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NEAR-PURE XYLENE CAUSING REVERSIBLE NEUROPSYCHIATRIC DISTURBANCE
273 lower with ball-and-cage valves’ and least with biological tissue prostheses.s Prevention of this complication demands meticulous control of anticoagulation. Clinical suspicion is the most important factor in the diagnosis. Any unexplained decrease in exercise tolerance, worsening dyspnoea, or heart failure should raise suspicion. Changes in the character of prosthetic valve clicks are a valuable sign. The diagnosis may be supported by echocardiography and fluorescent screening of the valve if it is radio-opaque (eg, Bjork Shiley prostheses made after March, 1975). Prosthetic valve occlusion is a life-threatening event; the outcome depends on how quickly the diagnosis is made’ and treatment is instituted. The condition is usually remediable. Department of Cardiology, John Radcliffe Hospital, Oxford OX3 9DU
S. BLOOM A. J. S. COATS O. J. M. ORMEROD
W, Nevelsteen A, Van Cauwelaert P. Nine years expenence with the Bjork Shiley prosthetic valve: Early and late results of 932 valve replacements. Ann Thorac Surg 1983; 35: 651-63. 2 Copans H, Lakier JB, Colsen PR, Fritz VU, Barlow JB, None N. Thrombosed Blork Shiley mitral valve prostheses. Circulation 1980; 61: 169-74. 3 Karp RB, Cyrus RJ, Blackstone EH, Kirklin JW, Kouchoukos NT, Pacifico AD. The Bjork Shiley valve: Intermediate term follow up. J Thorac Cardiovasc Surg 1981,
Central nervous system effects of industrial solvents are controversial.z3 There is evidence for psychological effects of acute high level exposure but chronic intellectual impairment is disputed.’ Poisoning following high-level xylene exposure is rare .5 Our case demonstrates an insidious onset of neuropsychiatric disorder over 6 months. Limited reports on xylene indicate non-specific neurological and intellectual impairment, including fatigue and giddiness, staggering gait, chronic residual insomnia, tremor, and feelings of drunkenness. In our case a direct toxic effect is the most likely explanation of this reversible acute organic brain syndrome. With occupational exposure to organic solvents subtle neurological manifestations invariably precede more widespread organic lesions, and the worker’s relatives may be aware of changes in mental state before he is.6 Clinicians should bear in mind solvent-induced neuropsychiatric impairment in the differential diagnosis of such vague presentations.
1 Daenan
81: 602-14
4 Pumphrey CW, Fuster V, Chesebro JH Systemic thromboembolism in valvular heart disease and prosthetic heart valves. Mod Concepts Cardiovasc Dis 1982; 51: 131-36. 5 Murphy DA, Levine FH, Buckley MJ. Mechanical valves. a comparative analysis of the Starr Edwards and the Blork Shiley prostheses J Thorac Cardiovasc Surg 1983; 86: 746-52. 6 Nunez L, Gil Aguado M, Celemm D, Iglesias A, Larrea JL. Aspirin or coumarin as the drug of choice for valve replacement with porcine bioprostheses. Ann Thorac Surg 1982; 33: 354-58
NEAR-PURE XYLENE CAUSING REVERSIBLE NEUROPSYCHIATRIC DISTURBANCE
SiR,—Xylene, in combination with toluene, is widely used in industry, and solvent mixtures have been reported to cause neurological and neuropsychiatric disorders in exposed workers.1 We report an unusual case in which exposure to 99-7% pure xylene gave rise to neuropsychiatric disturbance. A very shortsighted man (born Oct 2, 1927) who repaired catamaran hull moulds between 1977 and 1985 used xylene from mid-1983. From January to July, 1985, his work load increased and exposure increased significantly. In July, 1985, he was admitted to hospital. He had applied xylene with a brush dipped into an open bucket. The xylene tended to collect in the cup-shaped moulds in a room 12 x 6 x 4 m with air changes estimated at two to three per hour. He cleaned moulds for about 4 hours per day. Work exposure to xylene was assessed at several hundred parts per million (ppm); readings over a half-filled bucket registered 7000 ppm. Accepted exposure limits were thus grossly exceeded. Exposure to xylene was not doubted by the management of the company. He had no history of unexplained irritability or emotional lability and drank very little. However, throughout 1984 he had workrelated headaches; this was followed by tiredness (worse towards the end of the week but improving at weekends), and by May and June, 1985, the headaches were worse with irritability and dizziness, and he felt unsafe driving home. In July, 1985, he was admitted to hospital with agitation, breathlessness, extreme tiredness, lightheadedness, sensation of limbs shaking when lying or sitting, impaired concentration, and short-term memory and confusion. Dysphasia, fine tremor, hyperreflexia, and unstable gait were the only abnormal physical signs. Routine investigations were normal, as were nerve conduction studies. He gradually improved but by December he still experienced transient lightheadedness and unsteadiness in crowds. In February, 1986, he was aware of only occasional imbalance and the only neurological abnormality was residual unsteadiness in walking or tuming. Psychological assessment excluded gross intellectual or memory impairment but concentration and attention were impaired. Psychiatric examination in February and April, 1986, excluded significant psychiatric morbidity. By April, 1986, the transient tension, indecision, lack of drive, variable concentration, increased sleep requirement, irritability, and noise sensitivity, described in February, had virtually remitted.
Health and Safety Executive, London W2 4TF; and King’s College Hospital and Institute of Psychiatry, London SE5
F. E. C. T.
P. ROBERTS G. LUCAS D. MARSDEN TRAUER
1. Waldron HA Solvents and the brain. Br J Ind Med 1986; 43: 73-74. 2. Grasso P, Sharratt M, Davies DM, Irvine D. Neurophysiological and psychological disorders and occupational exposure to organic solvents. Food Chem Toxicol 1984; 22: 819-52. 3. O’Flynn RR, Monkman SM, Waldron HA. Organic solvents and presenile dementia. a case reference study using death certificates. Br J Ind Med 1987; 44: 259-62. 4 Orback P, Lindgren M, Olivecrona H, Haeger-Aronsen B. Computed tomography and psychometric test performances in patients with solvent induced chronic toxic encephalopathy and healthy controls. Br J Ind Med 1987; 44: 175-79. 5. Browning E. Toxicity and metabolism of industrial solvents. Amsterdam; Elsevier, 1965. 6. Baker EL, White RF, Muraluski BJ. Clinical evaluation of neurobehavioural effects of occupational exposure to organic solvents and lead. Int J Ment Health 1985; 14: 135-58.
SEROCONVERSION AGAINST HUMAN HERPESVIRUS-6 (AND OTHER HERPESVIRUSES) AND CLINICAL ILLNESS
SIR,-It has been assumed that a mononucleosis-like disease or lymphoproliferative disorders could be manifestations of primary infection with human herpesvirus-6 (HHV -6)1-S but this assumption has yet to be strongly supported by clinical data. A clear relation between a specific disease (exanthem subitum) and acute HHV-6 infection has only lately been establishes 6 Although DNA homologies between HHV-6 and cytomegalovirus (CMV) have been described, serological cross-reactions have not yet been found. Few seroconversions, and no IgM seroconversion, have been recorded.6 We describe seroconversion (IgG and IgM) against HHV-6 in a patient with longlasting Epstein-Barr virus (EBV) infection-like symptoms and fatigue. From Jan 21,1988, a 29-year-old woman (a physician) felt unwell with joint and muscle pain and cervical lymphadenopathy. Laboratory findings (Feb 16) revealed lymphocytosis (499%) and thrombocytosis 307 00(?l). After about 3 months of fatigue and "migrating" lymphadenopathy the patient noticed dark urine, and she had headaches in the early morning. A week later, a maculopapular rash without itching appeared on hands, feet, knees, elbows, and left thigh. It lasted 10 days and was initially accompanied by fever (38’OOC). A sensation of abdominal pressure led to an ultrasonic examination, which revealed hepatosplenomegaly ; no abdominal nor thoracic lymphnode enlargements (X-ray) were found. Laboratory findings revealed raised erythrocyte sedimentation rate, haemolysis with no detectable haptoglobin, raised white blood cell count with mononuclear predominance, low titres of antinuclear antibodies, total IgM 492 mg/dl, and raised liver enzymes. On May 6, liver enzymes were normal, but a slight lymphocytosis was still present. The fatigue persisted. On May 17, the hepatosplenomegaly was no longer detected, and by the end of May the patient had completely other
recovered. HHV-6 immunofluorescence assays (IFA) were done on human cord blood lymphocytes (CBL) 9-22 days after infection with HHV-6 (gift of Dr R. W. Honess, London)." CBL were stimulated with phytohaemagglutinin for 4 days and cultivated with
S. BLOOM A. J. S. COATS O. J. M. ORMEROD
W, Nevelsteen A, Van Cauwelaert P. Nine years expenence with the Bjork Shiley prosthetic valve: Early and late results of 932 valve replacements. Ann Thorac Surg 1983; 35: 651-63. 2 Copans H, Lakier JB, Colsen PR, Fritz VU, Barlow JB, None N. Thrombosed Blork Shiley mitral valve prostheses. Circulation 1980; 61: 169-74. 3 Karp RB, Cyrus RJ, Blackstone EH, Kirklin JW, Kouchoukos NT, Pacifico AD. The Bjork Shiley valve: Intermediate term follow up. J Thorac Cardiovasc Surg 1981,
Central nervous system effects of industrial solvents are controversial.z3 There is evidence for psychological effects of acute high level exposure but chronic intellectual impairment is disputed.’ Poisoning following high-level xylene exposure is rare .5 Our case demonstrates an insidious onset of neuropsychiatric disorder over 6 months. Limited reports on xylene indicate non-specific neurological and intellectual impairment, including fatigue and giddiness, staggering gait, chronic residual insomnia, tremor, and feelings of drunkenness. In our case a direct toxic effect is the most likely explanation of this reversible acute organic brain syndrome. With occupational exposure to organic solvents subtle neurological manifestations invariably precede more widespread organic lesions, and the worker’s relatives may be aware of changes in mental state before he is.6 Clinicians should bear in mind solvent-induced neuropsychiatric impairment in the differential diagnosis of such vague presentations.
1 Daenan
81: 602-14
4 Pumphrey CW, Fuster V, Chesebro JH Systemic thromboembolism in valvular heart disease and prosthetic heart valves. Mod Concepts Cardiovasc Dis 1982; 51: 131-36. 5 Murphy DA, Levine FH, Buckley MJ. Mechanical valves. a comparative analysis of the Starr Edwards and the Blork Shiley prostheses J Thorac Cardiovasc Surg 1983; 86: 746-52. 6 Nunez L, Gil Aguado M, Celemm D, Iglesias A, Larrea JL. Aspirin or coumarin as the drug of choice for valve replacement with porcine bioprostheses. Ann Thorac Surg 1982; 33: 354-58
NEAR-PURE XYLENE CAUSING REVERSIBLE NEUROPSYCHIATRIC DISTURBANCE
SiR,—Xylene, in combination with toluene, is widely used in industry, and solvent mixtures have been reported to cause neurological and neuropsychiatric disorders in exposed workers.1 We report an unusual case in which exposure to 99-7% pure xylene gave rise to neuropsychiatric disturbance. A very shortsighted man (born Oct 2, 1927) who repaired catamaran hull moulds between 1977 and 1985 used xylene from mid-1983. From January to July, 1985, his work load increased and exposure increased significantly. In July, 1985, he was admitted to hospital. He had applied xylene with a brush dipped into an open bucket. The xylene tended to collect in the cup-shaped moulds in a room 12 x 6 x 4 m with air changes estimated at two to three per hour. He cleaned moulds for about 4 hours per day. Work exposure to xylene was assessed at several hundred parts per million (ppm); readings over a half-filled bucket registered 7000 ppm. Accepted exposure limits were thus grossly exceeded. Exposure to xylene was not doubted by the management of the company. He had no history of unexplained irritability or emotional lability and drank very little. However, throughout 1984 he had workrelated headaches; this was followed by tiredness (worse towards the end of the week but improving at weekends), and by May and June, 1985, the headaches were worse with irritability and dizziness, and he felt unsafe driving home. In July, 1985, he was admitted to hospital with agitation, breathlessness, extreme tiredness, lightheadedness, sensation of limbs shaking when lying or sitting, impaired concentration, and short-term memory and confusion. Dysphasia, fine tremor, hyperreflexia, and unstable gait were the only abnormal physical signs. Routine investigations were normal, as were nerve conduction studies. He gradually improved but by December he still experienced transient lightheadedness and unsteadiness in crowds. In February, 1986, he was aware of only occasional imbalance and the only neurological abnormality was residual unsteadiness in walking or tuming. Psychological assessment excluded gross intellectual or memory impairment but concentration and attention were impaired. Psychiatric examination in February and April, 1986, excluded significant psychiatric morbidity. By April, 1986, the transient tension, indecision, lack of drive, variable concentration, increased sleep requirement, irritability, and noise sensitivity, described in February, had virtually remitted.
Health and Safety Executive, London W2 4TF; and King’s College Hospital and Institute of Psychiatry, London SE5
F. E. C. T.
P. ROBERTS G. LUCAS D. MARSDEN TRAUER
1. Waldron HA Solvents and the brain. Br J Ind Med 1986; 43: 73-74. 2. Grasso P, Sharratt M, Davies DM, Irvine D. Neurophysiological and psychological disorders and occupational exposure to organic solvents. Food Chem Toxicol 1984; 22: 819-52. 3. O’Flynn RR, Monkman SM, Waldron HA. Organic solvents and presenile dementia. a case reference study using death certificates. Br J Ind Med 1987; 44: 259-62. 4 Orback P, Lindgren M, Olivecrona H, Haeger-Aronsen B. Computed tomography and psychometric test performances in patients with solvent induced chronic toxic encephalopathy and healthy controls. Br J Ind Med 1987; 44: 175-79. 5. Browning E. Toxicity and metabolism of industrial solvents. Amsterdam; Elsevier, 1965. 6. Baker EL, White RF, Muraluski BJ. Clinical evaluation of neurobehavioural effects of occupational exposure to organic solvents and lead. Int J Ment Health 1985; 14: 135-58.
SEROCONVERSION AGAINST HUMAN HERPESVIRUS-6 (AND OTHER HERPESVIRUSES) AND CLINICAL ILLNESS
SIR,-It has been assumed that a mononucleosis-like disease or lymphoproliferative disorders could be manifestations of primary infection with human herpesvirus-6 (HHV -6)1-S but this assumption has yet to be strongly supported by clinical data. A clear relation between a specific disease (exanthem subitum) and acute HHV-6 infection has only lately been establishes 6 Although DNA homologies between HHV-6 and cytomegalovirus (CMV) have been described, serological cross-reactions have not yet been found. Few seroconversions, and no IgM seroconversion, have been recorded.6 We describe seroconversion (IgG and IgM) against HHV-6 in a patient with longlasting Epstein-Barr virus (EBV) infection-like symptoms and fatigue. From Jan 21,1988, a 29-year-old woman (a physician) felt unwell with joint and muscle pain and cervical lymphadenopathy. Laboratory findings (Feb 16) revealed lymphocytosis (499%) and thrombocytosis 307 00(?l). After about 3 months of fatigue and "migrating" lymphadenopathy the patient noticed dark urine, and she had headaches in the early morning. A week later, a maculopapular rash without itching appeared on hands, feet, knees, elbows, and left thigh. It lasted 10 days and was initially accompanied by fever (38’OOC). A sensation of abdominal pressure led to an ultrasonic examination, which revealed hepatosplenomegaly ; no abdominal nor thoracic lymphnode enlargements (X-ray) were found. Laboratory findings revealed raised erythrocyte sedimentation rate, haemolysis with no detectable haptoglobin, raised white blood cell count with mononuclear predominance, low titres of antinuclear antibodies, total IgM 492 mg/dl, and raised liver enzymes. On May 6, liver enzymes were normal, but a slight lymphocytosis was still present. The fatigue persisted. On May 17, the hepatosplenomegaly was no longer detected, and by the end of May the patient had completely other
recovered. HHV-6 immunofluorescence assays (IFA) were done on human cord blood lymphocytes (CBL) 9-22 days after infection with HHV-6 (gift of Dr R. W. Honess, London)." CBL were stimulated with phytohaemagglutinin for 4 days and cultivated with