264
RELAXATION TIMES OF NON-DOMINANT CEREBRAL HEMISPHERE AFTER REPEATED ECT
Transient aplastic anaemia associated with legionnaires’ disease SiR,—A 69-year-old woman was admitted with dyspnoea, fever, and an acute confusional state. 10 years earlier type IIdiabetes had been diagnosed. In the emergency room, the diagnosis was dehydration, diabetic ketoacidosis, and left lung pneumonia complicated by respiratory distress. Laboratory data showed a creatine phosphokinase value of 847 V/I (normal up to 180) with a normal MB component and myoglobinuria, consistent with rhabdomyolysis. The white-cell count was 1200/ul, the platelet count was 34 000/ui and the haemoglobin was 8-2 g/dl. She was intubated and mechanical ventilation was started. Legionella pneumophila was identified in a bronchial aspirate by direct immunofluorescence antibody (DFA) test and culture. Intravenous erythromycin had been started on admission and 24 h later oral rifampicin and intravenous ciprofloxacin were added. Bone marrow examination on admission disclosed a hypoplastic bone marrow with increased numbers of immature cells. L pneumophila was shown in bone marrow by DFA and culture. The patient improved slowly. By the second week the white-cell and platelet counts were normal (6500 and 250 000/jl, respectively) and the haemoglobin had risen to 105 g/dl. Bone marrow aspiration at this time showed a reactive plasmacytosis and monoblastosis, but no L pneumophila by DFA or culture. The patient was discharged with normal blood counts after 4 weeks. Legionella spp can produce disseminated infection. The organ most often involved is the lung, but diarrhoea, nausea,
headache, myalgia, confusion, lethargy, disorientation, depression, hallucinations, delirium, and retrograde amnesia reflect multisystem involvement,l and legionellae have been found in blood, kidney, liver, brain, pericardium, heart prostheses, haemodialysis fistulae, perirectal and cutaneous abscesses, postoperative wound infection, lymph nodes, spleen, bone marrow, thyroid, pancreas, muscle, prostate, and testes. Leukocytosis is the most frequent haematological finding, though leukopenia can develop and indicates a poor prognosis.2 Other rare haematological abnormalities are thrombocytopenia,3thrombotic thrombocytopenic purpura,4autoimmune haemolydc anaemia,s5 and disseminated intravascular coagulation.6 This case of aplastic anaemia further extends the spectrum of clinical manifestations of legionnaires’ disease. Department of Internal Medicine, Hospital de la Santa Creu i Sant Pau, Universitat Autónoma de Barcelona, 08025 Barcelona, Spain
ESTEBAN MARTÍNEZ PERE DOMINGO DOMINGO RUIZ
1. Winn WC Jr. Legionnaires’ disease: historical perspective. Clin Microbiol Rev 19881; 1: 60-81. 2. Meyer RD, Edelstein PH, Kirby BD, et al. Legionnaires’ disease: unusual clinical and laboratory features. Ann Intern Med 1980; 93: 240-43. 3. Gasper TM, Famdon PA, Davies R. Thrombocytopenia associated with Legionnaires’ disease. Br Med J 1978; ii: 1611-12. 4. Riggs SA, Wray NP, Waddell CC, Rossen RD, Gyorkey F. Thrombotic thrombocytopenic purpura complicating legionnaires’ disease. Arch Intern Med 1982; 142: 2275-80. 5. Strikas R, Seifert MR, Lentino JR. Autoimmune hemolytic anemia and Legionella pneumophila pneumonia. Ann Intern Med 1983; 99: 345. 6. Kirby BD, Snyder KM, Meyer RD, Finegold SM. Legionnaires’ disease: report of sixty-five nosocomially acquired cases and review of the literature. Medicine
only after repeated courses of ECT. We therefore report a prospective MRI study of five patients treated by 12-24 (median 21) ECTs over 6-30 (median 13) months. Between June, 1987, and July, 1988, five patients who had had ECT previously consented to MRI assessment and to future imaging should they require further ECT. All had primary depressive illnesses; none had a history of head injury, epilepsy, alcohol abuse, hypertension, or diabetes. Imaging was done when patients were euthymic, taking only oral antidepressant drug therapy, and at least 10 days after their last ECT. A 0-08 T resistive MRI system was used. The scans were presented in a random order (patients’ names concealed) to a radiologist (L. W. T.). Spin-lattice (Tl) and spin-spin (T2) relaxation times were calculated for each cerebral hemisphere (excluding CSF) from 12 mm thick transverse sections obtained 10 mm above the widest point of the lateral ventricle 6 Eight consecutive transverse T1-weighted images were obtained on three of the five patients, which allowed the calculation of the Huckman, ventricular, and sella media indices (ratios of brain parenchyma to ventricular space).’ Bilateral electrodes were used for all but 1 course of non-dominant unilateral ECT (patient 3). All patients had at least 2 further courses of ECT and three had 3 further courses. Repeated ECT produced no consistent changes in relaxation times of the non-dominant hemisphere (table). There were no changes in the mean Huckman, ventricular, or sella media indices to suggest any cerebral atrophy (first scan 2-15, 1-11, and 3-91 ; second scan 2.20, 1.11 and 4’ 17). A 2 mm diameter high-signal focus in the right internal capsule developed in patient 4 between occur
the first and second scans. This is the first prospective MRI study of brain structure before and after repeated courses of ECT. ECT produced no consistent change in T or T relaxation times of the cerebral hemispheres and, allowing for slight variations in scan positions, no structural abnormality was demonstrable. The aetiology of the high-signal focus seen in one patient is unknown, but is likely to represent deep white-matter ischaemia. Such hyperdensities are found in up to 30% of the brains of healthy elderly patients8 and their significance is uncertain. Departments of Psychiatry and Radiology, University of Edinburgh, Royal Edinburgh Hospital, Edinburgh EH10 5HF, UK
A. I. F. SCOTT L. W. TURNBULL A. BLANE R. H. B. DOUGLAS
(Baltimore) 1980; 59: 188-205. 1. Weiner RD. Does electroconvulsive
Electroconvulsive therapy and brain
damage
SiR,—The occasional loss of personal memories after electroconvulsive therapy (ECT) has never been adequately explained.’ The National Institute of Mental Health concluded that neuronal cell death was unlikely2 but others have claimed that ECT does cause brain damage.3,4 Magnetic resonance imaging (MRI) is the most sensitive imaging technique currently available for the detection of parenchymal disorders of the brain and prospective MRI may be informative about long-term changes induced by ECT. The only quantitative prospective study to date found that an average of 5 ECTs over 2 weeks had no effect on T relaxation time,s but detectable cerebral changes may take longer to evolve or may
therapy cause brain damage? Behav Brain Sci 1984; 7: 1-54. 2. Rose RM, Burt RA, Clayton PJ, et al. Consensus Conference: electroconvulsive therapy. JAMA 1985; 254: 2103-08. 3. Hartelius H. Cerebral changes following electrically induced convulsions. Acta Psychiatr Neurol Scand 1952; 77 (suppl). 4. Friedberg J. Shock treatment, brain damage, and memory loss m neurological perspective. Am JPsychiatry 1977; 134: 1010-14. 5. Mander AJ, Whitfield A, Kean DM, et al. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging. Br J Psychiatry 1987; 151: 69-71 6. Scott AIF, Douglas RHB, Whitfield A, Kendell RE. Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990; 156: 551-53.
Skjodt T, Svendsen J, Jacobsen EB, Torfing KF. Cerebral atrophy in younger persons: a comparative study between clinical examinations and computed tomography. Clin Radiol 1987; 38: 367-70. 8. Kirkpatrick JB, Hayman LA. White-matter lesions in MR imaging of clinically healthy brains of elderly subjects: possible pathologic basis. Radiology 1987; 162: 7.
509-11.
RELAXATION TIMES OF NON-DOMINANT CEREBRAL HEMISPHERE AFTER REPEATED ECT
Transient aplastic anaemia associated with legionnaires’ disease SiR,—A 69-year-old woman was admitted with dyspnoea, fever, and an acute confusional state. 10 years earlier type IIdiabetes had been diagnosed. In the emergency room, the diagnosis was dehydration, diabetic ketoacidosis, and left lung pneumonia complicated by respiratory distress. Laboratory data showed a creatine phosphokinase value of 847 V/I (normal up to 180) with a normal MB component and myoglobinuria, consistent with rhabdomyolysis. The white-cell count was 1200/ul, the platelet count was 34 000/ui and the haemoglobin was 8-2 g/dl. She was intubated and mechanical ventilation was started. Legionella pneumophila was identified in a bronchial aspirate by direct immunofluorescence antibody (DFA) test and culture. Intravenous erythromycin had been started on admission and 24 h later oral rifampicin and intravenous ciprofloxacin were added. Bone marrow examination on admission disclosed a hypoplastic bone marrow with increased numbers of immature cells. L pneumophila was shown in bone marrow by DFA and culture. The patient improved slowly. By the second week the white-cell and platelet counts were normal (6500 and 250 000/jl, respectively) and the haemoglobin had risen to 105 g/dl. Bone marrow aspiration at this time showed a reactive plasmacytosis and monoblastosis, but no L pneumophila by DFA or culture. The patient was discharged with normal blood counts after 4 weeks. Legionella spp can produce disseminated infection. The organ most often involved is the lung, but diarrhoea, nausea,
headache, myalgia, confusion, lethargy, disorientation, depression, hallucinations, delirium, and retrograde amnesia reflect multisystem involvement,l and legionellae have been found in blood, kidney, liver, brain, pericardium, heart prostheses, haemodialysis fistulae, perirectal and cutaneous abscesses, postoperative wound infection, lymph nodes, spleen, bone marrow, thyroid, pancreas, muscle, prostate, and testes. Leukocytosis is the most frequent haematological finding, though leukopenia can develop and indicates a poor prognosis.2 Other rare haematological abnormalities are thrombocytopenia,3thrombotic thrombocytopenic purpura,4autoimmune haemolydc anaemia,s5 and disseminated intravascular coagulation.6 This case of aplastic anaemia further extends the spectrum of clinical manifestations of legionnaires’ disease. Department of Internal Medicine, Hospital de la Santa Creu i Sant Pau, Universitat Autónoma de Barcelona, 08025 Barcelona, Spain
ESTEBAN MARTÍNEZ PERE DOMINGO DOMINGO RUIZ
1. Winn WC Jr. Legionnaires’ disease: historical perspective. Clin Microbiol Rev 19881; 1: 60-81. 2. Meyer RD, Edelstein PH, Kirby BD, et al. Legionnaires’ disease: unusual clinical and laboratory features. Ann Intern Med 1980; 93: 240-43. 3. Gasper TM, Famdon PA, Davies R. Thrombocytopenia associated with Legionnaires’ disease. Br Med J 1978; ii: 1611-12. 4. Riggs SA, Wray NP, Waddell CC, Rossen RD, Gyorkey F. Thrombotic thrombocytopenic purpura complicating legionnaires’ disease. Arch Intern Med 1982; 142: 2275-80. 5. Strikas R, Seifert MR, Lentino JR. Autoimmune hemolytic anemia and Legionella pneumophila pneumonia. Ann Intern Med 1983; 99: 345. 6. Kirby BD, Snyder KM, Meyer RD, Finegold SM. Legionnaires’ disease: report of sixty-five nosocomially acquired cases and review of the literature. Medicine
only after repeated courses of ECT. We therefore report a prospective MRI study of five patients treated by 12-24 (median 21) ECTs over 6-30 (median 13) months. Between June, 1987, and July, 1988, five patients who had had ECT previously consented to MRI assessment and to future imaging should they require further ECT. All had primary depressive illnesses; none had a history of head injury, epilepsy, alcohol abuse, hypertension, or diabetes. Imaging was done when patients were euthymic, taking only oral antidepressant drug therapy, and at least 10 days after their last ECT. A 0-08 T resistive MRI system was used. The scans were presented in a random order (patients’ names concealed) to a radiologist (L. W. T.). Spin-lattice (Tl) and spin-spin (T2) relaxation times were calculated for each cerebral hemisphere (excluding CSF) from 12 mm thick transverse sections obtained 10 mm above the widest point of the lateral ventricle 6 Eight consecutive transverse T1-weighted images were obtained on three of the five patients, which allowed the calculation of the Huckman, ventricular, and sella media indices (ratios of brain parenchyma to ventricular space).’ Bilateral electrodes were used for all but 1 course of non-dominant unilateral ECT (patient 3). All patients had at least 2 further courses of ECT and three had 3 further courses. Repeated ECT produced no consistent changes in relaxation times of the non-dominant hemisphere (table). There were no changes in the mean Huckman, ventricular, or sella media indices to suggest any cerebral atrophy (first scan 2-15, 1-11, and 3-91 ; second scan 2.20, 1.11 and 4’ 17). A 2 mm diameter high-signal focus in the right internal capsule developed in patient 4 between occur
the first and second scans. This is the first prospective MRI study of brain structure before and after repeated courses of ECT. ECT produced no consistent change in T or T relaxation times of the cerebral hemispheres and, allowing for slight variations in scan positions, no structural abnormality was demonstrable. The aetiology of the high-signal focus seen in one patient is unknown, but is likely to represent deep white-matter ischaemia. Such hyperdensities are found in up to 30% of the brains of healthy elderly patients8 and their significance is uncertain. Departments of Psychiatry and Radiology, University of Edinburgh, Royal Edinburgh Hospital, Edinburgh EH10 5HF, UK
A. I. F. SCOTT L. W. TURNBULL A. BLANE R. H. B. DOUGLAS
(Baltimore) 1980; 59: 188-205. 1. Weiner RD. Does electroconvulsive
Electroconvulsive therapy and brain
damage
SiR,—The occasional loss of personal memories after electroconvulsive therapy (ECT) has never been adequately explained.’ The National Institute of Mental Health concluded that neuronal cell death was unlikely2 but others have claimed that ECT does cause brain damage.3,4 Magnetic resonance imaging (MRI) is the most sensitive imaging technique currently available for the detection of parenchymal disorders of the brain and prospective MRI may be informative about long-term changes induced by ECT. The only quantitative prospective study to date found that an average of 5 ECTs over 2 weeks had no effect on T relaxation time,s but detectable cerebral changes may take longer to evolve or may
therapy cause brain damage? Behav Brain Sci 1984; 7: 1-54. 2. Rose RM, Burt RA, Clayton PJ, et al. Consensus Conference: electroconvulsive therapy. JAMA 1985; 254: 2103-08. 3. Hartelius H. Cerebral changes following electrically induced convulsions. Acta Psychiatr Neurol Scand 1952; 77 (suppl). 4. Friedberg J. Shock treatment, brain damage, and memory loss m neurological perspective. Am JPsychiatry 1977; 134: 1010-14. 5. Mander AJ, Whitfield A, Kean DM, et al. Cerebral and brain stem changes after ECT revealed by nuclear magnetic resonance imaging. Br J Psychiatry 1987; 151: 69-71 6. Scott AIF, Douglas RHB, Whitfield A, Kendell RE. Time course of cerebral magnetic resonance changes after electroconvulsive therapy. Br J Psychiatry 1990; 156: 551-53.
Skjodt T, Svendsen J, Jacobsen EB, Torfing KF. Cerebral atrophy in younger persons: a comparative study between clinical examinations and computed tomography. Clin Radiol 1987; 38: 367-70. 8. Kirkpatrick JB, Hayman LA. White-matter lesions in MR imaging of clinically healthy brains of elderly subjects: possible pathologic basis. Radiology 1987; 162: 7.
509-11.
