Epinephrine increases the neurotoxic potential of intrathecally administered lidocaine in the rat. (Department of Anesthesia and Preoperative Care, University of California, San Francisco, CA) Anesthesiology. 2001;94:876–881.

This study investigated whether adding epinephrine increases functional impairment or histologic damage induced by spinal administration of lidocaine in the rat. Eighty rats were divided into 4 groups to receive an intrathecal injection of normal saline containing 5% lidocaine, 5% lidocaine with 0.2 mg/mL of epinephrine, 0.2 mg/mL of epinephrine, or normal saline alone. Animals were assessed for persistent sensory impairment using the tail‐flick test administered 4 to 7 days after infusion. Animals were then killed, and the spinal cord and nerve roots were prepared for neuropathologic evaluation. Rats given 5% lidocaine developed persistent sensory impairment and histologic damage, and the addition of epinephrine resulted in a further significant increase in injury. Sensory function in animals given epinephrine without anesthetic was similar to baseline and did not differ from saline. Histologic changes in animals treated with epinephrine alone did not differ significantly from saline controls. Conclude the neurotoxicity of intrathecally administered lidocaine is increased by the addition of epinephrine. When making clinical recommendations for maximum safe intrathecal dose of this anesthetic, one may need to consider whether the solution contains epinephrine. Comment by Octavio Calvillo, M.D., Ph.D. The authors studied the neurotoxicity of epinephrine added to lidocaine injected intrathecally in rats. The animals were allocated to four groups of 20 rats each, receiving: normal saline alone, normal saline and 5% lidocaine, 5% lidocaine with epinephrine [0.2 mg/ml] in saline or epinephrine 0.2 mgml in saline. The animals were assessed for sensory deficits 4 and 7 days after infusion and then sacrificed. The spinal cords and nerve roots were prepared for neuropathological evaluation. Sections obtained from animals treated with lidocaine, lidocaine with epinephrine. Rats given 5% lidocaine developed persistent sensory impairment and histological evidence of damage, the addition of epinephrine, resulted in further damage. Histological changes in animals treated with epinephrine alone did not differ significantly from saline controls. The authors concluded that the neurotoxicity of intrathecally‐administered lidocaine is increased by the addition of epinephrine. They raised the possibility that the neurotoxicity of commercially available epinephrine may be due to the bisulfite contained therein, this chemical has been associated with neurotoxicity.     

Obtaining informed consent for clinical pain research: patients'' concerns and informational needs. (University of Pennsylvania Center for Bioethics, Philadelphia, PA) Pain. 2001;92:71–79.

The object of this study was to clarify the existence of dorsal root ganglion (DRG) neurons with dichotomizing axons projecting to the lumbar facet joint and to the sciatic nerve in rats. Two kinds of neurotracers (Dil and FG) were used in the study. Dil crystals were placed in the left F5-F6 facet joint, and FG was applied to the ipsilateral sciatic nerve or along the midline of the F% dermatome. Bilateral DRGs T13-S1 were observed by fluorescence microscope. DRG neurons double labeled with Dil and FG were recognized only in the ipsilateral DRGs from L3-L6 levels. Approximately 3% of DRG neurons innervating the L5-L6 facet joint had other axons to the sciatic nerve. By contrast, no double-labeled neurons were observed after FG was applied to the L5 dermatome. Conclude that in rats approximately 3% of DRG neurons innervating the lumbar facet joints have dichotomized axons projecting to the sciatic nerve.     

Postoperative epidural analgesia and possible transient anterior spinal artery syndrome. (HaEmek Medical Center, Afula, Israel) Reg Anesth Pain Med 2001;26:274–277.

An unusual complication of epidural analgesia used to facilitate postoperative pain relief while mobilizing a patient is presented in this case report. A 65‐year‐old woman with a history of chronic obstructive pulmonary disease, atherosclerotic cardiovascular disease, chronic renal failure, and degenerative vertebral anatomy underwent resection of the left ureter due to an obstructing tumor. The day following the surgery, mobilization to an armchair was started, followed by a decrease in blood pressure. Soon after, flaccid paralysis was sparing of sensory functions, consistent with anterior spinal artery syndrome, was diagnosed. This complication should be taken into account, especially in patients at risk, when considering epidural analgesia techniques in the postoperative period. Comment by Pedro F. Bejarano, M.D. Fortunately infrequent, the Anterior Spinal Artery Syndrome (ASAS) has been described in the early postoperative period in association with surgery involving the retroperitoneum (specially on the left side), as well as unexpectedly with regional anesthesia procedures (Spinal, Epidural and Celiac Plexus Blocks) in the vicinity of the T6 to L2 “critical zone” of medulary arterial blood flow.^1,2 This case highlights the importance of a proper evaluation and prevention when feasible, of combining risk factors (besides type of surgery and anesthetic technique) that may potentiate otherwise subclinical—but certainly prevalent—vascular, circulatory or spinal anatomy aging derangements leading to ASAS. As the authors state in the discussion of this case, it is remarkable the aethiological association with an apparently uncomplicated and retrospectively “preventable” hypotensive episode, whether it be a consequence of a relative hypovolemia, a pharmacological (postanesthetic or not) impairment of baropressor responses, or to an excessive local anesthetic sympathetic blockade. Learning from unexpected negative outcomes in anesthesia makes us more sensible to risk factors that are not specially highlighted in daily practice. In this sense, a case with so multiple patient's risk factors including the diagnosis of spinal stenosis, may had lead to other postop analgesia choices, namely systemic or even sole epidural opioid analgesia (that maybe was not considered here due to the COPD) as has been suggested before.³ Moreover, in the scope of an obstructive coronary disease high‐risk patient, a more aggressive treatment to the hypotensive episode including quick return to the recumbent or trendelemburg position limiting the isquemia could have favored this neurological adverse outcome. 1. Hong DK, Lawrence HM: Anterior Spinal Artery Syndrome following total Hip Artroplasty. Anesth Intensive Care. 2001;29:62–66. 2. Hachisuka K, Ogata H, Kohshi K: Postoperative Paraplegia with spinal myoclonus possibly caused by epidural anaesthesia: case report. Paraplegia. 1991 Feb;29(2):131–136. 3. Linz SM, Charbonnet C, Mikhail MS, et al.: Spinal artery syndrome masked by postoperative epidural analgesia. Can J Anaesth. 1997;44(11):1178–1181.     

Activation of brainstem N-methyl-D-aspartate receptors is required for the analgesic actions of morphine given systemically. (Oregon Health Sciences University, Portland, OR) Pain. 2001;92:129–138.

This study was designed to characterize the contribution of N-methyl-D-aspartate (NMDA) and non-NMDA-mediated excitatory transmission within the rostral ventromedial medulla (RVM) to activation of brainstem inhibitory output neurons and analgesia produced by systemic morphine administration. The results highlight 2 important aspects of RVM pain modulatory circuits. First, morphine given systemically produces it analgesic effect at least in part by recruiting an NMDA-mediated excitatory process to activate off-cells within the RVM. This excitatory process plays a role in the analgesic synergy produced by simultaneous μ-opioid activation at different levels of the neuraxis. Second, reflex-related activation of on-cells is medicated by a non-NMDA receptor, and this activation does not appear to play a significant role in regulating reflex responses to acute noxious stimuli. Excitatory amino acid-mediated excitation, thus, has 2 distinct roles within the RVM, activating off-cells and on-cells under different conditions.     

Microsurgical DREZotomy for pain due to spinal cord and/or cauda equina injuries: long-term results in a series of 44 patients. (University of Lyon, Lyon, France) Pain. 2001;92:159–171.

This article reported on the long‐term results of the microsurgical approach to the dorsal root entry zone (DREZotomy) in a series of 44 patients suffering from unbearable neuropathic pain secondary to spine injury. The follow‐up ranged from 1 to 20 years. The series included 25 cases with conus medullaris, 12 with thoracic cord, 4 with cauda equina and 3 with cervical cord injuries. Surgery was performed in 37 cases at the pathological spinal cord levels that corresponded to the territory of the so‐called “segmental pain,” and in 7 cases, on the spinal cord levels below the lesion for “infralesional pain,” syndromes. Regarding pain characteristics, a good result was obtained in 88% of the cases with predominately paroxysmal pain as compared with 26% with continuous pain. There were no perioperative mortalities. Morbidity included cerebrospinal fluid leak (3 patients), wound infection (2 patients), subcutaneous hematoma (1 patient), and bacteremia (1 patient). Conclude that the inclusion of DREZ‐lesioning surgery in the neurosurgical armamentarium for treating “segmental” pain due to spinal cord injuries is justified. Comment by Ron Pawl, M.D., FAC This is a seminal report, because it provides long‐term (greater than 1 year, 71 months average) outcome from the dorsal root entry zone lesioning, at the site of and one level above and below the site of injury, for pain after spinal cord injury. This procedure was performed using a microsurgical open technique. Results were good (greater than 75% relief) in patients with regional pain syndromes, in the body segments related to the site of cord injury, that was paroxysmal pain, and after conus medullaris lesions, which were the greatest number of cases treated. Continuous pain, burning pain, and infralesional pain syndromes, below the site of the cord injury, were not significantly benefited. Unfortunately, the authors did not report on the psychological make‐up of the patients, which might provide some insight into good versus bad outcome.     

Analgesia after thoracotomy in children: a comparison of interpleural, epidural, and intravenous analgesia.

The cohort for this study included 39 patients, between the ages of 8 and 20 years, who had had thoracotomy. Postoperative analgesia was provided by one of three techniques: intravenous narcotics (20 patients), thoracic epidural catheter (10 patients), or interpleural analgesia (IPA) (nine patients). Both IPA and epidural analgesia were administered according to a specific protocol. The efficacy of the three methods was evaluated using two indicators: the total intravenous narcotic requirements for the initial 72 hours and the number of times a dose of intravenous narcotic or supplemental epidural fentanyl was administered to each patient. Patients in the IPA group required significantly less intravenous narcotics (P less than .05) during the first three postoperative days (2.2 +/- 0.4, 1.9 +/- 0.6, and 1.4 +/- 0.5 mg of meperidine/kg/day) than patients in the intravenous narcotic group (8.1 +/- 1.2, 7.2 +/- 0.9, and 5.6 +/- 1.2 mg of meperidine/kg/day). When comparing epidural analgesia and IPA, the number of interventions in the patients receiving epidural analgesia was significantly less (P less than .05) than in the group receiving IPA. Four of 10 patients in the epidural group and two of nine in the IPA group required no interventions during the initial 72-hour postoperative course. In the epidural analgesia group, there were 19 days (of a total of 30 days) during which patients required no interventions. This percentage was significantly greater (P less than .05) than that of the IPA group, in which there were 9 days (of a total of 27 days), during which no interventions were required.     

The analgesic effect of codeine as compared to imipramine in different human experimental pain models. (University of Southern Denmark, Odense, Denmark) Pain. 2001;92:277–282.

In this article several complementary therapies were identified as particularly relevant to palliative cancer care. Exemplary studies were discussed. Although it was found that some promising results for treatment existed, the article concluded that there is a great deal of potential for complementary medicine in palliative care. The article also discussed the need for more rigorous research into the value of such treatments in palliative and supportive cancer care.     

TNF-alpha expression in painful and nonpainful neuropathies. (University Hospital, Basel, Switzerland) Neurology. 2001;56:1371–1377.

The objective of this study was to determine whether the cytokine tumor necrosis factor α (TNF-α) acts as a pain mediator in neuropathic pain in humans. Patients with painful neuropathies showed a stronger TNF-α immunoreactivity in myelinating Schwann cells relative to the epineurial background staining compared with patients with nonpainful neuropathy. Although there was no difference in sTNF-RI levels between painful and nonpainful neuropathies, patients with a mechanical allodynia had elevated serums sTNF-RI as compared to patients without allodynia. Conclude that TNF-α expression of human Schwann cells may be up-regulated in painful neuropathies. The elevation of sTNF-RI in patients with centrally mediated mechanical allodynia suggests that systemic sTNF-RI levels may influence central pain processing mechanisms.     

Orexin-A, an hypothalamic peptide with analgesic properties. (SmithKline Beecham Pharmaceuticals, Harlow, Essex, United Kingdom) Pain. 2001;92:81–90.

This study investigated the effects of acute and chronic tramadol treatment on T lymphocyte function and natural killer (NK) cell activity in rats receiving chronic constriction injury (CCI) of the sciatic nerve. T lymphocyte function was evaluated based on concanavalin-A (ConA)-induced and phytohemagglutinin (PHA)-induced splenocyte proliferation. NK cell activity was measured by lactic acid dehydrogenase release assay. The effects of tramadol on thermal hyperalgesia were also assessed by measuring paw withdrawal latency (PWL) in the rats. PWL was dose-dependently reversed by tramadol after acute treatment (single subcutaneous injection) with 10, 20, and 30 mg/kg, respectively. There was no significant change among acute treatments groups in NK cell activity, whereas splenocyte proliferation induced by ConA and PHA was significantly suppressed starting from a dose of 20 mg/kg. The reversal of the thermal hyperalgesia persisted throughout a period of chronic tramadol treatment of 40 and 80 mg/kg per day, respectively, with continuous subcutaneous infusion for 7 days at a uniform rate via osmotic minipumps. No modulation of NK cell activity was found in either dose group. However, the activity of splenocyte proliferation was decreased in the 80 mg/kg per day group when compared with the saline and 40 mg/kg per day groups. Suggest that tramadol treatment has an immunological profile different from pure μ-opioid agonists like morphine, which is known to suppress both NK cell activity and T lymphocyte proliferation at a subanalgesic dose in CCI rats. Conclude that tramadol treatment may be a better choice than morphine for treatment of chronic neuropathic pain, particularly in patients with compromised immunity.     

Continuous peripheral nerve block for ambulatory surgery. (Duke University, Durham, NC) Reg Anesth Pain Med 2001;26:209–214.

In this study data was prospectively gathered for 1 year from 228 patients in an ambulatory surgery center. All continuous peripheral nerve blocks (CPNB) were performed using the Contiplex system to provide anesthesia and postoperative analgesia. CPNB were performed using 5 upper and lower extremity techniques. Postsurgery local anesthetic was infused and at 24 hours, a rebolus of local anesthetic was performed. The CPNB catheter was removed and patients were examined for a loss of sensation. Patients were then discharged. The initial peripheral block was successful in 94% of the patients. Failed nerve block requiring general anesthesia occurred in 6%. The catheter was patent and functional in 90% of the patients at 24 hours, and 8% of the patients required more than 10 mg of intravenous morphine by 24 hours postsurgery. In the postanesthesia care unit, only 4 patients (1.7%) required treatment for nausea. At 24 hours and 7 days postsurgery, no patient reported a dysesthesia. Conclude that CPNB using the insulated Tuohy catheter system offered acceptable anesthesia and prolonged pain relief postsurgery. There were few side effects. Comment by Alan David Kaye, M.D., Ph.D., Erin Bayer, M.D. This study demonstrates the efficacy of the Contiplex system (CPNB) in providing surgical anesthesia and postoperative analgesia through CPNB. Despite the efficacy of CPNB, which could provide longer duration of postoperative analgesia than single injection block, it is not widely used due to lack of available equipment. Contiplex system utilizes a connector for a nerve stimulator attached to a 18‐gauge Tuohy needle. It allows for aspiration of blood, injection of local anesthesia and passage of a peripheral nerve catheter. This study demonstrated in an ambulatory surgery center with 228 patients, CPNB was used for 27 different types of surgical procedures which involved 5 different block sites. Success rates were 94% for initial peripheral block while 6% required general anesthesia. Patients required less postoperative analgesia. The incidence of postoperative side effects such as nausea and vomiting were minimal. Not a single patient reported dissatisfied with a 7‐day telephone follow‐up. A disadvantage of this technique is the use of an 18‐gauge needle and potential for vascular and/or nerve injuries, which did not occur in this study. Though previous studies have demonstrated the efficacy of the CPNB in inpatients, this is an important study focused on outpatients. A larger study group will be valuable in future studies.     

Herpes zoster in older adults. (Duke University Medical Center, Durham, NC) Clinical Infectious Diseases. 2001;32:1481–1486.

Herpes zoster (HZ) strikes millions of older adults annually worldwide and disables a substantial number of them via postherpetic neuralgia (PHN). Key aged‐related clinical, epidemiological, and treatment features of zoster and PHN are reviewed in this article. HZ is caused by renewed replication and spread of the varicella‐zoster virus (VZV) in sensory ganglia and afferent peripheral nerves in the setting of age‐related, disease‐related, and drug‐related decline in cellular immunity to VZV. VZV‐induced neuronal destruction and inflammation causes the principal problems of pain, interference with activities in daily living, and reduced quality of life in elderly patients. Recently, attempts to reduce or eliminate HZ pain have been bolstered by the findings of clinical trials that antiviral agents and corticosteroids are effective treatment for HZ and that tricyclic antidepressants, topical lidocaine, gabapentin, and opiates are effective treatment for PHN. Although these advances have helped, PHN remains a difficult condition to prevent and treat in many elderly patients. Comment by Miles Day, M.D. This article reviews the epidemiology clinical features diagnosis and treatment of acute herpes zoster. It also describes the treatment of postherpetic neuralgia. While this is a good review for the primary care physician, the discussion for the treatment for both acute herpes zoster and postherpetic neuralgia do not mention invasive therapy. It is well documented in pain literature that sympathetic blocks with local anesthetic and steroid as well as subcutaneous infiltration of active zoster lesions not only facilitate the healing of acute herpes zoster but also prevents or helps decrease the incidence of postherpetic neuralgia. All patients who present to the primary care physician with acute herpes zoster should have an immediate referral to a pain management physician for invasive therapy. The treatment of postherpetic neuralgia is a challenging experience both for the patient and the physician. While the treatments that have been discussed in this article are important, other treatments are also available. Regional nerve blocks including intercostal nerve blocks, root sleeve injections, and sympathetic blocks have been used in the past to treat postherpetic neuralgia. If these blocks are helpful, one can proceed with doing crynourlysis of the affected nerves or also radio‐frequency lesioning. Spinal cord stimulation has also been used for those patients who are refractory to noninvasive and invasive therapy. While intrathecal methylprednisolone was shown to be effective in the study quoted in this article one must be cautious not to do multiple intrathecal steroid injections in these patients. Multilple intrathecal steroid injections can lead to archnoiditis secondary to the accumulation of the steroid on the nerve roots and in turn causing worsening pain.     

The behavioral importance of dynamically activated descending inhibition from the nucleus reticularis gigantocellularis pars alpha. (University Hospital of Wales, Cardiff, United Kingdom) Pain 2001;92:53–62.

This study demonstrates the effects of nucleus reticularis gigantocellularis pars alpha (GiA) on the behavioral response during application of standardized noxious stimuli. As this system is activated in response to noxious stimulation, it is possible that chronic pain states may also activate GiA. Therefore, this study investigated this possibility in animals following partial sciatic nerve ligation (an animal model of chronic pain). Male Wistar rats (280–310 g) were anesthetized with halothane (0.5% to 2% in O₂). Guide cannulae for microinjections were stereotaxically placed above GiA. In one group of animals the sciatic nerve was partially litigated. Animals were allowed to recover for 4–6 days. The responses of each animal during the formalin test and the tail flick test were recorded on different days. Microinjections (0.5 μl) of either γ‐aminobutyric acid (GABA, 200 mM), D‐L homocysteic acid (DLH, 25 mM), or 0.9% saline (as control) into GiA were preformed during these tests in a randomized, blind manner. In animals without sciatic nerve ligation, microinjection of GABA to GiA did not significantly affect the animal's response during the tail flick test. However, microinjection of DLH significantly increased the latency of tail flick from 6.2 ± 0.8 to 8.4 ± 0.5 seconds for up to 15 minutes. Microinjection of GABA to GiA increased the behavioral response to formalin between 10 and 20 minutes postinjection, while microinjection of DLH reduced this response at all time points except 10 minutes postinjection (n = 8, p < 0.05, Mann‐Whitney U‐test). In animals with sciatic nerve ligation, microinjections (0.5 μl) of either GABA (200 mM), or saline (as control) into GiA contralateral to the partial sciatic ligation were performed during these tests in a randomized, blind manner. Partial sciatic ligation significantly reduced the behavioral response to contralaterally applied formalin from 15 minutes postinjection onwards, compared to controls without sciatic nerve ligation. Microinjection of GABA GiA significantly increased the behavioral response to formalin from 20 to 50 minutes postinjection. The inactivation of GiA only causes behavioral effects in nociceptive tests of a long enough duration to activate the system (ie, the formalin test but not the tail flick test). Chemical activation of the system affects both tests. Conclude that these data strongly support the concept of an important analgesic system that is activated in response to noxious stimulation, and subsequently acts to reduce behavioral responses to noxious stimuli. Comment by Leland Lou, M.D. This is a rat study that looked at the presence of inhibitory spinal multireceptive cells modifying and decreasing the behavioural response to noxious stimuli. While no direction was given as to the source of noxious stimuli inhibition in chronic pain, great effort was made to report a possible differential response of the C‐fiber pain system versus the large sensory fibers. After review it seems that the authors believed that the nucleus reticularis gigantocellularis pars alpha maybe a central processor of the inhibitory response. It is still too early to assess the clinical impact of this study.     

Lumbar sympathetic block for pain relief in two patients with interstitial cystitis. (Shimane Medical University, Izumo, Japan) Reg Anesth Pain Med 2001;26:271–273.

This case report discussed the effective treatment of interstitial cystitis (IC) with regard to a 63-year-old woman and a 78-year-old woman. Medical therapy with nonsteroidal anti-inflammatory drugs, anticholinergics, and hydrodistention of the bladder failed to improve their symptoms. Subsequently, a continuous lumbar epidural block using 1% mepivacaine was used in these patients. A transient reduction of the symptoms in both patients was achieved. A lumbar sympathetic block with a neurolytic agent produced almost complete and long-lasting relief of their symptoms. Conclude that lumbar sympathetic block using a neurolytic agent produced long-lasting pain relief in 2 patients with IC.
Comment by Pedro F. Bejarano, M.D. Chronic visceral pain association to the neurovegetative system and to sympathetically-maintained mechanisms has been well documented nowadays. The multiple neural connections among different abdominal nerve plexus has also been described, and this anastomoses may account for the observed analgesic effects in this case obtained without specific blockade of the superior hypogastric plexus. Despite the reported good results, the use of the lumbar approach may be controversial in this cases, as the uncomfortable peripheral effects of a permanent lumbar sympathetic neurolytic block (i.e.: lower limb vasodilation) favors a more anatomically restricted (visceral) area like that obtained with a superior hypogastric approach.
We must remark that the existence of Sympathetically mediated and/or maintained pain is not enough phenomenae to fit the diagnostic criteria of a RCPS, as suggested by the authors, but it is less so in the case of an evidently persistent, organic source of visceral nociception like in the Intersticial Cystitis disease.     

Axillary brachial plexus block with patient controlled analgesia for complex regional pain syndrome type I: a case report. (National Cheng Kung University, Tainan, Taiwan) Reg Anesth Pain Med 2001;26:68–71.

A 32-year-old man who suffered from complex regional pain syndrome type I (CRPS I) of the right upper limb after surgical release of carpal tunnel syndrome of the right hand is the subject of this case report. Symptoms and signs over the right hand were alleviated under rehabilitation and conventional pharmacological management, but severe painful swelling of the right wrist persisted. Axillary brachial plexus block (BPB) with patient controlled analgesia (PCA) was performed on the 32^nd postoperative day, which soon resulted in significant reduction of pain with gradual improvement of function of the right wrist. Conclude that axillary BPB with PCA may provide patients with CRPS I of the upper limb a feasible and effective treatment.     

An in vivo rat model to study calcitonin gene related peptide release following activation of the trigeminal vascular system. (Department of Neurology, University of Essen, Essen, Germany) Pain. 2001;92:101–106.

Neuropathic pain, due to peripheral nerve damage, can include allodynia (perception of innocuous stimuli as being painful), hyperalgesia (increased sensitivity to noxious stimuli) and spontaneous pain, often accompanied by sensory deficits. Plasticity in transmission and modulatory systems are implicated in the underlying mechanisms. The Kin and Chung rodent model of neuropathy employed involved unilateral tight ligation of 2 (L5 and L6) of the 3 (L4, L5, and L6) spinal nerves of the sciatic nerve and reproducibly induced mechanical and cold allodynia in the ipsilateral hindpaw over the 14 day postoperative period. In vivo electrophysiological techniques have then been used to record the response of dorsal horn neurones to innocuous and noxious electrical and natural (mechanical and thermal) stimuli after spinal nerve ligation (SNL). Activation of voltage-dependent calcium channels (VDCCs) is critical for neurotransmitter release and neuronal excitability, and antagonists can be antinociceptive. Here, for the first time, the effect of N-type and P-type VDCC antagonists (ω-conotoxin-GVIA and ω-agatoxin-IVA, respectively) on the evoked dorsal horn neuronal responses after neuropathy have been investigated. Conclude both presynaptic and postsynaptic VDCCs appear to be important.     

α-1 and α-2 adrenergic antagonists relieve thermal hyperalgesia in experimental mononeuropathy from chronic constriction injury. (Emory University School of Medicine, Atlanta, GA) Anesth Analg. 2001;92:1558–1562.

Two groups of 12 patients had a sciatic nerve block performed with 20 mL of either ropivacaine 7.5 mg mL⁻¹ or bupivacaine 5 mg mL⁻¹. There was no statistically significant difference in the mean time to onset of complete anesthesia of the foot or to the first request for postoperative analgesia. The quality of the block was the same in each group. Although there is no statistically significant difference in the mean time to peak plasma concentrations the mean peak concentration of ropivacaine was significantly higher than that of bupivacaine. There were no signs of systemic local anesthetic toxicity in any patient in either group.     

Periradicular infiltration for sciatica: a randomized controlled trial. (University Hospital of Oulu, Helsinki, Finland). Spine. 2001;26:1059–1067.

In this study, 160 consecutive, eligible patients with sciatica who had unilateral symptoms of 1 to 6 months duration, and who never underwent surgery were randomized for a double-blinded injection with methylprednisolone bupivacaine combination or saline. Objective and self-reported outcome parameters and costs were recorded at baseline, at 2 and 4 weeks, at 3 and 6 months, and at 1 year. Recovery was better in the steroid group at 2 weeks for leg pain, straight leg raising, lumbar flexion, and patient satisfaction. Back pain was significantly lower in the saline group at 3 and 6 months. Sick leave and medical costs were similar for both treatments, except for cost of therapy visits and drugs at 4 weeks, which were in favor of the steroid injection. By 1 year, 18 patients in the steroid group and 15 in the saline group underwent surgery. Conclude improvement during the follow-up was found in both the methylprednisolone and saline groups. The combination of methylprednisolone and bupivacaine seems to have a short-term effect, but at 3 and 6 months, the steroid group seems to experience a "re-bound" phenomenon.     

Subdural hematoma after dural puncture headache treated by epidural blood patch. (St. Thomas Hospital, London, United Kingdom) British J Anesth. 2001;86:720–723.

This case study discussed an accidental dural puncture in a 39-year-old patient during the siting of an epidural catheter for pain relief in labor. Twenty hours after the puncture, the mother developed a typical postdural headache, which increased in severity over the subsequent 24-hour period. An epidural blood patch was performed at 48 hours, and this initially relieved the headache. After discharge from the hospital, and 14 days after the dural puncture, the headache recurred, together with expressive dysphasia, poor coordination, and sensory loss in the right arm. A magnetic resonance imaging scan demonstrated a left-sided subdural hematoma, which drained successfully with complete recovery.