Although sensory impairment is considered to be one of the initial symptoms of organic mercury poisoning [1, 2] and, possibly, may be the only presenting symptom [3], there have been few electrophysiological studies of the peripheral nerves in these patients. A recent investigation [4] reported that, despite persistent clinical sensory deficit, both amplitude and velocity of the sensory nerve action potentials were normal, suggesting that the sensory impairment is due, primarily, to lesions of the central nervous system. Similarly, Von Burg and Rustam [5] did not find any abnormal motor and sensory conduction in patients exposed to methylmercury even though they found central lesions and myasthenic-like responses that suggested peripheral nerve involvement. They attributed the negative results to clinical improvement of the patients during the seven months that elapsed between examination and exposure. Since, to our knowledge, there have been no published results of electrophysiological studies of patients intoxicated with elemental mercury, we present a report of a patient with chronic elemental mercury poisoning and the apparent successful treatment with penicillamine.

REPORT OF A CASE

A 53-year-old male dentist noted in October 1973 that he felt like a "senile old man" after some years of emotional instability and depression. He was examined by an internist who could not find any physical abnormalities and advised psychiatric evaluation. The patient did see a psychiatrist and undertook a therapeutic program for about four months, without any changes in either physical or mental status. In November 1973, the patient noticed development of tingling and numbness of both feet that was exagger- ated by walking even half a block. In March 1974, he returned to his internist for further laboratory tests, and all results were reported as normal. Later that year, in May, he became subjectively aware of difficulty in differentiating between hot and cold while bathing; the "entire body" seemed to be involved. At that time, a question arose as to whether he had peripheral vascular disease, and he sought the advice of a friend (J.G.) who detected no evidence of peripheral vascular disease, but noted that there was diminished to absent vibration and position sense in both lower extremities. On the same day, he was seen by a consultant neurologist who found trace deep tendon reflexes in both lower extremities and confirmed absence of vibration sense below knees, bilaterally. Otherwise, the findings from neurological examination were normal. Electrodiagnostic studies led to a diagnosis of sensory polyneuropathy on the basis of abnormal sensory nerve action potentials in the lower extremities. One week after this study, he noticed the onset of similar complaints in the hands, and he began to drop instruments and other objects frequently. A search for toxic poly-neuropathy was made, and only after detailed persistent questioning was a history of handling mercury in the preparation of amalgam for fillings revealed. Twenty-four-hour urinary mercury level was found to be abnormal. The patient was then removed from exposure for five weeks and treated with penicillamine, 250 mg given orally four times a day, until November 1974. Subsequently, there has been a slow but progressive improvement to normal physical as well as mental status of the patient to permit a return to full- time professional activity. The vibration sense, position sense, and deep tendon reflexes in the lower extremities have returned to normal. He is able to differentiate hot and cold, and he does not drop small objects.

RESULTS

All the electrodiagnostic studies were performed by the same investigator (K.I.). Latencies and motor conduction velocities measured in the median, ulnar, peroneal, and tibial nerves before and after treatment were normal. Similarly, latencies and amplitudes of the antidromic sensory nerve action potentials of the median and ulnar nerves were normal. A typical examination showed a latency and amplitude, when stimulation was applied to the wrist, of 3.5 msec and 19 microvolts for the left median nerve and 2.5 msec and 34 microvolts for the right ulnar nerve.

Prior to medication, sensory nerve action potentials could not be elicited from the superficial peroneal nerves bilaterally, and the amplitude of the evoked potential from the sural nerves was lower than normal. In May 1974, conduction velocity and amplitude in the right sural nerve were 51.8 m/sec and 8 microvolts, respectively. (In our laboratory, normal values for conduction velocity and amplitude of the sensory nerve fibers in the lower extremities are 47.0 m/sec [SD, 3.0] and 17.0 microvolts [SD, 4.5], respectively).

Starting in September 1974, mercury levels in the urine were monitored almost daily (Table). Prior to medication, the concentrations were 33 micrograms and 40 micrograms/liter, which are high values even for dental practitioners. About 10 micrograms/liter is considered the upper limit for urinary mercury excretion of nonoccupationally exposed individuals [6]; whereas, a recent environmental study of mercury contamination in dental offices set 30 micrograms/liter as the maximum acceptable limit for personnel employed in dentistry [7]. On Sept 22, 1974, the patient started a daily regimen of penicillamine. Since acute sensitivity reactions, such as fever, rashes, leukopenia, eosinophilia, and thrombocytopenia, have been reported with this drug, white and red blood cell counts were monitored during the course of the therapy. No untoward effects were noted.

During the course of treatment, mercury excretion increased, especially in October, reaching a peak of 60 micrograms/liter. Sensory nerve action potentials could then be evoked in the right superficial peroneal nerve; however, the conduction velocity was slow, and the amplitude of the response was very low (Table). Penicillamine therapy was continued through Nov 20, 1974, at which time urinary excretion of mercury stabilized below the accepted limit (30 micrograms/liter) for dentists.

In January 1975, normal latency and sensory conduction velocity were observed in the right superficial peroneal nerve; however, the amplitude of the evoked potential continued low, and the nerve on the left side was still nonresponsive. Repeat tests in May and September 1975 demonstrated normal sensory responses in both the right and left superficial peroneal nerves.

COMMENT

Dental office personnel may suffer either acute or chronic mercury intoxication mainly because of inhalation of mercury vapor while they prepare and handle dental amalgam [8]. The immediate vicinity of such handling operations as well as spilled mercury or improperly stored mercury-containing wastes are also sources of exposure. Since our patient was a dentist and subject to some degree of exposure to such mercury vapor, we consider this a case of elemental mercury poisoning.

This case demonstrates that elemental mercury intoxication can measurably alter conduction along the sensory nerve fibers. The peripheral nerves in the lower extremities appear to be most sensitive, especially the superficial peroneal, which was completely nonresponsive. Early involvement of the sensory nerve fibers in the lower limbs is not an unusual finding in polyneuropathy. The first signs of a polyneuropathy are most frequently elicited in the sensory fibers of the distal parts of the lower extremities [8], while conduction velocities of motor fibers may be normal. DiBenedetto [8] found that, in patients with clinical symptoms of peripheral neuropathy, 82% of sensory nerve action potentials of the superficial peroneal nerve and 68% of the sural nerve responses were absent. There was no difficulty in evoking a good sensory response from normal adults, which is also true in our laboratory.

It is recommended that in suspected cases of chronic mercury poisoning, either organic or elemental, the superficial peroneal (sensory) and sural nerves be carefully examined electrophysiologically for evidence of neuropathy. In this patient, the efficacy of penicillamine in the treatment of elemental mercury intoxication is substantiated. [9, 10]

This investigation was supported in part by a grant from the Muscular Dystrophy Associations of America.

NONPROPRIETARY NAME AND TRADEMARK OF DRUG

Penicillamine -- CUPRIMINE.

*No response
**Obtained by electronic averaging

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