Biomedical subjects

Perry N Fuchs

Publications and source records attributed to Perry N Fuchs.

3 recordsLinked to original sources

PubMed2001

Enhanced formalin nociceptive responses following L5 nerve ligation in the rat reveals neuropathy-induced inflammatory hyperalgesia.

The development of mechanical and thermal hypersensitivity following peripheral nerve injury is well known and a great deal of research has been directed towards understanding the mechanisms underlying these phenomena. However, there has been very little research examining if hypersensitivity to an inflammatory condition following nerve injury also develops. Therefore, the purpose of the present study was to determine if hypersensitivity to an inflammatory condition produced in the formalin test develops following ligation of the L5 spinal nerve. Male Sprague-Dawley rats received tight ligation of the L5 spinal nerve or were given sham surgery. Following a 14-day recovery period, the threshold to produce a withdrawal response to a mechanical stimulus was measured using von Frey monofilaments and then formalin behavioral responses were measured. Compared to sham animals, L5 ligated animals exhibited significantly lower mechanical paw withdrawal thresholds as well as elevated and prolonged nociceptive responses during the second phase (20-60 min) of the formalin test. These results reveal enhanced inflammatory nociceptive processes following peripheral nerve damage and might provide a useful approach to study underlying neural mechanisms associated with clinical neuropathic pain syndromes.

Animals↗

PubMed2000

Intradermal injection of norepinephrine evokes pain in patients with sympathetically maintained pain.

Tissue injuries, with or without involvement of nerves, may lead to ongoing pain and hyperalgesia to external stimuli. In a subset of patients, the pain is maintained by sympathetic efferent activity (SMP). We investigated if the peripheral administration of the alpha-adrenergic agonist, norepinephrine (NE), in physiologically relevant doses resulted in pain in patients with SMP. To establish the dose of intradermal NE required to induce cutaneous vasoconstriction, NE (1 nM-10 microM, 30 microl) was injected under a laser Doppler probe on the volar forearm of seven normal subjects. A decrease in blood flow was evident at a dose of 10 microM. Twelve patients (five male, seven female) diagnosed to have SMP based on the decrease in pain by a local anesthetic sympathetic blockade (70+/-6%) were enrolled in the study. Pain ratings were obtained continuously for 5 min after intradermal injections of saline and NE (0.1-10 microM) into their hyperalgesic zone and the mirror-image contralateral side. Injections were done during the period of pain relief following a local anesthetic sympathetic blockade. Similar injections were made in eight control subjects. On the affected side of the patients, the two highest concentrations of NE (1 and 10 microM) caused significantly more pain than saline (P<0.05, ANOVA). In contrast, there was no significant pain induced by the NE injections in the unaffected side and in control subjects. Six of nine patients tested reported a marked decrease in pain and hyperalgesia following infusion of phentolamine (1 mg/kg over 10 min). Two of the three patients who did not receive pain relief following phentolamine infusion also did not report pain to the NE injections. We conclude that NE injections produce pain in SMP patients at doses that are at the threshold for producing vasoconstriction. These studies support a role for cutaneous adrenoceptors in the mechanisms of sympathetically maintained pain.

Adrenergic alpha-Agonists↗

PubMed1999

Topical EMLA pre-treatment fails to decrease the pain induced by 1% topical capsaicin.

Topical capsaicin has been reported to be beneficial for the treatment of neurogenic pain. However, due to the burning pain associated with topical capsaicin, many patients discontinue treatment before therapeutic benefits are obtained. This study assessed the efficacy of EMLA (eutectic mixture of 2.5% prilocaine and 2.5% lidocaine) to block pain induced by the topical application of 1% capsaicin. Nine healthy subjects (five males and four females) participated in the study. High dose topical capsaicin (1%) was applied to a 2.5 x 2.5 cm region of both volar forearms for 6 h. One arm was pretreated (for 2 h) and cotreated with EMLA, and the other arm served as vehicle control. Average and peak pain ratings were recorded at 15-min intervals using a 0 (no pain) to 10 (worst possible pain) scale. Average and peak pain ratings were significantly lower at the EMLA site during the first 15-30 min of capsaicin treatment. However, for the remaining 5.5 h of capsaicin treatment, the pain ratings at the EMLA and vehicle sites were not significantly different. The 6 h treatment with high dose topical capsaicin (1%) produced significant desensitization to heat stimuli that was not affected by EMLA treatment. EMLA fails to produce a long lasting attenuation of the pain induced by topical application of 1% capsaicin. These results argue against the use of EMLA to block pain to topical capsaicin during the treatment of neurogenic pain.

Administration, Topical↗