- Email: [email protected]
CEREBRAL ATROPHY AND COGNITIVE IMPAIRMENT IN CHRONIC SCHIZOPHRENIA
1303
including the controls, had heparin, so our conclusions are valid. Heparin was needed to prevent clotting in indwelling vascular cannulae and in isolated vascular segments (especially venous) during a period of clamping. Normal concentrations of A.T.P. in renal tissue were reestablished only after renal blood-flow had been restored’ indicating that the fundamental tubular enzyme systems remained intact. The continuing insult to the kidney in the glycerol and mercuric-chloride models and the inactivation of essential enzyme systems would obviously prevent inosine from exerting any beneficial effect on such a severely and peculiarly damaged tubular system. There is nothing in the results of Baker et al. that precludes the possibility that inosine may prevent acute renal failure from renal ischaemia.
Departments of Urology and Medicine, St Bartholomew’s
Hospital, and
Department of Chemistry and Biochemistry, Medical College of St Bartholomew’s Hospital, London ECIA 7BE
A. R. FERNANDO D. M. G. ARMSTRONG J. R. GRIFFITHS W. F. HENDRY E. P. N. O’DONOGHUE D. PERRETT J. P. WARD J. E. A. WICKHAM
RECURRENT ULCER AFTER VAGOTOMY to serial Hollander tests after vagotomy; the reason
SIR,—You refer (Nov. 6, p. 1005)
showing a steady
rise in
positivity
for this is obscure. After truncal vagotomy approximately 50% of those with negative responses at the initial test were found to have positive responses 3 months to 4 years later,’ and a reversal from insulin-negative to insulin-positive responses has been reported after parietal-cell vagotomy in sixteen of seventeen cases at 3 years.2 This change after truncal vagotomy may be due to ingrowth of nerve fibres from the proximal intact vagus through the oesophageal wall into Auerbach’s and Meissner’s plexuses and subsequently along these into the parietal-cell area. In addition to this proximal innervation, following highly selective vagotomy reinnervation may occur by ingrowth across the antral-corpus junction as well as via the oesophagus, giving rise to the increased incidence of reversal of insulin status which seems to follow this operation. Jordan compared parietal-cell vagotomy with selective vagotomy and antrectomy and showed that, only 2 months after operation, 41% of the parietal-cell vagotomy patients and none of the antrectomy group had a positive Hollander test. This result may support the above hypothesis since the vagotomy technique for the proximal part of the stomach was the same in each case. The degree of reinnervation along these lines will be variable, but may well be greater and more rapid across the antral-corpus junction than along the œsophageal plexuses, since there is a larger area and a shorter distance required for reinnervation to take place from the antrum. This type of reinnervation would at best be only partial because most vagal fibres are sensory, making motor reinnervation along the original lines unlikely. In a study of forty-one recurrent-ulcer patients with insulin-positive status after truncal vagotomy, intact vagus-nerve trunks were found along the oesophagus in all but one at re-Qperation.4. In contrast to this the incidence of recurrent ulceration after parietal-cell vagotomy reported by the Leeds group remains low,5 though the reversal of insulin status is extremely high. Dragstedt et al .6 state that recurrent ulceration due to incomplete vagotomy rarely happens after 5 years, and in our 1 2.
4.
6
Gillespie, G. Elder, J.
B.
Gillespie,
I. E.
Kay, A.
W.
Campbell,
Department of Gastroenterology Manchester Royal Infirmary, Manchester M13 9WL
T. V. TAYLOR K. W. PEARSON
CEREBRAL ATROPHY AND COGNITIVE IMPAIRMENT IN CHRONIC SCHIZOPHRENIA
SIR,-As
an
epidemiologist
I have been very interested in
Dr
Johnstone and her colleagues (Oct. 30, p. 924) and the comments by Professor Marsden (Nov. 15, p. the report
by
1079). Professor Marsden details, in his order of preference, the three likely causes of the cerebral atrophy detected: (i) treatment with neuroleptics of a non-dementing mental illness; (ii) an incidental dementing illness, such as Alzheimer’s disease; and (iii) a causal pathological process as yet unknown. While agreeing with this analysis, I suspect that, in time, the order of preference will be reversed. For, well before the wide use of neuroleptic drugs, neurosurgeons operating on patients with schizophrenia and other psychoses reported abnormalities of the meninges and apparent cortical atrophy.’ The results of air encephalography also indicated cortical atrophy.2 Later, evidence of cerebral atrophy was similarly demonstrated in a small series of young patients with mental illness and histories of consistent cannabis smoking.3 But, as Professor Marsden points out, it has always been difficult to reconcile these and similar findings in the living with macroscopically negative post-mortem observations. General paresis of the insane is clearly a disease of an organ produced by a microorganism and needing medical _care. On the other hand, anxiety, depression, and paranoia are often likely to be a normal reaction to the stuff of everyday life. The problem is where should schizophrenia and other severe disabling mental conditions without neurological signs be placed-as diseases of the brain for the attention of psychiatrists or as part of the broad spectrum of human behaviour and a charge on society itself? For some time I have been developing a hypothesis that the genesis of all severe disabling mental disorders is related to the cumulative effects of neuron damage in the cerebral cortex, irrespective of whether or not there are associated neurological signs. Now, computerised tomography offers a quick, accurate, and ethically acceptable method of measuring cerebral atrophy, so it should be possible to test this hypothesis. To the epidemiologist the traditional psychiatric classification based on signs and symptoms of abnormal mental behaviour seems analogous to the clinical classification of cardiac failure into "right-sided" and "left-sided" failure: the psychiatric equivalent being the schizophrenias and manic depressive reactions, as described by Bleuler and Kraepelin. The basic task in psychiatry remains to define an ætiological classification of the severe disabling conditions: the equivalent of identifying rheumatic carditis, coronary-artery disease, &c. If this stage in classification can be reached then it may be possible for epidemiologists to define more narrowly the causal factors underlying the disease processes. While I agree that the prescription of large and prolonged doses of neuroleptics should be approached with caution, it seems retrograde to discredit the use of these-drugs in general .
psychiatric practice.
E. H. G. Gas-
troenterology, 1970, 58, 625. Lyndon, P. J., Greenall, M. J., Smith, R. B., Goligher, J. C., Johnston, D. ibid 1975, 69, 1188. 3. Jordan, P. H. Ann. Surg 1976, 183, 619. Taylor, T. V., Pearson, K. W., Torrance, B. Unpublished. 5. Johnston, D., Pickford, I. R., Walker, B. E., Goligher, J. C. Br. med. J. 1975, i, 716. O’Leary, J P , Woodward, E. R., Hollenbeck, J. I., Dragstedt, L. R. Ann
Surg, 1976, 183, 613.
series 80% developed recurrent ulcers within 2 years of the initial operation. It would seem, therefore, that reinnervation along the lines suggested is partial and though being capable of reversing insulin status is less ulcerogenic than incomplete vagotomy per se. own
Wolverhampton Area Health Authority, New Cross Hospital, Wolverhampton WV10 0QP 1. 2.
F. N. GARRATT
Pool, J. L. Lancet, 1949, ii, 776. Donovan, J. S., Galbraith, J. S., Jackson, H. J. ment. Sci. 1949, 95, 655. 3. Campbell, A. M. G., Evans, M., Thomson, J L. G., Williams, M. J. Lancet, 1971, ii, 1219.
1304
SIR,-Writing in response to the report by Johnstone et al. Professor Marsden (Nov. 13, p. 1079) suggests that the observed cortical atrophy may be due to long-term neuroleptic treatment. Using computerised tomography to examine eight schizophrenic patients with antipsychotic-induced tardive dyskinesia, I was unable to find any significant cortical abnormality.’ The brain changes in schizophrenia, as well as in tardive dyskinesia, remain to be explained. Department of Psychiatry, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts 02114, U.S.A.
roxocobalamin. The results of the normal. Department of Pathology, Staffordshire General Infirmary, Stafford ST16 2PA
B12
and serum-folate
were
T. A. J. PHAURE A. R. MALTBY
RIFAMPIN-RESISTANT LEPROSY ALAN J. GELENBERG
SIR The rifamycin antibiotics have been used in the treatof leprosy since 1963.’ The orally active rifamycin, rifampicin, or rifampin has been utilised more recently.’-° Rifampin exerts a rapid bactericidal effect on Mycobacterium the leprce in man,35 but concern has been expressed regarding 3467 M. of possible development rifampin-resistant leprce. We have seen a patient with sulphone-resistant lepromatous leprosy who experienced clinical and bacteriological relapse
ment
PATIENTS’ PREFERENCE ON COMPULSORY ADMISSIONS
SIR,—The consultative document Review of the Mental Health Act 1959 suggests that there might be restriction of the treatment that could be given against a patient’s wishes under Section 25. This might result in an increase in the use of Section 26 (treatment order). We have attempted to ascertain the views of a small sample of patients. All patients on Sections 25 and 26 in the admission wards at Banstead Hospital and St Mary Abbots psychiatric unit during one week were interviewed and asked their preference, assuming they had to be readmitted against their wishes. Patients were told that Section 25 allowed doctors to give treatment against their wishes without any right of appeal, and that the order lasted for twenty-eight days and that Section 26 gave them a right of appeal but lasted for a year, though most patients are discharged as soon as they are better. They were also told that at the end of a Section 25, doctors might then think it necessary to apply for a Section 26 (treatment
DRUG SENSITIVITIES IN MOUSE FOOT PADS
order). Eighteen patients were interviewed. Three patients were cooperative but did not understand the questions. Five understood but expressed no preference. Of the remaining ten, who both understood the questions and expressed a preference, all stated that they would prefer to be admitted on Section 25. This preliminary finding, if repeated elsewhere, would suggest that patients have a strong preference for a shorter order even if this involves treatment against their wishes with no right of appeal. P. D. ROHDE S. RIPPINGALE
Banstead
Hospital, Sutton, Surrey SM2
5PA
>0001, Student’s t test, compared with controls. 0.01>P>0.001, A21, test with Yates’ correction, compared with controls and compared with any group with 6 of 6 positive harvests. Values are means (is.D.) of acid-fast bacilli harvested from individual animals 61months after inoculation with 5 x 103 M. lepra.
* 0.01>P
VITAMIN-B12 STATUS IN NEUROPSYCHIATRIC DISORDER
SIR,-We read with interest Dr Rose’s letter (Nov. 27, p. the value of serum-vitamin-B12 measurements in 1191) with patients neuropsychiatric disorders. His experience must be shared by most haematologists. Eighteen months ago this department formulated a policy, in agreement with the medical staff of our psychiatric hospital. If, in the absence of a macrocytosis whether defined by the human eye or by the Coulter model S, a vitamin-B12 assay is requested to investigate neuropsychiatric disorder, blood is taken for assay of serum-vitamin-B12’ red-cell folate, and serum-folate. Hæmatinics, hydroxocobalamin (’Neo-Cytamen’) in particular, are tried, and the clinical response is evaluated. If the patient responds then the pre-treatment sample is assayed. In the year before this policy was introduced, some 150 vitamin-B12 assays were done on patients with neuropsychiatric disorders. Since this policy has been in operation, we have done one B12/folate assay on a patient with normal peripheralblood indices who showed an apparent clinical response to hydon
1.
Gelenberg, A. J. Am. J. Psychtat. 1976, 133,
578.
while on rifampin monotherapy. The patient is a 49-year-old male of Scandinavian extraction who has had lepromatous leprosy since the age of 18. He was treated with sulphones, glucosulphones (’Promine’), and, later, sulfoxone (’Diasone’) both of which he took irregularly from 1946 until 1968. In 1968 he developed clinical relapse despite sulfoxone therapy and mousefoot-pad studies by Dr Charles Shepard in Atlanta, Georgia showed intermediate levels of sulphone resistance (multiplication in mice fed 0.0001% and 0 - 00 1% w/w dapsone in the diets but no growth in animals fed 0.01% dietary dapsone). The patient was put on high doses of dapsone (up to 200 mg daily’ D. V. A., de Souza Lima, L. Caprara, G. Lepr. Rev. 1965, 36, 123. 2. Rees, R. J. W., Pearson, J. M. H., Waters, M. F. R. Br. med. J. 1970, 1. 89. 3. Shepard, C. C., Levy, L., Fasal, P. Am. J. trop. Med. Hyg. 1972, 21, 446. 4. Opromolla, D. V. A., Tonello, C. J. S. Lep. Rev. 1975, 46, suppl p 141 5. Levy, L., Shepard, C. C., Fasal. P. Int. J. Lepr. 1976, 44, 183. 6. Ellard, G. A. Lepr Rev. 1975, 46, suppl p. 141. 7. Rees, R. J. W., Waters, M. F. R., Pearson, J. M. H Int. J. Lepr 1976. 44, 159.
1.
Opromolla,
including the controls, had heparin, so our conclusions are valid. Heparin was needed to prevent clotting in indwelling vascular cannulae and in isolated vascular segments (especially venous) during a period of clamping. Normal concentrations of A.T.P. in renal tissue were reestablished only after renal blood-flow had been restored’ indicating that the fundamental tubular enzyme systems remained intact. The continuing insult to the kidney in the glycerol and mercuric-chloride models and the inactivation of essential enzyme systems would obviously prevent inosine from exerting any beneficial effect on such a severely and peculiarly damaged tubular system. There is nothing in the results of Baker et al. that precludes the possibility that inosine may prevent acute renal failure from renal ischaemia.
Departments of Urology and Medicine, St Bartholomew’s
Hospital, and
Department of Chemistry and Biochemistry, Medical College of St Bartholomew’s Hospital, London ECIA 7BE
A. R. FERNANDO D. M. G. ARMSTRONG J. R. GRIFFITHS W. F. HENDRY E. P. N. O’DONOGHUE D. PERRETT J. P. WARD J. E. A. WICKHAM
RECURRENT ULCER AFTER VAGOTOMY to serial Hollander tests after vagotomy; the reason
SIR,—You refer (Nov. 6, p. 1005)
showing a steady
rise in
positivity
for this is obscure. After truncal vagotomy approximately 50% of those with negative responses at the initial test were found to have positive responses 3 months to 4 years later,’ and a reversal from insulin-negative to insulin-positive responses has been reported after parietal-cell vagotomy in sixteen of seventeen cases at 3 years.2 This change after truncal vagotomy may be due to ingrowth of nerve fibres from the proximal intact vagus through the oesophageal wall into Auerbach’s and Meissner’s plexuses and subsequently along these into the parietal-cell area. In addition to this proximal innervation, following highly selective vagotomy reinnervation may occur by ingrowth across the antral-corpus junction as well as via the oesophagus, giving rise to the increased incidence of reversal of insulin status which seems to follow this operation. Jordan compared parietal-cell vagotomy with selective vagotomy and antrectomy and showed that, only 2 months after operation, 41% of the parietal-cell vagotomy patients and none of the antrectomy group had a positive Hollander test. This result may support the above hypothesis since the vagotomy technique for the proximal part of the stomach was the same in each case. The degree of reinnervation along these lines will be variable, but may well be greater and more rapid across the antral-corpus junction than along the œsophageal plexuses, since there is a larger area and a shorter distance required for reinnervation to take place from the antrum. This type of reinnervation would at best be only partial because most vagal fibres are sensory, making motor reinnervation along the original lines unlikely. In a study of forty-one recurrent-ulcer patients with insulin-positive status after truncal vagotomy, intact vagus-nerve trunks were found along the oesophagus in all but one at re-Qperation.4. In contrast to this the incidence of recurrent ulceration after parietal-cell vagotomy reported by the Leeds group remains low,5 though the reversal of insulin status is extremely high. Dragstedt et al .6 state that recurrent ulceration due to incomplete vagotomy rarely happens after 5 years, and in our 1 2.
4.
6
Gillespie, G. Elder, J.
B.
Gillespie,
I. E.
Kay, A.
W.
Campbell,
Department of Gastroenterology Manchester Royal Infirmary, Manchester M13 9WL
T. V. TAYLOR K. W. PEARSON
CEREBRAL ATROPHY AND COGNITIVE IMPAIRMENT IN CHRONIC SCHIZOPHRENIA
SIR,-As
an
epidemiologist
I have been very interested in
Dr
Johnstone and her colleagues (Oct. 30, p. 924) and the comments by Professor Marsden (Nov. 15, p. the report
by
1079). Professor Marsden details, in his order of preference, the three likely causes of the cerebral atrophy detected: (i) treatment with neuroleptics of a non-dementing mental illness; (ii) an incidental dementing illness, such as Alzheimer’s disease; and (iii) a causal pathological process as yet unknown. While agreeing with this analysis, I suspect that, in time, the order of preference will be reversed. For, well before the wide use of neuroleptic drugs, neurosurgeons operating on patients with schizophrenia and other psychoses reported abnormalities of the meninges and apparent cortical atrophy.’ The results of air encephalography also indicated cortical atrophy.2 Later, evidence of cerebral atrophy was similarly demonstrated in a small series of young patients with mental illness and histories of consistent cannabis smoking.3 But, as Professor Marsden points out, it has always been difficult to reconcile these and similar findings in the living with macroscopically negative post-mortem observations. General paresis of the insane is clearly a disease of an organ produced by a microorganism and needing medical _care. On the other hand, anxiety, depression, and paranoia are often likely to be a normal reaction to the stuff of everyday life. The problem is where should schizophrenia and other severe disabling mental conditions without neurological signs be placed-as diseases of the brain for the attention of psychiatrists or as part of the broad spectrum of human behaviour and a charge on society itself? For some time I have been developing a hypothesis that the genesis of all severe disabling mental disorders is related to the cumulative effects of neuron damage in the cerebral cortex, irrespective of whether or not there are associated neurological signs. Now, computerised tomography offers a quick, accurate, and ethically acceptable method of measuring cerebral atrophy, so it should be possible to test this hypothesis. To the epidemiologist the traditional psychiatric classification based on signs and symptoms of abnormal mental behaviour seems analogous to the clinical classification of cardiac failure into "right-sided" and "left-sided" failure: the psychiatric equivalent being the schizophrenias and manic depressive reactions, as described by Bleuler and Kraepelin. The basic task in psychiatry remains to define an ætiological classification of the severe disabling conditions: the equivalent of identifying rheumatic carditis, coronary-artery disease, &c. If this stage in classification can be reached then it may be possible for epidemiologists to define more narrowly the causal factors underlying the disease processes. While I agree that the prescription of large and prolonged doses of neuroleptics should be approached with caution, it seems retrograde to discredit the use of these-drugs in general .
psychiatric practice.
E. H. G. Gas-
troenterology, 1970, 58, 625. Lyndon, P. J., Greenall, M. J., Smith, R. B., Goligher, J. C., Johnston, D. ibid 1975, 69, 1188. 3. Jordan, P. H. Ann. Surg 1976, 183, 619. Taylor, T. V., Pearson, K. W., Torrance, B. Unpublished. 5. Johnston, D., Pickford, I. R., Walker, B. E., Goligher, J. C. Br. med. J. 1975, i, 716. O’Leary, J P , Woodward, E. R., Hollenbeck, J. I., Dragstedt, L. R. Ann
Surg, 1976, 183, 613.
series 80% developed recurrent ulcers within 2 years of the initial operation. It would seem, therefore, that reinnervation along the lines suggested is partial and though being capable of reversing insulin status is less ulcerogenic than incomplete vagotomy per se. own
Wolverhampton Area Health Authority, New Cross Hospital, Wolverhampton WV10 0QP 1. 2.
F. N. GARRATT
Pool, J. L. Lancet, 1949, ii, 776. Donovan, J. S., Galbraith, J. S., Jackson, H. J. ment. Sci. 1949, 95, 655. 3. Campbell, A. M. G., Evans, M., Thomson, J L. G., Williams, M. J. Lancet, 1971, ii, 1219.
1304
SIR,-Writing in response to the report by Johnstone et al. Professor Marsden (Nov. 13, p. 1079) suggests that the observed cortical atrophy may be due to long-term neuroleptic treatment. Using computerised tomography to examine eight schizophrenic patients with antipsychotic-induced tardive dyskinesia, I was unable to find any significant cortical abnormality.’ The brain changes in schizophrenia, as well as in tardive dyskinesia, remain to be explained. Department of Psychiatry, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts 02114, U.S.A.
roxocobalamin. The results of the normal. Department of Pathology, Staffordshire General Infirmary, Stafford ST16 2PA
B12
and serum-folate
were
T. A. J. PHAURE A. R. MALTBY
RIFAMPIN-RESISTANT LEPROSY ALAN J. GELENBERG
SIR The rifamycin antibiotics have been used in the treatof leprosy since 1963.’ The orally active rifamycin, rifampicin, or rifampin has been utilised more recently.’-° Rifampin exerts a rapid bactericidal effect on Mycobacterium the leprce in man,35 but concern has been expressed regarding 3467 M. of possible development rifampin-resistant leprce. We have seen a patient with sulphone-resistant lepromatous leprosy who experienced clinical and bacteriological relapse
ment
PATIENTS’ PREFERENCE ON COMPULSORY ADMISSIONS
SIR,—The consultative document Review of the Mental Health Act 1959 suggests that there might be restriction of the treatment that could be given against a patient’s wishes under Section 25. This might result in an increase in the use of Section 26 (treatment order). We have attempted to ascertain the views of a small sample of patients. All patients on Sections 25 and 26 in the admission wards at Banstead Hospital and St Mary Abbots psychiatric unit during one week were interviewed and asked their preference, assuming they had to be readmitted against their wishes. Patients were told that Section 25 allowed doctors to give treatment against their wishes without any right of appeal, and that the order lasted for twenty-eight days and that Section 26 gave them a right of appeal but lasted for a year, though most patients are discharged as soon as they are better. They were also told that at the end of a Section 25, doctors might then think it necessary to apply for a Section 26 (treatment
DRUG SENSITIVITIES IN MOUSE FOOT PADS
order). Eighteen patients were interviewed. Three patients were cooperative but did not understand the questions. Five understood but expressed no preference. Of the remaining ten, who both understood the questions and expressed a preference, all stated that they would prefer to be admitted on Section 25. This preliminary finding, if repeated elsewhere, would suggest that patients have a strong preference for a shorter order even if this involves treatment against their wishes with no right of appeal. P. D. ROHDE S. RIPPINGALE
Banstead
Hospital, Sutton, Surrey SM2
5PA
>0001, Student’s t test, compared with controls. 0.01>P>0.001, A21, test with Yates’ correction, compared with controls and compared with any group with 6 of 6 positive harvests. Values are means (is.D.) of acid-fast bacilli harvested from individual animals 61months after inoculation with 5 x 103 M. lepra.
* 0.01>P
VITAMIN-B12 STATUS IN NEUROPSYCHIATRIC DISORDER
SIR,-We read with interest Dr Rose’s letter (Nov. 27, p. the value of serum-vitamin-B12 measurements in 1191) with patients neuropsychiatric disorders. His experience must be shared by most haematologists. Eighteen months ago this department formulated a policy, in agreement with the medical staff of our psychiatric hospital. If, in the absence of a macrocytosis whether defined by the human eye or by the Coulter model S, a vitamin-B12 assay is requested to investigate neuropsychiatric disorder, blood is taken for assay of serum-vitamin-B12’ red-cell folate, and serum-folate. Hæmatinics, hydroxocobalamin (’Neo-Cytamen’) in particular, are tried, and the clinical response is evaluated. If the patient responds then the pre-treatment sample is assayed. In the year before this policy was introduced, some 150 vitamin-B12 assays were done on patients with neuropsychiatric disorders. Since this policy has been in operation, we have done one B12/folate assay on a patient with normal peripheralblood indices who showed an apparent clinical response to hydon
1.
Gelenberg, A. J. Am. J. Psychtat. 1976, 133,
578.
while on rifampin monotherapy. The patient is a 49-year-old male of Scandinavian extraction who has had lepromatous leprosy since the age of 18. He was treated with sulphones, glucosulphones (’Promine’), and, later, sulfoxone (’Diasone’) both of which he took irregularly from 1946 until 1968. In 1968 he developed clinical relapse despite sulfoxone therapy and mousefoot-pad studies by Dr Charles Shepard in Atlanta, Georgia showed intermediate levels of sulphone resistance (multiplication in mice fed 0.0001% and 0 - 00 1% w/w dapsone in the diets but no growth in animals fed 0.01% dietary dapsone). The patient was put on high doses of dapsone (up to 200 mg daily’ D. V. A., de Souza Lima, L. Caprara, G. Lepr. Rev. 1965, 36, 123. 2. Rees, R. J. W., Pearson, J. M. H., Waters, M. F. R. Br. med. J. 1970, 1. 89. 3. Shepard, C. C., Levy, L., Fasal, P. Am. J. trop. Med. Hyg. 1972, 21, 446. 4. Opromolla, D. V. A., Tonello, C. J. S. Lep. Rev. 1975, 46, suppl p 141 5. Levy, L., Shepard, C. C., Fasal. P. Int. J. Lepr. 1976, 44, 183. 6. Ellard, G. A. Lepr Rev. 1975, 46, suppl p. 141. 7. Rees, R. J. W., Waters, M. F. R., Pearson, J. M. H Int. J. Lepr 1976. 44, 159.
1.
Opromolla,