469

the loss of beds reported merely reflected seasonal staffing difficulties or if staff played down their vacancies to deflect possible admissions from outside their catchment area or to ease the pressure on themselves during a stressful and understaffed period. On the other hand, the survey was done in the middle of a four-day holiday. The situation probably worsened over the ensuing days when there would have been further admissions but no discharges. The implementation of community care by closing non-acute services is affecting acute psychiatric services, and as ward closures accelerate the shortages our survey revealed may become a chronic bed famine. The loss of flexibility could lead to an increase in premature discharges and the "revolving door" syndrome; and junior doctors will have to spend ever longer trying to "borrow" admission beds from other districts. The homeless mentally ill, who are being neglected by community care provision, will be denied the treatment and sanctuary they periodically require, resulting in more misery, suicide, petty crime, and fuller prisons. Plans for community care should be reconsidered to take account of the need for preserving non-acute services alongside acute services. If they are not, pressure on acute psychiatic services in inner-city areas will become intolerable, with appalling social consequences.

DORIS HOLLANDER ROBIN POWELL

Friern Hospital, London N11 3BP, UK

SIR,-Dr Whitehead (Jan 20, p 172) believes that "overcrowded" psychiatric hospitals are no better than workhouses. Any overcrowding is unneccessary since we have discharged half the long-stay population since 1954. However, as he says, if psychiatric hospitals are to be kept functioning "vast amounts of money need to be spent on their fabric, their furnishing, and their staffing". However, the value of land and the buildings are attractive to health authorities which are overspent generally, and Government assurances that the proceeds of any sales will be applied to mental illness are not being honoured. It is assumed to be self-evident that hospital closures are beneficial. In one of the few cases where any evaluation of this policy is being done it is becoming increasingly difficult to obtain an inpatient control population that is matched for severity with patients selected for relocation in the community. The mentally ill have long wandered the streets, rotating between destitution, psychiatric hospital, and prison. However, even though we fail to keep adequate statistics and so cannot properly assess trends, the impression of twenty-eight voluntary organisations at a recent meeting of CONCERN (Guardian Dec 19, 1989) was that numbers are growing as fewer psychiatric beds are available. Whitehead believes that, without

investment,

the

quality of life in

hospitals have been closed and the proceeds dispersed? The 1975 white-paper Better 5’grMc for the Mentally Ill recognised (para 2.27) that families and relatives and the public in general would not tolerate the discharge to community care of chronic patients without proper aftercare so that these patients spend their days wandering the streets or become an unbearable burden on their families. Nor would they tolerate hostels that are so selective that they are only half-full while people needing residential care are turned away or appeals for help go unanswered in a crisis while the boundaries of responsibility are debated. Friern Hospital, London N11 3BP, UK

MALCOLM P. I. WELLER

1. Weller BGA, Weller MPI, Cheyne A. Long-term psychiatric patients m the community. Br J Psychiatry 1986, 151: 862. 2. Weller MPI, Weller BGA, Badenoch D. Mentally abnormal pnsoners on remand. Br Med J 1988; 297: 559-60. 3. Weller MPI, Tobiansky RI, Hollander D, Ibrahimi S. Psychosis and destitution at Christmas 1985-88. Lancet 1989; ii: 1509-11. 4. Bluglass RS.A psychiatric study of Scottish prisoners. MD thesis, University of St

Andrews, 1966. 5. Gunn J, Robertson

G, Dell S, Way C. Psychiatric aspects of imprisonment. London: Academic Press, 1978. 6. Gibbens TCN. Female offenders. Br J Hosp Med 1971; 6: 279-86. 7. Turner TH, Tofler DS. Indications of psychiatric disorder among women admitted to prison. Br Med J 1986; 292: 651-53. 8. Boothroyd J. The prisoners we are failing. Police Rev 1988; July 8. 1426-27.

Safety of transcranial magnetic stimulation SiR,—Dr Homberg and Dr Netz (Nov 18, p 1223) describe epilepsy during transcranial magnetic stimulation in a patient with stroke. Using the method of Barker et aP and the Novametrix ’Magstim 200’ stimulator, we have done more than 800 transcranial magnetic stimulation studies on controls and on patients with neurological conditions (including 76 tests on stroke patients) without ever observing seizures. Because little is known about long-term side-effects of magnetic stimulation we sent a questionnaire to 218 people who had been tested 3-21 months previously. We asked about their health since the tests and received replies from 154 patients (multiple sclerosis 108, Parkinson’s disease 19, stroke 6, and other neurological conditions 21) and from 9 healthy volunteers. Epileptic seizures were recorded by 2 patients with multiple sclerosis. A 60-year-old man had a single jacksonian seizure 4 weeks after magnetic stimulation. He was given phenytoin and had no further seizures. During stimulation he had received 24 cortical stimuli. A 30-year-old woman had two grand-mal seizures on the same day, 3 weeks after magnetic stimulation. An electroencephalogram (EEG) showed runs of high-voltage rhythmic and sharp activity, which were enhanced by overbreathing, suggesting an abnormally low epileptic threshold. Phenytoin was prescribed and she had no further seizures. During magnetic stimulation at the session before the convulsions she had

psychiatric hospitals may be no better than life "in a box under the arches". We found that the quality of life was superior for long-stay patients in hospital than for those housed in the community and receiving regular visits from community psychiatric nurses.1 The impetus for building asylums in the 19th century in Britain was a recognition that it was disgraceful to care for pauper lunatics in debtor prisons. The relation between psychiatric hospital bed occupancy and prison statistics has three components: (1) the high inverse correlation between the two;2 (2) the close relation between present or previous psychosis and imprisonment; and (3) the

received 50 cortical stimuli. This was her fifth series of tests; on all four earlier ones over the previous 6 months, 40 cortical stimuli had been administered. The prevalence of epilepsy in the general population is about 0-5%. In MS the prevalence is 1’1 %2 to 45%,3 so seizures in 2 among 108 patients with MS who replied to our questionnaire is not

consistency in prison surveys of the proportion of mental illness found.7 It is difficulty to get bail for the mentally ill, unemployed, and homeless, and the result is prolonged custody on remand. Prison conditions for those on remand and for those convicted of an offence differ little and the use of police cells with frequent moves8 can make remand very stressful. A flexible range of options is desirable, and previous reliance on a room in the home of a "caring" landlady was less satisfactory than current initiatives. Enthusiasm and change itself can be beneficial. Despite the lowered skill requirements and staff changes, showcase community units, taking the least severely ill patients, can work well, especially for patients who want to move from hospital. But what of those who do not wish to leave or are too disturbed? And what happens when the original hostel staff have changed and enthusiasms wane and when the money runs out when, at least, fifty

surprising. Other possible side-effects from magnetic stimulation included headache in 5 patients with no history of headaches. 3 patients described memory loss, although all had a neurological condition that could have accounted for deteriorating memory. Other complaints, less likely to be due to magnetic stimulation, included carcinoma of the colon, hair loss, increased "static electricity", and neck pain with diminished libido. All the other patients remained well or had been troubled only by their original illness. There is some evidence’ that accidental electric shocks can precipitate relapse in multiple sclerosis. However, of the 108 patients with multiple sclerosis only 20 had had a relapse during follow-up-a relapse rate of 018 over 12 to 21 months, this being less than the 115 observed by Thygesens in patients followed up for 18 months. Nonetheless convulsions developing in 2 multiple

470

sclerosis

patients within a month of magnetic stimulation is worrying. Bridgers and Delaney; found no harmful EEG changes in healthy individuals after magnetic stimulation but some patients with neurological disease may have a lowered epileptic threshold so that magnetic stimulation could trigger seizures. Further studies of the effects of magnetic stimulation in multiple sclerosis, with EEG before magnetic stimulation and periodically afterwards, may be helpful. Department of Clinical Neurophysiology, Royal Hallamshire Hospital,

ROSALIND KANDLER

Sheffield S10 2JF, UK

1. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimulation of the human motor cortex. Lancet 1985; i: 1106-07. 2. Elian M, Dean G. Multiple sclerosis and epilepsy. In: Perry JK, ed. Epilepsy: the eighth international symposium. New York: Raven Press, 1977. 3. Drake WE, Macrae D. Epilepsy in multiple sclerosis. Neurology 1961; 11: 810-16.

4. Bamford CR, Sibley WA, Cole Thies MSPH, Laguna JF, Smith MS, Clark K. Trauma as an etiologic and aggravating factor in multiple sclerosis. Neurology 1981; 31: 1229-34. 5. Thygesen P. The course of disseminated sclerosis: a close up of 105 attacks. Copenhagen: Rosenkilde & Bagger, 1953. 6. Bridgers SL, Delaney RC. Transcranial magnetic stimulation: an assessment of cognitive and other cerebral effects. Neurology 1989; 39: 417-19.

Buspirone metabolite and panic attacks SiR,—Dr Norman and Dr Judd (Sept 9, p 615) argue that the buspirone metabolite 1-(2-pyrimidinyl)piperazine (1-PP) was probably not involved in panic attacks precipitated by the addition of a single dose of buspirone to a tricyclic antidepressant. Dr Chignon and Dr Lepnie (July 1, p 46) had suggested that this metabolite might be involved via a2-adrenergic receptors. Norman and Judd claim that Gammans et all had found that the metabolite "is only 20% as potent as buspirone, has low penetration into brain, and can account for no more than 2% of the activity of busprione". What Gammans et al said was that the metabolite is only 20% as potent as buspirone "in a biologic system predictive of clinical anxiolytic action". At the a2 receptor, suggested to be involved in panic attacks, 1-PP is much more potent than buspirone.2-4 Nor did Gammans et al say that the metabolite has poor penetration into brain; they merely noted that brain levels of 1-PP were lower after buspirone than after 1-PP. Caccia et all had measured 1-PP and buspirone levels in rat brain and found the total area

under the

curve

of the metabolite

to

be 64 times that of

buspirone. In the rat given buspirone, the brain is therefore exposed to much more of the metabolite than of the parent drug. Caccia et al showed that in rats the ratio of 1-PP/buspirone is even higher in brain than it is in plasma, suggesting the metabolite penetrates into brain at least as well as the parent drug does. The plasma ratio of 1-PP/buspirone was similar in man and in rats’ (ie, the metabolite predominates in both species). Norman and Judd feel that involvement of the metabolite is also unlikely because a panic attack was precipitated within a few hours of the addition of buspirone. However, Caccia et al showed that the metabolite predominates over buspirone in plasma within minutes after an oral dose of buspirone. Whether 1-PP has a role in the panic attacks reported with buspirone remains speculative, but the reasons Norman and Judd gave for discounting a role of 1-PP are not valid. Lilly Research Laboratories, Eli Lilly and Company, Lilly Corporate Center, Indianapolis, Indiana 46285, USA

RAY W. FULLER

1. Gammans

RE, Mayol RF, LaBudde JA. Metabolism and disposition of buspirone. Am J Med 1986; 80 (suppl 3B): 41-51. 2. Gower AJ. In vivo &agr;2-adrenoceptor antagonist activity of buspirone and its metabolite, 1-(2-pyrimioinyl)-piperazine (1-PP) in the rat. Br J Pharmacol 1986; 89: 726P. 3. Rimele TJ, Henry DE, Lee DKH, Geiger G, Heaslip RJ, Grimes D. Tissuedependent alpha adrenoceptor activity of buspirone and related compounds. J Pharmacol Exp Ther 1987; 241: 771-78. 4. Bianchi G, Crarattini S. Blockade of &agr;2-adrenceptors by 1-(2-pyrimidinyl)-piperazine (PmP) in vivo and its relation to the activity of buspirone. Eur J Pharmacol 1988; 147: 343-50.

S, Conti I, Vigano G, Garattini S. 1-(2-pyrimidinyl)-piperazine metabolite of busprione in man and rat. Pharmacology 1986; 33: 46-51.

5. Caccia

as

active

Microwave

heating of milk

SIR,-Professor Lubec and collegues (Dec 9, p 1392) report the presence of D-proline and cis-3 and cis-4 hydroxyproline in milk formulae after microwave heating. It is claimed that D-proline is neurotoxic. However, in the study cited1 by Lubec et al the neurotoxicity resulted when D-proline was injected intraventricularly into the brains of 2 and 5 day old chicks. The gastrointestinal absorption of D-proline would be followed by its rapid conversion to a-keto-8-amino-M-valeric acid2 by the action of D-aminoacid oxidase, a broad specificity enzyme mainly present in kidneys and liver. Further metabolism of the valeric acid derivative would produce useful metabolites or energy. We are continually ingesting and effectively metabolising and utilising D-amino-acids. These come from the degradation of bacterial cell walls, which contain a range ofD-aminoacids.3 Lubec et al also seem concerned that cis-aminoacids (presumably cis-hydroxyprolines) might lead to "structural, functional, and immunological changes" if incorporated into proteins. In studies on the incorporation of proline analogues into procollagen Uitto and Prockop4 found about 17% replacement of proline by cishydroxyproline. However, this was in cell culture with a cishydroxyproline concentration of 1 -53 mmol/1, a high concentration that would favour incorporation into polypeptides in vitro. Plasma concentrations of proline are typically 2-3 mg/dl or so,5 corresponding to 0-2 mmol/1 or one-eighth the concentration of cis-hydroxyproline used by Uitto and Prockop.4 Lubec and colleagues reported that after microwave heating milk formulae the concentration of cis-hydroxyproline isomers was 1-2 my/1. From the protein concentration of milk formulae6 (about 1 -7 g/dl) and the proline content of cows’ milk protein7 (9-8 g per 100 g) one can calculate that an infant consuming 1 litre of milk formula per day would ingest about 1g proline. This is about 1000 times more than the 1-2 mg cis-hydroxyprolines reported in 1 litre of milk formula after microwave heating. In the normal in-vivo synthesis of collagen and other

hydroxyproline-containing proteins, hydroxyprolines, though present intracellularly, are not incorported during synthesis. The hydroxyprolines in proteins result from the enzymatic hydroxylation of prolyl residues in polypeptide or protein chains.8 cis-hydroxyprolines derived from microwave-heating of milk formula would not be significantly substituted for proline in protein synthesis. Department of Biochemistry, University of Western Australia, Nedlands, Western Australia 6009

WOLFE SEGAL

A, David JL, Garman MW. D-proline: stereo-specificity and sodium chloride dependence of lethal convulsant activity in the chick. Pharmacol Biochem Behav 1978; 8: 623-25. 2. Krebs HA. Oxidation of ammo adds. In: Sumner JB, Myrback K, eds. The enzymes, chemistry and mechanism of action. Vol II (1). New York: Academic Press, 1951: 530. 3. Lehninger AL. Biochemistry, 2nd ed. New York: Worth, 1975: 268. 4. Uitto J, Prockop DJ. Incorporation of proline analogs into procollagen. Arch Biochem Biophys 1977; 181: 293-99. 5. Dien K, ed. Documenta Geigy-scientific tables, 6th ed. Crows’ Nest, NSW: Geigy, 1962: 557. 6. Wharton BA. Infant formulae. Br Nutr Found Nutr Bull 1984; 9: 83: 7. Dien K, ed. Documenta Geigy-scientific tables, 6th ed. Crow’s Nest, NSW: Geigy, 1962: 500. 8. Lebninger AL. Biochemistry, 2nd ed. New York: Worth, 1975: 968. 1. Cherkin

"Doctor fish" and psoriasis SIR,-Dr Warwick and Dr Warwick (Nov 4, p 1093) are sceptical about the "doctor fish of Kangul". The species of fish have been identified. There are two types, both being members of the Cyprinidae family adapted to warm milieu—namely, "strikers" (Cyprinion macrostomus macrostomus) with a terminal mouth and "lickers" (Garra rufa obtusa) with a ventral mouth. (The "jabber" is an immature striker, losing its lateral spots during maturation.) Both fish are omnivorous, a well-known feature of Cyprinidae.3 The orientation of these fish to the human body is insufficient feeding, as a consequence of inadequate amounts of phytoplankton

Safety of transcranial magnetic stimulation.

469 the loss of beds reported merely reflected seasonal staffing difficulties or if staff played down their vacancies to deflect possible admissions...
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