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In animal neuroma models the application of alpha-adrenergic agonists causes a burst of spontaneous afferent activity. The increased activity has been hypothesized to generate nociceptive input. Corroborative work in humans, however, has not been done. Nine subjects with chronic nerve end neuromas received perineuromal injections of normal saline, epinephrine (5 micrograms), and lidocaine in a blinded manner. Qualitative and quantitative pain assessments were performed with each injection. Epinephrine, but not saline, caused an intense increase in reported pain with subjects often commenting that the appendage was "on fire". Lidocaine significantly reduced but did not completely abolish the reported pain. The chemosensitivity of the neuroma to epinephrine may explain some of the clinical responses noted after sympathetic system manipulation. It is likely that alpha-adrenergic sensitivity is only one of many components sustaining or exacerbating pain after nerve injury.

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The analgesic and adverse effects of intrathecal methadone 5 mg, 10 mg and 20 mg were assessed and compared with intrathecal morphine 0.5 mg. The study was conducted on 38 patients who underwent total knee or hip replacement surgery. The intrathecal opioid was administered at the end of surgery and assessments began 1 h thereafter and continued for 24 h. Pain measurements, supplementary analgesia requirements, and adverse effects were recorded. Intrathecal morphine 0.5 mg provided effective and prolonged analgesia. Intrathecal methadone 5 mg, 10 mg, and 20 mg produced good analgesia of 4 h duration. Thereafter the median pain scores with intrathecal methadone were consistently higher (worse) than those with intrathecal morphine (P less than 0.05). The time to the onset of discomfort severe enough to require supplemental morphine was longer after intrathecal morphine than following methadone (15 h with morphine 0.5 mg; 6.25 h, 6.5 h and 6 h with methadone 5 mg, 10 mg, and 20 mg respectively: P less than 0.05). Central nervous system depression manifesting as respiratory depression, hypotension, and excessive drowsiness occurred in 3 of 8 patients injected with methadone 20 mg intrathecally. Generalized pruritus, nausea, vomiting, and urinary retention were common and equally distributed among the treatment groups. We conclude that both intrathecal morphine 0.5 mg and methadone 5, 10, and 20 mg provide excellent analgesia but that morphine has a more prolonged effect. Methadone 20 mg produced unacceptable side effects. Clinical evidence for rostral spread of methadone within the CSF, as indicated by facial itching and excessive drowsiness, was less apparent with 5 mg than with 10 and 20 mg. Various explanations for the observed differences between the drugs are discussed.

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Eight patients with established lower limb postamputation stump pain were given lumbar intrathecal fentanyl 25 micrograms and lidocaine 70 mg 2 weeks apart in an attempt to better understand the role of peripheral and central mechanisms in this condition. Baseline pain was recorded and then analgetic and side effects and their duration were assessed. Three self-administered questionnaires with appropriate psychometric proprieties were given to the patients. Intrathecal fentanyl always abolished the pain. Its onset was rapid being heralded within 1-2.5 min by a pleasant sensation of warmth involving the lower trunk and legs. Analgesia was complete by 5-10 min and had a median duration of 8 h. The patients had a sense of well being and were unable to elicit discomfort by pain aggravating maneuvers. Normal motor and sensory functions were retained. Pruritus was the only adverse effect unique to intrathecal fentanyl. Intrathecal lidocaine usually relieved the discomfort but was unable to abolish it in 3 of 8 patients despite adequate neural blockade. Its onset of action was slower and duration of effect shorter than fentanyl. Intrathecal fentanyl provided profound analgesia associated with normalization of stump sensations and euphoria, probably due to a segmental spinal action. The effects of lidocaine were inferior to fentanyl due to the associated motor and sensory paralyses as well as the absence of euphoria. This study suggests that, while peripheral mechanisms played a role, central mechanisms involving the spinal cord were more important in the modulation of established stump pain in the 8 subjects evaluated.

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Two patients with postamputation stump and phantom limb pain respectively responded favorably to intrathecal fentanyl which temporarily abolished the pain, normalized sensations and produced euphoria without supraspinal effects. One of the patients subsequently received intrathecal, extradural and intravenous fentanyl as well as intrathecal lidocaine. The neuraxial (intrathecal and epidural) fentanyl temporarily abolished the pain. Intravenous fentanyl and intrathecal lidocine were unable to reproduce this effect. Neuraxial fentanyl apparently produced its effects by a segmental spinal action. Spinal modulation of postamputation pain was important in these patients.

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Rat neurons have shown an increase of spontaneously active fibers to systemically administered potassium channel blocking agents such as tetraethylammonium chloride (TEA) and gallamine. Neuroma formation and spontaneous activity have been associated with autotomy in rats and pain in humans. To evaluate the chemosensitivity of human neurons to potassium channel blocking agents, 9 subjects with neuroma pain underwent perineuromal injection in a single-blinded fashion of normal saline, gallamine, and lidocaine. Sodium had no effect on control pain levels, while gallamine significantly increased and lidocaine significantly decreased pain from control levels. Three of 4 patients with accompanying phantom limb pain noted an increase in pain after the injection of gallamine. The data suggest that peripheral input plays a modulating but not solitary role in both neuroma and phantom limb pain. Agents which increase potassium channel permeability or decrease sodium influx would be predicted to decreased perceived pain.

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