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A 41-year-old female developed spontaneous burning pain (causalgia) and stimulus-induced dysesthesia (allodynia) of the dorso-lateral part of her right foot following trauma. An L3 and L4 sympathectomy eliminated the spontaneous burning pain for only 1 year, but did not affect the stimulus-induced dysesthesia. We evaluated her two years post-sympathectomy with grouped sequential anesthetic blocks and sensory testing. Sympathetic blocks at L1 and L2 eliminated the burning pain and normalized heat perception from baseline hyperalgesia, indicating that the causalgia had been reactivated via more rostral sympathetic ganglia. Anesthetic block of the sural nerve eliminated both the burning pain and the stimulus-induced dysesthesia. During the sural nerve block, perception of touch and pin, but not heat, was preserved in the sural distribution. All perception was lost following subsequent block of the peroneal branches. When the peroneals were blocked first, perception of touch, pin and heat remained in the sural distribution. With peroneal block the burning pain was eliminated, but the stimulus-induced dysesthesia remained, even in the anesthetic peroneal territory. When sural block was added to the peroneal block the stimulus-induced dysesthesia was eliminated, and sensation in the sural distribution was lost. We conclude that the sural distribution received overalapping innervation for touch and pin-prick perception, but that heat perception, burning pain and the stimulus-induced dysesthesia were sural nerve dependent. Further, we were able to dissociate causalgia pain from allodynia in this patient.

The efficacy of amitriptyline was evaluated in 28 patients with chronic oral-facial pain. Most of the patients had evidence of musculoskeletal pain while some had a history suggesting pain of neurogenic origin. Two patients had mixed elements of neurogenic and musculoskeletal pain. Amitriptyline was more effective than placebo in reducing pain after 4 weeks of treatment. No effect was found after only 1 week of drug administration in either dose range. When the patients were divided into depressed and non-depressed groups based on their Hamilton depression scores, amitriptyline reduced pain in the depressed and in the non-depressed groups as compared to placebo. Amitriptyline reduced the depression scores in the depressed group but had no effect on the depression scores in the non-depressed group. Thus, pain reduction was not associated with a change in mood in the non-depressed group. Amitriptyline had no effect on patients' ratings of the intensity of experimental heat stimuli. We conclude that amitriptyline is effective in the treatment of chronic oral-facial pain and that its efficacy is independent of its effects on depression. It appears that tricyclic antidepressants act in a fashion different from opiate drugs that alter the sensory discriminative component of pain.