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Biomedical subjects

Howard L Fields

Publications and source records attributed to Howard L Fields.

44 records · Page 3Linked to original sources

Post-herpetic neuralgia: the relation of pain complaint, sensory disturbance, and skin temperature.

Twelve otherwise healthy patients with longstanding postherpetic neuralgia (PHN) were prospectively studied using clinical examination, infrared thermography and response to local anesthetic skin infiltration. All had at least 2 of 3 possible components to their PHN pain: continuous, neuralgic, or allodynic. In patients with allodynia, maximal reported pain and the location of maximal allodynia on sensory examination were largely overlapping and were often warm thermographically. Areas of dense sensory loss and skin scarring without allodynia were usually cool thermographically. Local anesthetic skin infiltration produced substantial pain relief in all 9 patients (essentially complete relief in 7) with allodynia: the 3 patients with predominantly continuous pain were not relieved. In 7 of 8 skin infiltration responders, the same dose of lidocaine i.m. in the deltoid muscle also produced significant, though less complete pain relief. These results suggest that PHN patients can be divided into at least 2 clinical groups: those with predominantly continuous pain localized to a region of significant sensory loss and those in whom allodynia is the most prominent sensory disturbance. The latter group has pain localized to areas with relatively preserved sensation. The differences in clinical features and response to lidocaine suggest that there are at least 2 different mechanisms contributing to the pain of PHN.

Aged↗

Topical lidocaine reduces pain in post-herpetic neuralgia.

We report the results of a single session, non-blinded, trial of topical application of 10% lidocaine in gel form to the painful skin of 11 patients with well established post-herpetic neuralgia (PHN). Pain decreased as measured by 100 mm VAS pain scale and 100 mm VAS pain relief scale in both trigeminal and thoracic PHN patients.

Administration, Topical↗

Synergy between the antinociceptive effects of intrathecal clonidine and systemic morphine in the rat.

These experiments tested the hypothesis that intrathecal alpha 2-adrenergic antinociception could be potentiated by the concurrent administration of systemic morphine. Thirty-four male rats, implanted with chronic indwelling intrathecal catheters, received a subcutaneous injection of either morphine sulfate or an equal volume of saline, followed by an intrathecal injection of clonidine HCl or an equal volume of vehicle. Antinociception was assessed using the tail-flick test. Tail-flick latencies following subcutaneous morphine plus intrathecal vehicle, or subcutaneous saline plus intrathecal clonidine were not significantly different from baseline. However, the combination of subcutaneous morphine plus intrathecal clonidine produced a significant antinociceptive effect. Such potentiation may prove to be a useful clinical strategy to help maximize analgesia, minimize side effects and attenuate the development of tolerance.

Analgesics↗

Potentiation of morphine antinociception by monoamine reuptake inhibitors in the rat spinal cord.

Potentiation of the antinociceptive effects of morphine by the tricyclic antidepressants was assayed in awake restrained rats using the tail-flick test. Intrathecally administered amitriptyline, desipramine or sertraline at doses that had no effect themselves (25-30 micrograms) potentiated a subthreshold parenteral dose of morphine (0.5 mg/kg). The morphine potentiating effect of amitriptyline was prevented by prior administration of parachlorophenylalanine (PCPA). This effect of PCPA was not restored by 5-hydroxytryptophan (5-HTP) but was restored when the animals were left for 14 days to replete. The morphine potentiating effects of amitriptyline, desipramine and sertraline were blocked by intrathecal administration of low doses of the serotonin antagonist methysergide and the alpha-adrenergic antagonists yohimbine and phentolamine but not by the beta-adrenergic antagonist propranolol. The results are consistent with the hypothesis that the potentiation of morphine's antinociceptive effect by tricyclic antidepressants depends on activation of both spinopetal serotonin and adrenergic neurons.

1-Naphthylamine↗

Analgesic responses to morphine and placebo in individuals with postoperative pain.

The effects of placebo and varying doses of intravenous morphine were studied in 74 patients. All patients underwent extraction of impacted mandibular third molars. Two hours after onset of anesthesia all patients received a placebo (intravenous saline). One hour after the placebo administration each patient received either a second placebo or, 4, 6, 8 or 12 mg of morphine, double blind, via a hidden intravenous line. Pain level was evaluated 50 min after morphine administration using a visual analog scale. Pooled data from all patients produced a dose-response curve asymptotic by 8 mg. The mean pain relief following the second placebo was found to be between that obtained following hidden administration of 4 and 6 mg of morphine. When pain level reports for individuals were plotted two unexpected features appeared. First, no patient reported complete relief, even at the highest dose of morphine (12 mg). Second, pain level reports 50 min following each dose of morphine tended to be in two clusters. Within each cluster the average pain was independent of the dose of morphine administered. However, in groups receiving progressively higher doses of morphine, the percentage of patients within the low pain level cluster increased. These latter observations are most consistent with the concept that there is a step component for narcotic analgesia.

Adolescent↗