- Email: [email protected]
AUTOANTIGENICITY OF SUBCELLULAR MEMBRANES
228 to have occurred because of a ten-day postal in the delivery of the diluent. A second series of 131 tests was carried out with the Wellcome H.A. test using fresh diluent and the false-positive rate was considerably lower in this second series (table i). It was concluded that the delayed diluent (which contains 7% mixed serum) may have been responsible for many of the false positives in the first series of Wellcome H.A. tests. Diluent is not supplied with hepanosticon since physiological saline solution is used. Prozoning did not occur in either test. We agree that these H.A. tests satisfy most of the requirements for mass-screening tests for HBAg, especially those of speed and simplicity, and are considerably more sensitive than the most commonly used technique (i.e., ’counterwas
thought
delay
irmnunoelectrophoresis). 1-5 We conclude that they would be very suitable for massscreening (and ideal in individually urgent situations in hospitals), provided that adequate neutralisation procedures are carried out on positive samples or that positive results are confirmed by a different test. The 35% increase in the number of positive sera detected by the i.D. test (table i) when sera are routinely concentrated eightfold should be noted. Department of Medical
Microbiology, University College, Stillorgan Road,
disorders include: (a) serum " muscle " enzymes (especicreatine phosphokinase, as well as glutamic-oxaloacetic . and glutamic-pyruvic transaminases, lactic dehydrogenase, and aldolase); (b) electromyography (with an awareness of changing views on interpretation) 9,12,13 and measurement of maximum motor-nerve conduction velocity, and distal latency and maximum sensory conduction velocity when
ally
indicated; (c) cerebrospinal-fluid analysis, and, particularly, (d) muscle biopsy studied by histochemical techniques. The muscle-biopsy histochemical studies are often of most diagnostic value.8,9 Biopsy of a limb muscle, such as quadriceps femoris or biceps brachialis, will often reveal the diagnosis of a mild generalised disorder. To biopsy a muscle near the vertebral column might be sampling in or nearer to a scoliosis-provoking weak muscle, but most histochemicopathologists do not yet have enough experience with those muscles to properly interpret subtle changes in them. The muscle biopsy must be of adequate size, undamaged at time of biopsy or before (e.g., by electromyographic 14 or acupuncture 15 needles), and with proper orientation of muscle fibres in it. As more of the idiopathic " scoliosis patients are fully studied, the number remaining idiopathic should greatly diminish. Treatment might be better planned knowing the underlying cause of the patient’s scoliosis. "
A. G. SHATTOCK A. N. SMITH.
Dublin 4.
Medical Neurology Branch, National Institutes of Health,
Bethesda, Maryland 20014, U.S.A.
THE MANY CAUSES OF " IDIOPATHIC SCOLIOSIS
Institute for Rehabilitation Medicine, New York University Medical Center, New York, New York 10016, U.S.A.
"
W. K. ENGEL S. C. BEAN. V. ASKANAS.
"
unexplained " cause, actually SIR.-Apropos the causes, of idiopathic " scoliosis, mentioned in your editorial of Nov. 2 (p. 1055), we wish to state our thesis that "
any neuromuscular disease must be considered as the possible cause in a given patient, either by (a) unequally
affecting symmetrical muscles responsible for holding the vertebrae in alignment or (b) by causing abnormal gait, pelvic tilt, &c., for which scoliosis is either beneficially compensatory or an unwanted consequence. Viewing it from a unit interested in neuromuscular diseases, we have found scoliosis, to a variable degree, in many types of diffuse neuromuscular diseases affecting children. These include: (a) neuropathic disorders, such as poliomyelitis, idiopathic relapsing polyneuropathy, chronic infantile and juvenile spinal muscular atrophy, and the various spinocerebellar ataxias; (b) myopathic conditions such as Duchenne muscular distrophy, congenital morphologically non-specific myopathy, and post-infantile acid-maltase deficiency; and (c) other early-onset conditions of yet-uncertain neuropathic-v.-myopathic pathokinesis, including rod disease, central-core disease, type-i muscle-fibre hypotrophy with and without " central nuclei, the form of benign congenital hypotonia with type-n fibre paucity, HgO syndrome (Prader-Willi), oculocranio-somatic neuromuscular disease with ragged-red " fibres, and myotonic atrophy.8-11 When an underlying neuromuscular disease is flagrant it is not likely to be missed, but the more subtle examples, which can occur in any of these, might be over"
"
looked
of the scoliosis. in all children with " idiopathic " scoliosis these diseases must be sought as possible underlying causes. (Of course one must also consider possible developmental and acquired focal lesions of the spine and spinal cord.) The proper diagnostic studies for neuromuscular as
the
cause
Consequently,
Engel, W. K. Pediat. Clin. N. Am. 1967, 14, 963. Engel, W. K. in New Developments in Electromyography and Clinical Neurophysiology (edited by J. E. Desmedt); p. 141. Basel, 1973. 10. Engel, W. K. Birth Defects: Orig. 7, 1971, no. 2, 18. 11. Olson, W., Engel, W. K., Walsh, G. O., Einaugler, R. Archs Neurol. 1972, 26, 193. 8. 9.
AUTOANTIGENICITY OF SUBCELLULAR MEMBRANES
SiR,-Dr Hickman 16 extends speculation of possible pathological involvement of mitochondrial D.N.A. from oncogenesis 17 to autoimmunity. This latter suggestion is based on
the concept that mitochondrial membrane components
might always be autoantigenic if exposed to the extracellular environment. Indeed, this premise was also the basis of the experiment reported as a preliminary test of the hypothesis of mitochondrial role in oncogenesis.18 What we are now prompted to stress is that, although the suggested involvement of mitochondrial D.N.A. in disease processes is highly speculative, mitochondria and certain other subcellular components may legitimately be considered as potential autoantigens. For example, in work in progress in our laboratory we have shown that, under appropriate conditions, immunisation with mitochondrial membrane fragments from livers of syngeneic mice can stimulate the production of specific complement-fixing antibodies. Similarly, complement-fixing antimicrosomal antibodies can be demonstrated following immunisation with a syngeneic microsomal membrane fraction. Furthermore, syngeneic liver microsomes also stimulate the production of antibodies that can be shown, by immunofluorescence, to bind strongly to nuclei of a variety of tissues of the host animal.19 Moreover, as has already been reported, mice immunised with syngeneic microsomes (plus Corynebacterium parvum) developed a severe dermatosis.18 Hence, it should always be borne in mind that any trauma that releases subcellular components without prior autolysis might provoke an autoimmune response. Indeed, the a
12. Engel, W. K. New Engl. J. Med. 1973, 289, 485. 13. Engel, W. K. Neurology (in the press). 14. Engel, W. K. Archs Neurol. 1967, 16, 509. 15. Engel, W. K., Zee, D. S. New Engl. J. Med. 1974, 16. Hickman, J. A. Lancet, 1974, ii, 1579. 17. Baum, H. ibid. 1973, ii, 738. 18. Baum, H., Baum, M. ibid. 1974, ii, 1397. 19. Blake, M., Sayers, T. J. Unpublished.
291, 801.
229 increased incidence of certain cancers in patients with autoimmune diseases, as cited by Dr Hickman, might conceivably be interpreted in terms of the autoimmunity being a secondary response to the tissue damage associated with
the cancerous
state.
Basic Medical Sciences Group, Chelsea College, Manresa Road, London SW3 6LX.
M. J. DAVEY T. J. SAYERS H. BAUM.
TREATMENT OF MALIGNANT HÆMOPATHIES ‘
AND URATE OXIDASE
SIR,—We fully agree with the statement in your editorial hyperuricaemic renal failure is caused by precipitation of uric acid in the distal tubules and collecting ducts ".1The danger of therapeutic hyperuricaemia arises because in many haemopathies the kidney. is often already injured, either because of a chronic increase in uricasmia (polycythaemia vera, chronic myelocytic leukaemia), or because of the basic disease itself (myeloma). We use rehydration, alkalinisation of urine, and hsemodialysis or peritoneal dialysis to combat the hyperuricxmia induced by chemotherapy. You state that " Acute hyperuricaemia during chemotherapy cannot entirely be prevented, but the severity can be kept to a minimum " by starting allopurinol therapy (300-500 mg. per day) as long as possible before chemotherapy". Allopurinol prevents xanthine oxidase from converting xanthine and hypoxanthine into uric acid. Xanthine and hypoxanthine both have urinary clearances similar to that of uric acid, and the risk of precipitation is lessened. However, anuria due to precipitation of xanthine in kidney tubules during the treatment of malignant haemopathies by allopurinol has been reported.2 We have been using urate oxidase, an enzyme which turns
that " acute
Uricaemia, whatever the initial level, was reduced to less than 60 mg. per litre in all cases, and often fell to about 25 mg. per litre. In the anuric case described above, uncaemia was 400 mg. per litre: after 3 days’ treatment at 3000 u per day, it dropped to 13 mg. per day, and diuresis started again. Uricuria and uricxmia always fell in parallel. Allantoinuria increased in every case from the start of urate-oxidase treatment, this increase continued for some days after treatment was stopped. Tolerance of urate oxidase was always satisfactory. Eventually there were some local, although temporary and only slightly painful, reactions at the injection site. We believe that the results obtained with urate oxidase in the treatment of therapeutically induced hyperuricaemia in malignant haemopathies are better than those obtained with allopurinol. Clinique Médicale B, C.H.U. de Brabois, 54000 Vandoeuvre, France.
P. G. R. P.
KISSEL MAUUARY ROYER TOUSSAIN.
CLOSURE OF ST. WULSTAN’S HOSPITAL SiR,—St. Wulstan’s Hospital has been the Birmingham region’s psychiatric rehabilitation unit since 1961. 1000 patients have come here from other hospitals, 700 have done well, and over 300 are successfully resettled in the community. The extent to which such a success-rate enables rehabilitation to pay for itself has been demonstrated.1
"
The members of the regional authority in Birmingham have conceded that a good job has been done at St. Wulstan’s. At a meeting held last March, it was acknowledged that, " The hospital had pioneered advances which had extended the scope of rehabilitation to patients who had earlier been considered beyond its reach and which had made St. Wulstan’s a centre of nationwide But the minutes of this meeting interest in the specialty." continue by saying: " The prospect of very considerable capital expenditure on the hospital however compelled consideration of the following factors: (a) Rehabilitation was done to some extent in other mental illness hospitals in the region. In view of this, was the specialist regional unit at St. Wulstan’s as necessary as it had been hitherto ? The demands on the region’s capital and revenue resources
uric acid into allantoin. Since allantoin is 10 times more soluble than uric acid, urate oxidase is safer than allopurinol. Urate oxidase was extracted by Laboureur and Langlois3 from a selected strain of Aspergillus fiavus, and first used pharmacologically in animals, and then in man. We first used it to treat gout,5 and then to treat the hyperuricaemia produced by chemotherapy of malignant haemopathies.s Lyophilised urate oxidase is available in sealed ampoules containing 1000 u. The normal dose is between 500 and 800 u., and is equally effective when given by either intraIts efficiency can be venous or intramuscular injection. assessed by the levels of uricaemia, uricuria, and allantoinuria produced. Eleven patients with treated chronic or acute haemopathies were given urate oxidase. The prescribed doses ranged from 800 to 1000 u per day; in the patient with anuria, who did not respond to any therapy, including peritoneal dialysis, we successfully used 3000 u of urate oxidase per day. The duration of the cure varies according to how long the hsemopathy has been treated. In those cases in which chemotherapeutic treatments were repeatedly used, we obtained several successive cures. In every case, the use of urate oxidase allowed the hsemopathy to be treated without any renal complication. In a female patient who had had a unilateral nephrectomy, splenic radiotherapy was required. Urate oxidase lowered uricaemia from 90 to 45 mg., maintained it at this level, and allowed radiotherapy to be used without endangering the kidney.
were
many and it
and
more
might be that rehabilitation might be better economically carried out by running down the specialist unit and developing the units in the other hospitals in the region with the expertise built up by St. Wulstan’s. (b) ’Ideally patients should be rehabilitated in local units. (c) The Worcester Development Project represented the future pattern of mental illness services for the region and the whole country. St. Wulstan’s did not relate in any meaningful way to the project."
Lancet, 1974, i, 1266. Band, P. R., Silverberg, D. S., Henderson, J. F., Ulan, R. A., Wensel, R. H., Banerjec, T. K., Little, A. S. New Engl. J. Med 1970, 283, 354. 3. Laboureur, P., Langlois, C. C. r. hebd. Séanc. Acad. Sci., Paris, 1967, 264, 2244. 4. Royer, R., Vindel, J., Lamarche, M., Kissel, P. Presse méd. 1968 . 76, 2325. 5. Kissel, P., Lamarche, M., Royer, R. Nature, 1968, 76, 2317. 6. Kissel, P., Schmitt, J., Streiff, F., Mauuary, G., Schmidt, C. Toussain, P. Annls Méd., Nancy, 1972, 11, 529.
1. 2.
,
.
The regional team of officers is now proposing to recommend closure of the hospital, probably in 1976 to coincide with the opening of the new unit in Worcester; the reasons given are said to be those quoted above. The decision will be made within a few months. The " very considerable capital expenditure " referred to in the minutes amounts to about E400.000. That includes the cost of conversion of our boilers from coal to oil firing (which surely no longer makes sense) and improvements in staff accommodation which we have said are unnecessarily lavish. We say the repairs could be done much more cheaply. Our suggestion that money could be raised by selling some of the hospital’s surplus land has beeen ignored. To close the regional unit and make the parent hospitals once more undertake all their own rehabilitation amounts to turning the clock back 13 years. It would throw away the advantages of specialisation and break up an experienced team of people. It would deny to many chronically ill patients all chance of access to skilled rehabilitation, since several of the parent hospitals cannot be said to have deve1.
Cheadle, A. J., Morgan, R. Br. J. Psychiat. 1974, 125, 193.
thought
delay
irmnunoelectrophoresis). 1-5 We conclude that they would be very suitable for massscreening (and ideal in individually urgent situations in hospitals), provided that adequate neutralisation procedures are carried out on positive samples or that positive results are confirmed by a different test. The 35% increase in the number of positive sera detected by the i.D. test (table i) when sera are routinely concentrated eightfold should be noted. Department of Medical
Microbiology, University College, Stillorgan Road,
disorders include: (a) serum " muscle " enzymes (especicreatine phosphokinase, as well as glutamic-oxaloacetic . and glutamic-pyruvic transaminases, lactic dehydrogenase, and aldolase); (b) electromyography (with an awareness of changing views on interpretation) 9,12,13 and measurement of maximum motor-nerve conduction velocity, and distal latency and maximum sensory conduction velocity when
ally
indicated; (c) cerebrospinal-fluid analysis, and, particularly, (d) muscle biopsy studied by histochemical techniques. The muscle-biopsy histochemical studies are often of most diagnostic value.8,9 Biopsy of a limb muscle, such as quadriceps femoris or biceps brachialis, will often reveal the diagnosis of a mild generalised disorder. To biopsy a muscle near the vertebral column might be sampling in or nearer to a scoliosis-provoking weak muscle, but most histochemicopathologists do not yet have enough experience with those muscles to properly interpret subtle changes in them. The muscle biopsy must be of adequate size, undamaged at time of biopsy or before (e.g., by electromyographic 14 or acupuncture 15 needles), and with proper orientation of muscle fibres in it. As more of the idiopathic " scoliosis patients are fully studied, the number remaining idiopathic should greatly diminish. Treatment might be better planned knowing the underlying cause of the patient’s scoliosis. "
A. G. SHATTOCK A. N. SMITH.
Dublin 4.
Medical Neurology Branch, National Institutes of Health,
Bethesda, Maryland 20014, U.S.A.
THE MANY CAUSES OF " IDIOPATHIC SCOLIOSIS
Institute for Rehabilitation Medicine, New York University Medical Center, New York, New York 10016, U.S.A.
"
W. K. ENGEL S. C. BEAN. V. ASKANAS.
"
unexplained " cause, actually SIR.-Apropos the causes, of idiopathic " scoliosis, mentioned in your editorial of Nov. 2 (p. 1055), we wish to state our thesis that "
any neuromuscular disease must be considered as the possible cause in a given patient, either by (a) unequally
affecting symmetrical muscles responsible for holding the vertebrae in alignment or (b) by causing abnormal gait, pelvic tilt, &c., for which scoliosis is either beneficially compensatory or an unwanted consequence. Viewing it from a unit interested in neuromuscular diseases, we have found scoliosis, to a variable degree, in many types of diffuse neuromuscular diseases affecting children. These include: (a) neuropathic disorders, such as poliomyelitis, idiopathic relapsing polyneuropathy, chronic infantile and juvenile spinal muscular atrophy, and the various spinocerebellar ataxias; (b) myopathic conditions such as Duchenne muscular distrophy, congenital morphologically non-specific myopathy, and post-infantile acid-maltase deficiency; and (c) other early-onset conditions of yet-uncertain neuropathic-v.-myopathic pathokinesis, including rod disease, central-core disease, type-i muscle-fibre hypotrophy with and without " central nuclei, the form of benign congenital hypotonia with type-n fibre paucity, HgO syndrome (Prader-Willi), oculocranio-somatic neuromuscular disease with ragged-red " fibres, and myotonic atrophy.8-11 When an underlying neuromuscular disease is flagrant it is not likely to be missed, but the more subtle examples, which can occur in any of these, might be over"
"
looked
of the scoliosis. in all children with " idiopathic " scoliosis these diseases must be sought as possible underlying causes. (Of course one must also consider possible developmental and acquired focal lesions of the spine and spinal cord.) The proper diagnostic studies for neuromuscular as
the
cause
Consequently,
Engel, W. K. Pediat. Clin. N. Am. 1967, 14, 963. Engel, W. K. in New Developments in Electromyography and Clinical Neurophysiology (edited by J. E. Desmedt); p. 141. Basel, 1973. 10. Engel, W. K. Birth Defects: Orig. 7, 1971, no. 2, 18. 11. Olson, W., Engel, W. K., Walsh, G. O., Einaugler, R. Archs Neurol. 1972, 26, 193. 8. 9.
AUTOANTIGENICITY OF SUBCELLULAR MEMBRANES
SiR,-Dr Hickman 16 extends speculation of possible pathological involvement of mitochondrial D.N.A. from oncogenesis 17 to autoimmunity. This latter suggestion is based on
the concept that mitochondrial membrane components
might always be autoantigenic if exposed to the extracellular environment. Indeed, this premise was also the basis of the experiment reported as a preliminary test of the hypothesis of mitochondrial role in oncogenesis.18 What we are now prompted to stress is that, although the suggested involvement of mitochondrial D.N.A. in disease processes is highly speculative, mitochondria and certain other subcellular components may legitimately be considered as potential autoantigens. For example, in work in progress in our laboratory we have shown that, under appropriate conditions, immunisation with mitochondrial membrane fragments from livers of syngeneic mice can stimulate the production of specific complement-fixing antibodies. Similarly, complement-fixing antimicrosomal antibodies can be demonstrated following immunisation with a syngeneic microsomal membrane fraction. Furthermore, syngeneic liver microsomes also stimulate the production of antibodies that can be shown, by immunofluorescence, to bind strongly to nuclei of a variety of tissues of the host animal.19 Moreover, as has already been reported, mice immunised with syngeneic microsomes (plus Corynebacterium parvum) developed a severe dermatosis.18 Hence, it should always be borne in mind that any trauma that releases subcellular components without prior autolysis might provoke an autoimmune response. Indeed, the a
12. Engel, W. K. New Engl. J. Med. 1973, 289, 485. 13. Engel, W. K. Neurology (in the press). 14. Engel, W. K. Archs Neurol. 1967, 16, 509. 15. Engel, W. K., Zee, D. S. New Engl. J. Med. 1974, 16. Hickman, J. A. Lancet, 1974, ii, 1579. 17. Baum, H. ibid. 1973, ii, 738. 18. Baum, H., Baum, M. ibid. 1974, ii, 1397. 19. Blake, M., Sayers, T. J. Unpublished.
291, 801.
229 increased incidence of certain cancers in patients with autoimmune diseases, as cited by Dr Hickman, might conceivably be interpreted in terms of the autoimmunity being a secondary response to the tissue damage associated with
the cancerous
state.
Basic Medical Sciences Group, Chelsea College, Manresa Road, London SW3 6LX.
M. J. DAVEY T. J. SAYERS H. BAUM.
TREATMENT OF MALIGNANT HÆMOPATHIES ‘
AND URATE OXIDASE
SIR,—We fully agree with the statement in your editorial hyperuricaemic renal failure is caused by precipitation of uric acid in the distal tubules and collecting ducts ".1The danger of therapeutic hyperuricaemia arises because in many haemopathies the kidney. is often already injured, either because of a chronic increase in uricasmia (polycythaemia vera, chronic myelocytic leukaemia), or because of the basic disease itself (myeloma). We use rehydration, alkalinisation of urine, and hsemodialysis or peritoneal dialysis to combat the hyperuricxmia induced by chemotherapy. You state that " Acute hyperuricaemia during chemotherapy cannot entirely be prevented, but the severity can be kept to a minimum " by starting allopurinol therapy (300-500 mg. per day) as long as possible before chemotherapy". Allopurinol prevents xanthine oxidase from converting xanthine and hypoxanthine into uric acid. Xanthine and hypoxanthine both have urinary clearances similar to that of uric acid, and the risk of precipitation is lessened. However, anuria due to precipitation of xanthine in kidney tubules during the treatment of malignant haemopathies by allopurinol has been reported.2 We have been using urate oxidase, an enzyme which turns
that " acute
Uricaemia, whatever the initial level, was reduced to less than 60 mg. per litre in all cases, and often fell to about 25 mg. per litre. In the anuric case described above, uncaemia was 400 mg. per litre: after 3 days’ treatment at 3000 u per day, it dropped to 13 mg. per day, and diuresis started again. Uricuria and uricxmia always fell in parallel. Allantoinuria increased in every case from the start of urate-oxidase treatment, this increase continued for some days after treatment was stopped. Tolerance of urate oxidase was always satisfactory. Eventually there were some local, although temporary and only slightly painful, reactions at the injection site. We believe that the results obtained with urate oxidase in the treatment of therapeutically induced hyperuricaemia in malignant haemopathies are better than those obtained with allopurinol. Clinique Médicale B, C.H.U. de Brabois, 54000 Vandoeuvre, France.
P. G. R. P.
KISSEL MAUUARY ROYER TOUSSAIN.
CLOSURE OF ST. WULSTAN’S HOSPITAL SiR,—St. Wulstan’s Hospital has been the Birmingham region’s psychiatric rehabilitation unit since 1961. 1000 patients have come here from other hospitals, 700 have done well, and over 300 are successfully resettled in the community. The extent to which such a success-rate enables rehabilitation to pay for itself has been demonstrated.1
"
The members of the regional authority in Birmingham have conceded that a good job has been done at St. Wulstan’s. At a meeting held last March, it was acknowledged that, " The hospital had pioneered advances which had extended the scope of rehabilitation to patients who had earlier been considered beyond its reach and which had made St. Wulstan’s a centre of nationwide But the minutes of this meeting interest in the specialty." continue by saying: " The prospect of very considerable capital expenditure on the hospital however compelled consideration of the following factors: (a) Rehabilitation was done to some extent in other mental illness hospitals in the region. In view of this, was the specialist regional unit at St. Wulstan’s as necessary as it had been hitherto ? The demands on the region’s capital and revenue resources
uric acid into allantoin. Since allantoin is 10 times more soluble than uric acid, urate oxidase is safer than allopurinol. Urate oxidase was extracted by Laboureur and Langlois3 from a selected strain of Aspergillus fiavus, and first used pharmacologically in animals, and then in man. We first used it to treat gout,5 and then to treat the hyperuricaemia produced by chemotherapy of malignant haemopathies.s Lyophilised urate oxidase is available in sealed ampoules containing 1000 u. The normal dose is between 500 and 800 u., and is equally effective when given by either intraIts efficiency can be venous or intramuscular injection. assessed by the levels of uricaemia, uricuria, and allantoinuria produced. Eleven patients with treated chronic or acute haemopathies were given urate oxidase. The prescribed doses ranged from 800 to 1000 u per day; in the patient with anuria, who did not respond to any therapy, including peritoneal dialysis, we successfully used 3000 u of urate oxidase per day. The duration of the cure varies according to how long the hsemopathy has been treated. In those cases in which chemotherapeutic treatments were repeatedly used, we obtained several successive cures. In every case, the use of urate oxidase allowed the hsemopathy to be treated without any renal complication. In a female patient who had had a unilateral nephrectomy, splenic radiotherapy was required. Urate oxidase lowered uricaemia from 90 to 45 mg., maintained it at this level, and allowed radiotherapy to be used without endangering the kidney.
were
many and it
and
more
might be that rehabilitation might be better economically carried out by running down the specialist unit and developing the units in the other hospitals in the region with the expertise built up by St. Wulstan’s. (b) ’Ideally patients should be rehabilitated in local units. (c) The Worcester Development Project represented the future pattern of mental illness services for the region and the whole country. St. Wulstan’s did not relate in any meaningful way to the project."
Lancet, 1974, i, 1266. Band, P. R., Silverberg, D. S., Henderson, J. F., Ulan, R. A., Wensel, R. H., Banerjec, T. K., Little, A. S. New Engl. J. Med 1970, 283, 354. 3. Laboureur, P., Langlois, C. C. r. hebd. Séanc. Acad. Sci., Paris, 1967, 264, 2244. 4. Royer, R., Vindel, J., Lamarche, M., Kissel, P. Presse méd. 1968 . 76, 2325. 5. Kissel, P., Lamarche, M., Royer, R. Nature, 1968, 76, 2317. 6. Kissel, P., Schmitt, J., Streiff, F., Mauuary, G., Schmidt, C. Toussain, P. Annls Méd., Nancy, 1972, 11, 529.
1. 2.
,
.
The regional team of officers is now proposing to recommend closure of the hospital, probably in 1976 to coincide with the opening of the new unit in Worcester; the reasons given are said to be those quoted above. The decision will be made within a few months. The " very considerable capital expenditure " referred to in the minutes amounts to about E400.000. That includes the cost of conversion of our boilers from coal to oil firing (which surely no longer makes sense) and improvements in staff accommodation which we have said are unnecessarily lavish. We say the repairs could be done much more cheaply. Our suggestion that money could be raised by selling some of the hospital’s surplus land has beeen ignored. To close the regional unit and make the parent hospitals once more undertake all their own rehabilitation amounts to turning the clock back 13 years. It would throw away the advantages of specialisation and break up an experienced team of people. It would deny to many chronically ill patients all chance of access to skilled rehabilitation, since several of the parent hospitals cannot be said to have deve1.
Cheadle, A. J., Morgan, R. Br. J. Psychiat. 1974, 125, 193.