Case Study Psychiatric Manifestations of Mercury Poisoning GWEN E. FAGALA, M.D.,
AND
CINDY L. WIGG, M.D.
Abstract. Mercury and its compounds are toxic substances that are widely used in industry and agriculture. Mercury poisoning is an uncommon but important clinical entity that often presents with psychiatric disturbances as a prominent part of the clinical picture. In this paper, a case of mercury poisoning in a l2-year-old girl with prominent psychiatric manifestations is presented. Relevant literature concerning the psychiatric manifestations of mercury poisoning is discussed. The importance of considering mercury poisoning, and toxic conditions in general, in the differential diagnosis of psychiatric disorders is emphasized. J. Am. Acad. Child Adolesc. Psychiatry, 1992, 31,2:306-311. Key Words: toxicology, mercury poisoning, organic mental disorders. Mercury, or quicksilver, has been used for many purposes for 3,000 years. In the past, mercury and its compounds were used extensively in medicine as cathartics, antiparasitics, vermifuges, antisyphilitics, diuretics, and ointments for various skin conditions (Sunderman, 1988). It was also used for gilding and gold-plating metal objects and for making mirrors. Its use in the manufacture of felt hats gave rise to the expression "mad as a hatter," referring to symptoms of mercury poisoning among hatmakers (Hunter, 1978). Modern medicine has all but abandoned the use of mercurials, but mercury and mercury compounds are still widely used in industry and agriculture. Elemental mercury is used in the manufacture of thermometers, barometers, vacuum pumps, and various components of electrical apparatus. Mercury compounds are used as detonators, in paints, and as agricultural fungicides (Hunter, 1978). Mercury amalgams are used as dental fillings. Mercury is also released in the atmosphere during the combustion of fossil fuels (Gerstner and Huff, 1977). The toxicity of mercury and its compounds has also been recognized for many centuries. Early descriptions of mercury toxicity date back to the first century A.D. and beyond. The toxicity of mercury vapor was first described in 1473 by Ulrich Ellenborg of Germany (Goldwater, 1936). In the 1940s, mercury toxicity was identified as the cause of the Mad Hatter syndrome, also called erethism (Gowdy and Demers, 1978). Also in the 1940s, Warkany and others discovered that acrodynia, a serious disease of children, was caused by mercury poisoning. In the 1950s and 1960s massive epidemics of mercury poisoning occurred in Japan
Accepted August 22, 1991. Dr. Fagala isa Third Year Resident in the Department ofPsychiatry and Behavioral Sciences, University of Texas Medical Branch, Galveston. Dr. Wigg is Assistant Professor of Psychiatry and Behavioral Sciences and Medical Director ofAdolescent Inpatient Services, Division of Child and Adolescent Psychiatry, University of Texas Medical Branch, Galveston, Texas. Reprint requests to Dr. Wigg, Division of Child and Adolescent Psychiatry, University of Texas Medical Branch, Graves Building 1.108, Galveston, TX 77550. 0890-8567/92/3102-0306$03.00/0© 1992 by the American Academy of Child and Adolescent Psychiatry.
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and Iraq as a result of ingestion of organic mercury compounds in food (Goldwater, 1936). Mercury may enter the human body via the lungs, the gastrointestinal tract, or the skin. Elemental mercury vaporizes easily and the inhaled vapor is easily and almost completely absorbed through the lungs. Ingested elemental mercury passes through the gastrointestinal tract with virtually no systemic absorption, but ingestion of organic mercury compounds, especially alkyl mercury compounds, results in almost complete absorption. Absorption of mercury via the skin causes a severe dermatitis in some individuals. Elemental mercury, once it enters the bloodstream, is quickly circulated to all parts of the body. It has a particular affinity for the brain and crosses the blood-brain barrier easily. Once inside nerve cells, it is oxidized to mercuric ion, complexed with sulfhydryl groups on proteins, and retained. In this form it returns to the bloodstream extremely slowly (Gerstner and Huff, 1977). The tendency of mercury to accumulate in the brain explains why psychiatric disturbances are a major part of the clinical picture of elemental mercury poisoning. This paper deals with a case of elemental mercury poisoning with prominent psychiatric manifestations in a 12-year-old girl.
Case Presentation The patient was a 12-year-old Hispanic girl who was healthy and functioning normally until approximately 1 month before her initial admission to the University of Texas Medical Branch. At the time of her initial admission, she presented with a chief complaint of difficulty walking. She reported feeling dizzy when she walked and complained of multiple joint pains, weakness, nausea, sweating, and numbness and tingling of her palms. Physical findings at that time included truncal ataxia with a positive Romberg sign and a tendency to fall to the right. Possible mild chorea was noted. She had decreased strength in her lower extremities. Her right patellar reflex was absent and the left one was markedly decreased. It was noted in her chart that she walked better when she was unaware of being observed. She had a CT scan of the head, an EEG, and a lumbar puncture, the results of which were all normal. Her antinuclear antibody titer (ANA) was negative. Lower extremity electromyJ. Am. Acad. Child Adolesc. Psychiatry, 31 :2, March 1992
CASE REPORT: MERCURY POISONING
ograms were abnormal. A streptozyme test was positive and her antistreptolysin-O titer was I :625. She reported a history of a sore throat 2 weeks before admission. At this point she was given the diagnosis of rheumatic fever and was treated with aspirin and a 2-week course of oral penicillin. Her ataxia improved somewhat after she was started on penicillin and she was discharged after 5 days in the hospital. Over the next 6 weeks she made multiple visits to the emergency room and various clinics with a variety of complaints, including joint pains; a rash over her abdomen, buttocks, and thighs; abdominal pain; and bloody diarrhea. On one emergency room visit her pain was described as having "a strong hysterical component." On one clinic visit at another hospital she was found to have a positive ANA. When she presented with abdominal pain and bloody diarrhea, proctoscopy was performed. Ulceration of the rectal mucosa was found up to 10 cm from the anal opening. The mucosa appeared normal proximal to that point. Biopsies were taken and she was scheduled to be followed up after the biopsy results were available. Approximately 1 week later, the patient returned to the pediatric clinic with worsening abdominal pain and burning of her genital area. She appeared quite ill and was admitted to the hospital. The initial diagnostic impression at that time was rheumatic fever, dermatitis, and colitis. The possibility of systemic lupus erythematosus was considered. Abnormal findings on her initial physical examination included a diffuse, excoriated, infected rash located primarily on her abdomen, buttocks, and thighs. Rectal examination showed loose sphincter tone and a significant rectal prolapse occurring with the Valsava maneuver. Pelvic exam was normal and showed an intact hymen. Results of laboratory tests included a negative ANA with an erythrocyte sedimentation rate of 46 mm/hour. A complete blood count was normal except for a white blood cell count of 20,200/mm3• Urinalysis showed 1+ proteinuria. Her electrolytes were normal except for a potassium of 2.7 meql L. This eventually rose to 3.8 meq/L during her hospital stay. Her rapid plasma reagin was nonreactive. A fecal culture grew no pathogens. Cervical cultures for chlamydia and N. gonorrhea were negative. Examination of her stool for ova and parasites was negative. Complement and immunoglobulin studies were normal. The results of the rectal biopsies done before admission revealed that her rectum was completely denuded of mucosa up to 10 cm proximal to the anal opening. Several observations about the patient's behavior were made by the pediatric treatment team during her admission. It was noted in her chart that she often appeared to be in great pain when medical personnel entered the room but appeared much calmer and more comfortable when she was being observed without her knowledge. She scratched herself almost constantly, especially in her genital area. She was observed on several occasions putting her finger into her rectum while defecating. She also assumed bizarre positions in bed at times. A number of consultants were called in to evaluate the patient. She was seen by a pediatric immunologist whose assessment was that many of her physical findings, particuJ. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
larly her skin lesions, were factitious in nature and that there was no evidence of an immunological disorder. The most likely diagnosis was thought to be a psychiatric disorder. A gastroenterologist felt that her unusual rectal ulceration and prolapse could be due to ulcerative colitis, pseudomembranous colitis, or sexual abuse with anal intercourse. Because of the patient's rather strange behavior at times, sexual abuse was considered to be a strong possibility, and psychiatric consultation was requested. During the initial interview with a child psychiatrist, the patient lay in bed with one hand holding her abdomen and the other holding her genitalia. She complained of being in pain but her affect was not consistent with being in pain. She often grimaced when her mother spoke and seemed reluctant to speak with her mother present. When she was seen alone, she began to cry and abruptly blurted out a history of two incidents of sexual abuse. The first occurred several years previously when an uncle had exposed himself to her and possibly fondled her. The second incident occurred approximately 1 year before her hospitalization when her father came home intoxicated and fondled her while she was taking a shower. When this history came to light, it was felt that the patient could be suffering from a'somatoform disorder secondary to sexual abuse. She also reported some symptoms of major depression, such as insomnia, lack of energy, and poor appetite. At this point the decision was made to transfer the patient to the adolescent psychiatry unit for further evaluation. On admission to the adolescent psychiatry unit, the patient's physical examination showed several abnormalities. Her blood pressure was 130/90 mm Hg with a pulse of 96 beats per minute. She had lost 19 pounds since the onset of her illness. Abdominal exam showed moderate periumbilical tenderness without guarding or rebound tenderness. Rectal exam showed loose sphincter tone, rectal prolapse, and a large macerated, excoriated area of skin around the anus. The vulva was erythematous with multiple excoriations. The patient's skin had numerous excoriated lesions over her abdomen, buttocks, and thighs. She also had numerous hypopigmented scars in these areas. Peeling of the skin on her palms and soles was noted, and she had several black areas on her fingernails. Neurological examination revealed mildly decreased sensation of vibration and pinprick in the distal lower extremities. An intention tremor of both hands was noted. Her gait was normal, but she had difficulty with tandem walking and was unable to stand on one foot. At the mental status examination, the patient was neatly dressed and well groomed. She sat slumped in a chair and spoke in a soft voice. She made little eye contact. She was cooperative with the interview. Her speech was often whining and mumbling in character, which made it difficult to understand. She described her mood as "okay." Her affect was primarily flat with occasional tearfulness. Her thought processes were coherent. She described having auditory hallucinations consisting of voices laughing at her and making fun of her. She believed that her fellow patients were laughing and making fun of her. Her intellectual functions were intact. She was able to do multiplication problems up to 5 X 13 without difficulty. She subtracted serial 7s from 100 307
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with only two errors. She was fully oriented, and her recent and remote memory were intact. Her similarities were concrete. When asked to interpret proverbs, she replied' 'I don't know" to all of them. Laboratory findings at admission included a white blood cell count of 20,900/mm 3, hemoglobin of 12.5 g/dL, and hematocrit of 37.3%. Her erythrocyte sedimentation rate was 48 mm/hour. Urinalysis showed 3+ protein, greater than 50 WBC/hpf, and a large blood clot thought to be due to external trauma. Her urine culture was negative. Liver and renal functions tests were normal. The patient's behavior on the unit was quite unusual. When allowed to do what she wanted to do, she would lie in bed in her room with the lights off, the blinds closed, and her head covered up completely. She would lie either in a fetal position or on her back with her knees drawn up toward her head and her feet in the air. She often made herself a bed on the floor because she said she was used to sleeping on the floor at home. When she was compelled to come out of her room, she would sit slumped over with her head between her knees and her face covered with her hands or her hair. She ate very little despite the efforts of the staff to get her food that she liked. Her weight dropped from 91 to 84 pounds during this admission. She often complained of colicky abdominal pain that kept her from sleeping. She spent a great deal of time in the bathroom and could often be heard straining to have a bowel movement. She caused a significant amount of rectal bleeding by digging with her finger in her rectum. She was often observed to be masturbating and/or scratching her genital area in front of other patients and staff. She had temper tantrums quite frequently. These usually occurred after her requests to go home had been denied. She would then get down on her knees and beg and offer to give her doctor all of her worldly possessions if she could go home. When told that she could not go home, she would lie down on the bed or floor, kick her feet, hit herself on the head with her fists, throw things, and scream incoherently. Her mother reported that she had never behaved like this before she became ill. The patient's blood pressure and pulse were consistently elevated throughout her hospitalization. Her blood pressure averaged about 150190 mm Hg, and her pulse was always over 95 and often up to 120 beats per minute. These readings were consistent even while the patient was asleep. When she awakened in the morning, her bed linens and clothing were often soaked with perspiration. The patient's working diagnosis at this time was major depression with psychotic features. She met DSM-III-R criteria for this diagnosis except that the treatment team felt that an organic cause had not been ruled out, although the patient had come from the pediatric service and no organic cause had been found while she was there. An EEG was done that showed marked slowing of the background rhythm, suggesting diffuse cerebral dysfunction. Because the patient had abdominal pain associated with psychosis, the possibility of porphyria was considered. A 24-hour urine specimen was obtained for measurement of porphyrin excretion. This revealed a urinary coproporphyrin level of 236 /-lg/24 ° with the upper limit of normal being 56/-lg124 Other 0
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types of porphyrins were not detected. Reading about coproporphyrins revealed that this increased level was not specific for porphyria but could also occur in other conditions such as liver disease, malignancy, and toxic conditions, especially lead poisoning. Lead poisoning seemed like a strong possibility in this patient so a blood lead level and a urine toxic metal screen were ordered. Her blood lead level was 5/-lg1 dl. Her urine specimen was strongly positive for mercury. Pediatric consultation as well as consultation by a medical toxicologist were requested at this time. A 24-hour urine collection for mercury quantitation was begun. In the meantime, a meeting was held with the patient's family to try to determine the source of the patient's mercury exposure. Several possible sources of exposure were inquired about, including latex paint, water, soil, and the father's occupation as a welder's assistant. None of these possibilities seemed likely in this case. As the family session was about to end, the patient's 13-year-old brother related an incident that had occurred about 6 months previously. At that time, a friend of the brother had visited the patient's home, a small mobile home. He had brought a large metal cylinder that his father had obtained from the garbage of a local petrochemical plant. The patient and her brothers and sisters were playing with the cylinder and decided to crack it open to see what was inside. They cracked it open with a hammer and a silver liquid spilled out onto the living room carpet. The family was unaware that it was toxic. The parents scooped up what they could off of the carpet and put it in a glass. The children played with it for several days before their mother threw it away. Since that time, the family had been exposed to mercury vapor from the mercury remaining in the carpet. The patient had been the only one in the family to show symptoms of mercury poisoning because she slept on the floor where the concentration of the mercury vapor was highest. At this point, urine samples were obtained from all of the patient's immediate family members as well as several other relatives who had spent time in their home over the previous 6 months. All of the immediate family members were positive for mercury, and all had 24-hour urine mercury levels high enough to require treatment. All were treated with oral D-penicillamine. The patient's 24-hour urine mercury level was 686 /-lgl 24°. She was transferred to pediatrics for intravenous chelation therapy. She was treated with calcium disodium EDTA, acetylcysteine, D-penicillamine, and dimercaptosuccinic acid (DMSA), a new investigational oral chelating agent. She was given small doses of thioridazine for agitation while she was on the pediatric service. As her body burden of mercury decreased, her mental status returned to normal and the thioridazine was tapered and discontinued. Children's Protective Services closed the sexual abuse case after it was determined that all of the patient's physical and psychiatric symptoms could be explained by the mercury poisoning (Akabane, 1987). Unfortunately, the patient was lost to psychiatric follow-up after discharge. Discussion
This case exemplifies many of the psychiatric manifestaJ. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
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tions commonly reported in cases of mercury toxicity, as well as some less common ones. Disturbances of mood and personality are commonly associated with mercury poisoning, as are many complaints often thought to be "psychosomatic." Psychotic symptoms and bizarre behavior are apparently much less common. Certain types of cognitive impairments are also reported to be associated with mercury toxicity. The mood alterations most commonly reported in association with mercury toxicity are irritability and depression. Depression and irritability may be the first noticeable signs of mercury intoxication (Feldman, 1982). In a study of chlorine-alkali workers, Piikivi and Hanninen (1989) found significantly more subjective anger in mercury exposed workers than in controls. Studies by Roels et aI. (1985) and Skerfving and Vostal (1972) yielded similar results. In a series of cases of mercury toxicity among workers in a thermometer factory, Vroom and Greer (1972) reported irritability as a presenting symptom in six of nine cases. Similar findings are reported by Ross and Sholiton (1983) in a series of mercury-exposed laboratory workers. The patient described here certainly displayed irritability as evidenced by her frequent, violent temper tantrums. Depression is also frequently reported in cases of mercury toxicity, although it is less strongly associated than irritability. Subjective depression was reported in four of nine cases by Ross and Sholiton (1983). Soleo et aI. (1990) found a nonsignificant increase in Ipat depression scale scores in mercury-exposed workers in a fluorescent lamp factory compared with nonexposed workers in the same factory. Piikivi and Hanninen (1989), however, found no significant difference in reports of depression between exposed workers and controls. The patient in this case was quite depressed and, in fact, met DSM-III-R criteria for major depression with psychotic features. The condition of the patient is aptly summed up in Textbook of Pediatrics: "the child [with mercury poisoning) does not play or smile but appears dejected and melancholic, a picture of abject misery" (p. 1799). Personality disturbances are also common in cases of mercury toxicity. Historically, a particular personality syndrome, called erethism, has been described in hatters and other mercury-exposed workers. This syndrome consists of irritability, excitability, shyness, sensitivity, outbursts of temper, quarreling, and a tendency to perspire and blush. It is this blushing, or reddening, that gives the syndrome its name, "erethism" (Gerstner and Huff, 1977; Ross et aI., 1977). Some studies have been done using standardized personality inventories in patients with mercury toxicity. Vroom and Greer (1972) administered the Minnesota Multiphasic Personality Inventory to nine patients with mercury poisoning. They found that all were somewhat anxious and about half somatized their complaints. Forzi used the Eysenck Personality Inventory to study two groups of workers, one with higher and the other with lower exposure to mercury. He found the group with higher exposure to be more introverted and neurotic (Forzi et aI., 1976). Angotzi et aI. (1980) compared a mercury-exposed group with a control using the personality inventory of Cattell. They J. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
found a tendency toward anxiety and introversion in the mercury-exposed group. The largest difference between the two groups was in the trait of shyness. Personality testing was not possible with the case patient, but clinically she exhibited many of the characteristics of erethism, including irritability, outbursts of temper, shyness, sensitivity, and a tendency to perspire. Although the patient experienced auditory hallucinations, psychotic symptoms are apparently uncommon in patients with mercury toxicity. There are few reports of psychosis among cases of mercury poisoning reported in the literature (Sunderman, 1988; Vroom and Greer, 1972). The patient exhibited some strange behaviors that could be construed as being psychotic behaviors, such as assuming unusual postures and covering her face all the time. However, assumption of bizarre positions as a result of hypotonia and lax ligaments is a common symptom of acrodynia, as is photophobia, which would explain the patient's preference for darkness and tendency to cover her face (Akabane, 1987). Another common feature of mercury toxicity is a multiplicity of physical complaints that are often thought to be psychosomatic in origin. These symptoms include pain in various parts of the body, headache, fatigue, weakness, loss of appetite, insomnia, dizziness, difficulty walking, and diarrhea (Centers for Disease Control, 1990; Gerstner and Huff, 1977; Rosenman et al., 1986; Ross et aI., 1977; Smith et aI., 1970). Smith et aI. (1970) found a close correlation between the level of mercury exposure and the statistical incidence of certain complaints (loss of appetite, weight loss, diarrhea, and dizziness) among workers in a chlorine manufacturing plant. The case patient experienced virtually all of the abovementioned symptoms during the course of her illness and many of them were thought to be psychosomatic or "hystericaL" The effects of mercury exposure on various cognitive functions have been the subject of several studies. Most of these studies have used standard neuropsychiatric tests to study the effects of mercury exposure on intelligence, visualspatial skills, psychomotor functions, and memory (Camerino et aI., 1981; Hanninen, 1982; Piikivi and Hanninen, 1989; Shapiro et aI., 1982; Smith et aI., 1983; Soleo et aI., 1990; Uzzell and Oler, 1986; Vroom and Greer, 1972). Several studies used the Wechsler Adult Intelligence Scale (WAIS), or subtests thereof, to study the effects of mercury exposure on intelligence (Camerino et aI., 1981; Piikivi et aI., 1984; Shapiro et aI., 1982; Soleo et aI., 1990; Uzzell and Oler, 1986; Vroom and Greer, 1972). Most found no significant effect of mercury exposure on overall intelligence. However, Camerino et al. (1981) did find a significant decrease in perceptual intelligence, as measured using the Raven Progressive Matrices and WAIS Block Design tests, in mercury-exposed workers in a mercury extraction plant when compared with nonexposed workers. The effects of mercury exposure on visual-spatial skills has also been studied. Shapiro et aI. (1982) found a significant increase in the number of errors on the Bender-Gestalt test in dentists with high tissue mercury levels versus dentists with no detectable tissue mercury. Several investigators have studied the effects of mercury 309
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exposure on psychomotor functioning. Piikivi et al. (1984) used a modified version of the Santa Ana Dexterity Test and found that mercury-exposed chlorine-alkali workers performed significantly worse on the task using both hands than did nonexposed workers. Camerino et al. (1981) found significant differences in visuomotor skills, measured by simple reaction time and choice reaction time, between mercury-exposed and nonexposed subjects. They also found that visuomotor impairment was significantly correlated with urine mercury levels. Paradoxically, Piikivi and Hanninen (1989) found that mercury-exposed chlorine-alkali workers in their study had significantly better hand-eye coordination than nonexposed workers. The most consistent finding in studies of the effects of mercury on cognitive functions has been impairment of short-term memory. Smith et al. (1983) studied short-term memory using an estimate of the subjects' 50% threshold for correct serial recall on the Wechsler Digit Span forward test. They found a significant linear relationship between 50% threshold spans and urinary mercury concentrations, with short-term memory decreasing as urinary mercury increased. Williamson et al. (1982) discovered a correlation between short-term memory and length of exposure in mercury-exposed dentists. Camerino et al. (1981) found that short-term memory impairment was significantly correlated with urinary mercury levels in workers in a mercury extraction plant. Vroom and Greer (1972) studied employees of a thermometer manufacturing plant and found recent memory impairment similar to that found in temporal lobe lesions. Most of the above mentioned studies were done on workers exposed to mercury on their jobs and not on patients with clinical evidence of mercury poisoning. Neuropsychological testing was attempted with the patient in this report, but she was unable to cooperate with testing during her hospitalization and was lost to psychiatric follow-up after discharge. However, her recent and remote memory were intact on mental status examination on admission to the psychiatric unit. Cases of mercury poisoning are often misdiagnosed initially, as evidenced by this case and other case reports (Centers for Disease Control, 1990; Ross and Sholiton, 1983; Sunderman, 1988). The patient here was initially thought to have rheumatic fever because she had an elevated antistreptolysin-a titer and a history of a sore throat, and her other symptoms seemed to fit with this diagnosis. On her second admission she was thought to have a psychiatric disorder because of her prominent psychiatric symptomatology and the apparent lack of an organic etiology for her physical symptoms. Her history of sexual abuse along with the rectal prolapse seemed to confirm that she suffered from a psychiatric disorder resulting from severe sexual abuse. Unfortunately, all of these factors proved to be red herrings that delayed the correct diagnosis of this classic case of acrodynia (Akabane, 1987). This case underscores the importance of ruling out any organic condition before making a psychiatric diagnosis. It reminds us that it is important to "think organic" even when the patient has come from a medical service where an extensive work up has already been done. The assumption 310
that this patient had already been "medically cleared" resulted in failure to obtain a toxic metal screen on admission, although this would have been standard procedure for a child admitted directly to psychiatry with a first psychotic episode. This case also reminds us of the importance of inquiring about toxic exposure during history-taking. Although this patient's family was unaware of the toxicity of the silver liquid in their carpet and, therefore, probably would not have given this history without being extensively questioned about mercury, many patients and their families may be aware of toxic exposures and may be able to give important information when asked. In this age of increasing accumulation of toxins in our environment, it is becoming more and more important to consider toxic conditions in the differential diagnosis of psychiatric disorders. References Akabane, T. (1987), Acrodynia. In: Textbook of Pediatrics, eds. R. E. Behrman, V. C. Vaughan & W. E. Nelson. Philadelphia: W. B. Saunders Company, pp. 1506-1507. Angotzi, G., Cassitto, M. G., Camerino, D. & Cioni, R. (1980), Rapporti tra exposizione a mercurio e condizioni di salute in un gruppo di lavorti addeti all dritillazione di mercurio. Med. Lav., 6:463-480. Camerino, D., Cassitto, M. G., Desideri, E. & Angotzi G. (1981), Behavior of some psychological parameters in a population of a Hg extraction plant. Clinical Toxicology, 18:1299-1309. Centers for Disease Control. (1990) Elemental mercury poisoning in a household-Ohio, 1989. Morbidity and Mortality Weekly Report, 39:424-425. Feldman, R. G. (1982), Neurological manifestations of mercury intoxication. Acta Neurol. Sand., 66(suppl. 92):201-209. Forzi, M., Cassitto, M. G., Bulgheroni, C. & Foa, V. (1976), Psychological measures in workers occupationally exposed to mercury vapor: a validation study. In: Adverse Effects of Environmental Chemicals and Psychotropic Drugs, vol. 2, ed. M. Horvath. Amsterdam: Elsevier, pp. 169-171. Gerstner, H. B. & Huff, J. E. (1977), Clinical toxicology of mercury. J. Toxicol. Environ. Health, 2:491-526. Goldwater, L. J. (1936), From Hippocrates to Ramazzini: early history of industrial medicine. Annals of Medical History, 8:27-35. Gowdy, J. & Demers, F. (1978), The blood mercury levels in mental hospital patients. Am. J. Psychiatry, 135:115-116. Hanninen, H. (1982), Behavioral effects of occupational exposure to mercury and lead. Acta Neurol. Scand., 66(suppl. 92):167-175. Hunter, D. (1978), Diseases of Occupations. London: Hodder and Stoughton. Piikivi, L., & Hanninen, H. (1989), Subjective symptoms and psychological performance of chlorine-alkali workers. Scand. J. Work Environ. Health, 15:69-74. - - - - Martelin, T. & Mantere, P. (1984), Psychological performance and long-term exposure to mercury vapors. Scand. J. Work Environ. Health, 10:35-41. Roels, H., Gennart, J. P., Lauwerys, R., Buchet, J. P., Malchaire, J. & Bernard A. (1985), Surveillance of workers exposed to mercury vapor: validation of previously proposed biological threshold limit value for mercury concentration in urine. Am. J. Ind. Med., 7:45-71. Rosenman, K. D., Valciukas, J. A., Glickman, L., Meyers, B. R. & Cinotti, A. (1986), Sensitive indicators of inorganic mercury toxicity. Arch. Environ. Health, 41:208-215. Ross, W. D., Gechman, A. S., Sholiton, M. C. & Paul, H. S. (1977), Need for alertness to neuropsychiatric manifestations of inorganic mercury poisoning. Compr. Psychiatry, 18:595-598. Ross, W. D. & Sholiton, M. C. (1983), Specificity of psychiatric manifestations in relation to neurotoxic chemicals. Acta Psychiatr. Scand., 67(suppl. 303):100-104. Shapiro,1. M., Sumner, A. 1., Spitz, L. K., et al. (1982), Neurophysiological function in mercury-exposed dentists. Lancet, 1:1147-1150. J. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
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Skerfving, S. & Vostal, J. (1972), Symptoms and signs of intoxication. In: Mercury in the Environment, eds. L. Friberg & J. Vostal. Cleveland: CRC Press, pp. 93-107. Smith, P. 1., Lango1f, G. D. & Goldberg, 1. (1983), Effects of occupational exposure to elemental mercury on short term memory. Br. J.
Ind. Med., 40:413-419. Smith, R. G., Vorwald, A. J., PatH, L. S. & Mooney, T. F. (1970), Effects of exposure to mercury in the manufacture of chlorine. Am.
Ind. Hyg. Assoc. J., 31:687-700. Soleo, L., Urbano, M. L., Petrera, V. & Ambrosi, L. (1990), Effects of low exposure to inorganic mercury on psychological performance. Br. J. Ind. Med., 47:105-109.
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Sunderman, F. W. (1988), Perils of mercury. Ann. CUn. Lab. Sci., 18:89-101. Uzzell, B. P. & Oler, J. (1986), Chronic low-level mercury exposure and neuropsychological functioning. J. CUn. Exp. Neuropsychol., 8:581-593. Vroom, F. Q. & Greer, M. (1972), Mercury vapor intoxication. Brain, 95:305-318. Williamson, A. M., Teo, R. K. & Sanderson, J. (1982), Occupational mercury exposure and its consequences for behavior. Int. Arch.
Occup. Environ. Health, 50:273-286.
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CINDY L. WIGG, M.D.
Abstract. Mercury and its compounds are toxic substances that are widely used in industry and agriculture. Mercury poisoning is an uncommon but important clinical entity that often presents with psychiatric disturbances as a prominent part of the clinical picture. In this paper, a case of mercury poisoning in a l2-year-old girl with prominent psychiatric manifestations is presented. Relevant literature concerning the psychiatric manifestations of mercury poisoning is discussed. The importance of considering mercury poisoning, and toxic conditions in general, in the differential diagnosis of psychiatric disorders is emphasized. J. Am. Acad. Child Adolesc. Psychiatry, 1992, 31,2:306-311. Key Words: toxicology, mercury poisoning, organic mental disorders. Mercury, or quicksilver, has been used for many purposes for 3,000 years. In the past, mercury and its compounds were used extensively in medicine as cathartics, antiparasitics, vermifuges, antisyphilitics, diuretics, and ointments for various skin conditions (Sunderman, 1988). It was also used for gilding and gold-plating metal objects and for making mirrors. Its use in the manufacture of felt hats gave rise to the expression "mad as a hatter," referring to symptoms of mercury poisoning among hatmakers (Hunter, 1978). Modern medicine has all but abandoned the use of mercurials, but mercury and mercury compounds are still widely used in industry and agriculture. Elemental mercury is used in the manufacture of thermometers, barometers, vacuum pumps, and various components of electrical apparatus. Mercury compounds are used as detonators, in paints, and as agricultural fungicides (Hunter, 1978). Mercury amalgams are used as dental fillings. Mercury is also released in the atmosphere during the combustion of fossil fuels (Gerstner and Huff, 1977). The toxicity of mercury and its compounds has also been recognized for many centuries. Early descriptions of mercury toxicity date back to the first century A.D. and beyond. The toxicity of mercury vapor was first described in 1473 by Ulrich Ellenborg of Germany (Goldwater, 1936). In the 1940s, mercury toxicity was identified as the cause of the Mad Hatter syndrome, also called erethism (Gowdy and Demers, 1978). Also in the 1940s, Warkany and others discovered that acrodynia, a serious disease of children, was caused by mercury poisoning. In the 1950s and 1960s massive epidemics of mercury poisoning occurred in Japan
Accepted August 22, 1991. Dr. Fagala isa Third Year Resident in the Department ofPsychiatry and Behavioral Sciences, University of Texas Medical Branch, Galveston. Dr. Wigg is Assistant Professor of Psychiatry and Behavioral Sciences and Medical Director ofAdolescent Inpatient Services, Division of Child and Adolescent Psychiatry, University of Texas Medical Branch, Galveston, Texas. Reprint requests to Dr. Wigg, Division of Child and Adolescent Psychiatry, University of Texas Medical Branch, Graves Building 1.108, Galveston, TX 77550. 0890-8567/92/3102-0306$03.00/0© 1992 by the American Academy of Child and Adolescent Psychiatry.
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and Iraq as a result of ingestion of organic mercury compounds in food (Goldwater, 1936). Mercury may enter the human body via the lungs, the gastrointestinal tract, or the skin. Elemental mercury vaporizes easily and the inhaled vapor is easily and almost completely absorbed through the lungs. Ingested elemental mercury passes through the gastrointestinal tract with virtually no systemic absorption, but ingestion of organic mercury compounds, especially alkyl mercury compounds, results in almost complete absorption. Absorption of mercury via the skin causes a severe dermatitis in some individuals. Elemental mercury, once it enters the bloodstream, is quickly circulated to all parts of the body. It has a particular affinity for the brain and crosses the blood-brain barrier easily. Once inside nerve cells, it is oxidized to mercuric ion, complexed with sulfhydryl groups on proteins, and retained. In this form it returns to the bloodstream extremely slowly (Gerstner and Huff, 1977). The tendency of mercury to accumulate in the brain explains why psychiatric disturbances are a major part of the clinical picture of elemental mercury poisoning. This paper deals with a case of elemental mercury poisoning with prominent psychiatric manifestations in a 12-year-old girl.
Case Presentation The patient was a 12-year-old Hispanic girl who was healthy and functioning normally until approximately 1 month before her initial admission to the University of Texas Medical Branch. At the time of her initial admission, she presented with a chief complaint of difficulty walking. She reported feeling dizzy when she walked and complained of multiple joint pains, weakness, nausea, sweating, and numbness and tingling of her palms. Physical findings at that time included truncal ataxia with a positive Romberg sign and a tendency to fall to the right. Possible mild chorea was noted. She had decreased strength in her lower extremities. Her right patellar reflex was absent and the left one was markedly decreased. It was noted in her chart that she walked better when she was unaware of being observed. She had a CT scan of the head, an EEG, and a lumbar puncture, the results of which were all normal. Her antinuclear antibody titer (ANA) was negative. Lower extremity electromyJ. Am. Acad. Child Adolesc. Psychiatry, 31 :2, March 1992
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ograms were abnormal. A streptozyme test was positive and her antistreptolysin-O titer was I :625. She reported a history of a sore throat 2 weeks before admission. At this point she was given the diagnosis of rheumatic fever and was treated with aspirin and a 2-week course of oral penicillin. Her ataxia improved somewhat after she was started on penicillin and she was discharged after 5 days in the hospital. Over the next 6 weeks she made multiple visits to the emergency room and various clinics with a variety of complaints, including joint pains; a rash over her abdomen, buttocks, and thighs; abdominal pain; and bloody diarrhea. On one emergency room visit her pain was described as having "a strong hysterical component." On one clinic visit at another hospital she was found to have a positive ANA. When she presented with abdominal pain and bloody diarrhea, proctoscopy was performed. Ulceration of the rectal mucosa was found up to 10 cm from the anal opening. The mucosa appeared normal proximal to that point. Biopsies were taken and she was scheduled to be followed up after the biopsy results were available. Approximately 1 week later, the patient returned to the pediatric clinic with worsening abdominal pain and burning of her genital area. She appeared quite ill and was admitted to the hospital. The initial diagnostic impression at that time was rheumatic fever, dermatitis, and colitis. The possibility of systemic lupus erythematosus was considered. Abnormal findings on her initial physical examination included a diffuse, excoriated, infected rash located primarily on her abdomen, buttocks, and thighs. Rectal examination showed loose sphincter tone and a significant rectal prolapse occurring with the Valsava maneuver. Pelvic exam was normal and showed an intact hymen. Results of laboratory tests included a negative ANA with an erythrocyte sedimentation rate of 46 mm/hour. A complete blood count was normal except for a white blood cell count of 20,200/mm3• Urinalysis showed 1+ proteinuria. Her electrolytes were normal except for a potassium of 2.7 meql L. This eventually rose to 3.8 meq/L during her hospital stay. Her rapid plasma reagin was nonreactive. A fecal culture grew no pathogens. Cervical cultures for chlamydia and N. gonorrhea were negative. Examination of her stool for ova and parasites was negative. Complement and immunoglobulin studies were normal. The results of the rectal biopsies done before admission revealed that her rectum was completely denuded of mucosa up to 10 cm proximal to the anal opening. Several observations about the patient's behavior were made by the pediatric treatment team during her admission. It was noted in her chart that she often appeared to be in great pain when medical personnel entered the room but appeared much calmer and more comfortable when she was being observed without her knowledge. She scratched herself almost constantly, especially in her genital area. She was observed on several occasions putting her finger into her rectum while defecating. She also assumed bizarre positions in bed at times. A number of consultants were called in to evaluate the patient. She was seen by a pediatric immunologist whose assessment was that many of her physical findings, particuJ. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
larly her skin lesions, were factitious in nature and that there was no evidence of an immunological disorder. The most likely diagnosis was thought to be a psychiatric disorder. A gastroenterologist felt that her unusual rectal ulceration and prolapse could be due to ulcerative colitis, pseudomembranous colitis, or sexual abuse with anal intercourse. Because of the patient's rather strange behavior at times, sexual abuse was considered to be a strong possibility, and psychiatric consultation was requested. During the initial interview with a child psychiatrist, the patient lay in bed with one hand holding her abdomen and the other holding her genitalia. She complained of being in pain but her affect was not consistent with being in pain. She often grimaced when her mother spoke and seemed reluctant to speak with her mother present. When she was seen alone, she began to cry and abruptly blurted out a history of two incidents of sexual abuse. The first occurred several years previously when an uncle had exposed himself to her and possibly fondled her. The second incident occurred approximately 1 year before her hospitalization when her father came home intoxicated and fondled her while she was taking a shower. When this history came to light, it was felt that the patient could be suffering from a'somatoform disorder secondary to sexual abuse. She also reported some symptoms of major depression, such as insomnia, lack of energy, and poor appetite. At this point the decision was made to transfer the patient to the adolescent psychiatry unit for further evaluation. On admission to the adolescent psychiatry unit, the patient's physical examination showed several abnormalities. Her blood pressure was 130/90 mm Hg with a pulse of 96 beats per minute. She had lost 19 pounds since the onset of her illness. Abdominal exam showed moderate periumbilical tenderness without guarding or rebound tenderness. Rectal exam showed loose sphincter tone, rectal prolapse, and a large macerated, excoriated area of skin around the anus. The vulva was erythematous with multiple excoriations. The patient's skin had numerous excoriated lesions over her abdomen, buttocks, and thighs. She also had numerous hypopigmented scars in these areas. Peeling of the skin on her palms and soles was noted, and she had several black areas on her fingernails. Neurological examination revealed mildly decreased sensation of vibration and pinprick in the distal lower extremities. An intention tremor of both hands was noted. Her gait was normal, but she had difficulty with tandem walking and was unable to stand on one foot. At the mental status examination, the patient was neatly dressed and well groomed. She sat slumped in a chair and spoke in a soft voice. She made little eye contact. She was cooperative with the interview. Her speech was often whining and mumbling in character, which made it difficult to understand. She described her mood as "okay." Her affect was primarily flat with occasional tearfulness. Her thought processes were coherent. She described having auditory hallucinations consisting of voices laughing at her and making fun of her. She believed that her fellow patients were laughing and making fun of her. Her intellectual functions were intact. She was able to do multiplication problems up to 5 X 13 without difficulty. She subtracted serial 7s from 100 307
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with only two errors. She was fully oriented, and her recent and remote memory were intact. Her similarities were concrete. When asked to interpret proverbs, she replied' 'I don't know" to all of them. Laboratory findings at admission included a white blood cell count of 20,900/mm 3, hemoglobin of 12.5 g/dL, and hematocrit of 37.3%. Her erythrocyte sedimentation rate was 48 mm/hour. Urinalysis showed 3+ protein, greater than 50 WBC/hpf, and a large blood clot thought to be due to external trauma. Her urine culture was negative. Liver and renal functions tests were normal. The patient's behavior on the unit was quite unusual. When allowed to do what she wanted to do, she would lie in bed in her room with the lights off, the blinds closed, and her head covered up completely. She would lie either in a fetal position or on her back with her knees drawn up toward her head and her feet in the air. She often made herself a bed on the floor because she said she was used to sleeping on the floor at home. When she was compelled to come out of her room, she would sit slumped over with her head between her knees and her face covered with her hands or her hair. She ate very little despite the efforts of the staff to get her food that she liked. Her weight dropped from 91 to 84 pounds during this admission. She often complained of colicky abdominal pain that kept her from sleeping. She spent a great deal of time in the bathroom and could often be heard straining to have a bowel movement. She caused a significant amount of rectal bleeding by digging with her finger in her rectum. She was often observed to be masturbating and/or scratching her genital area in front of other patients and staff. She had temper tantrums quite frequently. These usually occurred after her requests to go home had been denied. She would then get down on her knees and beg and offer to give her doctor all of her worldly possessions if she could go home. When told that she could not go home, she would lie down on the bed or floor, kick her feet, hit herself on the head with her fists, throw things, and scream incoherently. Her mother reported that she had never behaved like this before she became ill. The patient's blood pressure and pulse were consistently elevated throughout her hospitalization. Her blood pressure averaged about 150190 mm Hg, and her pulse was always over 95 and often up to 120 beats per minute. These readings were consistent even while the patient was asleep. When she awakened in the morning, her bed linens and clothing were often soaked with perspiration. The patient's working diagnosis at this time was major depression with psychotic features. She met DSM-III-R criteria for this diagnosis except that the treatment team felt that an organic cause had not been ruled out, although the patient had come from the pediatric service and no organic cause had been found while she was there. An EEG was done that showed marked slowing of the background rhythm, suggesting diffuse cerebral dysfunction. Because the patient had abdominal pain associated with psychosis, the possibility of porphyria was considered. A 24-hour urine specimen was obtained for measurement of porphyrin excretion. This revealed a urinary coproporphyrin level of 236 /-lg/24 ° with the upper limit of normal being 56/-lg124 Other 0
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types of porphyrins were not detected. Reading about coproporphyrins revealed that this increased level was not specific for porphyria but could also occur in other conditions such as liver disease, malignancy, and toxic conditions, especially lead poisoning. Lead poisoning seemed like a strong possibility in this patient so a blood lead level and a urine toxic metal screen were ordered. Her blood lead level was 5/-lg1 dl. Her urine specimen was strongly positive for mercury. Pediatric consultation as well as consultation by a medical toxicologist were requested at this time. A 24-hour urine collection for mercury quantitation was begun. In the meantime, a meeting was held with the patient's family to try to determine the source of the patient's mercury exposure. Several possible sources of exposure were inquired about, including latex paint, water, soil, and the father's occupation as a welder's assistant. None of these possibilities seemed likely in this case. As the family session was about to end, the patient's 13-year-old brother related an incident that had occurred about 6 months previously. At that time, a friend of the brother had visited the patient's home, a small mobile home. He had brought a large metal cylinder that his father had obtained from the garbage of a local petrochemical plant. The patient and her brothers and sisters were playing with the cylinder and decided to crack it open to see what was inside. They cracked it open with a hammer and a silver liquid spilled out onto the living room carpet. The family was unaware that it was toxic. The parents scooped up what they could off of the carpet and put it in a glass. The children played with it for several days before their mother threw it away. Since that time, the family had been exposed to mercury vapor from the mercury remaining in the carpet. The patient had been the only one in the family to show symptoms of mercury poisoning because she slept on the floor where the concentration of the mercury vapor was highest. At this point, urine samples were obtained from all of the patient's immediate family members as well as several other relatives who had spent time in their home over the previous 6 months. All of the immediate family members were positive for mercury, and all had 24-hour urine mercury levels high enough to require treatment. All were treated with oral D-penicillamine. The patient's 24-hour urine mercury level was 686 /-lgl 24°. She was transferred to pediatrics for intravenous chelation therapy. She was treated with calcium disodium EDTA, acetylcysteine, D-penicillamine, and dimercaptosuccinic acid (DMSA), a new investigational oral chelating agent. She was given small doses of thioridazine for agitation while she was on the pediatric service. As her body burden of mercury decreased, her mental status returned to normal and the thioridazine was tapered and discontinued. Children's Protective Services closed the sexual abuse case after it was determined that all of the patient's physical and psychiatric symptoms could be explained by the mercury poisoning (Akabane, 1987). Unfortunately, the patient was lost to psychiatric follow-up after discharge. Discussion
This case exemplifies many of the psychiatric manifestaJ. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
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tions commonly reported in cases of mercury toxicity, as well as some less common ones. Disturbances of mood and personality are commonly associated with mercury poisoning, as are many complaints often thought to be "psychosomatic." Psychotic symptoms and bizarre behavior are apparently much less common. Certain types of cognitive impairments are also reported to be associated with mercury toxicity. The mood alterations most commonly reported in association with mercury toxicity are irritability and depression. Depression and irritability may be the first noticeable signs of mercury intoxication (Feldman, 1982). In a study of chlorine-alkali workers, Piikivi and Hanninen (1989) found significantly more subjective anger in mercury exposed workers than in controls. Studies by Roels et aI. (1985) and Skerfving and Vostal (1972) yielded similar results. In a series of cases of mercury toxicity among workers in a thermometer factory, Vroom and Greer (1972) reported irritability as a presenting symptom in six of nine cases. Similar findings are reported by Ross and Sholiton (1983) in a series of mercury-exposed laboratory workers. The patient described here certainly displayed irritability as evidenced by her frequent, violent temper tantrums. Depression is also frequently reported in cases of mercury toxicity, although it is less strongly associated than irritability. Subjective depression was reported in four of nine cases by Ross and Sholiton (1983). Soleo et aI. (1990) found a nonsignificant increase in Ipat depression scale scores in mercury-exposed workers in a fluorescent lamp factory compared with nonexposed workers in the same factory. Piikivi and Hanninen (1989), however, found no significant difference in reports of depression between exposed workers and controls. The patient in this case was quite depressed and, in fact, met DSM-III-R criteria for major depression with psychotic features. The condition of the patient is aptly summed up in Textbook of Pediatrics: "the child [with mercury poisoning) does not play or smile but appears dejected and melancholic, a picture of abject misery" (p. 1799). Personality disturbances are also common in cases of mercury toxicity. Historically, a particular personality syndrome, called erethism, has been described in hatters and other mercury-exposed workers. This syndrome consists of irritability, excitability, shyness, sensitivity, outbursts of temper, quarreling, and a tendency to perspire and blush. It is this blushing, or reddening, that gives the syndrome its name, "erethism" (Gerstner and Huff, 1977; Ross et aI., 1977). Some studies have been done using standardized personality inventories in patients with mercury toxicity. Vroom and Greer (1972) administered the Minnesota Multiphasic Personality Inventory to nine patients with mercury poisoning. They found that all were somewhat anxious and about half somatized their complaints. Forzi used the Eysenck Personality Inventory to study two groups of workers, one with higher and the other with lower exposure to mercury. He found the group with higher exposure to be more introverted and neurotic (Forzi et aI., 1976). Angotzi et aI. (1980) compared a mercury-exposed group with a control using the personality inventory of Cattell. They J. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
found a tendency toward anxiety and introversion in the mercury-exposed group. The largest difference between the two groups was in the trait of shyness. Personality testing was not possible with the case patient, but clinically she exhibited many of the characteristics of erethism, including irritability, outbursts of temper, shyness, sensitivity, and a tendency to perspire. Although the patient experienced auditory hallucinations, psychotic symptoms are apparently uncommon in patients with mercury toxicity. There are few reports of psychosis among cases of mercury poisoning reported in the literature (Sunderman, 1988; Vroom and Greer, 1972). The patient exhibited some strange behaviors that could be construed as being psychotic behaviors, such as assuming unusual postures and covering her face all the time. However, assumption of bizarre positions as a result of hypotonia and lax ligaments is a common symptom of acrodynia, as is photophobia, which would explain the patient's preference for darkness and tendency to cover her face (Akabane, 1987). Another common feature of mercury toxicity is a multiplicity of physical complaints that are often thought to be psychosomatic in origin. These symptoms include pain in various parts of the body, headache, fatigue, weakness, loss of appetite, insomnia, dizziness, difficulty walking, and diarrhea (Centers for Disease Control, 1990; Gerstner and Huff, 1977; Rosenman et al., 1986; Ross et aI., 1977; Smith et aI., 1970). Smith et aI. (1970) found a close correlation between the level of mercury exposure and the statistical incidence of certain complaints (loss of appetite, weight loss, diarrhea, and dizziness) among workers in a chlorine manufacturing plant. The case patient experienced virtually all of the abovementioned symptoms during the course of her illness and many of them were thought to be psychosomatic or "hystericaL" The effects of mercury exposure on various cognitive functions have been the subject of several studies. Most of these studies have used standard neuropsychiatric tests to study the effects of mercury exposure on intelligence, visualspatial skills, psychomotor functions, and memory (Camerino et aI., 1981; Hanninen, 1982; Piikivi and Hanninen, 1989; Shapiro et aI., 1982; Smith et aI., 1983; Soleo et aI., 1990; Uzzell and Oler, 1986; Vroom and Greer, 1972). Several studies used the Wechsler Adult Intelligence Scale (WAIS), or subtests thereof, to study the effects of mercury exposure on intelligence (Camerino et aI., 1981; Piikivi et aI., 1984; Shapiro et aI., 1982; Soleo et aI., 1990; Uzzell and Oler, 1986; Vroom and Greer, 1972). Most found no significant effect of mercury exposure on overall intelligence. However, Camerino et al. (1981) did find a significant decrease in perceptual intelligence, as measured using the Raven Progressive Matrices and WAIS Block Design tests, in mercury-exposed workers in a mercury extraction plant when compared with nonexposed workers. The effects of mercury exposure on visual-spatial skills has also been studied. Shapiro et aI. (1982) found a significant increase in the number of errors on the Bender-Gestalt test in dentists with high tissue mercury levels versus dentists with no detectable tissue mercury. Several investigators have studied the effects of mercury 309
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exposure on psychomotor functioning. Piikivi et al. (1984) used a modified version of the Santa Ana Dexterity Test and found that mercury-exposed chlorine-alkali workers performed significantly worse on the task using both hands than did nonexposed workers. Camerino et al. (1981) found significant differences in visuomotor skills, measured by simple reaction time and choice reaction time, between mercury-exposed and nonexposed subjects. They also found that visuomotor impairment was significantly correlated with urine mercury levels. Paradoxically, Piikivi and Hanninen (1989) found that mercury-exposed chlorine-alkali workers in their study had significantly better hand-eye coordination than nonexposed workers. The most consistent finding in studies of the effects of mercury on cognitive functions has been impairment of short-term memory. Smith et al. (1983) studied short-term memory using an estimate of the subjects' 50% threshold for correct serial recall on the Wechsler Digit Span forward test. They found a significant linear relationship between 50% threshold spans and urinary mercury concentrations, with short-term memory decreasing as urinary mercury increased. Williamson et al. (1982) discovered a correlation between short-term memory and length of exposure in mercury-exposed dentists. Camerino et al. (1981) found that short-term memory impairment was significantly correlated with urinary mercury levels in workers in a mercury extraction plant. Vroom and Greer (1972) studied employees of a thermometer manufacturing plant and found recent memory impairment similar to that found in temporal lobe lesions. Most of the above mentioned studies were done on workers exposed to mercury on their jobs and not on patients with clinical evidence of mercury poisoning. Neuropsychological testing was attempted with the patient in this report, but she was unable to cooperate with testing during her hospitalization and was lost to psychiatric follow-up after discharge. However, her recent and remote memory were intact on mental status examination on admission to the psychiatric unit. Cases of mercury poisoning are often misdiagnosed initially, as evidenced by this case and other case reports (Centers for Disease Control, 1990; Ross and Sholiton, 1983; Sunderman, 1988). The patient here was initially thought to have rheumatic fever because she had an elevated antistreptolysin-a titer and a history of a sore throat, and her other symptoms seemed to fit with this diagnosis. On her second admission she was thought to have a psychiatric disorder because of her prominent psychiatric symptomatology and the apparent lack of an organic etiology for her physical symptoms. Her history of sexual abuse along with the rectal prolapse seemed to confirm that she suffered from a psychiatric disorder resulting from severe sexual abuse. Unfortunately, all of these factors proved to be red herrings that delayed the correct diagnosis of this classic case of acrodynia (Akabane, 1987). This case underscores the importance of ruling out any organic condition before making a psychiatric diagnosis. It reminds us that it is important to "think organic" even when the patient has come from a medical service where an extensive work up has already been done. The assumption 310
that this patient had already been "medically cleared" resulted in failure to obtain a toxic metal screen on admission, although this would have been standard procedure for a child admitted directly to psychiatry with a first psychotic episode. This case also reminds us of the importance of inquiring about toxic exposure during history-taking. Although this patient's family was unaware of the toxicity of the silver liquid in their carpet and, therefore, probably would not have given this history without being extensively questioned about mercury, many patients and their families may be aware of toxic exposures and may be able to give important information when asked. In this age of increasing accumulation of toxins in our environment, it is becoming more and more important to consider toxic conditions in the differential diagnosis of psychiatric disorders. References Akabane, T. (1987), Acrodynia. In: Textbook of Pediatrics, eds. R. E. Behrman, V. C. Vaughan & W. E. Nelson. Philadelphia: W. B. Saunders Company, pp. 1506-1507. Angotzi, G., Cassitto, M. G., Camerino, D. & Cioni, R. (1980), Rapporti tra exposizione a mercurio e condizioni di salute in un gruppo di lavorti addeti all dritillazione di mercurio. Med. Lav., 6:463-480. Camerino, D., Cassitto, M. G., Desideri, E. & Angotzi G. (1981), Behavior of some psychological parameters in a population of a Hg extraction plant. Clinical Toxicology, 18:1299-1309. Centers for Disease Control. (1990) Elemental mercury poisoning in a household-Ohio, 1989. Morbidity and Mortality Weekly Report, 39:424-425. Feldman, R. G. (1982), Neurological manifestations of mercury intoxication. Acta Neurol. Sand., 66(suppl. 92):201-209. Forzi, M., Cassitto, M. G., Bulgheroni, C. & Foa, V. (1976), Psychological measures in workers occupationally exposed to mercury vapor: a validation study. In: Adverse Effects of Environmental Chemicals and Psychotropic Drugs, vol. 2, ed. M. Horvath. Amsterdam: Elsevier, pp. 169-171. Gerstner, H. B. & Huff, J. E. (1977), Clinical toxicology of mercury. J. Toxicol. Environ. Health, 2:491-526. Goldwater, L. J. (1936), From Hippocrates to Ramazzini: early history of industrial medicine. Annals of Medical History, 8:27-35. Gowdy, J. & Demers, F. (1978), The blood mercury levels in mental hospital patients. Am. J. Psychiatry, 135:115-116. Hanninen, H. (1982), Behavioral effects of occupational exposure to mercury and lead. Acta Neurol. Scand., 66(suppl. 92):167-175. Hunter, D. (1978), Diseases of Occupations. London: Hodder and Stoughton. Piikivi, L., & Hanninen, H. (1989), Subjective symptoms and psychological performance of chlorine-alkali workers. Scand. J. Work Environ. Health, 15:69-74. - - - - Martelin, T. & Mantere, P. (1984), Psychological performance and long-term exposure to mercury vapors. Scand. J. Work Environ. Health, 10:35-41. Roels, H., Gennart, J. P., Lauwerys, R., Buchet, J. P., Malchaire, J. & Bernard A. (1985), Surveillance of workers exposed to mercury vapor: validation of previously proposed biological threshold limit value for mercury concentration in urine. Am. J. Ind. Med., 7:45-71. Rosenman, K. D., Valciukas, J. A., Glickman, L., Meyers, B. R. & Cinotti, A. (1986), Sensitive indicators of inorganic mercury toxicity. Arch. Environ. Health, 41:208-215. Ross, W. D., Gechman, A. S., Sholiton, M. C. & Paul, H. S. (1977), Need for alertness to neuropsychiatric manifestations of inorganic mercury poisoning. Compr. Psychiatry, 18:595-598. Ross, W. D. & Sholiton, M. C. (1983), Specificity of psychiatric manifestations in relation to neurotoxic chemicals. Acta Psychiatr. Scand., 67(suppl. 303):100-104. Shapiro,1. M., Sumner, A. 1., Spitz, L. K., et al. (1982), Neurophysiological function in mercury-exposed dentists. Lancet, 1:1147-1150. J. Am. Acad. Child Adolesc. Psychiatry, 31:2, March 1992
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Skerfving, S. & Vostal, J. (1972), Symptoms and signs of intoxication. In: Mercury in the Environment, eds. L. Friberg & J. Vostal. Cleveland: CRC Press, pp. 93-107. Smith, P. 1., Lango1f, G. D. & Goldberg, 1. (1983), Effects of occupational exposure to elemental mercury on short term memory. Br. J.
Ind. Med., 40:413-419. Smith, R. G., Vorwald, A. J., PatH, L. S. & Mooney, T. F. (1970), Effects of exposure to mercury in the manufacture of chlorine. Am.
Ind. Hyg. Assoc. J., 31:687-700. Soleo, L., Urbano, M. L., Petrera, V. & Ambrosi, L. (1990), Effects of low exposure to inorganic mercury on psychological performance. Br. J. Ind. Med., 47:105-109.
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Sunderman, F. W. (1988), Perils of mercury. Ann. CUn. Lab. Sci., 18:89-101. Uzzell, B. P. & Oler, J. (1986), Chronic low-level mercury exposure and neuropsychological functioning. J. CUn. Exp. Neuropsychol., 8:581-593. Vroom, F. Q. & Greer, M. (1972), Mercury vapor intoxication. Brain, 95:305-318. Williamson, A. M., Teo, R. K. & Sanderson, J. (1982), Occupational mercury exposure and its consequences for behavior. Int. Arch.
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