Spinal anaesthesia inhibits central temporal summation

In a previous investigation we found that extradural anaesthesia did not adequately inhibit temporal summation of repeated electrical stimuli: pain to repeated stimuli was blocked in only one of 10 patients, and pain thresholds to repeated stimuli were significantly lower than pain thresholds to a single stimulus. In this study we have investigated in 10 patients the effect of spinal anaesthesia on temporal summation, assessed by repeated electrical stimulation of the sural nerve. Plain 0.5% bupivacaine 18 mg was injected at L2-3. The pain threshold to a single electrical stimulus, summation threshold (increase in perception during repeated electrical stimuli with five impulses of the same intensity at 2 Hz), pinprick and cold sensation were assessed. After spinal anaesthesia, pain to both single and repeated stimulation, and pinprick and cold sensation, disappeared in all patients. We conclude that spinal anaesthesia inhibits temporal summation elicited by repeated electrical stimulation.      

Temporal summation during extradural anaesthesia

We have investigated in 10 patients the effect of extradural anaesthesia on temporal summation by comparing pain thresholds to single and repeated (five impulses at 2 Hz) electrical stimuli and compared these tests with pinprick and cold stimulation. Bupivacaine 0.5% (20 ml) was injected at L2-3. After extradural anaesthesia the threshold to repeated stimuli was significantly lower than the threshold to single stimuli (P = 0.0007). Nine patients lost cold sensation and 10 patients pinprick sensation. Pain to single electrical stimulation disappeared in six patients and pain to repeated electrical stimulation in one. Pain may be evoked by temporal summation of repeated electrical stimuli even when pinprick sensation, cold sensation and pain to single electrical stimuli are inhibited. Thus temporal summation should be taken into consideration when extradural analgesia is assessed.      

Block of the sacral segments in lumbar epidural anaesthesia

Background. Block of the first sacral segment is often delayedin lumbar epidural anaesthesia. The addition of either epinephrineor sodium bicarbonate to the local anaesthetic enhances theefficacy of epidural block. We assessed the block of lumbo-sacralsegments in lumbar epidural anaesthesia adding epinephrine and/orbicarbonate to lidocaine. Methods. Twenty-seven patients undergoing lumbar epidural anaesthesiawith lidocaine 2%, 17 ml at L4-5 or L5-S1 were randomly dividedinto three groups. Plain lidocaine, lidocaine with 1:200 000epinephrine or lidocaine–epinephrine–bicarbonatewas administrated via an epidural catheter. The pain thresholdafter repeated electrical stimulation was used to assess thesensory block at the L2, S1, and S3 segments. Motor block wasevaluated using the Bromage scale. Results. Patient characteristics were comparable between thegroups. The pH of lidocaine in the lidocaine–epinephrine–bicarbonategroup was significantly higher than that in other groups. Painthresholds at the S1 and S3 segments in the lidocaine–epinephrine–bicarbonategroup were significantly higher than those in the lidocaine–epinephrinegroup. However, differences in the pain threshold at the L2segment between groups were insignificant. The time to onsetof sensory block at the S1 and S3 in the lidocaine–epinephrine–bicarbonategroup was significantly shorter than that in the lidocaine group.Pain threshold by pinprick test was approximately within the30–50 mA range. Conclusion. A combination of lidocaine, bicarbonate, and epinephrineincreases the pain threshold over the sacral segments. Br J Anaesth 2003; 90: 173–8     

Efficacy of 1% ropivacaine at sacral segments in lumbar epidural anesthesia

BACKGROUND AND OBJECTIVES: It is suggested that the potency of 1% ropivacaine is comparable to that of 0.75% bupivacaine and higher than that of 2% lidocaine. Alkalinized lidocaine reportedly enhances the block of sacral segments during lumbar epidural anesthesia. We hypothesized that 1% ropivacaine might also block at the lumbosacral segments adequately during lumbar epidural anesthesia. METHODS: Forty-two patients undergoing lumbar epidural anesthesia at L4-5 or L5-S1 were randomly divided into 3 groups and received either 14 mL 2% lidocaine (lidocaine group), 2% lidocaine with epinephrine 1:200,000 and bicarbonate (lidocaine-epinephrine-bicarbonate group), or 1% ropivacaine (ropivacaine group). Pain threshold after repeated electrical stimulation was used to assess sensory block at the L2, S1, and S3 segments while motor block was evaluated using the modified Bromage Scale. RESULTS: Demographic data were comparable between the groups. Significant differences in the pH of each local anesthetic solution were found between the 3 groups. Pain thresholds at the S1 and S3 segments in the lidocaine-epinephrine-bicarbonate group were significantly higher and sensory block onset faster than in the other groups. However, no significant differences were found in either the pain threshold or the onset of sensory block of the L2 segment between the groups. No significant differences in the pain threshold, onset of sensory block, or Bromage Scale were found between the lidocaine and ropivacaine groups. CONCLUSIONS: We conclude that 1% ropivacaine does not improve block of sacral segments within 20 minutes following epidural ropivacaine administration.     

Epidural bolus injection with alkalinized lidocaine improves blockade of the first sacral segment — a brief report

PURPOSE: It has been reported that the addition of epinephrine and/or bicarbonate to local anesthetic enhances the depth of epidural blockade and that initial partial bolus injection results in greater caudal spread. We evaluated the anesthetic effects of lidocaine with epinephrine and/or bicarbonate injected into the epidural space by bolus or catheter injection. METHODS: Forty-four patients undergoing epidural anesthesia with 17 mL of 2% lidocaine containing 1:200,000 epinephrine at L4-5 or L5-S1 were randomly divided into four groups. Lidocaine was administrated via epidural catheter [lidocaine catheter (LC) group] or Tuohy needle (lidocaine bolus group), lidocaine-bicarbonate was administrated via catheter (lidocaine-bicarbonate catheter group) or needle [lidocaine-bicarbonate bolus (LBB) group]. Pain threshold after repeated electrical stimulation was performed at L2 and S1 regions. Motor blockade was evaluated using the Bromage scale. Sympathetic blockade was assessed with plethysmographic waveforms from the toe. RESULTS: The pain threshold of the S1 dermatome in LBB group was significantly higher than in the lidocaine only groups, however, differences in the pain threshold at the L2 dermatome among the groups were insignificant. The onset of sensory blockade in the S1 dermatome in the LBB group was significantly shorter than in the LC group. Significantly greater motor blockade was achieved in the lidocaine-bicarbonate groups than in the lidocaine-only groups. The amplitude of plethysmographic waveforms significantly increased within each group. CONCLUSION: Epidural bolus injection of lidocaine-bicarbonate with epinephrine improves the pain threshold and speeds the onset of the blockade of the first sacral region.     

Epidural clonidine enhances postoperative analgesia from a combined low-dose epidural bupivacaine and morphine regimen.

In a randomized, double-blind, placebo-controlled trial, the value of adding clonidine to a low-dose epidural regimen for postoperative pain treatment was assessed. Twenty-four patients scheduled for hysterectomy during combined thoracic epidural (bupivacaine and morphine) and general anesthesia were studied. Postoperative analgesia consisted of epidural bupivacaine (5 mg/h) and morphine (0.1 mg/h) for 12 h. In addition, the patients randomly received clonidine (75 micrograms), followed by an infusion of 18.75 micrograms/h or saline solution (placebo) epidurally. Pain was evaluated at rest, during cough, and during mobilization every hour. Sensory level of analgesia was evaluated by pinprick. We found no significant difference in pain scores at rest between the clonidine and placebo groups but an enhanced analgesic effect by clonidine during cough and mobilization (P less than 0.05). Arterial blood pressure decreased significantly during clonidine infusion and remained lower than in the control group throughout the study. We conclude that a continuous low-dose epidural clonidine infusion enhances analgesia from a combined low-dose epidural bupivacaine and morphine regimen after hysterectomy; however, the concomitant decrease in arterial blood pressure during epidural clonidine deserves further study before such a regimen can be recommended.     

The combination of epidural clonidine and S(+)-ketamine did not enhance analgesic efficacy beyond that for each individual drug in adult orthopedic surgery

STUDY OBJECTIVES: To evaluate the benefit of epidural clonidine and S(+)-ketamine combination through the epidural route in adult orthopedic surgery. DESIGN: Randomized double-blinded study. SETTING: Teaching hospital. PATIENTS: Scheduled to undergo knee surgery, 56 American Society of Anesthesiologists physical status 1 and 2 adult patients. INTERVENTIONS: Patients were randomized to 1 of 4 groups to receive the combined epidural-intrathecal technique. A 10-mL epidural injection of either study drug or normal saline was first administered to all patients. Intrathecal anesthesia was performed with 15 mg of bupivacaine. The control group (CG) received epidural saline. The 0.1-mg/kg S(+)-ketamine epidural group received 0.1 mg/kg epidural S(+)-ketamine. The 0.5-microg/kg clonidine epidural group received 0.5 microg/kg epidural clonidine. The S(+)-ketamine/clonidine group received 0.1 mg/kg epidural S(+)-ketamine plus 0.5 microg/kg epidural clonidine. MEASUREMENTS AND MAIN RESULTS: Pain and adverse effects were evaluated by visual analog scale. Rescue analgesics were available to patients. The groups were demographically similar. Sensory level to pinprick, surgical and anesthetic time, and visual analog scale scores for pain at first rescue medication were similar among the groups. The time to first rescue analgesic (minute) was lowest in CG (P < .005). The CG required more rescue analgesics in 24 hours than any of the other groups (P < .0005). Patients who received either epidural clonidine, S(+)-ketamine, or both displayed similar analgesia. The frequency of adverse effects was similar among groups (P > .05). CONCLUSIONS: The association of epidural clonidine or S(+)-ketamine did not result in a greater analgesic effect in the model of acute postoperative pain studied, although the interaction of epidural clonidine and S(+)-ketamine is not attributable to sharing of a common second messenger system.     

Effects of gabapentin on experimental somatic pain and temporal summation

BACKGROUND AND OBJECTIVES: Gabapentin is used for treatment of neuropathic pain, but its effect on different somatic pain modalities and integrative mechanisms are not completely understood. The aim of this double-blind, placebo-controlled experimental pain study, conducted on 20 healthy volunteers, was to examine the effect of a single dose of 1200 mg gabapentin on multi-modal experimental cutaneous and muscle pain models. METHODS: The following pain models were applied: (1) pain thresholds to single and repeated cutaneous and intramuscular electrical stimulation (temporal summation to 5 stimuli delivered at 2 Hz); (2) stimulus-response function relating pain intensity scores (visual analog scale, VAS) to increasing current intensities for electrical skin and muscle stimuli (single and repeated, determined at baseline); and (3) the pain intensity (VAS) and pain areas after intramuscular injection of hypertonic saline. Pain assessments were performed prior to, and at 4, 6, and 8 hours after medication. RESULTS: When responses were averaged across the post-dose times, gabapentin: (1) significantly increased the temporal summation pain threshold in skin compared with placebo (P = .03); (2) significantly reduced the area under the pain intensity curve to hypertonic saline injections in the muscle (P = .02); and (3) significantly reduced the area of pain evoked by hypertonic saline (P = .03). CONCLUSIONS: Gabapentin reduces temporal summation of skin stimuli at pain threshold intensities; this may have potential as a biomarker for drugs with efficacy on neurogenic pain. The data also suggest that tonic muscle pain is responsive to gabapentin treatment and suggest further clinical studies.     

Effects of volume and concentration of lidocaine on epidural anaesthesia in pregnant females

BACKGROUND AND OBJECTIVE: The effects of altering the concentration of a local anaesthetic on the development of epidural anaesthesia in pregnant females are unclear. We compared the anaesthetic effects of a constant dose of two different concentrations of epidural lidocaine for Caesarean section. METHODS: After Institutional Review Board approval and informed consent, patients undergoing elective Caesarean section were randomized to receive either lidocaine 1% 30 mL (+epinephrine 5 microg mL(-1)) or lidocaine 2% 15 mL (+epinephrine 5 microg mL(-1)) (n = 20 each) for epidural anaesthesia at the L1-L2 interspace. The spread of the sensory block to pinprick and the degree of motor block (modified Bromage scale) were measured at 5, 10, 15, 20 and 30 min after injection. RESULTS: No significant differences in the progression of analgesia and motor block were observed at any time between 1 and 2% lidocaine. The maximum cephalad spread was observed 30 min after injection; the median was at T4 (range T3-T5) and at T4 (range T3-T6) for lidocaine 1 and 2%, respectively. CONCLUSIONS: The same doses but different volumes of lidocaine 1 and 2% produced comparable anaesthetic effects in pregnant females. The effects of epidural anaesthesia depend primarily on the total dose of the local anaesthetic.     

The addition of epinephrine increases intensity of sensory block during epidural anesthesia with lidocaine

BACKGROUND AND OBJECTIVES: Little is known about the effect of adding epinephrine to local anesthetic solutions on the intensity of sensory block during epidural anesthesia. This study examined development of sensory block during lumbar epidural anesthesia using a cutaneous current perception threshold (CPT) quantitative sensory testing device. METHODS: Twenty ASA I patients who were randomly divided to receive 10 mL 1% lidocaine with (group E) or without (group P) epinephrine 1:200,000. Current perception threshold at 2,000, 250, and 5 Hz stimulation at the trigeminal (V), ninth thoracic (T9), and second lumbar (L2) dermatomes, and the dermatomal levels of block of light touch, temperature, and pinprick discrimination were measured before and every 5 minutes, until 60 minutes after injection of epidural lidocaine. RESULTS: After epidural administration of lidocaine with epinephrine, all CPT significantly increased at T9 and L2, whereas no increase was detected after epidural plain lidocaine. Areas under the curves, calculated to express overall magnitude and duration of CPT values, were significantly larger in group E than those in group P at 2,000 and 250 Hz at T9. No differences were observed in the maximal levels of loss of cold, pinprick, and touch sensations between both groups. CONCLUSIONS: These results suggest that lumbar epidural anesthesia using 10 mL 1% lidocaine with epinephrine produces a more intense block of both large and small diameter sensory nerve fibers than that with plain lidocaine. It appears, therefore, that the addition of epinephrine improves the quality of sensory block during epidural anesthesia with lidocaine.     

Lumbar epidural fentanyl: segmental spread and effect on temporal summation and muscle pain

Background. Despite extensive use, different aspects of thepharmacological action of epidural fentanyl have not been clarified.We applied a multi-modal sensory test procedure to investigatethe effect of epidural fentanyl on segmental spread, temporalsummation (as a measure for short-lasting central hyperexcitability)and muscle pain. Methods. Thirty patients received either placebo, 50 or 100µg single dose of fentanyl epidurally (L2–3), ina randomized, double-blind fashion. Heat pain tolerance thresholdsat eight dermatomes from S1 to fifth cranial nerve (assessmentof segmental spread), pain threshold to transcutaneous repeatedelectrical stimulation of the sural nerve (assessment of temporalsummation) and pain intensity after injection of hypertonicsaline into the tibialis anterior muscle (assessment of musclepain) were recorded. Results. Fentanyl 100 µg, but not 50 µg, producedanalgesia to heat stimulation only at L2. Surprisingly, no effectat S1 was detected. Both fentanyl doses significantly increasedtemporal summation threshold and decreased muscle pain intensity. Conclusions. The findings suggest that a single lumbar epiduraldose of fentanyl should be injected at the spinal interspacecorresponding to the dermatomal site of pain. Increased effecton L2 compared with S1 suggests that drug effect on spinal nerveroots and binding to opioid receptors on the dorsal root gangliamay be more important than traditionally believed for the segmentaleffect of epidurally injected fentanyl. Epidural fentanyl increasestemporal summation threshold and could therefore contributeto prevention and treatment of central hypersensitivity states.I.M. injection of hypertonic saline is a sensitive techniquefor detecting the analgesic action of epidural opioids. Br J Anaesth 2003; 90: 467–73     

The analgesic effect of tramadol after intravenous injection in healthy volunteers in relation to CYP2D6

Tramadol analgesia results from a monoaminergic effect by tramadol itself and an opioid effect of its metabolite (+)-M1 formed by O-demethylation of tramadol by CYP2D6. In this study we sought to determine the impact of (+)-M1 on the analgesic effect of tramadol evaluated by experimental pain models. The effect of an IV injection of 100 mg tramadol on experimental pain was studied 15-90 min after dosing in volunteers, 10 extensive metabolizers with CYP2D6 and 10 poor metabolizers without CYP2D6 in 2 placebo-controlled trials. The pain tests included detection and tolerance threshold to single electrical sural nerve stimulation, pain summation threshold to repetitive electrical sural nerve stimulation (temporal summation), and the cold pressor test. In extensive metabolizers, tramadol reduced discomfort experienced during the cold pressor test (P = 0.002). In poor metabolizers, the pain tolerance thresholds to sural nerve stimulation were increased (P = 0.04). (+)-M1 could be detected in the serum samples from all extensive metabolizers except one, but (+)-M1 was below the limit of determination in all poor metabolizers. The opioid effect of (+)-M1 appears to contribute to the analgesic effect of tramadol, but the monoaminergic effect of tramadol itself seems to create an analgesic effect.     

Oral Clonidine Premedication Does Not Alter the Efficacy of Simulated Intravenous Test Dose Containing Low Dose Epinephrine in Awake Volunteers

Background: Clonidine premedication modifies the hemodynamic responses to sympathomimetics. The present study was designed to test whether clonidine altered the response to a small intravenous dose of epinephrine, such as that which might be used in an epidural test dose.

Methods: In 18 healthy volunteers, four series of determinations were performed in random order and were separated by a minimum 72 h: (1) no premedication followed by intravenous saline 3 ml, (2) no premedication followed by intravenous test dose containing 3 ml of 1.5% lidocaine + 15 micro gram epinephrine, (3) oral clonidine (5 micro gram/kg 1.5 h before hemodynamic determinations) followed by intravenous saline, and (4) oral clonidine followed by intravenous epinephrine-containing test dose. Systolic blood pressure (SBP) and heart rate (HR) were measured continuously, and symptoms associated with central nervous system toxicity were noted.

Results: After the test dose injections, HR and SBP increased with or without clonidine premedication. The 95% confidence intervals for the maximum HR increases with and without clonidine were 49-61 and 44-54 beats/min, respectively, indicating that one could not be absolutely certain that everyone would develop a positive HR response. The HR increase was >or= to 20 beats/min in 18 of 18 volunteers given epinephrine with or without clonidine and in 0 of 18 volunteers given saline. Calculated sensitivities, specificities, and positive and negative predictive values were all 100% based on the conventional HR criterion and were unaltered by clonidine. Subjective symptoms were not affected by clonidine.     

Effect of epidural clonidine on somatosensory evoked potentials to dermatomal stimulation

The effect of lumbar epidural clonidine 150 micrograms on early (less than 0.5 s) somatosensory evoked potentials (SEP) to electrical stimulation of the L1 and S1 dermatomes was examined in twelve cancer patients. Epidural clonidine led to a minor but significant decrease in amplitude of two components (N1 and N3) following S1 stimulation while SEP latency was prolonged only in the P1 and P3 components (P less than 0.05). In all patients the pain score decreased, mean score at rest from 4.9 +/- 0.5 to 0.6 +/- 0.2 and during mobilization from 7.4 +/- 0.6 to 1.3 +/- 0.5 (P less than 0.01). Mean systolic and diastolic blood pressures decreased from 118 +/- 4/72 +/- 5 mmHg to 99 +/- 5/60 +/- 3 mmHg (P less than 0.01), respectively. It is concluded that epidural clonidine has a minor effect on the early SEPs to electrical dermatomal stimulation. Additionally, a pronounced effect on cancer pain was seen.     

The effect of intravenous infusion of adenosine on electrically evoked hyperalgesia in a healthy volunteer model of central sensitization

Human pain models invoking central sensitization, one of the key mechanisms of chronic pain, may be useful for characterizing new analgesics. A new model of electrical hyperalgesia can detect the efficacy of several analgesic mechanisms. Because IV adenosine can alleviate neuropathic pain, we investigated its effect on experimental sensitization. This was a double-blinded, randomized, two-period crossover study in 20 healthy volunteers. Current pulses (0.5 ms; 1 Hz) were applied intracutaneously to achieve pain rating of approximately 5 on a 0-10 numeric rating scale. Pain, areas of pinprick hyperalgesia, and tactile allodynia were assessed during the 2.5-h stimulation period. Adenosine (50 microg. kg(-1). min(-1)) and placebo were infused IV over 60 min. Additional testing was performed 24 h after each treatment. Adenosine reduced the area of pinprick hyperalgesia during the infusion compared with placebo; there was no significant effect on tactile allodynia or pain rating. The effect on hyperalgesia developed over 15 min and was significant (P < or = 0.05) for the rest of the infusion period. There was no difference between treatments at 24 h. Thus, in accordance with reports on neuropathic pain, adenosine reduced central sensitization in the human model of electrical hyperalgesia. However, adenosine did not have the long-term effects seen in patients. The model can investigate mechanisms of drugs for the treatment of chronic pain.     

Analgesic effects of epidural morphine, fentanyl and lidocaine

The analgesic effects of epidurally administered morphine 5 mg (group M, n = 15), fentanyl 100 micrograms (group F, n = 15), 2% lidocaine 60 mg (group L, n = 15) and normal saline (group S, n = 10) were investigated in 55 patients scheduled for abdominal surgery. Each drug was prepared in 3 ml solution and was injected though an epidural catheter introduced 3 cm cephalad into the epidural space at T10-11. Analgesic effects were assessed by changes in the dull pain sensation induced by electrical stimulation at 3 Hz through a pair of stainless needles which were placed subcutaneously at T7 and T10 dermatomes. In group M, analgesic effects at T10 were demonstrated in 12 of 15 subjects and the onset of analgesia was more rapid at T10 than at T7. The mean onset time of analgesia was 7.8 +/- 3.6 (mean +/- SD) min. There were 5 subjects in group F and 6 in group L who showed more rapid onset of analgesic effects at T10 than at T7, respectively. There were 2 subjects in group F and 5 in group L, with more rapid onset of analgesia at T7 than at T10. There were several subjects in group F and L with simultaneous onset of analgesia at T7 and T10. In group L, the mean distribution of analgesic area, confirmed with pinprick, was 5.2 +/- 1.9 (mean +/- SD) dermatomal segments. Hypercapnea, associated with somnolence, was frequently seen in group F. None of the subjects in group M, L or S showed such incidents. These results suggest that the main site of action of epidural morphine is located in the spinal cord while that of epidural fentanyl in the brain.     

Lumbar Epidural Morphine in Humans and Supraspinal Analgesia to Experimental Heat Pain

Background: Epidural administration of morphine is a common analgesic technique to manage pain. Morphine spreads from the epidural space to the cerebrospinal fluid and then rostrally, causing side effects mediated by the brain stem. However, data on the rostral spread of morphine-mediated analgesia are sparse. This study examined the rostral spread of analgesic effects on heat and electrical pain after epidural administration of morphine.

Methods: In a randomized, double-blinded, placebo-controlled, crossover study, 5 mg morphine or saline placebo were injected into the lumbar epidural space in nine healthy volunteers. Correct needle placement was confirmed with fluoroscopy. Analgesia to experimental nociceptive heat and electrical stimuli was measured at lumbar (L4), thoracic (T10), cervical (C2), and trigeminal (V2) levels before and 2, 5, 10, and 24 h after epidural injection. Plasma samples for assaying morphine concentrations were drawn before and after each analgesic evaluation.

Results: Epidural morphine significantly attenuated experimental heat pain at all dermatomes tested compared with saline placebo. Analgesic effects were significant at L4 after 2, 5, and 10 h, at T10 after 5, 10, and 24 h, and at V2 after 10 h. Electrical pain was attenuated at the lumbar and thoracic but not at the cervical dermatome. Analgesic effects were significant at L4 after 2, 5, and 10 h and at T10 after 5 and 10 h. Morphine plasma concentrations were below the detection limit (1 ng/ml) in eight of the nine subjects 10 h after epidural injection.     

Epidural administration of low-dose morphine combined with clonidine for postoperative analgesia after lumbar disc surgery.

This study evaluates the efficacy and side effects of a low dose of epidural morphine combined with clonidine for postoperative pain relief after lumbar disc surgery. In 36 of 51 patients who accepted the procedure, an epidural catheter was inserted (L1-L2 level). General anesthesia was induced with propofol and sufentanil, and maintained with sevoflurane in O2/N2O. After emergence from anesthesia, epidural analgesia was initiated according to two randomly assigned protocols: 1 mg of morphine with 75 microg of clonidine (Group M) or 12.5 mg of bupivacaine with 75 microg of clonidine (Group B), in 10 mL saline. Piritramide was administered during the first postoperative 24 hours using a patient-controlled analgesia device (PCA). The following parameters were recorded: piritramide consumption during the first 24 hours; pain at rest during the first postoperative hours (D0), during the first night (D1), and during the first mobilization; [visual analogue scale (VAS)]; and the occurrence of drowsiness, motor blockade, respiratory depression, nausea, vomiting, itching, micturition problems, and bladder catheterization during D0 and D1. Epidural administration of morphine-clonidine significantly improved postoperative pain relief and reduced piritramide consumption as compared to epidural bupivacaine-clonidine. Side effects did not differ between groups except for a higher incidence of micturition problems in Group M during D1. The occurrence of bladder catheterization was not significantly higher in that group. We conclude that a low dose of epidural morphine combined with clonidine offers a better postoperative analgesia than does bupivacaine-clonidine. The excellent analgesic conditions were obtained at the expense of a higher incidence of difficulties in initiating micturition.     

Improved analgesia with clonidine when added to local anesthetic during combined spinal-epidural anesthesia for hip arthroplasty: a double-blind, randomized and placebo-controlled study

Background: The perioperative effects of intrathecal and epidural clonidine combined with local anesthetic were evaluated in 60 patients undergoing hip arthroplasty. Methods: This was a double‐blinded study and the patients were randomized into three groups, with 20 patients in each group. All patients received spinal anesthesia with 17.5 mg of plain bupivacaine with 15 µg of clonidine (Group BC‐RC) or without clonidine (Groups B‐R and B‐RC). Postoperatively, epidural infusion was administered in the following way: Group B‐R – ropivacaine 4 mg h^?1; Groups B‐RC and BC‐RC: ropivacaine 4 mg h^?1 and clonidine 40 µg h^?1. Sensory block was assessed with light touch, pinprick, transcutaneous electrical stimulation at T12 and L2 dermatomes, and perception of thermal stimuli. Results: The maximal upper level of sensory block measured by pin‐prick (T6–T7) did not differ between the groups while the partial sensory block for cold and warmth were increased two dermatomes above pin‐prick level in the group with intrathecal clonidine compared to the other two groups (P < 0.05). Duration of anesthesia, analgesia and motor block were longer in Group BC‐RC compared to Groups B‐R and B‐RC (P < 0.02). Postoperatively, both VAS score on movement and PCA‐morphine consumption were higher in Group B‐R than in Groups B‐RC and BC‐RC (P < 0.01). The arterial pressure and heart rate in Groups B‐RC and BC‐RC were significantly lower than in Group B‐R at 10–24 and 15–24 h, respectively, after spinal injection. Conclusion: Low‐dose intrathecal clonidine provided a better quality of anesthesia and longer‐lasting analgesia. Epidural clonidine‐ropivacaine infusion resulted in improved postoperative analgesia but was associated with a moderate decrease in blood pressure.     

Sensory function and pain in a population of patients treated for breast cancer

Background: Chronic pain is often reported after surgery for breast cancer. This study examined pain and sensory abnormalities in women following breast cancer surgery.
Methods: Sensory tests were carried out on the operated and contra-lateral side in 55 women with chronic pain after breast cancer treatment and in a reference group of 27 pain-free women, who had also undergone treatment for breast cancer. Testing included a numeric rating score of spontaneous pain, detection and pain threshold to thermal and dynamic mechanical stimuli and temporal summation to repetitive pinprick stimulation. The neuropathic pain symptom inventory was applied for participants with chronic pain.
Results: The mean age was 58.6 years for the pain patients and 60.6 years for the pain-free patients. Thermal thresholds were significantly higher on the operated side than on the contra-lateral side in both groups and side difference in warmth detection threshold was significantly higher in the pain group than in the pain-free group (mean 3.8 °C vs. 1.1 °C, P =0.01). The frequency of cold allodynia was higher in participants with pain than in pain-free participants (15/53 vs. 1/25, P =0.01), and the frequency of temporal summation evoked by repetitive pinprick was higher in participants with pain than in pain-free participants (23/53 vs. 2/25, P =0.0009). The frequency of dynamic mechanical allodynia did not differ significantly between the two groups.
Conclusion: These findings suggest that chronic pain after surgery for breast cancer is associated with sensory hyperexcitability and is a neuropathic pain condition.