Great Auricular Neuralgia
Harvey J. Blumenthal, M.D.
Clinical Professor of Neurology, Oklahoma University College of Medicine, Tulsa Reprint requests to: Harvey J. Blumenthal, M.D., 6565 S. Yale, Suite 312, Tulsa, OK 74136 Accepted for publication: June 16, 1992 SYNOPSIS
An unusual neuralgia of the great auricular nerve resulting from a skin incision to Insert a cardiac pacemaker is described. The anatomy and presumed pathophysiology are discussed. Key words: Neuralgia, great auricular nerve. (Headache 1992; 32:413-415) Tic Douloureux, post-herpetic neuralgia and glossopharyngeal neuralgia are three of the most common painful facial neuralgias, but I could not find any description of neuralgia of the great auricular nerve; herein, is reported great auricular neuralgia resulting from implanting a cardiac pace-maker. CASE REPORT
A 73 year old man had a cardiac pacemaker inserted in October, 1988, for bradyarrhythmia with heart block. Three months later, he developed tingling neuralgic discomfort in his left shoulder and radiating up the lateral side of his neck to the angle of his jaw and behind his ear. This occurred every two or three days at the outset, but within three or four months, the frequency increased and he had repeated neuralgic paresthesias several times a day. He found these neuralgic paresthesias were more likely to occur at rest than when he was up and active, although they could occur at any time. The discomfort began immediately above the skin incision for the pacemaker insertion. The mildly painful paresthesias lasted 15 to 30 seconds and sometimes would re-occur after another 5 to 15 minutes. He did not find any changes in position or movement provoked the discomfort. He experienced several of the neuralgic paresthesias while in my office waiting room and also in the examination room. The patient described the paresthesia, "like 100 little bugs crawling," without intense pain. Occasionally, the paresthesia awakened him from a sound sleep. Sometimes his neck itched and he would rub the area. Occasionally the discomfort would begin behind the ear and radiate to the angle of the jaw and neck. On examination, the skin incision was slightly above the inferior margin of the manubrium, just above the second rib and below the left clavicle. I could not provoke the discomfort by palpating the skin over the pacemaker, the incision site, or pressing in the left supraclavicular space where the paresthesias were the most keenly felt. Touching the lower half of his ear, mastoid region or angle of the jaw did not provoke discomfort. There was no mass in his neck and the scar of the skin incision was not tender. Light touch and cutaneous pain sensations were intact over the mastoid, the pinna of the ear, the neck and supraclavicular region. These sensory inputs did not provoke paresthesia or neuralgic pain. There were no abnormal neurological signs. I asked the patient if he would be willing to have a simple operation, cutting the cutaneous nerves above the pacemaker incision, and he replied he would "consider it." He was willing to try car-bamazepine and he took 100 mg three times daily. One week later, the patient and his wife reported the carbamazepine helped the discomfort substantially. One month later, the patient reported that he did not think the medication helped at all. Upon re-examination, cutaneous pain testing just at and above the incision site caused a tingling dysesthesia and mild neuralgic discomfort in the typical distribution of the great auricular nerve up the neck to the angle of the jaw and the lower half of the ear. The carbamazepine was increased to 200 mg three times daily. One month later, the patient considered himself at least "50% improved" with both the intensity and frequency of the paresthesias diminished. Deep pressure and palpation at the incision line caused an uncomfortable itching sense over the pinna of the ear and mastoid region. Touching the pinna, mastoid or neck did not provoke the discomfort. The medication was stopped and one month later the patient reported he continued to have mild
neuralgic pain, but not as intense as previously and he preferred not taking the medication further, nor would he consider surgery. By telephone report six months later, the patient reported the neuralgic paresthesia quit completely for about four or five months, only to return with mild tingling lasting one or two seconds, two or three times daily. He did not wish further treatment. DISCUSSION Recent thorough reviews of the "classical neuralgias''1,2 and pain syndromes make no mention of "great auricular neuralgia." In fact, this nerve receives scant attention in any medical or neuro-logical texts1,3-5 and merits a review of the anatomy and presumed pathophysiology of this unusual neuralgia. Anatomy: The cervical plexus is formed by the union of the ventral rami of the first, second, third and fourth cervical nerves. Sensation of skin and subcutaneous tissue of the superior anterior chest is supplied by the supraclavicular nerves, cutaneous branches of the cervical plexus. These nerves consist of sensory fibers joining the third and fourth cervical roots (Figure 1). Another branch of the cervical plexus is the great auricular nerve, a sensory nerve supplying the skin overlying the angle of the mandible, the lower one-third of the auricle and skin covering the mastoid process (Figure 1). The great auricular nerve is composed of fibers of the second and third cervical nerves and ascends from the posterior triangle of the neck. All the sensory branches of the cervical plexus merge behind the scalenus anterior muscle, enter their respective cervical nerve roots, and carry their afferent impulses into the nerve soma, the dorsal root ganglion.6
Thus, there is overlap of the great auricular nerve and supraclavicular nerves with these two peripheral nerves joining the cervical plexus and having the third cervical root in common (Figure 1). Wyburn-Mason, in his classic paper on "The Nature of Tic Douloureux," speculated that there may be an overlap of sensory supply of one area from neighboring spinal nerve roots; furthermore, he believed that, "at least in a proportion of cases, tic douloureux is a disturbance of the great auricular nerve and other branches of the cervical plexus."7 Wyburn-Mason described treatment of 56 cases of tic douloureux by alcohol block or surgical section of the great auricular nerve!7 Experimental Electrophysiologic Evidence: The neuralgic pain in this case was probably triggered by local irritation of severed cutaneous sensory nerves, perhaps trapped in scar tissue, and possibly with microneuroma formation with resultant spontaneous afferent nerve action potentials. Wall and Gutnick found that small fibers arising from neuromas had spontaneous electrophysiological activity recorded nine days to four months after the injury, and they speculated this activity might be the basis by which some neuromas were painful.8 Experimental studies show that under certain conditions, a "conditioning" impulse may result in "autoexcitation;" this autoexcitation has been attributed to depolarization of hypersensitive fibers that respond to subnormal triggering stimuli caused by the transient change in extra-cellular current flow.9 Neilsen found that orthodromic (motor) nerve impulses and damaged nerve fibers might be altered in at least three ways: (1) Conduction was increased; (2) There was lateral spread of impulses to other nerve fibers; (3) Passage of a single impulse may give rise to after potentials immediately after the reflex response, or "late activity."10 Similar aberrant sensory nerve impulses may reach the dorsal root ganglion asynchronously, resulting in summation of after potentials immediately following the initial response and cause lateral spread of impulses to other nerve fibers which join the third cervical root, or nearby nerve terminals which ordinarily bring impulses from the great auricular nerve.10 This lateral spread of impulses has been studied extensively. Howe et al described chronic injury experiments resulting in focal demyelination which extends several millimeters. Here, ectopic generation of nerve impulses cause development of generator potentials, resulting in repetitive firing at regions of "spatial inhomogeneity.''11 REFERENCES
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