Mercury Poisoning in Kamla

Iyer, MD; Joseph Goodgold, MD;

\s=b\ We examined a dentist with chronic elemental mercury poisoning electrophysiologically. Motor conduction in the upper and lower limbs was normal. Sensory nerve action potentials in the ulnar and median nerves were normal, but could not be elicited in the superficial peroneal nerves. Conduction velocity of the sural nerves was normal, but the action potential amplitude was abnormal. Following treatment with penicillamine, sensory conductions in the lower limbs returned to normal. (Arch Neurol 33:788-790, 1976)

sensory impairment is considered to be one of the initial symptoms of organic mercury poisoning1·- and, possibly, may be the only presenting symptom,'- there have been few electrophysiological studies of the peripheral nerves in these patients. A recent investigation4 re¬ ported that, despite persistent clinical sensory deficit, both amplitude and velocity of the sensory nerve action

Although

Xi.

potentials

were

that the sensory

normal, suggesting impairment is due,

Accepted

for publication June 15, 1976. Departments of Rehabilitation Medicine (Drs Iyer, Goodgold, and Eberstein) and Medicine (Dr Berg), New York University From the

Medical Center.

Reprint requests to Institute of Rehabilitation Medicine, 400 E 34th St, New York, NY 10016 (Dr Iyer).

a

Arthur Eberstein,

primarily, nervous

Dentist PhD; Perry Berg, MD

to lesions of

the central

system. Similarly, Von Burg

and Rustams did not find any abnor¬ mal motor and sensory conduction in

patients exposed to methylmercury even though they found central lesions and myasthenic-like responses that suggested peripheral nerve in¬ volvement. They attributed the nega¬ tive 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 pa¬ tients

intoxicated

mercury,

we

with

present

a

elemental

report of

a

patient with chronic elemental mercu¬ ry poisoning and the apparent suc¬ cessful 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 insta¬ bility and depression. He was examined by an internist who could not find any phys¬ ical abnormalities and advised psychiatric evaluation. The patient did see a psychia¬ trist 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 exaggerated by walking even half a block. In March 1974, he returned to his internist for further labora-

tory tests, and all results

were

reported

as

normal. Later that year, in May, he became subjectively aware of difficulty in differ¬ entiating 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 extremi¬ ties. On the same day, he was seen by a consultant neurologist who found trace deep tendon reflexes in both lower extrem¬ ities and confirmed absence of vibration sense below knees, bilaterally. Otherwise, the findings from neurological examina¬ tion were normal. Electrodiagnostic stud¬ ies led to a diagnosis of sensory polyneuropathy on the basis of abnormal sensory the lower nerve action potentials in extremities. One week after this study, he noticed the onset of similar complaints in the hands, and he began to drop instru¬ ments and other objects frequently. A search for toxic polyneuropathy was made, and only after detailed persistent ques¬ tioning was a history of handling mercury in the preparation of amalgam for fillings revealed. Twenty-four-hour urinary mer¬ cury 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 improve¬ ment to normal physical as well as mental status of the patient to permit a return to full-time professional activity. The vibra¬ tion sense, position sense, and deep tendon reflexes in the lower extremities have returned to normal. He is able to differen¬ tiate hot and cold, and he does not drop small objects.

RESULTS All the were

electrodiagnostic performed by the same

gator (K.I.). Latencies and

studies investi¬ 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 19µ for the left median nerve and 2.5 msec and 34µ for the right ulnar nerve.

Mercury

Concentration in Urine and

Sensory

Nerve Action Potentials

Superficial

Peroneal

Right

Left

Date May 1974

July Sept

Mercury in Urine, ug/Lhter Treatment

16

33

40

25 26 Oct

26 21

11 14

Ti"

28

Yes

15 20 22

38 23

Yes Yes No No No

22

27 40 22

July 16 Sept 24

14

No No No No No No No

10

*No response. fObtained by electronic

NR NR

4Ï-

No

20

20 15

m/sec

Yes Yes Yes Yes Yes

Feb26 April 9 May 14

NR NR

Yes Yes Yes Yes

20 26 48 60 34 31 40 26

19 26

NR NR

Velocity,

Yes Yes

23 30 Nov 6

28 Dec 18 Jan 1975 12

Amplitude,

m/sec

Yes No

45 9

Velocity,

Yes Yes Yes

55

10

Amplitude, NR* NR

20 22 23 24

Conduc¬ tion

Conduction

NR

NR

10.0

58.8

10.0

53.3

8.0

11

averaging.

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 8µ , respectively. (In our labora¬ tory, 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 17.0µ

[SD, 4.5], respectively.)

Starting in September 1974, mercu¬

ry levels in the urine

were monitored almost daily (Table). Prior to medica¬ tion, the concentrations were 33/tg and 40µg/liter, which are high values even for dental practitioners. About 10µg/ liter is considered the upper limit for urinary mercury excretion of nonoccu-

exposed

pationally

individuals";

environmental contamination in mercury dental offices set 30µg/liter as the maximum acceptable limit for person¬ nel employed in dentistry.7 On Sept

whereas, study of

a

recent

22, 1974, the patient started

a daily regimen of penicillamine. Since acute sensitivity reactions, such as fever, rashes, leukopenia, eosinophilia, and thrombocytopenia, have been re¬ ported 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, especial¬ ly in October, reaching a peak of 60µg/ 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 thera¬ py was continued through Nov 20, 1974, at which time urinary excretion

of

mercury

stabilized

below

accepted limit (30µg/liter) for

the den¬

tists. In January 1975, normal latency and sensory conduction velocity were observed in the right superficial peroneal nerve; however, the ampli¬ tude of the evoked potential continued low, and the nerve on the left side was still nonresponsive. Repeat tests in May and September 1975 demon-

strated normal sensory responses in both the right and left superficial

peroneal

nerves.

COMMENT

Dental office personnel may suffer either acute or chronic mercury intox¬ ication mainly because of inhalation of mercury vapor while they prepare and handle dental amalgam/ The immediate vicinity of such handling operations as well as spilled mercury or improperly stored mercury-con¬ taining 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 ele¬ mental mercury intoxication can mea¬

surably alter conduction along the sensory nerve fibers. The peripheral in the lower extremities appear to be most sensitive, especially

frequently

elicited in the sensory fibers of the distal parts of the lower extremities," while conduction veloci¬ ties of motor fibers may be normal. DiBenedettos 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 effi¬ cacy of penicillamine in the treatment of elemental mercury intoxication is

substantiated.1'1"

nerves

the

was superficial peroneal, completely nonresponsive. Early in¬

which

volvement of the sensory nerve fibers in the lower limbs is not an unusual finding in polyneuropathy. The first signs of a polyneuropathy are most

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

of America.

Nonproprietary Name and Trademark of Drug Penicillamine—Cuprimine.

References 1. Tsubaki T: Organic mercury intoxication in the Agano river area studied by Niigata University research group. Clin Neurol 8:511-520, 1968. 2. Miyakawa K: Experimental study on the pathogenesis of the so-called "Minamata disease." Psychiatr Neurol Jap 62:1887-1913, 1960. 3. Miyakawa T, Deshimaru M, Sumiyoshi S, et al: Experimental organic mercury poisoning: Pathological changes in peripheral nerves. Acta Neuropathol 15:45-55, 1970. 4. Le Quesne PM, Damluji SF, Rustam H: Electrophysiological studies of peripheral nerves

in patients with organic mercury poisoning. J Neurol Neurosurg Psychiatry 37:333-339, 1974. 5. Von Burg R, Rustam H: Electrophysiological investigation of methylmercury intoxication in humans: Evaluation of peripheral nerve by conduction velocity and electromyography. Elec-

troencephalogr Clin Neurophysiol 37:381-392,

1974. 6. Goldwater LJ: Occupational exposure to mercury. J R Inst Pub Health 27:279-283, 1964. 7. Schneider M: An environmental study of mercury contamination in dental offices. J Am

Dent Assoc 89:1092-1098, 1974. 8. DiBenedetto M: Sensory nerve conduction in lower extremities. Arch Phys Med 51:253-258, 1970. 9. Smith ADM, Miller JW: Treatment of inorganic mercury poisoning with N-acetyl-D, L-penicillamine. Lancet 1:640-642, 1961. 10. Hirschman SZ, Feingold M, Boylen G: Mercury in house paint as a cause of acrodynia: Effect of therapy with N-acetyl-D, L-penicillamine. N Engl J Med 269:889-893, 1963.

Mercury poisoning in a dentist.

Mercury Poisoning in Kamla Iyer, MD; Joseph Goodgold, MD; \s=b\ We examined a dentist with chronic elemental mercury poisoning electrophysiologicall...
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