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Biomedical subjects

Elon Eisenberg

Publications and source records attributed to Elon Eisenberg.

At least 19 recordsLinked to original sources
PubMed2006

Effect of early administration of the N-methyl-d-aspartate receptor antagonist amantadine on the development of postmastectomy pain syndrome: a prospective pilot study.

UNLABELLED: Postmastectomy pain syndrome (PMPS) is a neuropathic pain syndrome that might develop after breast surgery. Like many other forms of neuropathic pain, it is relatively resistant to treatment and negatively affects the quality of life. A double-blind, randomized, placebo-controlled pilot trial was conducted to study the analgesic efficacy of perioperative administration of the N-methyl-D-aspatrate (NMDA) receptor antagonist amantadine in preventing PMPS after mastectomy plus axillary lymph node dissection (ALND). In the study group, a regimen of 200 mg/day of amantadine was started 1 day before surgery and continued for 14 days, whereas the control group received a placebo. Patients were required to indicate the exact location of their pain and to record its level at 1, 3, and 6 months after surgery. Neurologic examination and Quantitative Thermal Testing (QTT) were performed 1 and 6 months after surgery. On both the neurologic examination and the QTT, all patients, regardless of the perioperative intervention (amantadine or placebo), presented evidence for nerve injury, manifested primarily by painful hypoesthesia (anesthesia dolorosa) in the axilla or inner arm. PMPS persisted for the entire duration of the study in 82% of the patients who were available for follow-up. The average intensity of the pain was moderate in both groups and tended not to decline over time. No differences between the 2 groups in any of the outcome parameters reached statistical significance. According to the results of the present pilot study, the NMDA antagonist amantadine does not prevent the development of PMPS in patients who undergo breast surgery with ALND. PERSPECTIVE: Breast surgery that involves ALND seems to uniformly cause nerve injury, which cannot be prevented by the perioperative administration of 200 mg of amantadine. It is most commonly presented by painful hypoesthesia or anesthesia dolorosa in the axillary/inner arm area, which is moderate in intensity and likely to persist for at least 6 months.

Adolescent↗
PubMed2006

Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome.

Complex regional pain syndromes (CRPS, type I and type II) are devastating conditions that can occur following soft tissue (CRPS type I) or nerve (CRPS type II) injury. CRPS type I, also known as reflex sympathetic dystrophy, presents in patients lacking a well-defined nerve lesion, and has been questioned as to whether or not it is a true neuropathic condition with an organic basis. As described here, glabrous and hairy skin samples from the amputated upper and lower extremity from two CRPS type I diagnosed patients were processed for double-label immunofluorescence using a battery of antibodies directed against neural-related proteins and mediators of nociceptive sensory function. In CRPS affected skin, several neuropathologic alterations were detected, including: (1) the presence of numerous abnormal thin caliber NF-positive/MBP-negative axons innervating hair follicles; (2) a decrease in epidermal, sweat gland, and vascular innervation; (3) a loss of CGRP expression on remaining innervation to vasculature and sweat glands; (4) an inappropriate expression of NPY on innervation to superficial arterioles and sweat glands; and (5) a loss of vascular endothelial integrity and extraordinary vascular hypertrophy. The results are evidence of widespread cutaneous neuropathologic changes. Importantly, in these CRPS type I patients, the myriad of clinical symptoms observed had detectable neuropathologic correlates.

Adult↗
PubMed2006

Can personality traits and gender predict the response to morphine? An experimental cold pain study.

The aim of the present study was to examine the possible role of personality traits, in accordance with Cloninger's theory, and gender, in the variability of responsiveness to opioids. Specifically, it was intended to test whether or not the three personality dimensions - harm avoidance (HA), reward dependence (RD) and novelty seeking (NS) - as suggested by Cloninger, can predict inter-personal differences in responsiveness to morphine after exposure to experimental cold pain. Thirty-four healthy volunteers (15 females, 19 males) were given the cold pressor test (CPT). Pain threshold, tolerance, and magnitude (VAS) were measured before and after (six measures, 30 min apart) the administration of either 0.5 mg/kg oral morphine sulphate (n=21) or 0.33 mg/kg oral active placebo (diphenhydramine) (n=13) in a randomized, double blind design. Assessment of the three personality traits, according to Cloninger's Tridimensional Personality Questionnaire, was performed before the CPT. A high HA score (but not RD, NS, or baseline values of the three pain parameters) predicted a significantly larger pain relief following the administration of morphine sulphate (but not of the placebo). Women exhibited a larger response in response to both treatments, as indicated by a significantly increased threshold and tolerance following morphine sulphate as well as significantly increased tolerance and decreased magnitude following placebo administration. The present study confirms the existence of individual differences in response to analgesic treatment. It suggests that high HA personality trait is associated with better responsiveness to morphine treatment, and that females respond better than men to both morphine and placebo.

Adolescent↗
PubMed2006

Quantitative sensory testing for spinal cord stimulation in patients with chronic neuropathic pain.

OBJECTIVE: A prospective pilot study was conducted, attempting to identify objective tests that would help clinicians to assess the efficacy of spinal cord stimulation (SCS) trial preceding permanent device implantation. SETTING: Four university hospitals in the United States and Israel. PARTICIPANTS: Thirteen patients with radicular leg pain due to failed back surgery syndrome (FBSS) or leg pain due to complex regional pain syndrome (CRPS) who were candidates for SCS. METHODS: PARTICIPANTS underwent a series of quantitative sensory tests prior to, and seven days after the initiation of SCS trial. These tests included: vibration threshold (conducted using the VSA 3000; Medoc Inc., Ramat Ishay, Israel), cold threshold, warm threshold, heat pain threshold, phasic heat pain threshold, tonic heat pain threshold (conducted using the TSA 2001; Medoc Inc.), and electrical pain tolerance at 5, 250 and 2000 Hz (administered using the NerveScan 2000; Neurotron, Inc., Baltimore, MD, USA). RESULTS: Useful data were obtained from 12 patients. The results of the vibration threshold and the tolerance to electrical stimulation at 5 and 250 Hz changed with an SCS trial. These results also correlated with the decision regarding the permanent implantation, which was made independently of them. In contrast, the results of thermal thresholds and tolerance to electrical stimulation at 2000 Hz tests did not change with the SCS trial. CONCLUSIONS: Our findings, which agree with those of a few other studies, suggest that the vibration threshold and the tolerance to electrical stimulation at 5 and 250 Hz tests can assist the clinician to select the right patients for permanent stimulation.

Adolescent↗
PubMed2005

Efficacy of mu-opioid agonists in the treatment of evoked neuropathic pain: Systematic review of randomized controlled trials.

UNLABELLED: Several reviews of randomized controlled trials (RCTs) have shown the efficacy of mu-opioids in reducing spontaneous neuropathic pain (NP). However, relatively little is known about their specific efficacy for evoked pain, which is a significant problem for many patients with NP. The present systematic review assesses the efficacy of opioid agonists for the treatment of evoked NP based upon published RCTs. We searched articles in any language using the MEDLINE database (1966 to December 2004), the Cochrane Central Register of Controlled Trials (4th quarter, 2004) and the reference lists of retrieved papers, employing search terms for RCTs, opioids and NP. Only RCTs in which opioid agonists were given to treat NP of any etiology, and evoked pain was assessed were included. Data were extracted by two independent investigators. Nine articles met inclusion criteria and were classified as short-term (less than 24h; n=7) or intermediate-term trials (4 weeks; n=2). Although the scarcity of retrieved data precluded formal meta-analysis of short-term trials, we found that the intensity of dynamic mechanical allodynia was significantly attenuated by opioids relative to placebo in all studies. In contrast, no consistent effects on the magnitude of static allodynia, the threshold for mechanical allodynia or the threshold or magnitude of heat allodynia were found. The threshold and magnitude of cold-induced allodynia generally responded positively to opioid treatments in patients with peripheral pain syndromes, but not central pain syndromes. Evoked pain was studied in only two intermediate-term trials, in both of which oxycodone was significantly superior to placebo. The results of the two trials were combinable for a meta-analysis that showed an overall 24 points difference in endpoint pain intensities between patients given opioids and those treated with placebo (95% CI -33 to -15; p<0.00001). IN CONCLUSION: short-term studies show that opioids can reduce the intensity of dynamic mechanical allodynia and perhaps of cold allodynia in peripheral NP. Insufficient evidence precludes drawing conclusions regarding the effect of opioids on other forms of evoked NP. A meta-analysis of intermediate-term studies demonstrates the efficacy of opioids over placebo for evoked NP. These findings are clinically relevant because dynamic mechanical allodynia and cold allodynia are the most prevalent types of evoked pain in NP.

Analgesics, Opioid↗
PubMed2005

Effects of cold stimulation on secondary hyperalgesia (HA) induced by capsaicin in healthy volunteers.

Little is known about the sensory characteristics and underlying mechanisms behind secondary hyperalgesia (HA) (2 degrees HA). The aim of the present study was to investigate the relationships between two different noxious stimuli, mechanical and cold on capsaicin-induced 2 degrees HA. Fourteen healthy volunteers were exposed to three different cold stimuli (20, 10, 0 degrees C) 30 s each, on both forearms. The cold stimuli were applied before (baseline) and 8 min after intradermal administration of 50-microg capsaicin to the forearm, distally to the injection site in the inspected area of 2 degrees HA. Pain intensities were assessed immediately after each cold stimulus by means of a visual analogue scale (cold-VAS). Additionally, areas of mechanical HA (cm(2)) were assessed distally and proximally to the injection site at three different time points: 5, 8 (right after the second series of cold stimuli), and 30 min after the injection. No significant differences in cold-VAS were found between pre- and post-capsaicin injection at the tested forearm (P= 0.334), whereas significant reduction from pre- to post-injection was found in cold-VAS in the control forearm (P= 0.024). Further, 8 min after the injection, the cold stimulation led to an expansion of 2 degrees HA area (from 5.1+/-1.38 to 11.4+/-1.72 cm(2)) to punctuate stimuli distally but not proximally to the injection site (P<0.05). It is concluded that there is no HA to cold stimuli within the area of mechanical 2 degrees HA. However, cooling acts as a conditioning stimulus and expands the area of capsaicin-induced punctuate HA.

Adult↗
PubMed2005

Opioids and abnormal pain perception: New evidence from a study of chronic opioid addicts and healthy subjects.

Recent evidence reported on increased pain sensitivity in animals following parenteral opioid administration and in humans subsequent to intravenously of short-acting opioids and possibly in drug addicts. The aims of the present study were to explore the possibilities that (1) pain perception is altered in chronic opioid addicts (OAs); (2) if indeed so, the cessation of opioid consumption resets their altered pain perception. Sixty heroin or methadone OAs who attended a 4-week inpatient detoxification program were exposed to the cold pressor test (CPT) upon entrance to the program, at 7 and 28 days subsequent to the cessation of opioid consumption (verified by repeated urine toxicology tests). Latency of pain onset (s), pain intensity (0-100 VAS), and tolerance (time for hand withdrawal) in response to the CPT were measured. In comparison with 70 healthy controls, the OAs demonstrated prolonged latency (6.6+/-3.5s versus 10.9+/-7.7s; p < 0.0001); decreased VAS (74+/-16 versus 55+/-20; p < 0.0001); shorter tolerance (56.4+/-51.3s versus 31.7+/-40.7s; p = 0.001). No differences between the three time points in any of the three measures were detected in the OAs. The results provide further evidence of opioid-induced hyperalgesia in the OA population, as manifested by their quicker hand withdrawal. In addition, it appears that detoxification from opioids does not reset pain perception for at least 1 month.

Chronic Disease↗
PubMed2005

Efficacy and safety of opioid agonists in the treatment of neuropathic pain of nonmalignant origin: systematic review and meta-analysis of randomized controlled trials.

CONTEXT: In the United States, an estimated 2 million persons have neuropathic pain that is often resistant to therapy. The use of opioids for neuropathic pain remains controversial, in part because studies have been small, have yielded equivocal results, and have not established the long-term risk-benefit ratio of this treatment. OBJECTIVE: To assess the efficacy and safety of opioid agonists for the treatment of neuropathic pain based on published randomized controlled trials (RCTs). DATA SOURCES: We searched MEDLINE (1966 to December 2004) and the Cochrane Central Register of Controlled Trials (fourth quarter, 2004) for articles in any language, along with reference lists of reviews and retrieved articles, using a combination of 9 search terms for RCTs with 32 terms for opioids and 15 terms for neuropathic pain. STUDY SELECTION: Trials were included in which opioid agonists were given to treat central or peripheral neuropathic pain of any etiology, pain was assessed using validated instruments, and adverse events were reported. Studies in which drugs other than opioid agonists were combined with opioids or opioids were administered epidurally or intrathecally were excluded. DATA EXTRACTION: Data were extracted by 2 independent investigators and included demographic variables, diagnoses, interventions, efficacy, and adverse effects. DATA SYNTHESIS: Twenty-two articles met inclusion criteria and were classified as short-term (less than 24 hours; n = 14) or intermediate-term (median = 28 days; range = 8-56 days; n = 8) trials. The short-term trials had contradictory results. In contrast, all 8 intermediate-term trials demonstrated opioid efficacy for spontaneous neuropathic pain. A fixed-effects model meta-analysis of 6 intermediate-term studies showed mean posttreatment visual analog scale scores of pain intensity after opioids to be 14 units lower on a scale from 0 to 100 than after placebo (95% confidence interval [CI], -18 to -10; P<.001). According to number needed to harm (NNH), the most common adverse event was nausea (NNH, 3.6; 95% CI, 2.9-4.8), followed by constipation (NNH, 4.6; 95% CI, 3.4-7.1), drowsiness (NNH, 5.3; 95% CI, 3.7-8.3), vomiting (NNH, 6.2; 95% CI, 4.6-11.1), and dizziness (NNH, 6.7; 95% CI, 4.8-10.0). CONCLUSIONS: Short-term studies provide only equivocal evidence regarding the efficacy of opioids in reducing the intensity of neuropathic pain. Intermediate-term studies demonstrate significant efficacy of opioids over placebo for neuropathic pain, which is likely to be clinically important. Reported adverse events of opioids are common but not life-threatening. Further RCTs are needed to establish their long-term efficacy, safety (including addiction potential), and effects on quality of life.

Analgesics, Opioid↗
PubMed2005

Skeletonized versus pedicled internal mammary artery: impact of surgical technique on post CABG surgery pain.

OBJECTIVE: Recent evidence suggests that coronary artery bypass graft (CABG) surgery often results in chronic chest wall pain, termed: 'post CABG pain syndrome' (PCP). Direct injury to intercostal nerves during the surgical procedure was presumed to underlie this syndrome. The aim of this study was to investigate the effect of two harvesting techniques of the internal mammary artery (IMA)-skeletonization (S-LIMA) and pedicle (P-LIMA) on the occurrence and incidence of PCP. METHODS: A mailed questionnaire enquiring about the presence and characteristics of PCP was sent to all 482 patients who had undergone CABG in our institution in the years 1999-2000. A randomly chosen subgroup of IMA patients reporting PCP were summoned for evaluations of pain localization and intensity, thermal and tactile sensitivity, and disability assessment using recognized tests and indices. RESULTS: Of the 380 responders (S-LIMA: 221, P-LIMA: 125, veins only V-34) 169 (44%) reported having PCP. Its prevalence was similar between the two IMA groups (S-LIMA: 45%, P-LIMA: 50%) but significantly lower in the V group (18%, P=0.003). Physical assessment in the subgroup of 43 IMA patients (S-LIMA: 22, P-LIMA: 21) performed 40.2+/-8.7 months after surgery confirmed equal occurrence of mostly left and midline chest wall neuropathic pain in both IMA groups. No significant differences were found between the two groups in respect to indices of pain intensity, thermal and tactile sensitivity and disability. CONCLUSIONS: PCP is a prevalent finding in post CABG patients. The skeletonization technique of IMA harvesting although causing significantly less inner chest wall trauma does not appear to reduce the occurrence of PCP. This finding may imply that ischemic injury rather than direct mechanical injury to the intercostal nerves is the putative mechanism underlying PCP.

Aged↗
PubMed2005

Vasomotor response to cold stimulation in human capsaicin-induced hyperalgesic area.

Cooling the skin induces sympathetically driven vasoconstriction, with some vasoparalytic dilatation at the lowest temperatures. Neurogenic inflammation, on the other hand, entails vasodilatation. In this study we investigated the balance between vasoconstriction and vasodilatation in an area of experimentally induced secondary hyperalgesia (2 degrees HA), in response to low-temperature stimulations. Fourteen healthy volunteers were exposed to three 30-s long cold stimuli (20, 10, and 0 degrees C) applied, at three adjacent sites, before (baseline) and 8 min after intradermal injection of 50 microg capsaicin to the volar forearm. The cold stimuli were applied distally to the injection site within the 2 degrees HA. Blood flux (BF) and skin temperatures were measured at four different regions (proximally, and distally to the capsaicin injection and at the 0, 10, and 20 degrees C thermode sites) all within the 2 degrees HA. The vascular measurements were conducted five times. Results showed a marked increase in BF after baseline cold stimulation (P<0.001) at the 0 degrees C compared with the three other sites. In addition, vasodilatory effect (elevated BF) was found following the capsaicin injection compared with baseline for all regions (P<0.001): the non-cooled area was dilated by 450+/-5.1%; The vasoconstrictive effect for the 10 and 20 degrees C did not overcome the capsaicin vasodilatation, but did reduce it, with dilatation of 364+/-7.0% and 329+/-7.3%, respectively. For 0 degrees C, a dilatation of 407+/-6.5% was seen. It is concluded that in this experimental model, and potentially in the equivalent clinical syndromes, vasodilatation induced by the inflammation is only slightly reduced by cold stimulation such that it is still dominant, despite some cold-induced vasoconstriction.

Adult↗
PubMed2005

Evidence for cortical hyperexcitability of the affected limb representation area in CRPS: a psychophysical and transcranial magnetic stimulation study.

Functional alterations in noxious, sensory and motor circuits within the central nervous system may play an important role in the pathophysiology of complex regional pain syndrome (CRPS). The aim of the present study was to search for further evidence of hyperexcitability in the hemisphere contralateral to the affected limb in patients with CRPS by employing both psychophysical and transcranial magnetic stimulation (TMS) methods. Twelve patients with CRPS type I, confined to the distal part of a limb (six in an upper-limb and six in a lower-limb), were enrolled in the study. The quantitative thermal, mechanical and 'wind-up' like pain testing was performed at the most painful site in the affected limb and in the ipsilateral limb. Results were then compared to those found at mirror sites in the contralateral limbs. TMS was used to assess the inter-hemispheric difference in parameters of corticospinal excitability, intracortical inhibition, and intracortical facilitation. The quantitative thermal and mechanical testing showed significant differences in cold, heat and mechanical pain thresholds, as well as in the first and last 'wind-up' stimuli between the affected and the contralateral limbs of the CRPS patients. No significant differences between the ipsilateral unaffected limbs and their contralateral pair limbs were found. A significant reduction in the short intracortical inhibition associated with a significant increase of the I-wave facilitation was found in the hemisphere contralateral to the affected side in the upper-limb CRPS group. No significant inter-hemispheric asymmetry between the affected and the non-affected sides was revealed in the lower-limb CRPS group. Taken together, these results suggest that in patients with well-localized CRPS, there is evidence for sensory and motor CNS hyperexcitability, though it seems to involve only corresponding regions within the CNS rather than the entire hemisphere.

Adult↗
PubMed2005

Oral opioid administration and hyperalgesia in patients with cancer or chronic nonmalignant pain.

AIMS: Previous research has reported on reduced paw withdrawal latencies to heat and mechanical stimuli after parenteral administration of opioids in animals and on increased pain sensitivity in humans subsequent to postoperative infusions of short-acting opioids or in drug addicts. The aim of the present study was to explore the possibility that oral opioid treated patients with cancer-related or chronic nonmalignant pain differ in their pain sensitivity from patients treated with non-opioid analgesics. METHODS: The study population consisted of 224 patients, including 142 in the opioid-treated group and 82 in the non-opioid-treated group. Pain thresholds for punctuate measured by von Frey filaments (g), mechanical pressure measured by pressure algometer (mmHg), heat stimuli measured by quantitative sensory testing (degrees C), as well as suprathreshold tonic heat pain intensity (46.5 degrees C for 1 min) measured by 0-10 numerical pain scale (NPS) were obtained at a nonpainful site (thenar eminence) in all patients. RESULTS: No differences between the groups were found for gender, age, duration of pain, or duration of treatment (independent variables). No significant differences between the groups were found in punctuate (difference = 17.0 g (95% CI -8.8, 42.8), P = 0.19), pressure (2.2 mmHg (-28.7, 33.2), P = 0.89) and heat (-0.3 degrees C (-1.5, 0.9), P = 0.70) pain thresholds, or in suprathreshold heat pain intensity (difference between maximal pain intensities -0.4 NPS units (95% CI -1.2, 0.4), P = 0.31). Pearson correlations within the opioid-treated group failed to show significant relationships between any of the independent variables and the outcome measures. A further comparison of the outcomes between the 'weak' opioid-treated subgroup and the 'strong' opioid-treated subgroup again revealed insignificant results. CONCLUSIONS: These results suggest that the administration of 'commonly used' dosages of oral opioids does not result in abnormal pain sensitivity beyond that of patients receiving non-opioid analgesia.

Administration, Oral↗
PubMed2005

Lamotrigine for neuropathic pain.

Lamotrigine is an antiepileptic drug that stabilizes neural membranes by blocking the activation of voltage-sensitive sodium channels and inhibiting the presynaptic release of glutamate. Full length reports of five open trials and six out of seven randomized controlled trials (plus two abstracts) have demonstrated the efficacy of lamotrigine in the treatment of various forms of neuropathic pain. The present drug profile provides a review of the pharmacologic properties of lamotrigine, the clinical evidence related to its efficacy and safety, and discusses the current and future role of the drug in the treatment of neuropathic pain.

Analgesics↗
PubMed2004

Plasma endothelin-1 levels in patients with complex regional pain syndrome.

The clinical characteristics of complex regional pain syndrome (CRPS)--spontaneous and stimulus-evoked pain, autonomic abnormalities, motor dysfunction, and trophic changes in the affected limb--are well known. However, its pathogenesis is unclear, and the diagnosis is often delayed, in part due to lack of objective laboratory tests. Endothelin-1 (ET-1) is a potent vasoconstrictor that has recently been shown to produce pain, allodynia, edema, and muscle weakness, as well as to exert a direct excitatory effect on nociceptive afferents. Furthermore, new evidence indicates that ET-1 is involved in various cancer- and non-cancer-related painful conditions. The aim of the present explorative study was to determine the ET-1 plasma levels in patients with CRPS in an attempt to identify a 'laboratory marker' for CRPS and to search for evidence suggesting that ET-1 may be involved in the pathogenesis of CRPS. ET-1 plasma levels were determined in 20 severely affected CRPS patients, in eight patients with non-CRPS chronic painful conditions, and in 10 healthy volunteers. The results showed that there were no significant differences in ET-1 plasma levels between the three groups. We conclude that the plasma level of ET-1 cannot be regarded as a 'marker' for CRPS. Yet, the possibility that ET-1 is involved in the pathophysiology of CRPS has not been excluded and deserves further investigation.

Adult↗