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.