabalin approval. Japanese claims data were used to identify patients aged 18 years or more with PHN, postherpetic trigeminal neuralgia or postherpetic polyneuropathy who were initiated on their first PHN-associated prescription through May 2010 (before approval) or from June 2010 (after approval). From these claims, 6-month treatment patterns from first prescription were compared for the periods before and after approval. These patterns included pain-related medications and the frequency of pain-relief procedures. All-cause and pain-related medical costs were also compared for these periods. The number of PHN patients who were initiated on treatment before and after approval were 107 (mean age, 47.4 ± 13.0 years) and 505 (45.9 ± 13.0), respectively. Post-approval, significant reductions were observed for prescription of non-steroidal anti-inflammatory drugs, tricyclic antidepressants and neurotrophin relative to before approval. Excluding pregabalin acquisition costs, mean costs per patient for medications associated with PHN for 6 months from the first prescription were significantly lower after approval, ¥2882 vs ¥4185. Total medical costs were similar in both periods. Approval of pregabalin appeared to result in a treatment paradigm toward use of an approved therapy with demonstrated efficacy.

It is unknown whether flumazenil antagonizes the decrease in cerebral blood flow or the alteration in dynamic cerebral autoregulation induced by midazolam. We, therefore, investigated the effects on cerebral circulation of flumazenil administered after midazolam, to test our hypothesis that, along with complete reversal of sedation, flumazenil antagonizes the alterations in cerebral circulation induced by midazolam.Sixteen healthy young male subjects received midazolam followed by flumazenil. The modified Observer's Assessment of Alertness/Sedation (OAA/S) scale and bispectral index (BIS) were used to assess levels of sedation/awareness. For evaluation of cerebral circulation, steady-state mean cerebral blood flow velocity (MCBFV) was measured by transcranial Doppler ultrasonography. In addition, dynamic cerebral autoregulation was assessed by spectral and transfer function analysis between mean arterial pressure (MAP) variability and MCBFV variability.During midazolam sedation, defined by an OAA/S score of 3 (responds only after name is called loudly and/or repeatedly), BIS, steady-state MAP, steady-state CBFV, and transfer function gain decreased significantly compared with baseline. After flumazenil administration, an OAA/S score of 5 (responds readily to name spoken in a normal tone) was confirmed. Then, BIS and MAP returned to the same level as baseline. However, steady-state MCBFV showed a further significant decrease compared with that under midazolam sedation, and the decreased transfer function gain persisted.Contrary to our hypothesis, the present results suggest that despite complete antagonism of the sedative effects of midazolam, flumazenil would not reverse the alterations in cerebral circulation induced by midazolam.

BACKGROUND:In Japan, routine clinical care does not normally involve the use of a monitoring device to guide the administration of neuromuscular blocking drugs or their antagonists. Although most previous reports demonstrate that sugammadex offers more rapid and reliable antagonism from rocuronium-i

Introduction The mechanism of complex regional pain syndrome (CRPS) was reported as being related to both the central and peripheral nervous systems. Recurrence of CRPS was, reportedly, induced by hand surgery in a patient with upper limb CRPS. However, there is no documentation of mechanical allodynia and burning abdominal pain induced by Cesarean section under spinal anesthesia in patients with upper limb CRPS. Case We report the case of a patient who suffered from burning abdominal pain during Cesarean section under spinal anesthesia 13 years after the occurrence of venipuncture-induced CRPS of the upper arm. The patient's pain characteristics were similar to the pain characteristics of her right arm during her previous CRPS episode 13 years earlier. In addition, mechanical allodynia around the incision area was confirmed after surgery. We provided ultrasound-guided rectus sheath block using 20 mL of 0.4% ropivacaine under ultrasound guidance twice, which resulted in the disappearance of the spontaneous pain and allodynia. Discussion The pain relief was probably related to blockade of the peripheral input by this block, which in turn would have improved her central sensitization. Conclusion Our report shows that attention should be paid to the appearance of neuropathic pain of the abdomen during Cesarean section under spinal anesthesia in patients with a history of CRPS.

Two well-studied conditions of peripheral neuropathic pain are postherpetic neuralgia (PHN) and painful diabetic peripheral neuropathy (DPN). Several pregabalin trials for peripheral neuropathic pain have been conducted in the West, but limited data are available for Japan. As ethnicity may influence health risks, differences may be evident in safety data from pregabalin trials in Japan and in the West. The objectives of this review were to compare large pooled safety data from randomized controlled trials evaluating pregabalin for the treatment of PHN or DPN in the West with data from two (one PHN, N = 371; one DPN, N = 314) similar trials in Japan. Longer-term safety data from Japanese open-label extension studies were also reviewed in these neuropathic pain populations. Published and unpublished Pfizer-supported pregabalin trials were identified and sourced from internal Pfizer records. A PubMed search to check for inclusiveness was conducted on 2 November 2011 using the following criteria: 'diabetic peripheral neuropathy' OR 'postherpetic neuralgia' OR 'neuropathic pain' AND 'pregabalin', with limits set for clinical and randomized controlled trials published in English. Five PHN trials (N = 1250) and nine DPN trials (N = 2554) were identified as suitable for inclusion based on methodological comparability. Descriptive safety data from the original trials were reviewed and the most commonly reported adverse events (AEs; dizziness, somnolence, peripheral oedema and weight gain) were identified to be of primary interest. The majority of AEs were of mild to moderate severity in Japanese and Western populations. The most commonly reported AE data (all-causality) with pregabalin (regardless of dose) in Japan (dizziness: PHN = 31.1%; DPN = 24.6%, and somnolence: PHN = 28.6%; DPN = 25.7%) were compared with pooled data from the Western trials (dizziness: PHN = 24.9%; DPN = 23.0%, and somnolence: PHN = 15.1%; DPN = 13.4%). Further assessment of these pooled AE (all-causality) data showed that dizziness and somnolence appeared early in the course of pregabalin treatment, but resolved before the end of the treatment in the majority of PHN and DPN patients (maximum duration of trials was 13 weeks). The slightly higher incidence of dizziness and somnolence in the two Japanese trials than that seen in the Western trials may reflect an increased exposure to pregabalin per fixed dose due to the lower mean bodyweight of the Japanese versus Western populations (on a mg/kg basis). However, of the participants who experienced these AEs (all-causality), the proportion who withdrew from the trials in Japan (dizziness: PHN = 23.5%; DPN = 18.2%, and somnolence: PHN = 10.3%; DPN = 10.9%) were comparable with the proportion who withdrew from trials in the West (dizziness: PHN = 16.0%; DPN = 29.3%, and somnolence: PHN = 19.4%; DPN = 34.2%). In Japan, 12.5% (PHN) and 15.1% (DPN) of patients experienced peripheral oedema as an AE (all-causality) compared with 8.8% (PHN) and 10.3% (DPN) in the West. Weight gain as an AE (all-causality) was experienced in 11.7% (PHN) and 13.4% (DPN) of patients in Japan compared with 3.8% (PHN) and 7.0% (DPN) in the West, but stabilized with continued treatment. Despite the lower mean bodyweight in Japanese versus Western patients, the PHN and DPN patients in Japan had stable blood glucose and HbA(1c) levels throughout the trials. The results of this review indicate safety outcomes in pregabalin trials are comparable between patients in Japan and those in the West. While managing peripheral neuropathic pain with pregabalin treatment, all patients should be observed closely for the incidence of dizziness and somnolence, especially at the beginning of treatment. These patients should also be monitored for evidence of peripheral oedema and weight gain during stable treatment, regardless of the source of neuropathic pain.

Background Increasing age is associated with a longer duration of action of neuromuscular block. The aim of this study was to determine the influence of ageing on the recovery of the post-tetanic count (PTC) from rocuronium-induced neuromuscular block. Methods Twenty-two younger (20–60 years) and 22 older (> 70 years) patients were enrolled in this study. After induction of anaesthesia with fentanyl and propofol, all patients initially received 1 mg/kg rocuronium and neuromuscular block were evaluated by contractions of the adductor pollicis muscle to ulnar nerve train-of-four stimulation using an acceleromyograph. Subsequently, intense rocuronium-induced block was determined every 6 min using the PTC during 1.0–1.5% sevoflurane and remifentanil anaesthesia. When the first response to the PTC stimulus was detected, 0.2 mg/kg rocuronium was additionally administered, and again, spontaneous recovery of neuromuscular function was monitored until the first response to the PTC reappeared. Results Median values (range) of the times from the administration of 1 mg/kg and 0.2 mg/kg rocuronium until recovery of the first detectable PTC were significantly longer in the older [51.0 (27–100) min, P

We report a patient with myotonic dystrophy who showed prolonged rocuronium-induced neuromuscular blockade, although with a fast recovery with sugammadex. During general anesthesia with propofol and remifentanil, the times to spontaneous recovery of the first twitch (T1) of train of four to 10% of control values after an intubating dose of rocuronium 1 mg/kg and an additional dose of 0.2 mg/kg were 112 min and 62 min, respectively. Despite the high sensitivity to rocuronium, sugammadex 2 mg/kg administered at a T1 of 10% safely and effectively antagonized rocuronium-induced neuromuscular block in 90 s.

Background The aim of this study was to evaluate the correlation between cardiac output (CO) and reversibility of rocuronium-induced moderate neuromuscular block with sugammadex in elderly patients. Methods Fifty elderly (≥ 65 years) patients were enrolled in this study. During 1.0–1.5% end-tidal sevoflurane and remifentanil anaesthesia, contraction of the adductor pollicis muscle in response to ulnar nerve stimulation was acceleromyographically quantified. All patients initially received 1 mg/kg rocuronium followed by 0.2 mg/kg whenever the second twitch T2 of the train-of-four (TOF) response reappeared. CO was measured throughout the study using a FloTrac™/Vigileo™ monitor. After completion of surgery and at the reappearance of T2, the time required for a bolus dose of 2 mg/kg sugammadex to facilitate recovery to a TOF ratio of 0.9 was recorded, and its correlation with CO was analysed. Results Adequate recovery of neuromuscular block was achieved after sugammadex in all patients. Mean CO at the time of reversal with sugammadex was 5.3 l/min (1.3), and recovery time to a TOF ratio of 0.9 was 173.4 s (54.8). A statistically significant inverse correlation was seen between the time to recovery to a TOF ratio of 0.9 and CO [reversal time (s) = −27.7·CO + 298.7, R2 = 0.461, P

To describe a case of complete neurological recovery from cauda equina syndrome lasting ten months following spinal anesthesia with 0.5% hyperbaric bupivacaine and epidural anesthesia with ropivacaine, and to discuss the possible mechanisms involved.A 79-yr-old man with Paget's disease was scheduled for surgery to remove a skin tumour below his scrotum. He had no history of radicular pain or back pain and no pre-existing neurologic disorder. Surgery was performed with the patient in the supine position. He received 0.5% hyperbaric bupivacaine intrathecally for the procedure and ropivacaine through an epidural catheter for postoperative pain management. After catheter removal, the patient developed urinary retention, fecal incontinence, and perianal hypoesthesia. A lumbosacral magnetic resonance imaging (MRI) revealed no tumour, infarction, degeneration, spinal stenosis, or compression on the cauda equina nerve roots. A diagnosis of cauda equina syndrome was made, and the etiology was thought to be toxicity of bupivacaine either alone or in combination with ropivacaine. After three months, the patient reported some return of sensation at the perianal area, with complete resolution at four months. At the ten-month follow-up visit, the patient had recovered from his urinary retention and fecal incontinence.This case suggests that spinal anesthesia, even with an ordinary dose of hyperbaric 0.5% bupivacaine, might induce cauda equina syndrome in older patients.

The aim of this study was to investigate whether monitoring neuromuscular block at the masseter muscle (MM) would allow faster tracheal intubation when compared with that at the adductor pollicis muscle (APM).Twenty female patients undergoing gynecological surgery were enrolled into this study. Immediately after inducing anesthesia with fentanyl and propofol, both the left masseter and ulnar nerves were stimulated in a 2 Hz train-of-four (TOF) mode using peripheral nerve stimulators. Contractions of the MM were felt with the anesthesiologist's left hand lifting the patient's jaw and holding an anesthesia facemask, while those of the APM were visually observed. Immediately after the contracting responses of the muscles were confirmed, all of the patients received an iv bolus of vecuronium 0.1 mg kg(-1). Onset times after vecuronium were defined as the duration until the contractions became impalpable at the MM or invisible at the APM. When the contraction of the MM could no longer be felt, the conditions for laryngoscopy and tracheal intubation were assessed.Onset time evaluated tactually at the MM (mean +/- SD, 108.4 +/- 27.7 s) was significantly shorter than that evaluated visually at the APM (181.2 +/- 32.1 s, P0.0001). The intubating conditions for all patients were graded as either excellent or good.Tactual evaluation of muscle paralysis of the MM during induction of anesthesia is clinically useful since it leads to faster tracheal intubation.

Background Dexmedetomidine, which is often used in intensive care units in patients with compromised circulation, might induce further severe decreases in cerebral blood flow (CBF) with temporal decreases in arterial pressure induced by various stimuli if dynamic cerebral autoregulation is not improved. Therefore, the authors hypothesized that dexmedetomidine strengthens dynamic cerebral autoregulation. Methods Fourteen healthy male subjects received placebo, low-dose dexmedetomidine (loading, 3 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.2 microg x kg(-1) x h(-1) for 60 min), and high-dose dexmedetomidine (loading, 6 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.4 microg x kg(-1) x h(-1) for 60 min) infusions in a randomized, double-blind, crossover study. After 70 min of drug administration, dynamic cerebral autoregulation was estimated by transfer function analysis between arterial pressure variability and CBF velocity variability, and the thigh cuff method. Results Compared with placebo, steady state CBF velocity and mean blood pressure significantly decreased during administration of dexmedetomidine. Transfer function gain in the very-low-frequency range increased and phase in the low-frequency range decreased significantly, suggesting alterations in dynamic cerebral autoregulation in lower frequency ranges. Moreover, the dynamic rate of regulation and percentage restoration in CBF velocity significantly decreased when a temporal decrease in arterial pressure was induced by thigh cuff release. Conclusion Contrary to the authors' hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.

A novel transdermal matrix patch delivery system for fentanyl has been developed to deliver improved management of cancer pain compared with that obtained using current fentanyl reservoir patches. This study was carried out to assess the efficacy, safety and pharmacokinetic profiles of a 12.5 microg/h transdermal matrix fentanyl patch administered with the objective of replacing morphine, oral oxycodone or fentanyl injection formulations. The study also evaluated how the pharmacokinetic profiles of higher dose fentanyl patches (25, 37.5 and 50 microg/h) changed following dose adjustments to optimize management of cancer pain.This open-label, multicentre study involved 87 patients of both sexes (or =20 years) with a confirmed diagnosis of cancer. Patients were receiving any one of the following at the time of enrollment for the management of their cancer pain: (a) morphine45 mg/day orally,30 mg/day as suppositories, or15 mg/day by injection; (b) oral oxycodone30 mg/day; or (c) fentanyl injectable preparations0.3 mg/day. The patients were administered a 3-day course of fentanyl transdermal matrix patch application three times. The initial dose was 12.5 microg/h, which could be increased when a new patch was applied if the physician deemed this to be appropriate based on pain intensity ratings and use of rescue medications. Efficacy outcomes included patients' global assessment scores (primary efficacy endpoint) measured on a five-step scale and dichotomous scores for physicians' global assessment. The occurrence of adverse events and changes in laboratory tests were evaluated as safety variables. Serum fentanyl levels were measured immediately after removal of the old patch on days 4, 7 and 10 to obtain data on trough serum concentrations.The percentage of patients in category 3 or higher (very satisfied, satisfied, or neither satisfied nor dissatisfied) for the patient's global assessment score was 89.4% (76/85), indicating high patient satisfaction and attainment of sufficient pain control after patients switched from their previously used opioid analgesics. Similar findings were obtained on physicians' global assessment scores. A total of 316 adverse events occurred in 78 (90.7%) of 86 patients who were administered at least one patch. These included nausea (31 [36.0%]), somnolence (26 [30.2%]), vomiting (22 [25.6%]), diarrhoea (17 [19.8%]), constipation (14 [16.3%]), pyrexia (11 [12.8%]) and insomnia (9 [10.5%]). The mean (+/- SD) serum fentanyl concentration determined on day 4 was 169.9 +/- 103.4 pg/mL (n = 83). Serum fentanyl measurement results indicated that the same fentanyl patch dose resulted in similar serum fentanyl levels, while increased doses produced higher serum fentanyl concentrations.The fentanyl matrix transdermal patch formulation employed in this study demonstrated sufficient cancer pain control for patients switching from morphine or oral oxycodone preparations. The patch tested was well tolerated and its use did not result in any increased incidence of adverse drug reactions over those commonly found with opioid analgesics.

Study Objective To evaluate the different effects on autonomic circulatory control during volatile induction/maintenance of anesthesia (VIMA) vs total intravenous anesthesia (TIVA). Design Prospective study. Setting Operating theater of a university hospital. Patients Twenty patients, with American Society of Anesthesiologists physical status of I or II, were randomly allocated into the VIMA group (n = 10) or the TIVA group (n = 10). Interventions In the VIMA group, anesthesia was induced with 5% sevoflurane and 60% N 2 O in oxygen and maintained with 2% sevoflurane and 60% N 2 O in oxygen. In the TIVA group, anesthesia was induced with propofol 2.0 mg/kg intravenously by bolus injection and fentanyl 2 μg/kg, and maintained with an intravenous infusion of propofol 5 mg/kg·per hour and air-oxygen mixture. Measurements Monitoring included recordings of electrocardiographic and arterial blood pressure waveforms. Autonomic nervous activity and arterial cardiac baroreflex function were evaluated by analysis of blood pressure variability, heart rate variability, and transfer function analysis between these 2 variables. Main Results In the VIMA group, the low-frequency component of blood pressure variability (LF SBP ) and low- and high-frequency components of the R-R interval variability (LF RR and HF RR ) decreased significantly during anesthesia. In the TIVA group, LF SBP and LF RR decreased significantly. The degree of reduction in LF SBP was greater in the VIMA group than in the TIVA group. However, changes in R-R interval variability and cardiac baroreflex indices were not significantly different between the 2 groups. Conclusions Our results demonstrated that although reductions in autonomic nervous modulation to the heart might not be so different between the 2 groups, reduction in sympathetic nervous modulation to peripheral vasculature is greater in the VIMA group than in the TIVA group.

The aim of the present study was to clarify the neurophysiological changes associated with analgesic and behavioral effects of low-dose ketamine HCl in patients suffering from chronic neuropathic pain. Ten in-patients with neuropathic pain participated in this single-blind, placebo-controlled study after giving written informed consent. Following intravenous injections of a saline solution (placebo), three bolus injections of 5 mg ketamine HCl were administered at 5 min intervals. Changes in pain perception were assessed using a numerical rating scale for pain. Behavioral changes, including psychotomimetic effects, were assessed using the Brief Psychiatric Rating Scale (BPRS). Electroencephalograms (EEG) and electrooculograms (EOG) were recorded continuously throughout the testing period. One minute EEG and closed-eye eye movements were quantified. The effects of ketamine were evaluated by comparing the neurophysiological and behavioral parameters obtained from the placebo and ketamine trials. Pain reduction was significantly correlated with ketamine-induced changes in hallucinatory behavior and excitement as measured by the BPRS. Ketamine injections caused a significant decrease in the EEGα amplitude without an accompanying reduction in EEG frequency. The EEGα amplitude reduction at the right central electrode was significantly related to subjective pain relief. Subanesthetic doses of ketamine significantly decreased rapid eye movements, but did not initiate slow eye movements. In conclusion, the present EEG-EOG/behavioral results indicate that ketamine-induced failure of neural integration between cortical–subcortical regions induces psychotic symptoms and alters pain perception on neuropathic pain.

Background: During partial neuromuscular blockade indirect repetitive nerve stimulation causes fade in the response of the muscle. We studied the intensity of the fade induced by intravenous administration of three steroidal muscle relaxants, and investigated the mechanism of fade by comparing with results obtained during partial blockade with animal toxins and vesamicol. Methods: In 60 cats, we measured the fade in the compound action potentials of the gastrocnemius muscle evoked by repetitive sciatic nerve stimulation at 100 Hz during partial neuromuscular blockade with rocuronium, vecuronium, pancuronium, α-bungarotoxin, μ-conotoxin and vesamicol, respectively. Results: Profound fade was induced by all three non-depolarising muscle relaxants (rocuronium=vecuronium

平成元年1月から平成6年5月までに,静脈注射や採血時などに注射針による神経損傷が原因で発生したと考えられる疼痛および知覚障害を主訴として当院ペインクリニック科を受診した患者6例について調査,検討した.穿刺部位では手関節橈側,肘関節屈側,示指部であった.症状としては火傷様疼痛,しびれ,冷感などを訴えhypesthesia, allodyniaなどの知覚障害が認められた.神経損傷によるinjury dischargeや炎症による侵害刺激伝播を抑制するため,損傷部への局所麻酔薬浸潤や抗炎症薬が有用であった.医療従事者へ対する患者の不満も痛みを長引かせる重要な因子であり,発生直後からの適切な対処が必要であると思われた.

Objective. The purpose of this study was to determine the incidence and prognosis of persistent and neuropathic pain induced by venipuncture for blood sampling in clinical practice. Design & Setting. We investigated the incidence of persistent and neuropathic pain after venipuncture for blood sampling and evaluated the prognosis of patients with neuropathic pain at Nihon University Itabashi Hospital, Japan, based on an observational study. Subjects. Outpatients who required venipuncture for blood sampling at the laboratory room of Nihon University Itabashi Hospital between 2004 and 2008 were included as study subjects. Results. In the present study, of the 587,551 venipunctures performed at our hospital between 2004 and 2008, the incidences of persistent and neuropathic pain after venipuncture were 1 in every 4,418 venipunctures (133/587,551) and 1 in every 30,923 venipunctures (19/587,551), respectively. All the 19 patients who were identified as having neuropathic pain recovered completely. Conclusions. We demonstrated that the incidence of persistent pain after venipuncture for blood sampling is low and that its prognosis is good.

We used near-infrared spectroscopy (NIRS) to evaluate cerebral blood oxygenation changes in subjects undergoing cesarean section under spinal anesthesia (SP) with hyperbaric bupivacaine (group H, 27 subjects) or isobaric bupivacaine (group I, 15 subjects). In group H, total-Hb, oxy-Hb, and mean blood pressure (MBP) within 20 min after SP were significantly lower than the baseline values. In contrast, there was no significant change from baseline in total-Hb, oxy-Hb, or MBP in group I after SP. Total-Hb and MBP in group H were significantly lower than those in group I within 10 min after SP. There was no significant change of deoxy-Hb, tissue oxygen index, or heart rate from baseline in either of the groups. These results suggest that isobaric bupivacaine may be superior to hyperbaric bupivacaine for preventing a decrease of maternal cerebral blood flow after SP for cesarean section.

The twitch responses evoked from the abductor hallucis muscle (AHM) and the adductor pollicis muscle (APM) were examined simultaneously in 20 anesthetized patients following a single bolus intravenous administration of 0.04 mg·kg−1 of vecuronium bromide. The mean onset time of vecuronium-induced depression of AHM twitch responses was significantly slower than that of APM twitch responses (4.9±1.5 minvs 3.7±1.2 min, mean±SD,P

The α(2)-adrenergic receptor agonist dexmedetomidine reportedly weakens heart rate (HR) responses to 'rapid' (during a few seconds) reduction in arterial pressure, but does not affect HR responses to 'gradual' (during 60 s) reduction in arterial pressure. As the speed of neurotransmission along the parasympathetic nerve is relatively rapid, alteration of parasympathetic-mediated arterial-cardiac baroreflex function plays a more important role in HR responses to 'rapid' changes in arterial pressure. We therefore hypothesized that dexmedetomidine attenuates parasympathetic-mediated arterial-cardiac baroreflex function.Twelve healthy men received placebo, low-dose (loading, 3 μg/kg/h for 10 min; maintenance, 0.2 μg/kg/h for 60 min) (low-DEX), or moderate-dose (loading, 6 μg/kg/h for 10 min; maintenance, 0.4 μg/kg/h for 60 min) (moderate-DEX) dexmedetomidine infusions in a randomized, double-blind, crossover study. Before and after 70 min of infusion, arterial-cardiac baroreflex function was assessed by spectral and transfer function analysis between arterial pressure variability and HR variability.The high-frequency power of systolic arterial pressure (SAP) variability increased significantly with low-DEX and moderate-DEX infusions (significant interaction effects, P = 0.005), whereas the high-frequency power of R-wave-R-wave interval (RRI) variability (as an index of cardiac parasympathetic activity) did not change significantly at any dose infusions. Then, transfer function gain in the high-frequency range (as an index of parasympathetic arterial-cardiac baroreflex) decreased significantly with low-DEX and moderate-DEX infusions (significant interaction effects, P = 0.007).The present results suggest that dexmedetomidine attenuates parasympathetic-mediated arterial-cardiac baroreflex function, implying weakened HR response to 'rapid' reduction in arterial pressure.

The main aim of this study was to compare the onset times of rocuronium evaluated subjectively and by acceleromyography at the masseter muscle (MM). Forty female patients were sequentially enrolled in this study. In the first 20 patients, neuromuscular block was evaluated subjectively. After induction of anesthesia with fentanyl and propofol, both the left masseter and ulnar nerves were stimulated in 2-Hz train-of-four (TOF) mode using peripheral nerve stimulators. Contractions of the MM were felt with an anesthesiologist’s left hand holding an anesthesia facemask; those of the adductor pollicis (APM) were visually observed. All the patients received a bolus of rocuronium, 0.6 mg/kg. Onset times after rocuronium were defined as the duration until the contractions became impalpable at the MM or invisible at the APM. At the time contraction of the MM had not been felt, intubating conditions were assessed. In the next 20 patients, contractions of the MM and the APM were concurrently quantified using acceleromyography after induction of anesthesia and laryngeal mask insertion. Following 0.6 mg/kg rocuronium, onset of the action was recorded. Onset of the action of rocuronium at the MM evaluated subjectively [mean (SD), 70.3 (17.7) s] was similar to that monitored acceleromyographically [73.3 (27.6) s, P > 0.05], and significantly shorter than that at the APM acceleromyographically [111.0 (34.8) s, P = 0.016]. Intubating conditions of 20 patients were graded either excellent or good. Subjective evaluation of contractions of the MM by an anesthesiologist’s hand may be reliable to determine faster timing for safe tracheal intubation.

Background Although midazolam and propofol reduce cerebral blood flow (CBF) similarly, they generate different effects on the autonomic nervous system and endothelium-induced relaxation. Midazolam induces sympathetic dominance, whereas propofol induces parasympathetic dominance. Midazolam has no effect on endothelium-dependent relaxation, whereas propofol suppresses endothelium-dependent relaxation. Moreover, midazolam apparently constricts cerebral arterioles. We therefore hypothesized that midazolam and propofol have different effects on dynamic cerebral autoregulation. Methods Ten healthy male subjects received midazolam, propofol, and placebo administrations in a randomized, single-blind, crossover study. The modified Observer's Assessment of Alertness/Sedation scale was used to assess sedation depth. After reaching a target depth of sedation (Observer's Assessment of Alertness/Sedation scale score 3, responds only after name is called loudly and/or repeatedly) or after 15 minutes of normal saline administration as placebo, dynamic cerebral autoregulation was evaluated by spectral and transfer function analyses between mean arterial blood pressure variability in the radial artery measured by tonometry, and CBF velocity variability in the middle cerebral artery measured by transcranial Doppler ultrasonography. Results Steady-state CBF velocity decreased significantly with midazolam and propofol administration (significant interaction effects, P = 0.024). However, transfer function gain in the low-frequency range decreased significantly only with midazolam administration (significant interaction effects, P = 0.015), suggesting a reduced magnitude of transfer from mean arterial blood pressure oscillations to CBF fluctuations during midazolam sedation. Conclusion Our results suggest that midazolam and propofol sedation have different effects on dynamic cerebral autoregulation despite causing equivalent decreases in steady-state CBF velocity. Only midazolam sedation is likely to improve dynamic cerebral autoregulation.

The main purpose of this study was to examine the effectiveness of the timing principle with 1 mg kg(-1) rocuronium for rapid sequence intubation. As secondary outcomes, propofol and lidocaine with or without remifentanil were examined to note their effects on the cardiovascular responses to laryngoscopy and intubation.Thirty patients were randomly allocated to one of two groups of 15 patients each: a lidocaine-treated group (L) and a lidocaine/remifentanil-treated group (LR). Thirty seconds after lidocaine 1 mg kg(-1) with or without infusion of remifentanil 1 microg kg(-1) min(-1), all patients received a bolus of rocuronium 1 mg kg(-1). Shortly afterwards, patients were given propofol 2-2.5 mg kg(-1). Intubating conditions and cardiovascular responses were observed 60 s after rocuronium. The time to spontaneous recovery of visible train-of-four (TOF) counts of 4 was observed at the thumb during 1.0-1.5% end-tidal sevoflurane and remifentanil anesthesia.All patients had excellent or good intubating conditions. Hypertension and tachycardia during laryngoscopy were well prevented in group LR, whereas they were significantly observed in group L. The times to reappearance of TOF counts of 4 were comparable in all groups [mean (SD); 63.6 (8.6) min in group L and 63.5 (11.6) min in group LR].Application of the timing principle with 1 mg kg(-1) rocuronium is beneficial for rapid tracheal intubation. Co-administered lidocaine, remifentanil and propofol can definitely suppress cardiovascular responses during laryngoscopy and intubation.

Introduction: During and immediately following a 2-wk spaceflight, dynamic cerebral autoregulation is improved, leading to stable cerebral blood flow velocity (CBFV). However, the factors inducing this improved cerebral autoregulation remain unclear. Although mild reduction of plasma volume (one of the key adaptations to spaceflight) may lead to improved cerebral autoregulation, there have been no reports estimating the alteration of dynamic cerebral autoregulation during mild dehydration. We, therefore, investigated the effect of mild intravascular dehydration on dynamic cerebral autoregulation. Methods: Furosemide, 0.2 mg · kg ―1 , was administered to 14 men. Dynamic cerebral autoregulation was estimated before and approximately 45 min after furosemide administration using spectral and transfer function analyses between mean blood pressure (MBP) variability and mean CBFV variability. We then assessed the degree of dehydration as plasma volume changes, and/or central venous pressure (CVP). Results: Furosemide administration caused an approximate 10% reduction in plasma volume, with CVP decreasing by 1.2 mmHg. Steady state MBP and mean CBFV did not change. However, transfer function gain in the low-frequency range significantly decreased, implying a decrease in the magnitude of transfer from MBP oscillations to mean CBFV fluctuations. Discussion: The present degree of dehydration was similar to the alteration observed after short-term spaceflight, and enhanced dynamic cerebral autoregulation in the low-frequency range with unchanged steady state mean CBFV. Consequently, these results on cerebral circulation were consistent with those of a previous spaceflight study. Thus, it is suggested that mild intravascular dehydration partly explains the improved dynamic cerebral autoregulation observed during and immediately after spaceflight.

Two patients with spinocerebellar ataxia received epidural analgesia with no exacerbation of their symptoms. The patients developed transient, but extremely severe, low back pain as a result of the epidural analgesia.

The aim of this study was to examine the effect of landiolol hydrochloride, an ultrashort-acting beta(1)-blocker, on suxamethonium-induced neuromuscular block.Thirty patients were randomly allocated to receive a loading dose of landiolol, 0.125 mg x kg(-1) x min(-1) for 1 min, followed by an infusion at 0.04 mg x kg(-1) x min(-1), or placebo. Twenty minutes after the infusion of landiolol or placebo, suxamethonium 1 mg x kg(-1) was administered during propofolfentanyl-nitrous oxide anesthesia. Neuromuscular block was monitored by train-of-four (TOF) responses of the adductor pollicis muscle, applying acceleromyographic stimuli to the ulnar nerve.The onset of neuromuscular block did not differ between the groups. The time from administration of suxamethonium to spontaneous recovery to the first twitch of TOF (T1) of control was significantly longer in the landiolol group (mean [SD]; 12.2 [2.5] min), when compared with the control group (9.8 [2.6] min). However, the TOF ratios measured when the T1 had spontaneously recovered to 10%, 25%, 50%, 75%, 90%, and 100% of control was comparable between the groups.Landiolol delayed recovery from suxamethonium-induced paralysis. However, the interaction between the drugs seemed to be small in the clinical setting.

Frequent changes in the perioperative central blood volume could affect cerebral autoregulation through alterations in sympathetic nerve activity, cardiac output, blood viscosity, and cerebral vasomotor tone. However, the effect of dynamic cerebral autoregulation has not been studied during acute wide-ranging changes in central blood volume, especially with respect to central hypervolemia with hemodilution.We evaluated dynamic cerebral autoregulation during central hypovolemia and central hypervolemia with hemodilution using spectral and transfer function analysis between mean arterial blood pressure (MBP) and cerebral blood flow (CBF) velocity variability in 12 individuals. Rapid changes in central blood volume were achieved using two levels of lower body negative pressure (-15 and -30 mm Hg) and two discrete infusions of normal saline (15 mL/kg and total 30 mL/kg). We then estimated changes in central blood volume as central venous pressure (CVP) and/or cardiac output using impedance cardiography.Steady-state CBF velocity and cardiac output decreased at -30 mm Hg lower body negative pressure (changes of CVP approximately -4 mm Hg) or were increased by each saline infusion (changes of CVP 4-6 mm Hg), without a significant change in MBP. However, transfer function gain (magnitude of transfer) between MBP and CBF velocity variability significantly increased only after saline infusion, suggesting an increased magnitude of transfer from MBP oscillations to CBF fluctuations during central hypervolemia with hemodilution.Our results suggest that, although steady-state CBF velocity changes under both central hypervolemia and hypovolemia, only hypervolemic hemodilution impairs dynamic cerebral autoregulation.

BACKGROUND: Although intrathecal midazolam has been reported to produce antinociceptive effects mediated by -aminobutyric acid type A-benzodiazepine receptor complexes in the spinal cord, the effects of systemic midazolam on nociception remain unclear. We performed this study to examine the effects of IV-administered midazolam on somatosympathetic A and C reflex discharges in brain-intact cats and decerebrate cats (with transection at midbrain level). METHODS: Somatosympathetic A and C reflexes were elicited in the inferior cardiac sympathetic nerve by electrical stimulation of myelinated (A) and unmyelinated (C) afferent fibers of the superficial peroneal nerve in 28 mature cats. After control somatosympathetic reflex responses were obtained, midazolam was administered IV to four groups of randomly allocated cats as follows: brain-intact cats at a dose of 0.03 mg/kg, brain-intact cats at a dose of 0.1 mg/kg, brain-intact cats at a dose of 0.5 mg/kg, and decerebrate cats at a dose of 0.1 mg/kg. RESULTS: C reflex discharges were significantly augmented at the dose of 0.03 mg/kg and significantly depressed at the dose of 0.1 and 0.5 mg/kg in brain-intact cats. C reflex discharges were also significantly depressed at the dose of 0.1 mg/kg in decerebrate cats. CONCLUSIONS: We have demonstrated that IV midazolam produces dose-related effects on somatosympathetic reflex discharges. The clinical implication of these findings is that the effect of midazolam on nociception depends on its dosage. It also appears that the infra-midbrain region plays a major role in mediating the depressive effects of midazolam on somatosympathetic C reflex discharges. (Anesth Analg 2007;105:832‐7)

A surgical patient with ventricular septal rupture after acute myocardial infarction is presented. The primary concern of general anesthesia was in the maintenance of systemic arterial pressure and reduction of afterload. General anesthesia was induced with a combination of fentanyl, ketamine, and propofol, which successfully suppressed fluctuations of hemodynamic variables associated with induction of anesthesia and tracheal intubation. Intravenous milrinone was used for inotropic support and reduction of systemic vascular resistance. The ventricular septal rupture was successfully repaired.

Sevoflurane reduces autonomic neural control, which plays a significant role in cerebral autoregulation. Therefore, we hypothesized that sevoflurane influences cerebral autoregulation. We investigated the effects of sevoflurane on dynamic cerebral blood flow (CBF) autoregulation by using spectral and transfer function analysis between blood pressure variability and CBF velocity variability. Eleven healthy male subjects received 0.5%, 1.0%, and 1.5% sevoflurane via facemask. Dynamic cerebral autoregulation was evaluated by transfer function gain, phase, and coherence between CBF velocity in the middle cerebral artery measured by transcranial Doppler, and blood pressure in the radial artery. Coherence in the very low-frequency range (0.02-0.07 Hz) increased above 0.5 during administration of 0.5% and 1.0% sevoflurane. Transfer function gain in this frequency range (0.02-0.07 Hz), as an index of dynamic cerebral autoregulation, increased significantly with 0.5% and 1.0% sevoflurane. Transfer function gain and coherence in the low- and high-frequency ranges, however, remained unchanged during administration of sevoflurane. These results suggest that sevoflurane impairs dynamic cerebral autoregulation in the very-low-frequency range even with small concentrations, whereas dynamic cerebral autoregulation in the low- and high-frequency ranges remained unchanged.

IT is well known that phantom limb pain can reappear or be exacerbated transiently during spinal anesthesia in amputees. 1 However, to the best of our knowledge, the reappearance of phantom limb pain immediately after nonamputation surgery in an amputee has not been reported. We herein present a patient with chief complaint of reactivation of phantom limb pain the day immediately after cervical myelopathy surgery.

We report a case of recurrent ST-segment elevations totaling 7 times over 3 hours during subtotal gastrectomy and the early postoperative period in a patient with no history of coronary artery disease. Possible contributing factors include cold stimulus, epidural anesthesia, and inadequate depth of anesthesia. The first episode almost resulted in cardiac arrest and was treated with intravenous epinephrine. The second episode was associated with ventricular fibrillation, which was treated with defibrillation and intravenous verapamil. The third to the seventh episodes were successfully treated with intravenous nitrate. The electrocardiographic changes and postoperative coronary angiography were consistent with a clinical diagnosis of coronary artery spasm. This case suggests that coronary artery spasm is capable of occurring repeatedly in a cyclic pattern during perioperative periods.

The purpose of this study was to clarify the relationship between skin temperature over the thenar muscles and the duration of action of vecuronium measured acceleromyographically at the thumb in anesthetized patients.In 15 patients undergoing elective open abdominal surgery under propofol, fentanyl, and nitrous oxide anesthesia, train-of-four (TOF) stimuli were delivered over the ulnar nerve at 2 Hz every 15 s, and the degree of neuromuscular block was measured acceleromyographically at the thumb. Each patient received an intubating dose of vecuronium 0.1 mg x kg(-1), followed by maintenance doses of 0.02 mg x kg(-1) administered repeatedly whenever the first twitch of TOF responses had recovered to 25% of control. The interval between maintenance doses was defined as the clinical duration (DUR25). The median values of skin temperature (ST) over the ipsilateral thenar muscles and esophageal temperature (ET) were recorded during the action of the first and all subsequent maintenance doses. The relationships between change in temperature and change in DUR25 were analyzed.Whereas ET showed only minor changes (median, -0.3 degrees C), ST fluctuated markedly between +0.9 degrees and -6.3 degrees C (median, -1.4 degrees C). Increase and decrease were also seen in a series of DUR25s, as expected from the changes in ST. The median values of DUR25 produced by the first and last maintenance vecuronium doses were 21.5 and 32.3 min, respectively. A negative linear correlation was found between the change in DUR25 and that in ST, demonstrating that DUR25 increased by 20% of baseline with each 1 degrees C decrease in ST.Our results show that peripheral ST decreases considerably during open abdominal surgery without reduction in core temperature, and the decrease contributes to the potentiation of neuromuscular block in the periphery during propofol, fentanyl, and nitrous oxide anesthesia.

To the Editor: During ultrasound-guided nerve blocks, physicians generally hold the ultrasound transducer in one hand while inserting the nerve block needle with the other. However, since it is sometimes difficult for the anesthesiologist to single-handedly manipulate the ultrasonographic transducer for simultaneous visualization of the nerve and the tip of the needle, anesthesiologists who perform ultrasound-guided nerve blocks usually require an assistant for local anesthetic injection and catheter insertion. A guideline for ultrasound-guided nerve blocks, jointly published by the American Society of Regional Anesthesia (ASRA) and European Society of Regional Anesthesia (ESRA) in 2009 [1], points out that for safety purposes, continuous visualization of the needle tip during advancement is important. On the other hand, Site et al. [2] reported that visualization of the needle tip is not easy. Several ultrasound transducer stabilization devices are already available to overcome the previously mentioned issues in clinical practice. These stabilizers are secured to the skin surface as desired by the physician. However, they lack portability. For example, the weight of one of the available stabilizers, ultraStand (Wellan Medical, Inc., NH, USA), is 7 kg. In addition, to the best of our knowledge, although the structures and characteristics of these devices have been described in brochures, they have not been described in any independent research papers. Hence, to improve the portability of the stabilizer, we developed a portable, lightweight (1.45 kg) ultrasound transducer stabilization device that can freely move in any direction and allow easier adherence of the transducer to the skin surface of the patient, as desired by the physician. Our unique patented device (patent number 2008-317507 in Japan) is more compact and portable than the devices currently available (Fig. 1). It was designed to accompany the infusion stands available in every operation room and outpatient pain clinic in Japan, unlike transducer stabilization devices, which require their own special stands. The device consists of both transducer and infusion stand holders (Fig. 2) and attaches to either linearor convextype transducers. Figure 3 demonstrates the use of the stabilization device to attach the linear-type transducer to the left neck for interscalene nerve block. Figure 4 demonstrates how it also enables continuous and unassisted catheter insertion for right interscalene nerve block in a patient with complex regional pain syndrome. In conclusion, our new portable ultrasound transducer stabilization device might facilitate unassisted local anesthetic injection and catheter insertion during ultrasoundguided nerve blocks.

A patient with severe right chest pain and mechanical allodynia induced by an intercostal drainage tube to his chest is presented. It was not relieved by treatment with diclofenac sodium and was worsened by movement and touch to the right chest wall. Mechanical allodynia was also present. The patient's wrenching pain disappeared immediately after stitch removal, but the dull pain and mechanical allodynia persisted, gradually decreasing to zero in 7 days.

A randomized, double-blind, controlled study was designed to evaluate the effect of presurgical local infiltration of bupivacaine in the surgical field on postsurgical wound pain relief and analgesic requirements in 28 healthy patients scheduled for laparoscopic gynecologic examinations.After induction of general anesthesia by routine methods, the patients were randomly divided into two groups. In the bupivacaine (B) group (n = 15), patients were injected with 5 ml of 0.25% bupivacaine at each incisional area (four sites, total of 20 ml) approximately 15 minutes before skin incision. In the control (C) group (n = 13), the surgical field was injected with an equal volume of physiologic saline solution (four sites, total of 20 ml).Postsurgical wound pain at rest was evaluated by a 10-cm visual analog pain scale at 1, 10, 24, and 72 hours and 1 month after surgery. The patients were interviewed via telephone 1 month after hospital discharge for re-evaluation of resting pain.The results indicated that the incidence of postsurgical wound pain for up to 10 hours after surgery in group B was significantly lower (p0.05) than in group C. Pain intensity ranged from mild to moderate (2-5 cm). In addition, the mean visual analog pain scale pain intensity was significantly less for group B (0.31 +/- 0.85 cm) than for group C (2.62 +/- 2.06 cm) for up to 10 hours after surgery (p0.05). The number of patients who requested analgesics and complained of sleep disturbances was significantly higher in group C (p0.05). The mean cumulative dose of diclofenac sodium at 24 hours was significantly (p0.05) lower in group B (6.67 +/- 17.6 mg) than in group C (30.8 +/- 25.3 mg). Prolonged postsurgical wound pain persisting 1 month after surgery was observed in one patient in group C.It is concluded that presurgical infiltration of 0.25% bupivacaine in the surgical field is a useful method for decreasing postsurgical wound pain for up to 10 hours and analgesic consumption for up to 24 hours after laparoscopic gynecologic examination.

Two techniques for evaluating human baroreflex sensitivity (BRS), i.e. the sequence technique and the cross-spectral technique, were compared during the following four different body positions; 6 degrees head-down tilt (HDT), supine (Sup), 60 degrees head-up tilt (HUT) and upright (Upr). The sequence technique is based on the slope of linear regression between beat-to-beat RR intervals and systolic blood pressures. The cross-spectral technique is based on the cross-spectral analysis of RR interval and systolic blood pressure variabilities, and the estimates of BRS were computed separately for the low-frequency region (0.04-0.15 Hz) and the high-frequency region (0.15-0.5 Hz). The BRS obtained by the sequence technique had a significant correlation to that obtained by the cross-spectral technique for the low-frequency region in HDT, Sup and HUT, but not in Upr. There was a significant correlation between the BRS obtained by the sequence technique and that obtained by the cross-spectral technique for the high-frequency region in every body position. It became clear that the sequence technique is mutually related to the cross-spectral technique for the high-frequency region, but not necessarily identical to the cross-spectral technique for the low-frequency region. Moreover, a comparison was also made between the baroreceptor activating sequence and the deactivating sequence in the sequence technique during the four different body positions. Although the estimates of BRS of the activating sequence and the deactivating sequence were similar in every body position, the numbers of their sequences were progressively separated in the order of HDT, Sup, HUT and Upr. The numbers of the activating sequence and the deactivating sequence in the sequence technique were found to be separated in a sympathetically dominant condition.

Recently, heart rate spectral analysis has become recognized as a powerful tool for quantitatively evaluating autonomic nervous system activity. The purpose of this study was to analyze parasympathetic nervous activity by heart rate spectral analysis after administration of atropine and neostigmine for reversal of residual neuromuscular blockade. For our study, 36 female patients (26–37 years of age), ASA physical status (PS) I, who were scheduled for laparoscopic examination, were randomly allocated to one of the following four groups: In group A (1∶1), 9 patients received 1.0mg atropine followed 4 min later by 1.0 mg neostigmine. In group B (1∶2), 9 patients received 0.5 mg atropine followed 4 min later by 1.0 mg neostigmine. In group C (1∶2.5), 9 patients received 1.0 mg atropine followed 4 min later by 2.5 mg neostigmine. In group D (1∶2 mix), 9 patients received a mixed solution of atropine 0.5 mg and neostigmine 1.0mg. After finishing the laparoscopic examination, additional anesthesia was maintained with 70% nitrous oxide, 30% oxygen, and 0.5% isoflurane. The control data were obtained 10 min after finishing the laparoscopic examination. After that, the data on atropine were obtained between 2 and 4min after administration of atropine, and the data on neostigmine were obtained between 5 and 7 min after administration of neostigmine. We selected power spectral density of the high-frequency component (HF-p) in heart rate spectral analysis as an index to assess parasympathetic activity. In groups A, B, and C, the HF-p decreased after administration of atropine. In groups B and C, the HF-p increased after administration of neostigmine as compared to the control. In group A, the HF-p increased after neostigmine but did not differ from the control. The difference between groups D and B was not statistically significant. From the results of this study, we concluded that the muscarinic effect of neostigmine could not be sufficiently blocked by atropine at 1/2 dosages of neostigmine, but could be sufficiently blocked by atropine at equivalent dosages of neostigmine, under light isoflurane anesthesia.

The effects of nitrous oxide on the late reflex potential, a medullary component of somato-sympathetic reflex potentials, induced from the lumbar sympathetic trunk by electrical stimulation of the femoral nerve was investigated in brain intact cats and midbrain decerebrated cats under adequate anaesthesia with intravenous urethane and α-chloralose. The late reflex potential was depressed by inhalation of 75% nitrous oxide in oxygen in brain intact cats. Midbrain decerebration itself caused marked potentiation of the late reflex potential, although subsequent inhalation of 75% nitrous oxide did not cause any depressive effect on the potentiated late reflex potential. No significant changes in arterial pressure and heart rate were seen during the experiments. From these results, we concluded that anaesthetic concentrations of nitrous oxide might activate the descending inhibitory system from higher areas in the central nervous system.

We evaluated vecuronium-induced neuromuscular block in both arms of a patient with cerebral palsy and hemiplegia. A remarkable resistance to vecuronium was observed in the hemiplegia side compared with cerebral palsy side. Complete recovery from neuromuscular block should be assessed in the cerebral palsy side that shows a delayed recovery.