469

the loss of beds reported merely reflected seasonal staffingdifficulties or if staff played down their vacancies to deflect possibleadmissions from outside their catchment area or to ease the pressureon themselves during a stressful and understaffed period. On theother hand, the survey was done in the middle of a four-day holiday.The situation probably worsened over the ensuing days when therewould 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 closuresaccelerate the shortages our survey revealed may become a chronicbed famine. The loss of flexibility could lead to an increase inpremature discharges and the "revolving door" syndrome; andjunior doctors will have to spend ever longer trying to "borrow"admission beds from other districts. The homeless mentally ill, whoare being neglected by community care provision, will be denied thetreatment and sanctuary they periodically require, resulting in moremisery, suicide, petty crime, and fuller prisons.

Plans for community care should be reconsidered to take accountof the need for preserving non-acute services alongside acuteservices. If they are not, pressure on acute psychiatic services ininner-city areas will become intolerable, with appalling social

consequences.

Friern Hospital,London N11 3BP, UK

DORIS HOLLANDERROBIN POWELL

SIR,-Dr Whitehead (Jan 20, p 172) believes that "overcrowded"psychiatric hospitals are no better than workhouses. Anyovercrowding is unneccessary since we have discharged half thelong-stay population since 1954. However, as he says, if psychiatrichospitals are to be kept functioning "vast amounts of money need tobe spent on their fabric, their furnishing, and their staffing".However, the value of land and the buildings are attractive to healthauthorities which are overspent generally, and Governmentassurances that the proceeds of any sales will be applied to mentalillness 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 policyis being done it is becoming increasingly difficult to obtain aninpatient control population that is matched for severity withpatients selected for relocation in the community.The mentally ill have long wandered the streets, rotating between

destitution, psychiatric hospital, and prison. However, even thoughwe fail to keep adequate statistics and so cannot properly assesstrends, the impression of twenty-eight voluntary organisations at arecent meeting of CONCERN (Guardian Dec 19, 1989) was thatnumbers are growing as fewer psychiatric beds are available.Whitehead believes that, without investment, the quality of life inpsychiatric hospitals may be no better than life "in a box under thearches". We found that the quality of life was superior for long-staypatients in hospital than for those housed in the community andreceiving regular visits from community psychiatric nurses. 1The impetus for building asylums in the 19th century in Britain

was a recognition that it was disgraceful to care for pauper lunatics indebtor prisons. The relation between psychiatric hospital bedoccupancy and prison statistics has three components: (1) the highinverse correlation between the two;2 (2) the close relation betweenpresent or previous psychosis and imprisonment; and (3) theconsistency in prison surveys of the proportion of mental illnessfound.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 anoffence differ little and the use of police cells with frequent moves8can 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 thancurrent initiatives. Enthusiasm and change itself can be beneficial.Despite the lowered skill requirements and staff changes, showcasecommunity units, taking the least severely ill patients, can workwell, especially for patients who want to move from hospital. Butwhat of those who do not wish to leave or are too disturbed? Andwhat happens when the original hostel staff have changed andenthusiasms wane and when the money runs out when, at least, fifty

hospitals have been closed and the proceeds dispersed? The 1975white-paper Better 5’grMc for the Mentally Ill recognised (para2.27) that families and relatives and the public in general would nottolerate the discharge to community care of chronic patients withoutproper aftercare so that these patients spend their days wanderingthe streets or become an unbearable burden on their families. Norwould they tolerate hostels that are so selective that they are onlyhalf-full while people needing residential care are turned away orappeals for help go unanswered in a crisis while the boundaries ofresponsibility are debated.

Friern Hospital,London N11 3BP, UK MALCOLM P. I. WELLER

1. Weller BGA, Weller MPI, Cheyne A. Long-term psychiatric patients m thecommunity. 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 atChristmas 1985-88. Lancet 1989; ii: 1509-11.

4. Bluglass RS.A psychiatric study of Scottish prisoners. MD thesis, University of StAndrews, 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 stimulationSiR,—Dr Homberg and Dr Netz (Nov 18, p 1223) describe epilepsyduring transcranial magnetic stimulation in a patient with stroke.Using the method of Barker et aP and the Novametrix ’Magstim200’ stimulator, we have done more than 800 transcranial magneticstimulation studies on controls and on patients with neurologicalconditions (including 76 tests on stroke patients) without everobserving seizures.

Because little is known about long-term side-effects of magneticstimulation we sent a questionnaire to 218 people who had beentested 3-21 months previously. We asked about their health sincethe tests and received replies from 154 patients (multiple sclerosis108, Parkinson’s disease 19, stroke 6, and other neurologicalconditions 21) and from 9 healthy volunteers.

Epileptic seizures were recorded by 2 patients with multiplesclerosis. A 60-year-old man had a single jacksonian seizure 4 weeksafter magnetic stimulation. He was given phenytoin and had nofurther seizures. During stimulation he had received 24 corticalstimuli. A 30-year-old woman had two grand-mal seizures on thesame day, 3 weeks after magnetic stimulation. An

electroencephalogram (EEG) showed runs of high-voltagerhythmic and sharp activity, which were enhanced byoverbreathing, suggesting an abnormally low epileptic threshold.Phenytoin was prescribed and she had no further seizures. Duringmagnetic stimulation at the session before the convulsions she hadreceived 50 cortical stimuli. This was her fifth series of tests; on allfour earlier ones over the previous 6 months, 40 cortical stimuli hadbeen 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 2among 108 patients with MS who replied to our questionnaire is notsurprising.

Other possible side-effects from magnetic stimulation includedheadache in 5 patients with no history of headaches. 3 patientsdescribed memory loss, although all had a neurological conditionthat could have accounted for deteriorating memory. Other

complaints, less likely to be due to magnetic stimulation, includedcarcinoma of the colon, hair loss, increased "static electricity", andneck pain with diminished libido.

All the other patients remained well or had been troubled only bytheir original illness. There is some evidence’ that accidental electricshocks can precipitate relapse in multiple sclerosis. However, of the108 patients with multiple sclerosis only 20 had had a relapse duringfollow-up-a relapse rate of 018 over 12 to 21 months, this beingless than the 115 observed by Thygesens in patients followed up for18 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 changesin healthy individuals after magnetic stimulation but some patientswith neurological disease may have a lowered epileptic threshold sothat magnetic stimulation could trigger seizures. Further studies ofthe effects of magnetic stimulation in multiple sclerosis, with EEGbefore magnetic stimulation and periodically afterwards, may behelpful.

Department of Clinical Neurophysiology,Royal Hallamshire Hospital,Sheffield S10 2JF, UK ROSALIND KANDLER

1. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimulation of the humanmotor cortex. Lancet 1985; i: 1106-07.

2. Elian M, Dean G. Multiple sclerosis and epilepsy. In: Perry JK, ed. Epilepsy: theeighth 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 thebuspirone metabolite 1-(2-pyrimidinyl)piperazine (1-PP) was

probably not involved in panic attacks precipitated by the additionof a single dose of buspirone to a tricyclic antidepressant. DrChignon and Dr Lepnie (July 1, p 46) had suggested that thismetabolite 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 penetrationinto brain, and can account for no more than 2% of the activity ofbusprione". What Gammans et al said was that the metabolite isonly 20% as potent as buspirone "in a biologic system predictive ofclinical anxiolytic action". At the a2 receptor, suggested to beinvolved in panic attacks, 1-PP is much more potent than

buspirone.2-4 Nor did Gammans et al say that the metabolite haspoor penetration into brain; they merely noted that brain levels of1-PP were lower after buspirone than after 1-PP. Caccia et all hadmeasured 1-PP and buspirone levels in rat brain and found the totalarea under the curve of the metabolite to be 64 times that of

buspirone. In the rat given buspirone, the brain is therefore exposedto much more of the metabolite than of the parent drug. Caccia et alshowed that in rats the ratio of 1-PP/buspirone is even higher inbrain than it is in plasma, suggesting the metabolite penetrates intobrain at least as well as the parent drug does. The plasma ratio of1-PP/buspirone was similar in man and in rats’ (ie, the metabolitepredominates in both species).Norman and Judd feel that involvement of the metabolite is also

unlikely because a panic attack was precipitated within a few hoursof the addition of buspirone. However, Caccia et al showed that themetabolite predominates over buspirone in plasma within minutesafter 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 Juddgave 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. Tissue-dependent 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.

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

Microwave heating of milkSIR,-Professor Lubec and collegues (Dec 9, p 1392) report thepresence of D-proline and cis-3 and cis-4 hydroxyproline in milkformulae after microwave heating. It is claimed that D-proline isneurotoxic. However, in the study cited1 by Lubec et al the

neurotoxicity resulted when D-proline was injectedintraventricularly into the brains of 2 and 5 day old chicks. Thegastrointestinal absorption of D-proline would be followed by itsrapid conversion to a-keto-8-amino-M-valeric acid2 by the action ofD-aminoacid oxidase, a broad specificity enzyme mainly present inkidneys and liver. Further metabolism of the valeric acid derivativewould produce useful metabolites or energy. We are continuallyingesting and effectively metabolising and utilising D-amino-acids.These come from the degradation of bacterial cell walls, whichcontain a range ofD-aminoacids.3Lubec et al also seem concerned that cis-aminoacids (presumably

cis-hydroxyprolines) might lead to "structural, functional, andimmunological changes" if incorporated into proteins. In studies onthe incorporation of proline analogues into procollagen Uitto andProckop4 found about 17% replacement of proline by cis-

hydroxyproline. However, this was in cell culture with a cis-

hydroxyproline concentration of 1 -53 mmol/1, a high concentrationthat would favour incorporation into polypeptides in vitro. Plasmaconcentrations of proline are typically 2-3 mg/dl or so,5corresponding to 0-2 mmol/1 or one-eighth the concentration ofcis-hydroxyproline used by Uitto and Prockop.4 Lubec andcolleagues reported that after microwave heating milk formulae theconcentration of cis-hydroxyproline isomers was 1-2 my/1. Fromthe protein concentration of milk formulae6 (about 1 -7 g/dl) and theproline content of cows’ milk protein7 (9-8 g per 100 g) one cancalculate that an infant consuming 1 litre of milk formula per daywould ingest about 1 g proline. This is about 1000 times morethan the 1-2 mg cis-hydroxyprolines reported in 1 litre of milkformula after microwave heating.

In the normal in-vivo synthesis of collagen and other

hydroxyproline-containing proteins, hydroxyprolines, thoughpresent intracellularly, are not incorported during synthesis. Thehydroxyprolines in proteins result from the enzymatichydroxylation of prolyl residues in polypeptide or protein chains.8cis-hydroxyprolines derived from microwave-heating of milkformula would not be significantly substituted for proline in proteinsynthesis.

Department of Biochemistry,University of Western Australia,Nedlands, Western Australia 6009 WOLFE SEGAL

1. Cherkin A, David JL, Garman MW. D-proline: stereo-specificity and sodiumchloride dependence of lethal convulsant activity in the chick. Pharmacol BiochemBehav 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.

"Doctor fish" and psoriasisSIR,-Dr Warwick and Dr Warwick (Nov 4, p 1093) are scepticalabout the "doctor fish of Kangul". The species of fish have beenidentified. There are two types, both being members of theCyprinidae 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" isan immature striker, losing its lateral spots during maturation.)Both fish are omnivorous, a well-known feature of Cyprinidae.3The orientation of these fish to the human body is insufficientfeeding, as a consequence of inadequate amounts of phytoplankton