Journal of Neurology, Neurosurgery, and Psychiatry, 1979, 43, 143-149

Accidental ethyl mercury poisoning with nervoussystem, skeletal muscle, and myocardium injuryI CINCA, IRINA DUMITRESCU, P ONACA, A SERBANESCU, AND B NESTORESCU

From the Clinic of Neurology and the Laboratory of the Clinic of Occupational Diseases,Colentina Hospital, Bucharest, Romania

SUMMARY Four case reports are presented of patients who ate the meat of a hog inadvertentlyfed seed treated with fungicides containing ethyl mercury chloride. The clinical, electrophysiological,and toxicological, and in two of the patients the pathological data, showed that this organic mercurycompound has a very high toxicity not only for the brain, but also for the spinal motoneurones,peripheral nerves, skeletal muscles, and myocardium.

Use of organic mercury compounds as fungicideshas bee,n noted in several countries to producesevere poisoning, occasionally epidemic in charac-ter. We had the opportunity to examine the firstcases of such poisoning ever to have appeared inRomania. They showed some features not yetdescribed in the literature on poisoning withvarious organic mercury compounds.

Case reports

In August 1974, a mother with her three childrenwas referred to our clinic by a provincial hospitalwhere they had treated for 17 days.

CASE 1This boy (MG), aged 15 years, one week beforehis first admission developed pain in the musclesand gait disturbance. He could neither stand norwalk. The tendon jerks were bilaterally hyper-active and there was a positive Babinski's signon the left side, clonus of the left foot, andtwitching of the thigh muscles. Severe cerebellarsigns were noted-that is, ataxia and dysarthria.Within a week he developed dysphagia andaphonia, B;abinski's sign appeared bilaterally, andthe overall status deteriorated. On referral tothis clinic we noted generalised muscle wasting,spasticity of the upper limb flexors and lower

Address for reprint requests: Professor I Cinca, Str Andrei Muresan 6,Sector I, Bucharest 71276, Romania.

Accepted 21 May 1979

limb extensors, bilateral mydriasis, and impairedswallowing. T1he patient was drowsy, unrespon-sive to comman,ds, and had loss of sphinctercontrol. The clinical picture deteriorated evenfurther: he developed a horizontal nystagmus,was agitated, and became comatose four dayslater. He required ventilatory assistance -anddied three days later from cardiac arrest, withinone month of the onset of the illness.The CSF was clear with 0-4 lymphocytes per

m,m3 and 0-28 g/l albumin. Haemoglobin was10-88 g/dl. The leucocyte count was 13 500/mm3with neutrophilia. The blood glucose was8-6 mmol/l, urea 17-3 mmol/l, creatinine248-5 pmol/l, sedimentation rate 55 mm in thefirst hour, 90 mm in the second hour. There weretraces of albumin in the urine.An electroencephalogram showed slow diffuse

dysrhythmia with predominance of delta waves.General necropsy revealed foci of broncho-

pneumonia and an abscess of the left lung. Thegross appearance of the brain was normal. Allover the cerebral cortex but mostly in the'calcarine cortex, there was nerve cell loss and adiffuse proliferation of neuroglia on micro-scopic examination of the brain.

In the midibrain and bulbar (especially thelateral nucleus) reticular formation, neurogliaactivation with nerve cell sa,tellitosis was apparent,extending to neuronal loss and formation ofneuronophagic nodules.Myelin preparations showed demyelination of

the nerve fibres in the ninth and tenth cranialnerve roots (fig 1) In the cerebellum there was

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I. Cinea, I. Dumitrescu, P. Onaca, A. Serbanescu and B. Nestorescu

Fig 1 Demyelination of nerve fibre bundles in thevagus nerve roots (case 1). Spielmeyer staining, originalmagnification x 100.

cell wasting of the granular layer. Purkinje'scells were more spared, though in certain areas

silver impregnation for neurofibrils showed

empty basket-cells and torpedo-shaped Purkinjecell axons (fig 2). The lesions were evenly distri-buted over the neo- and paleocerebellar cortex.Throughout its length the spinal cord showed a

highly abnormal picture of the ventral horns, withmotoneurone loss and presence of neurophago-cytic nodules (fig 3). Among the spared neuronesmany showed chromatolys,is or were shrunken or

hyperchromatic. The spinal and peripheral nerve

roots were normal in appearance.

Fig 2 Empty basket-cells and torpedo-like axon ofPurkinje cell in cerebellar cortex (case 1). Silverimpregnation Bielschowsky, original magnification x 240.

The skeletal (intercostal) muscles showed zones

of waxy segmental degeneration of the musclefibre, with interstitial proliferation of fibroblasts(fig 4).

f

..

horn (case 1). Nissl staining, original magnification- 400.

On microscopic examination of the otherviscera, the kidney showed stasis and interstitialinfiltration, with rarefaction of the glomerularelements he,re and there. The myocardiumshowed zones of interstitial chronic myocarditiswith proliferation of fibroblasts but absence ofsclerosis (fig 5). In the lung bronchopneumonicfoci were found. The liver was normal.

Fig 4 Intercostal muscle (case 1). Waxy degenerationol muscle fibre segments with interstitial fibroblastproliferation. Haematoxyline and eosine staining,original magnification x 100.

CASE 2This 10 year old boy (MM) had, five days beforeadmission, developed walking difficulty, musclepains, vomiting, and dysarthria. Neurologilcalexamination showed walking disability, weaknessof the limbs, general hypotonia, horizontal nys-tagmus, deglutition impairment, severe ataxia,and increased tendon reflexes.

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Accidental ethyl mercury poisoning with nervous system, skeletal muscle and myocardiuim injury

t~~~~~~~~-..jdSFX-.3,Fig 5 Interstitial chronic myocarditis with fibroblastproliferation (case 1). Haematoxyline and eosine stainingoriginal magnification x 240.

Over the next two weeks he developed psycho-motor agitation and a bilateral Babinski sign. Hebecame unable to speak and entered a subcomastate.He was still comatose when referred here. He

could not swallow, the pupils were bilaterallydilated, and there was generalised muscleatrophy and loss of sphincter control. His condi-tion deteriorated gradually. Within 10 days hedeveloped decortication posturing, fever, andvomiting. He died from cardiac arrest within a

month and a half of the onset of the disease.The CSF was clear, with 0-8 lymphocytes/mm;

albumin 0 16 g/l; blood contained 10-22 g/dlhaemoglobin. The white cell count was 10 000/mm3 with neutrophilia. Blood urea was at first6 7 mmol/l and then increased to 19-7 mmol/l.

Fig 6 Calcarine cortex: disappearance of neurones

with intense neuroglial proliferation and formation of'neuroglial nodules (case 2). Nissl staining, original

magnification X 100.

Sedimentation rate was 27 mm/ihr; urine albuminlevel was 3-3 g/l.

Electrocardiography showed S-T segmentdepression and T wave inversion in precordialleads. The electroencephalogram was of averagevoltage with lack of alpha rhythm and diffuseslow activity.On gross pathological examination, the bra,in

appeared normal. Microscopic examination ofthe cerebral cortex showed lesions which wereidentical to those found in case 1 but with a muchmore intense neuroglial proliferation that hadresulted in formation of neuroglial nodules inthe calcarine area (fig 6).The caudate nucleus and the putamen showed

an almost complete loss of the small cells withpreservation of most of the large cells and diffuseproliferation of glia. In the brainstem there wasglial proliferation in the midbrain periaqueductalgrey matter. In the cerebellum cell loss wasnoted in the granular layer. The spinal cordshowed alterations identical to those found incase 1.

Pathological examination of the viscerarevealed acute inflammation of the renal pelvis,stasis and tiny lesions of interstitial nephritis.

Chronic interstitial myocarditis lesions werefound as in case 1 (fig 7).

In the lung there was a picture of oedematousalveolitis. The liver was normal.

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admitted to the hospital accompanying her twosons had no pathological sign wha-tever. Witjhin48 hours she developed gait disturbances w,ith

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1L Cinca, I. Dumitrescu, P. Onaca, A. Serbanescu and B. Nestorescu

progressive weakness in the lower limbs andmuscular pains. Referred to this clinic, she wasnoticed to have spastic paraparesis, with bilateralBabinski sign and distal superficial hypoaesthesiaof the limbs. She was drowsy. Nine days latershe developed headache and vomiting, her sightdeteriorated and there was a horizontal nystagmusand intention tremor. She became agitated, con-fused and delirious. Within one month of theonset of symptoms she improved and wasable to walk again. The pyramidal tract signsremitted and so did the mental disturbance. Shecontinued to have headache and fatigue. Thevisual field was con-centrically narrowed.

Routine laboratory tests failed to show anyabnormality, except a slightly raised blood urea(7 3 mmol/l), while in the CSF tihere was a slightpleocytosis (15 lymphocytes/mm3) with analbumin level of 0-3 g/l.

Electrocardiography showed flattening of theT wave in precordial leads. An audiogramrevealed slight bilateral perceptive deafness. TheEEG tracing was of slighly decreased amplitude,with the alpha rhythm present and predominanceof fast waves.Two months later she was discharged home

much improved. She was readmitted for a reviewfour months later and was found to show only aconcentric narrowing of the visual fields.

CASE 4This 15 year old girl (MA), was admitted oneweek after her brother. Five days previously shehad developed gait and sight impairment and astate of drowsiness. Her gait was spastic andslightly ataxic. Babinski's sign was present onboth sides. Speech was dysarthric.When examined here she was found to have

marked amblyopia with bilateral mydriasis andslow pupillary reflexes. She could walk only ifsupported. Her gait was spastic and she hadspastic quadriparesis, drowsiness and disturbedsphincter control. Three days later, vomiting,intention tremor, staccato speech, and slownesscerebration developed. Within 10 days ofadmission the motor deficiency remitted, sheregained the ability to distinguish the shape ofthings, though she still had concentric narrowingof the visual fields. She recovered progressively;her sight improved as she was now able to see at5 m distance. She started to walk again and thecerebellar signs diminished.The CSF contained no cells, albumin 0 16 g/l.

Urine albumin was noted at a concentration of0-5 g/l.

Her electrocardiogram showed sinus rhythm at100 beats/min. In precordial leads the S-Tsegment was below the isoelectric line and theT wave was negative. There was evidence of leftventricular hypertrophy. The electroencephalo-gram showed slow dysrhythmia.The diagnosis established during hospitalisation

was organic mercury poisoning, and treatmentwith penicillamine 1 g/day for 21 days wasstarted one month after admission. She was dis-charged greatly improved after a stay of twomonths in the clinic. When reviewed four monthslater she still had a mild intention tremor andconcentric narrowing of the visual fields.The clinical diagnosis of organic mercury

poisoning was confirmed by the toxicologicaldeterminations performed on the blood, hair andurine immediately after admission (tables 1, 2).

Table 1 Mercury content of blood and hair

Control Case 1 Case 2 Case 3 Case 4

Mercury level in wholeblood (pg/ml) 0 - 5 1 3

(maximum permitted0.02 pg/ml)Mercury level in hair

(Wg/g) - - 542 160 152(maximum permitted 6 pg/g)

Table 2 Mercury in the urine (ptg/24 hr; maximumpermitted 100-120 jig/24 hr)

Period Case I Case 2 Case 3 Case 4

Mercury level inurine Admission 57 126 660 165

10 days later - 180 452 224Mercury level after After 7 days

starting treatment - - - 303penicillamine After 14 days

treatment - - - 193

Subsequent epidemiological data showed that10 days or so be,fore becoming ill the family hadeaten the meat of a hog that over the past fewdays had shown signs of disease, reeling andfalling. Some poultry died with the same signs.They had inadvertently been fed seed treated withfungicides containing alkyl mercury compounds-Cryptodin (a powder containing 2-5% ethylmercury chloride) and F.B7 (a powder containing1% ethyl meroury chloride).

ELECTROPHYSIOLOGICAL INVESTIGATION

In the two surviving patients the followingadditional investigations were performed.

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Accidental ethyl mercury poisoning with nervous system, skeletal muscle and myocardium injury1

In cases 3 and 4 EMG recordings were obtainedfrom the tibialis anterior, extensor digitorumbrevis of the foot and the first dorsal interos-seous muscle of the hands. They were all normal.Motor conduction velocity in cases 3 and 4

was measured in the median and ulnar nerves(segment elbow to wrist) and in the peronealnerve (segment knee to ankle). Standard tech-niques were used with recording of the evokedresponses in the abductor pollicis brevis, hypo-thenar, and extensor digitorum brevis musclesrespectively.Sensory conduction velocity was measured in

the median and ulnar nerves. The stimuli weredelivered to digits 1 and 5 respectively throughring electrodes. Recordings were made from thenerves at elbow and wrist. The results are shownin table 3.

Table 3 N'erve conduction velocity

Immediately Six monthsafter lateradmission

Motor conduction velocity m/s m/sMedian nerve (elbow to wrist)

case 3 60 -

case 4 62

Ulnar nerve (elbow to wrist)case 3 55case 4 60 -

Peroneal nerve (knee to ankle)case 3 47case 4 55

,Sensoiy conduction velocityMedian nerve (elbow to wrist)

case 3 38 59case 4 26 56

Ulnar nerve (elbow to wrist)case 3 42 60case 4 30 58

TOXICOLOGICAL INVESTIGATIONSThe level of mercury in the blood was measuredby an ultraviolet spectrometer method (table 1).

The levels of mercury in the hair, urine, and(in lethal cases) in the nervous system (table 4)and viscera (table 5), were measured by a photo-metric method with dithizone after decay of theorganic substances in an acid oxidant(Nestorescu's methodt). Unfortunately we werenot able to use more reliable methods (atomicabsorption and gas chromatography).

Discussion

In all our patients the symptoms appeared at least10 days after ingestion of mercury contaminatedfoodstuffs, as reported also by other authors inorganic mercury poisoning.2-5The initial symptoms were headache, fever,

diarrhoea, vomiting and myalgia, recallingespecially the symptomatology in a report onpoisoning by an ethyl mercury compound (ethylmercury p-toluene sulphonanilide) in the 1961Iraq epidemic.6Although the neurological symptoms of

poisoning by alkyl mercury compounds are wellknown especially after the 1953 Minamata epi-demic, it might be of interest to attempt tocorrelate certain phenomena noticed in ourpatients with the anatomical lesions and theelectrophysiological data. Thus, gross cerebellardamage was moderate, as noted by otherauthors. According to Okinaka et al7 the exten-sive cortical damage might also contribute toproducing ataxia. The gross phonation and de-glutition in case 1 might have been the result notonly of the bilateral pyramidal lesions but alsoof demyelination in the ninth and tenth cranialnerves. We have been unable to find previousreports of the latter. It is only experimentally inanimals with induced poisoning by methylmercury compounds that lesions could beproduced in the dorsal roots of the spinalnerves.2 8 9

Table 4 Mercutry in nervous system (wet tissue; j.g/g; maximum permitted 0 6 jg/g)

Occipital Cerebellar Frontal Lenticular Thalamus Optic Centrum Choroid Pons Spinal Callosumcortex cortex cortex nucleus nerve ovale plexuses cord

Case I - - 22 - - - - - - - -

Case 2 21.3 13.9 10.6 10.6 7.2 7.0 6.6 6.3 4.3 4.2 3.5

Table 5 Mercury in viscera (wet tissue; jig/g)

Kidney Adrenal Liver Stomach Lung Spleen Myocardium Skeletalmuscle

Case 1 28.6 - - - - - - -Case 2 84.0 28.3 28.2 23.3 18.2 10.0 6.7 4.2

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Sensory disturbances have also been disclosedby the slowing down of sensory nerve conduc-tion in cases 3 and 4 found on admission whichbecame normal six months later on clinicalrecovery (table 3). Electrophysiological data havehitherto invalidated the hypothesis of per-ipheral neuropathy produced by methyl mercurypoisoning.10

Wasting of muscles and twitching in cases Iand 2 were suggestive of spinal cord anteriorhorn lesions, which were confirmed by theanatomical evidence. Poisoning by methylmercury compounds has only very infrequentlybeen noted to produce spinal lesions and theseusually spare the ventral horn neurones." Yet incases of poisoning with other organic mercurycompounds, appearances like amyotrophic lateralsclerosis have been noted, as for example in ethylphenyl mercury poisoning"2 and in poisoning withethyl mercury compounds."3 Okinaka et al'consider that organic mercury compounds,according to the chemical nature of the sub-stance, produce two forms of poisoning, acerebro-cerebellar and a spinal form.Apart from the lesions located in the cerebral

cortex, striate nuclei, cerebellum, and mesence-phalon reported by numerous authors4 714-18, wenoticed some as yet unreported lesions. Thesewere the neuronal lesions of the bulbar reticularformation found in case 1 which we have notfound reported before, though certain modifica-tions in the lower brainstem were suspected tooccur in organic mercury poisoning by von Burgand Rustam1" in their electrophysiological studies.We also failed to find any report of anatomicaldamage to skeletal muscle or myocardium. Itshould be noted that, as we noted in our cases,electrocardiographic alterations are associatedwith ethyl mercury'! 19 much more frequentlythan with methyl mercury5 poisoning.

Toxicological determinations on our casesshowed greatly raised levels of mercury in theblood, hair, and urine (tables 1 and 2). Theurinary excretion appears to be a less reliableindex of the severity of the poisoning, since thehighest excretion of mercury was in case 3 wherethe course was favourable, but urinary excre-tion of mercury is known to be extremely vari-able.20` The levels of mercury in the blood andhair are the most reliable indices of the degreeof poisoning, and they were very much increasedin case 2 which had a fatal course.The brain, which is the crucial organ in intoxi-

cation by organic mercury compounds, alsoshowed greatly increased levels of mercury inour two necropsy cases. In case 2, when samples

were taken from various regions of the centralnervous system, the highest levels of mercurywere found in the occipital cortex, the cerebellarcortex, the lenticular nucleus, and the frontalcortex (table 4), which were also the regions withevident anatomical lesions.

In case 4 where treatment with penicillaminewas begun, urinary excretion of mercuryincreased and then slightly decreased, but noconclusion can be drawn concerning the effec-tiveness of such therapy, as case 3 also improvedwithout it.The published data on treatment with chelating

substances in organic mercury poisoning are notconclusive either, as certain authors have failedto obtain positive effects'3 23 while othersreported having obtained improvements.' 22According to Berlin and Ullberg24 accumulationof mercury in the brain is accelerated by experi-mental administration of dimercaprol (BAL).

Indirect poisoning after eating the meat of hogsfed by mistake with seed treated with methylmercury compounds has also been reported bysome American authors.25"From study of our cases, it appears that ethyl

mercury compounds display a very high toxicitynot only for the brain, but also for the spinalmotoneurones, peripheral nerves, skeletalmuscles, and myocardium.

References

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2 Hunter D, Bomford RR, Russell DS. Poisoningby methyl mercury compounds. Q J Med 1940;33:193-213.

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