Anesth Analg 2002 Jan;94(1):199-202
Department of Anaesthesia and The National Refractory Angina Centre, The Cardiothoracic Centre Liverpool NHS Trust, Liverpool, England.
[Medline record in process]
Despite receiving thoracic epidural analgesia, severe ipsilateral shoulder pain is common in patients after thoracotomy. We recruited 44 patients into a double-blinded randomized placebo-controlled study to investigate whether suprascapular nerve block would treat postthoracotomy shoulder pain effectively. All patients received a standard anesthetic with a midthoracic epidural. Thirty patients who experienced shoulder pain within 2 h of surgery were randomly assigned to receive a suprascapular nerve block with either 10 mL of 0.5% bupivacaine or 10 mL of 0.9% saline. Shoulder pain was assessed before nerve blockade, at 30 min, and then hourly for 6 h after the block using a visual analog scale (VAS) and a 5-point verbal ranking score (VRS). The incidence of shoulder pain before nerve block was 78%. There was no significant decrease in either VAS or VRS in the Bupivacaine group. These results suggest that this pain is unlikely to originate in the shoulder and lead us to question the role of a somatic afferent in referred visceral pain. We conclude that suprascapular nerve block does not treat ipsilateral shoulder pain after thoracotomy in patients with an effective thoracic epidural. IMPLICATIONS: This randomized, double-blinded, placebo-controlled trial showed that suprascapular nerve block does not treat the severe ipsilateral shoulder pain that patients experience after thoracotomy. This has implications for established theories of referred pain and indicates that this pain is unlikely to originate in the shoulder.
PMID: 11772828, UI: 21633745
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Anesth Analg 2002 Jan;94(1):11-5
Departments of Anesthesiology, Respiratory Diseases, and Surgery, Medical Faculty of Istanbul, University of Istanbul, Turkey.
In this clinical, randomized, prospective study, we compared the effects of three different analgesia techniques (thoracic epidural analgesia [TEA] with and without preoperative initiation and IV patient-controlled analgesia [IV-PCA]) on postthoracotomy pain in 69 patients. In two groups, a thoracic epidural catheter was inserted preoperatively. Group Pre-TEA had bupivacaine and morphine solution preoperatively and intraoperatively. Postoperative analgesia was maintained with epidural PCA with a similar solution. Group Post-TEA, with no intraoperative medication, had the same postoperative analgesia as Group Pre-TEA plus the bolus dose. Group IV-PCA received only IV-PCA with morphine for postoperative analgesia. Pain was evaluated every 4 h during the first 48 h at rest, cough, and movement. Pre-TEA was associated with decreased pain compared with the other groups. Six months later, the patients were asked about their pain. The incidence and the intensity of pain were most frequent in Group IV-PCA (78%) and were the least in Group Pre-TEA (45%) (Group Pre-TEA versus Group IV-PCA, P = 0.0233; Group Pre-TEA versus Group IV-PCA, P = 0.014). Patients having pain on the second postoperative day had 83% chronic pain. TEA with preoperative initiation is a preferable method in preventing acute and long-term thoracotomy pain. IMPLICATIONS: Preoperatively initiated thoracic epidural analgesia has the most satisfying results in controlling postthoracotomy pain in the acute and long-term period, and it is associated with a decreased incidence (and intensity) of chronic pain compared with postoperative (epidural or IV) analgesia. Chronic pain has an incidence of 62%.
PMID: 11772793, UI: 21633710
Anesthesiology 2002 Jan;96(1):35-44
Submitted for publication May 1, 2001.
BACKGROUND: Although pain-related activation was localized in multiple brain areas by functional imaging, the temporal profile of its signal has been poorly understood. The authors characterized the temporal evolution of such activation in comparison to that by conventional visual and motor tasks using functional magnetic resonance imaging. METHODS: Five right-handed volunteers underwent whole brain echo-planar imaging on a 3 T magnetic resonance imaging scanner while they received pain stimulus on the right and left forearm and performed visually guided saccade and finger tapping tasks. Pain stimulus on the right and left forearm consisted of four cycles of 15-s stimulus at 47.2-49.0 degrees C, interleaved with 30-s control at 32 degrees C, delivered by a Peltier-type thermode, and visually guided saccade and finger tapping of three cycles of 30-s active and 30-s rest conditions. Voxel-wise t statistical maps were standardized and averaged across subjects. Blood oxygenation level-dependent signal time courses were analyzed at local maxima of representative activation clusters (t > 3.5). RESULTS: Pain stimulus on the right forearm activated the secondary somatosensory (S2), superior temporal, anterior cingulate, insular, prefrontal cortices, premotor area, and lenticular nucleus. Pain stimulus on the left forearm activated similar but fewer areas at less signal intensity. The S2 activation was dominant on the contralateral hemisphere. Pain-related activation was statistically weaker and showed less consistent signal time courses than visually guided saccade- and finger tapping-related activation. Pain-related signals decayed earlier before the end of stimulus, in contrast to well-sustained signal plateaus induced by visually guided saccade and finger tapping. CONCLUSIONS: The authors speculate that pain-related blood oxygenation level-dependent signals were attenuated by the pain-induced global cerebral blood flow decrease or activation of the descending pain inhibitory systems.
PMID: 11752999, UI: 21621164
BMJ 2001 Dec 8;323(7325):1366
Publication Types:
PMID: 11776946, UI: 21632719
BMJ 2001 Dec 1;323(7324):1306-7
PMID: 11764758, UI: 21607385
BMJ 2001 Nov 24;323(7323):1250; discussion 1250-1
PMID: 11758522, UI: 21594037
PMID: 11758521, UI: 21594036
BMJ 2001 Nov 24;323(7323):1250-1
PMID: 11758520, UI: 21594038
Clin Orthop 2001 Dec;(393):345-9
Department of Orthopaedic Surgery, Okayama University Medical School, Faculty of Medicine, Japan.
PMID: 11764368, UI: 21606949
Clin Orthop 2001 Dec;(393):258-63
Department of Orthopaedic Surgery, Westfalische Wilheims-Universitat Munster, Germany.
Thirteen patients with osteoid osteoma were enrolled in a prospective trial to test whether rofecoxib, a selective cyclooxygenase-2 inhibitor, is as effective for pain control as acetylsalicylic acid. Each patient documented the pain level using a visual analog scale, with 0 being no pain and 10 being unbearable pain, during 2 days of no pain medication, 4 days of 500 mg acetylsalicylic acid three times a day, and 10 days of 25 mg rofecoxib once a day. Oral administration of 500 mg acetylsalicylic acid three times a day led to a significant decrease in pain at night, pain at rest, and pain induced by exercise. Twenty-five milligrams rofecoxib given once a day at midday showed the same remarkable improvement in pain at night, pain at rest, and pain induced by exercise. Rofecoxib in comparison with acetylsalicylic acid showed a trend toward lower pain levels in all categories. Rofecoxib offered a significantly better reduction in pain at rest during the day than did acetylsalicylic acid. Results of the current study suggest that pain induction in osteoid osteoma is related to cyclooxygenase-2, an enzyme that is blocked by acetylsalicylic acid and rofecoxib. Conservative medical treatment with rofecoxib for osteoid osteoma is recommended when percutaneous intervention is associated with significant morbidity.
PMID: 11764357, UI: 21606938
Geriatrics 2001 Dec;56(12):18-24
Harvard Medical School, USA.
Herpes zoster (shingles) is a localized infection that begins in the dorsal root ganglla of the cranial or spinal nerves and spreads as a rash over the corresponding dermatome. It usually is caused by reactivation of latent varicella-zoster virus remaining from childhood chicken pox. Postherpetic neuralgia (PHN) is a chronic neuropathic pain syndrome that occurs as a complication of shingles, most commonly in older persons. Acute zoster and PHN can be severe conditions associated with impaired sleep, decreased appetite, depression, anxiety disorder, and diminished libido. Management of zoster-related pain should begin as soon as possible after the onset of symptoms. Combination therapy--including antiviral, antidepressant, corticosteroid, opioid, and topical agents--provides the most effective analgesia.
PMID: 11766559, UI: 21616663
J Clin Oncol 2002 Jan 1;20(1):348-52
Department of Pain Medicine and Palliative Care, Beth Israel Medical Center, New York, NY.
PMID: 11773191, UI: 21635094
Neurology 2001 Dec 26;57(12):2179-84
Neurologische Klinik (Drs. Birklein and Weber), Institut fur Physiologie und experimentelle Pathophysiologie (Dr. Schmelz), Friedrich-Alexander-Universitat Erlangen, Germany.
OBJECTIVE: To test the contribution of neurogenic inflammation and neuropeptide release to the pathophysiology of complex regional pain syndrome (CRPS). BACKGROUND: CRPS is characterized by edema and increased skin temperature, sympathetic dysfunction and pain, or hyperalgesia. This investigation was prompted by a recent study by the authors that suggested a facilitated neurogenic inflammation in CRPS. METHODS: In addition to physical examination, calcitonin gene-related peptide (CGRP) serum concentrations were measured using a radioimmunoassay (RIA) for human CGRP in 19 patients with acute CRPS, on the affected and unaffected sides (n = 13), before and 9 months after therapy (n = 9). In addition, an age- and sex-matched group of 16 healthy controls was investigated. RESULTS: In blood from the cubital vein, CGRP levels in patients with CRPS (122.2 +/- 14.6 pmol/L) were increased (controls 83.8 +/- 6.7 pmol/L, p < 0.03). There was no difference between the affected and unaffected sides. There was, however, a reduction of serum CGRP after therapy (acute disease: 141.2 +/- 18.5 pmol/L, after therapy 106.7 +/- 11.3 pmol/L, p < 0.005); absolute CGRP levels then no longer differed from controls. Increased serum CGRP was correlated to the incidence of nerve lesions (p < 0.02) and hyperhidrosis (p < 0.04). There was no correlation to other clinical symptoms, duration of CRPS, or pain. However, normalization of CGRP after therapy was accompanied by clinical improvement of local inflammatory signs, but not by pain reduction. CONCLUSIONS: Increased systemic CGRP levels in patients with acute CRPS suggest neurogenic inflammation as a pathophysiologic mechanism contributing to vasodilation, edema, and increased sweating. However, pain and hyperalgesia, in particular in chronic stages, were independent of increased neuropeptide concentration.
PMID: 11756594, UI: 21630124
Neurology 2001 Dec 26;57(12):2166-7
PMID: 11756593, UI: 21630123
Neurology 2001 Dec 26;57(12):2161-2
Department of Anesthesia and Faculty of Dentistry, McGill University, Montreal, Quebec, Canada.
PMID: 11756591, UI: 21630121
Support Care Cancer 2002 Jan;10(1):13-35
Harry R. Horvitz Center for Palliative Medicine.
Morphine is the most practical and versatile analgesic for the relief of severe pain associated with advanced cancer. Information is available in the literature about its use in routine clinical practice. Morphine induces analgesia by reducing neurotransmitter release presynaptically and hyperpolarizing dorsal horn neurons at the postsynaptic level, thus preventing rostral transmission of nociception. Morphine has a unique metabolism via glucuronidation (UGT2B7), which results in an active metabolite (morphine-6-glucuronide). The pharmacokinetics of morphine relate to its hydrophilic characteristic, volume of distribution, route of administration and clearance. Renal failure alters its pharmacokinetics more than cirrhosis. The age of the patient and multiple medications will alter morphine pharmacokinetics. Morphine can be given by several different routes: oral, rectal, subcutaneous (s.c.), intravenous (i.v.), epidural and intrathecal. Recent experience confirms benefits of topical morphine for cutaneous pain associated with benign or malignant ulcers. Guidelines for morphine administration are reviewed, and in particular those of the Harry R. Horvitz Center for Palliative Medicine are outlined.
PMID: 11777184, UI: 21632924
Support Care Cancer 2001 Nov;9(8):606-10
Department of Palliative Medicine, St Vincent's University Hospital, Dublin, Ireland. e.tiernan@abdn.ac.uk
The objectives of this study were (i) to assess the level of knowledge with respect to pain and symptom management among doctors in their first year after graduation and (ii) to measure the impact of a structured teaching programme on their level of knowledge. All 34 newly qualified junior house officers in one teaching hospital were offered a six-session teaching programme in pain and symptom management. A multiple-choice questionnaire was used to assess their level of knowledge at the beginning and at the end of a 6-month period over which the teaching sessions took place. Attendance at and satisfaction with the programme were high. There was a significant improvement in the level of knowledge at the end of the programme, with the greatest improvement in those who attended most sessions. The low scores recorded for the questionnaire administered before the teaching programme suggest that there is a critical need for improved education in palliative care amongst newly qualified doctors. We have shown that a simple in-service case-based teaching programme can meet this need effectively.
PMID: 11762971, UI: 21597909
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