- Email: [email protected]
VIEWS OF BRITISH NEUROLOGISTS ON EPILEPSY, DRIVING, AND THE LAW
401
these closely related life-sustaining processes. Although we agree with Panksepp et al. 54 that "as with any complex mechanism, knowledge advances by the gradual refinement of oversimplifications", we believe we should emphasise that the modern-day Sir Galahads seeking the single holy grail to cure obesity may well search in vain. Obesity, like diabetes mellitus, may well have many different subtypes each with its own
Occasional
VIEWS OF BRITISH NEUROLOGISTS ON EPILEPSY, DRIVING, AND THE LAW PETER HARVEY
appropriate management.
1
Morley JE. The neuroendocrine control of appetite: the role of the endogenous opiates, cholecystokinin, TRH, gamma-ammo butyric acid and the diazepam receptor Life Sci 1980; 27: 355-68.
Powley TL, Laughton W. Neural pathways involved in the hypothalamic integration of autonomic responses. Diabetologia 1981; 20: 378-87. 3. Powley TL, MacFarlane BA, Markell MS, Opsahl CA. Different effects of vagotomy and atropine on hypothalamic stimulation of feeding. Behav Biol 1978; 23: 306-25. 4 Anand BK, Brobeck JR. Hypothalamic control of food intake in rats and cats. Yale J 2
Biol Med 1951; 24: 123-40. Bray GA, Inoue S, Nishizawa Y. Hypothalamic obesity: the autonomic hypothesis and the lateral hypothalamus. Diabetologia 1981; 20: 366-67. 6. Mayer J. Regulation of energy intake and the body weight: the glucostatic theory and 5.
lipostatic hypothesis. Ann NY Acad Sci 1955; 63: 15-43 Significance of glucose, insulin and free fatty acid on the hypothalamic feeding and satiety neurons. In: Novin D, Wyrwicka W, Bray G, eds. Hunger. basic
7. Oomura Y
mechanisms and clinical implications New York Raven Press, 1976: 145-57. LeMagnen J, Devos M, Gaudilliere J-P, Louis-Sylvestre J, Tallon S Role ofa lipostatic mechanism in regulation by feeding of energy balance in rats J Comp Physiol Psychol 1973; 84: 1-23. 9 Mellinkoff SM, Frankland M, Boyle D, Greipel M. Relationship between serum ammo acid concentrations and fluctuations in appetite J Appl Physiol 1956; 8: 535-38. 10. Levine AS, Morley JE. Purinergic regulation of food intake. Science 1982; 217: 77-79. 11. Kissileff HR, van Itallie TB. Physiology of the control of food intake. Ann Rev Nutr 1982, 2: 371-418. 12 Brobeck JR. Food intake as a mechanism of temperature regulation. Yale J Biol Med 8
1948; 20: 545-52. 13. Booth DA Prediction of feeding behaviour from energy flows in the rat. In: Booth DA, ed Hunger models-computable theory of feeding control. London: Academic Press, 1978. 227-78. 14 Mot1ey JE, Levine AS. The role ofihe endogenoun opiates as regu1ators of appetite. Am J Clin Nutr 1982; 35: 757-61. 15. Sanger DJ. Endorphinergic mechanisms in the control of food and water intake.
Appetite 1981; 2: 193-208 16. Jones JG, Richter JA. The site of Life Sci 1981,18: 2055-64.
naloxone in suppressing food and water intake in rats.
17 Atkinson RL Naloxone decreases food intake in obese humans. J Clin Endocrinol Metab 1982; 55: 196-98. 18. Kyriakides M, Silverstone T, Jeffcoate W, Laurance B. Effect of naloxone on hyperphagia in Prader-Willi syndrome. Lancet 1980; i: 876-77 19. Thompson DA, Welle SL, Lilavivat U, Penicaud L, Campbell RG. Opiate receptor blockade in man reduces 2-deoxy-d-glucose-induced food intake but not hunger, thirst and hypothermia. Life Sci 1982; 31: 847-52 20. Marks-Kaufman R, Kanarek RB. Morphine selectively influences macronutrient uptake in the rat Pharmacol Biochem Behav 1980; 12: 427-30. 21 Morley JE, Levine AS Dynorphin-(1-13) induces spontaneous feeding in rats. Life Sci
1981; 29: 1901-03. RJ Behavioral effects of dynorphin—a novel opioid neuropeptide. Neuropharmacology 1980; 19: 801-03. 23. Morley JE, Levine AS, Grace M, Kneip J. Dynorphin-( 1-13), dopamine and feeding in rats. Pharmacol Biochem Behav 1982; 16: 701-05 24 Morley JE, Levine AS, Grace M, Kneip J. An investigation of the role of kappa opiate receptor agonists in the initiation of feeding. Life Sci 1982, 31: 2617-26 25. Ferguson-Segall M, Flynn JJ, Walker J, Margules DL. Increased immunoreactive dynorphin and leu-enkephalin in posterior pituitary of obese mice (ob/ob) and supersensitivity to drugs that act at kappa receptors. Life Sci 1982; 31: 2233-36. 26. Morley JE, Elson MK, Levine AS, Shafer RB. The effects of stress on central nervous system concentrations of the opioid peptide, dynorphin Peptides 1983; 3: 901-06. 27. Reid LD, Konecka AM, Przewlocki R, Millan MH, Millan MJ, Herz A Endogenous opioids, circadian rhythms, nutrient deprivation, eating and drinking Life Sci 1982; 22. Katz
31: 1829-32. 28 Levine AS, Morley JE, Brown DM, Handwerger BS. Extreme sensitivity of diabetic mice to naloxone-induced suppression of food intake Physiol Behav 1982, 28: 987-89 29 Levine AS, Morley JE Peptidergic control of insulin-induced feeding Peptides 1981; 2: 261-64. 30 Morley JE, Levine AS Stress induced eating is mediated through endogenous opiates. Science 1980, 209: 1259-61. 31 Vaswani KK, Tejwani GA Opiate mediated, stress induced increase in the intake of high fat diet. Soc Neurosci Abstr 1982; 8: 224 32 Perlow MJ, Freed WJ, Carman JS, Wyatt RJ Calcitonin reduces feeding in man, monkey and rat. Pharmacol Biochem Behav 1980, 12: 609-12. 33 Levine AS, Morley JE. Reduction of feeding in rats by calcitonin. Brain Res 1981; 222: 187-91 34 Rizzo AJ, Goltzman D Calcitonin receptors in the central nervous system of the rat.
Endocrinology 1981; 108: 1672-77
ANTHONY HOPKINS
Departments of Neurological Sciences, Royal Free and St Bartholomew’s Hospitals, London
Correspondence should be addressed to J. E. M., VA Medical Center, 54th Street and 48th Avenue South, Minneapolis, Minnesota 55417, U.S.A. REFERENCES
Survey
good grounds for preventing some people with driving. The accident rate amongst licensed epilepsy drivers with epilepsy is 1’ 3 to 2’ 0 times that amongst agematched controls without epilepsy.’,2 In a study from Tasmania accidents resulting from previously undisclosed epilepsy accounted for no fewer than 33 out of 43 accidents due to seizures.The same study showed the value of sensible restrictions. Of 205 drivers who had declared previous seizures, 122 were granted a licence, and none had a seizure in the period of follow-up. 83 were initially ineligible, of whom 50 were eventually granted a licence. 5 of these subsequently had a seizure, resulting in an accident in 2 cases. Restrictions exist in many countries, but these vary considerably-for example, even amongst the United States of America.’ Unfortunately, there is good evidence from several countries that many currently ineligible people with epilepsy are driving. This evidence is based on: 1. A shortfall of people declaring epilepsy when applying for a licence compared with the expected figures derived from known figures of incidence and prevalence.2,3 2. A mismatch between referrals to an EEG department for THERE
are
from
35.
Levine AS. Corticotropin releasing factor, grooming and ingestive Life Sci 1982; 31: 1459-64 Stuckey JA, Gibbs J. Lateral hypothalamic injection of bombesin decreases food intake
Morley JE, behavior
36
Brain Res Bull 1982; 8: 617-21 Levine AS, Prasad C. Histidyl-proline diketopiperazine decreases food intake in rats. Brain Res 1981; 210: 475-78. 38 Hoebel BG, Hernandez L, McLean S, et al. Catecholamines, enkephalin and neurotensin in feeding and reward. In: Hoebel BG, Novin D, eds. The neural basis of feeding and reward. Brunswick, Massachusetts: Haer Institute, 1982: 465-78. 39. Della-Fera MA, Baile CA. Cerebral ventricular injections Of CCK-octapeptide and feed intake: the importance of continuous injection Physiol Behav 1980; 24: 1133-38. 40 Liebowitz SF. Neurochemical systems of the hypothalamus in control of feeding and drinking behavior and water electrolyte excretion. In: Morgane P, Panksepp J, eds. Handbook of the hypothalamus, vol 3. New York: Marcel-Dekker, 1980: 299-437. 41. Blundell JE. Serotonin and feeding. In: Esmon WB, ed. Serotonin in health and disease, vol 5, Clinical applications New York. Spectrum, 1979: 403-50. 42. Paul SM, Hulihan-Giblin B, Skolnick P. (+)-Amphetamine binding to rat hypothalamus: relation to anorexic potency of phenylethylamines. Science 1982; 218: 487-90. 43. Pollard H, Lorens C, Schwartz JC, Gras C, Dray F Localization of opiate receptors and enkephalins in the rat striatum in relationship with the nigrostriatal dopaminergic system. Brain Res 1978; 151: 392-98 44. Urwyler S, Tabakoff B. Stimulation of dopamine synthesis and release by morphine and D-ala-d-leu-enkephalin in the mouse striatum in vivo Life Sci 1981; 28: 2277-86. 45. Cooper SJ. Benzodiazepines as appetite enhancing compounds Appetite 1980; 1: 7-19. 46. Grandison S, Guidotti A. Stimulation of food intake by muscimol and beta endorphin. Neuropharmacology 1977; 16: 533-36 47. Morley JE, Levine AS, Kneip J Muscimol induced feeding: a model to study the hypothalamic regulation of appetite. Life Sci 1981; 29: 1213-18. 48 Mrosovsky N, Powley TL Set points for body weight and fat. Behav Biol 1977; 20: 205-23. 49. Wirtshafter D, Davis JD. Set points, settling points and the control of body weight. Physiol Behav 1977; 19: 75-78. 50. Armstrong S, Coleman G, Singer A. Food and water deprivation: changes in rat feeding, drinking, activity and body weight. Neurosci Biobehav Rev 1980; 4: 378-402. 51 Levine AS, Morley JE The effect of prostaglandins (PGE2and PGF2&agr;) on food intake in rats Pharmacol Biochem Behav 1981, 15: 735-38. 52. Porte D Jr, Woods SC. Regulation of food intake and body weight by insulin. Diabetologia 1981; 20: 274-80. 53. Morley JE, Levine AS, Murray SS, Kneip J, Grace M. Peptidergic regulation of stressinduced eating. Am JPhysiol 1982; 243: R159-63 54 Panksepp J, Bishop J, Rossi J. Neurohormonal and endocrine control of feeding. Psychoendocrinology 1979; 4: 89-106. in rats
37.
Morley JE,
402
epilepsy and the numbers of these patients subsequently found from licensing-authority records to hold a driving licence.5 An estimate that 9 out of 10 people with epilepsy applying for a licence concealed their epilepsy. 3. A comparison between information given about epilepsy at examination for military service in the Netherlands and subsequent driving-licence applications. Of those with a history of epilepsy at military examination, only 9% of those who by 5 years later had obtained a licence had declared their epilepsy when applying for the licence.6 4. Inquiries about driving, with promised confidence, of people with epilepsy in the community. 19 of 62 subjects (31070), currently ineligible to hold a licence7 under British regulations, admitted that they were driving. In Great Britain "an applicant for a licence suffering from epilepsy shall satisfy the conditions that: definite
(a) he shall have been free from any epileptic attack during the immediately preceding the date when the licence is to have effect; or (b) in the case of an applicant who has had such attacks whilst asleep during that period, he shall have had such attacks only whilst asleep during a period of at least three years immediately preceding the date when the licence is to have effect; and (c) the driving ofa vehicle by him in pursuance of8 the licence is not likely to be a source of danger to the public". two years
Prominently printed on each British driving licence is the "You are required by law to inform DVLC (Drivers and Vehicle Licensing Centre), Swansea, at once if you have any disability which is or may become likely to affect your
three o’clock in the morning. Assuming he has had no more seizures, when may he drive? (c) An engineer of 40 had ten grand mal seizures between the ages of 10 to 22, when his medication was changed to phenytoin, 400 mg daily; he has had no more seizures since. He holds a current driving licence. He is admitted to hospital for a minor surgical procedure, and the house surgeon finds that his serum phenytoin is 100 mol/1 (25 ug/ml) (upper limit of "therapeutic range" 72 J.lmol/l [18g/ml]). Despite there being no evidence of clinical toxicity, he reduces the dosage to 200 mg daily. Ten days later the engineer has a grand mal seizure whilst awake. He immediately goes back to taking 400 mg of phenytoin a day, and consults you four weeks later, having had no further seizures, and when his serum phenytoin is 100 mol/1 (25 g/m1). Assuming he has had no more seizures, when may he drive? (d) A woman of 45 is treated for depression with amitriptyline. Three weeks after starting this treatment she has two grand mal seizures in the space of three days, one whilst asleep, and one whilst awake. Physical examination and investigations revealed no structural abnormalities of the brain. You see her in outpatients one month after the second seizure. She has stopped the amitriptyline. Assuming she has no more seizures, when may she drive? (e) A municipal gardener of 37 has had epilepsy characterised by daily myoclonic jerks and weekly grand mal seizures from the age of 10. Five years ago he was put on sodium valproate, since when he has had no generalised seizures, but he continues to
sentence
fitness as a driver, unless you do not expect it to last for more than three months". The onus is therefore on the licence holder who has experienced a seizure to report it. Doctors may be presumed to have a duty to inform their patients of the diagnosis of epilepsy, or at least that the patient has a relevant disability, and to remind patients of the need to inform the DVLC, and their insurance company.9 When the DVLC is notified, it will usually obtain information from the patient’s family doctor, and sometimes a report from hospital doctors as well, before deciding on that patient’s eligibility to hold a driving licence. A small panel of neurologists and neurosurgeons advises the DVLC about general principles, and members of this panel are consulted about specific doubtful cases. The DVLC may recommend revocation of the licence, or grant a licence for a limited period. A licence to drive a private car may be allowed, but not a heavy goods or public service vehicle. If the patient is not satisfied, he has the right of appeal to a magistrate’s court. We have become increasingly aware of the number of "grey" areas into which some patients fall, of inconsistent advice given by colleagues, and of our inability to predict the DVLC’s rulings. In an attempt to identify the areas of confusion, we have investigated current practice and
understanding among neurologists. METHODS
We sent
to
all 233 clinical members of the Association of British
Neurologists 23 short case-histories, of which these are examples: (a) An insurance salesman aged 19 had his first grand mal seizure whilst awake at the office two months ago. Assuming he has had no more seizures, when may he drive? (b) A managing director has had epilepsy for many years, characterised by grand mal seizures whilst awake but which have now been controlled with phenytoin for over ten years. He holds a current driving licence renewed annually. He consults you with his wife who tells you that on four occasions in the past six months her husband had grand mal seizures whilst asleep at
Fig. I-Neurologists’ understanding of Driving Licence Regulations. Intervals refer to time when patients may resume driving, assuming no further seizures.
403
correspondence to neurologists and patients by the DVLC that patients may drive one year after a single seizure-advice that does not occur in the regulations-is illogical in the face
Fig. 2-Influence of abnormal EEG on advice given by neurologists about driving. have
myoclonic jerks within an hour of awakening or whilst nodding off to sleep. This is now his only symptom. (i) His EEG is now normal; when may he drive? (ii) His EEG continues to show 3 Hz spike-and-wave activity; when may he drive? As well as being asked when they thought the subject of each casehistory could become eligible to hold a driving licence under the regulations then currentl° (when the seizure-free period required was three years), the neurologists were asked to indicate their understanding of the regulations without referring to them. They were also asked when they would prefer each of these hypothetical patients to be allowed to drive, if this interval were different from
what they thought the
regulations required. RESULTS
130 neurologists replied, a response rate of 56%. Figs. 1 and 2 show the very considerable variation in their understanding of the regulations amongst neurologists. Similar variations occurred in the responses not shown here (these and the other case-histories sent out can be obtained from the authors). Although the neurologists were asked to express any preferences for duration of restriction they seemed satisfied with what they thought the regulations required. However, as the figures show, there were wide differences of opinion among neurologists and discrepancies between their interpretation of, and the apparent intent of, the regulations. 8, 10 DISCUSSION
Certain areas of confusion are obvious. The first seizure (fig. la).-After a first grand mal seizure, 12% of neurologists would allow the patient to continue driving, 27% would advise against this for one year after the seizure, and 28% for three years after the seizure. The regulations offer no comment about a first seizure. Current epidemiological definitions of epilepsy require "more than one non-febrile’ seizure". 7,11 One seizure is therefore not considered sufficient to justify a diagnosis of epilepsy. However, one study reported that the cumulative risks of recurrence after a first seizure are 16% after one year, 21% after two years, and 27% after three years. 12 In another study the recurrence rate was 15% in the first year and a further 20% in the second.13 The criteria for inclusion in these two studies were not identical. The advice often given in
of this evidence. The role of investigations.-Guidance proffered to us by the DVLC in respect of individual cases often refers to the normality or otherwise of investigations, a matter which is not mentioned in the regulations. Although Hauser and his colleagues’2 reported that seizures were more likely to recur in patients with generalised spike-and-wave abnormalities in the EEG, this is an unusual abnormality to find in those with epilepsy who are of an age to drive. Hauser et al. found no difference in recurrence rate between those with normal EEGs and those showing a focal abnormality. Although many British neurologists do not arrange an EEG after a first seizure, fig. 2 shows that some do take the EEG into account in other circumstances when advising about driving. Seizures precipitated by specific circumstances.-Is a single seizure precipitated by a tricyclic antidepressant epileptic or not? Fig. ld shows the wide range of interpretation by neurologists. What should be done if seizures recur on altering dosage of anticonvulsant drugs after a long seizurefree period? A strict interpretation of the new regulations would prevent driving for two years after a seizure that occurred soon after stopping or reducing anticonvulsant drugs. Fig. Ic shows that many neurologists took a more realistic line. We are informed that the DVLC will now allow a probationary period of 12 months after a single seizure if the patient has previously had five seizure-free years off anticonvulsants. This concession is not generally known because it has not been publicised; as neurologists interested in epilepsy, we discovered it only by chance. Sleep Mr.—Gibberd’ presented the cumulative risk of having a daytime seizure after a period of having seizures only whilst asleep, and the regulations are presumably meant to reflect this information. However, the wording of the regulations about epileptic attacks whilst asleep remains confusing. Take the situation of a single nocturnal attack occurring after a period of many years’ remission of seizures whilst awake. Can the patient drive now on the basis that the only attack he has had in the past three years has been whilst asleep; or can he drive in two years if he has no further attacks; or does he have to establish a new three-year history of asleeponly attacks? The old regulations were interpreted by the neurologists in either of two ways, nearly a third of all neurologists suggesting that the patient could continue
driving (fig. lb). In the absence of any published advice from the DVLC, doctors turn to quasi-official pamphlets such as that published by the Medical Commission on Accident Prevention.l5 The advice proffered seems to us to be often misleading, and to reflect only the views of the authors. It is, however, often interpreted as "the official view". It has been argued that since a doctor’s only obligation is to inform the patient of his duty to report his disability to the DVLC, he does not need to know what the regulations are, but patients naturally ask their doctors what they expect the DVLC’s ruling will be. It is churlish to refuse to reply, inadequate to plead ignorance, and positively harmful to give an inaccurate
reply. We believe that the situation could easily be improved by better communication. The advisory panel might usefully send all neurologists and neurosurgeons-if not all doctorsnotes of guidance about particular circumstances that we have discovered give rise to doubt. Difficult cases could still
404 to hospital. We have determined the frequency and of readmission to a modern geriatric medical unit to identify the problems and define the changes required in
be referred to the advisory panel, but the numbers would surely be reduced, and advice throughout the country would become more consistent. Above all, there is need for further studies of the risks of recurrence of seizures under various circumstances, so that the guidance given by the DVLC and its advisory panel may be more firmly based on fact.
people
Correspondence should be addressed to P. H., Department of Neurological Sciences, Royal Free Hospital, Pond Street, London NW3.
Details of all admissions, discharges, and deaths occurring in the four wards (one male; three female) of an 84-bedded geriatric medical unit at St Francis’ Hospital were analysed retrospectively each week during the year ending April 2, 1982. The age, sex, marital status, and nature of home support were noted for each patient. Case records were used to identify those who had been discharged from any hospital during the preceding twelve months, and the interval between discharge and readmission was noted. The reasons for readmission were determined (by H. G.) from information obtained from the patients, the hospital records, and individual medical, nursing, and remedial staff. Patients’ relatives and neighbours were also interviewed at the hospital when it was considered they could contribute helpful details. The patients were divided into two classes; class A patients had not been admitted to hospital during the preceding twelve months, and class B patients had been readmitted following discharge from a hospital in the King’s Health District at some time during the preceding twelve months. Thereclasses were compared to identify significant differences and to determine whether and how readmission could have been prevented. The readmitted patients were allocated to one of five groups according to the principal reason for readmission: group 1, unavoidable clinical deterioration; group 2, inadequate medical management; group 3, noncompliance of patient; group 4, social problems; and group 5, inadequate rehabilitation. Patients readmitted within two weeks of their previous discharge were studied separately. The frequency of readmission was also measured for each quarter to assess the effects of seasonal variations. The cumulative rate of readmission was determined for each group of patients. Statistical comparisons were made using the standard error of the difference between two means.
REFERENCES 1. Hormio A. Does
epilepsy mean higher susceptibility to traffic accidents? Acta Psychiatry Scand 1961; 150: suppl. 210-12. 2. Waller JA. Chronic medical conditions and traffic safety: review of the California experience. N Engl J Med 1965; 273: 1413-20. 3. Millengen KS. Epilepsy and driving. Proc Aust Assoc Neurol 1976; 13: 67-72. 4. Epilepsy International. Report of the Committee on Driving Licence Regulations in various countries (1980). Unpublished report. 5. Maxwell RDH, Leyshon GE. Epilepsy and driving. Br Med J 1971; 3: 12-15. 6. van der Lugt PJM. Is an application form useful to select patients with epilepsy who may drive? Epilepsia 1975; 16: 743-46. 7. Hopkins AP, Scambler G. How doctors deal with epilepsy. Lancet 1977; i: 183-86. 8. Statutory instrument 1982 no. 423. Road Traffic Act. Motor Vehicles (Driving Licences) (Amendment) (no. 3) Regulations (United Kingdom) 1982. 9. Editorial. Lancet 1980; i: 401. 10. Statutory instrument 1981 no. 952. Road Traffic Act. Motor Vehicles (Driving Licences) Regulations (United Kingdom) 1981. 11. Hauser BH, Kurland LT. The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967. Epilepsia 1975; 16: 1-68. 12. Hauser WA, Anderson VE, Loewnson RB, McRoberts S. Seizure recurrence after a first unprovoked seizure. 1982; 307: 522-28. 13. Cleland PG, Mosquera I, Steward WP, Foster JB. Prognosis of isolated seizures in adult life Br Med 1981; 283: 1364. J 14. Gibberd FB, Bateson MC. Sleep epilepsy, its pattern and prognosis. Br Med J 1974; ii: 403-07. 15. Medical Aspects of Fitness to Drive, 3rd ed. London: Medical Commission on Accident Prevention, 1976.
N Engl J Med
Hospital Practice CAN READMISSIONS TO A GERIATRIC MEDICAL UNIT BE PREVENTED?
HELEN GRAHAM
causes
patient care. PATIENTS AND METHODS
RESULTS
BRIAN LIVESLEY 617
Dulwich, London SE22 0SQ, and Department of Clinical Gerontology, St Francis’ Hospital, London SE22 8DF
Summary
During the year ending April 2, 1982, 153 patients readmitted to a geriatric
medical unit within twelve months of their previous discharge from any hospital in the district accounted for 24·8% of the 617 patients admitted. Readmission of the 153 patients was due to unavoidable clinical deterioration (32%), inadequate medical management (21%), non-compliance of patient (20·2%), social problems (18·3%), or inadequate rehabilitation (8·5%). Readmission could have been
prevented in 73 (47·7%) patients. These figures emphasise the importance of greater medical interest in the problems of the aged and support the need for a higher consultant/bed ratio in geriatric medical units to allow more effective management of patients aged 75 years and over. INTRODUCTION
DURING the past
decade, high-turnover geriatric medical
units have been increasing bed usage but despite this, the occupancy of non-maternity hospital beds by patients aged 75 years and over rose from 33% in 1973 to 39% in 1978. By the end of the century, however, the population aged 75 years and over will increase by 20%2 and place an even greater demand on the whole hospital service. One feature of this increasing demand is an apparently high rate of readmission of old
patients (220 men, 397 women; aged 59-101 years) admitted during the year. 464 patients (class A) were admitted for the first time and 153patients (class B) (24. 8% of all admissions; 56 men and 97 women) were readmitted. 106 patients had been discharged from the geriatric medical unit and 47 from non-geriatric wards. The period in which readmission was most likely to occur was two weeks after discharge; 43 of the 153 readmissions occurred within two weeks. The 49 patients (26 men and 23 women) in group 1 were admitted because of unavoidable clinical deterioration (a new medical event in 18, deterioration of an existing disorder in 19, and for terminal care in 12 patients who died from carcinoma or intractable disease within three weeks). 32 patients (10 men, 22 women; group 2) were admitted because of inadequate clinical management. In 17 the disorder was incompletely defined or controlled (e.g., Parkinson’s disease, falls). 6 patients had been discharged unwell (3 had exacerbation of existing bronchitis and 3 postoperative complications) and 2 with side-effects of drugs. In 2 cases drugs ordered by the consultant were not instituted by the junior medical staff and in a further 2 significant radiological evidence of bronchus carcinoma was overlooked. In 3 cases the general practitioner persistently refused to attend the patient. Of the 31 patients in group 3 (5 men, 26 women) 18 refused residential home or community services, 9 did not comply with therapy, and 4 discharged themselves from hospital. were
these closely related life-sustaining processes. Although we agree with Panksepp et al. 54 that "as with any complex mechanism, knowledge advances by the gradual refinement of oversimplifications", we believe we should emphasise that the modern-day Sir Galahads seeking the single holy grail to cure obesity may well search in vain. Obesity, like diabetes mellitus, may well have many different subtypes each with its own
Occasional
VIEWS OF BRITISH NEUROLOGISTS ON EPILEPSY, DRIVING, AND THE LAW PETER HARVEY
appropriate management.
1
Morley JE. The neuroendocrine control of appetite: the role of the endogenous opiates, cholecystokinin, TRH, gamma-ammo butyric acid and the diazepam receptor Life Sci 1980; 27: 355-68.
Powley TL, Laughton W. Neural pathways involved in the hypothalamic integration of autonomic responses. Diabetologia 1981; 20: 378-87. 3. Powley TL, MacFarlane BA, Markell MS, Opsahl CA. Different effects of vagotomy and atropine on hypothalamic stimulation of feeding. Behav Biol 1978; 23: 306-25. 4 Anand BK, Brobeck JR. Hypothalamic control of food intake in rats and cats. Yale J 2
Biol Med 1951; 24: 123-40. Bray GA, Inoue S, Nishizawa Y. Hypothalamic obesity: the autonomic hypothesis and the lateral hypothalamus. Diabetologia 1981; 20: 366-67. 6. Mayer J. Regulation of energy intake and the body weight: the glucostatic theory and 5.
lipostatic hypothesis. Ann NY Acad Sci 1955; 63: 15-43 Significance of glucose, insulin and free fatty acid on the hypothalamic feeding and satiety neurons. In: Novin D, Wyrwicka W, Bray G, eds. Hunger. basic
7. Oomura Y
mechanisms and clinical implications New York Raven Press, 1976: 145-57. LeMagnen J, Devos M, Gaudilliere J-P, Louis-Sylvestre J, Tallon S Role ofa lipostatic mechanism in regulation by feeding of energy balance in rats J Comp Physiol Psychol 1973; 84: 1-23. 9 Mellinkoff SM, Frankland M, Boyle D, Greipel M. Relationship between serum ammo acid concentrations and fluctuations in appetite J Appl Physiol 1956; 8: 535-38. 10. Levine AS, Morley JE. Purinergic regulation of food intake. Science 1982; 217: 77-79. 11. Kissileff HR, van Itallie TB. Physiology of the control of food intake. Ann Rev Nutr 1982, 2: 371-418. 12 Brobeck JR. Food intake as a mechanism of temperature regulation. Yale J Biol Med 8
1948; 20: 545-52. 13. Booth DA Prediction of feeding behaviour from energy flows in the rat. In: Booth DA, ed Hunger models-computable theory of feeding control. London: Academic Press, 1978. 227-78. 14 Mot1ey JE, Levine AS. The role ofihe endogenoun opiates as regu1ators of appetite. Am J Clin Nutr 1982; 35: 757-61. 15. Sanger DJ. Endorphinergic mechanisms in the control of food and water intake.
Appetite 1981; 2: 193-208 16. Jones JG, Richter JA. The site of Life Sci 1981,18: 2055-64.
naloxone in suppressing food and water intake in rats.
17 Atkinson RL Naloxone decreases food intake in obese humans. J Clin Endocrinol Metab 1982; 55: 196-98. 18. Kyriakides M, Silverstone T, Jeffcoate W, Laurance B. Effect of naloxone on hyperphagia in Prader-Willi syndrome. Lancet 1980; i: 876-77 19. Thompson DA, Welle SL, Lilavivat U, Penicaud L, Campbell RG. Opiate receptor blockade in man reduces 2-deoxy-d-glucose-induced food intake but not hunger, thirst and hypothermia. Life Sci 1982; 31: 847-52 20. Marks-Kaufman R, Kanarek RB. Morphine selectively influences macronutrient uptake in the rat Pharmacol Biochem Behav 1980; 12: 427-30. 21 Morley JE, Levine AS Dynorphin-(1-13) induces spontaneous feeding in rats. Life Sci
1981; 29: 1901-03. RJ Behavioral effects of dynorphin—a novel opioid neuropeptide. Neuropharmacology 1980; 19: 801-03. 23. Morley JE, Levine AS, Grace M, Kneip J. Dynorphin-( 1-13), dopamine and feeding in rats. Pharmacol Biochem Behav 1982; 16: 701-05 24 Morley JE, Levine AS, Grace M, Kneip J. An investigation of the role of kappa opiate receptor agonists in the initiation of feeding. Life Sci 1982, 31: 2617-26 25. Ferguson-Segall M, Flynn JJ, Walker J, Margules DL. Increased immunoreactive dynorphin and leu-enkephalin in posterior pituitary of obese mice (ob/ob) and supersensitivity to drugs that act at kappa receptors. Life Sci 1982; 31: 2233-36. 26. Morley JE, Elson MK, Levine AS, Shafer RB. The effects of stress on central nervous system concentrations of the opioid peptide, dynorphin Peptides 1983; 3: 901-06. 27. Reid LD, Konecka AM, Przewlocki R, Millan MH, Millan MJ, Herz A Endogenous opioids, circadian rhythms, nutrient deprivation, eating and drinking Life Sci 1982; 22. Katz
31: 1829-32. 28 Levine AS, Morley JE, Brown DM, Handwerger BS. Extreme sensitivity of diabetic mice to naloxone-induced suppression of food intake Physiol Behav 1982, 28: 987-89 29 Levine AS, Morley JE Peptidergic control of insulin-induced feeding Peptides 1981; 2: 261-64. 30 Morley JE, Levine AS Stress induced eating is mediated through endogenous opiates. Science 1980, 209: 1259-61. 31 Vaswani KK, Tejwani GA Opiate mediated, stress induced increase in the intake of high fat diet. Soc Neurosci Abstr 1982; 8: 224 32 Perlow MJ, Freed WJ, Carman JS, Wyatt RJ Calcitonin reduces feeding in man, monkey and rat. Pharmacol Biochem Behav 1980, 12: 609-12. 33 Levine AS, Morley JE. Reduction of feeding in rats by calcitonin. Brain Res 1981; 222: 187-91 34 Rizzo AJ, Goltzman D Calcitonin receptors in the central nervous system of the rat.
Endocrinology 1981; 108: 1672-77
ANTHONY HOPKINS
Departments of Neurological Sciences, Royal Free and St Bartholomew’s Hospitals, London
Correspondence should be addressed to J. E. M., VA Medical Center, 54th Street and 48th Avenue South, Minneapolis, Minnesota 55417, U.S.A. REFERENCES
Survey
good grounds for preventing some people with driving. The accident rate amongst licensed epilepsy drivers with epilepsy is 1’ 3 to 2’ 0 times that amongst agematched controls without epilepsy.’,2 In a study from Tasmania accidents resulting from previously undisclosed epilepsy accounted for no fewer than 33 out of 43 accidents due to seizures.The same study showed the value of sensible restrictions. Of 205 drivers who had declared previous seizures, 122 were granted a licence, and none had a seizure in the period of follow-up. 83 were initially ineligible, of whom 50 were eventually granted a licence. 5 of these subsequently had a seizure, resulting in an accident in 2 cases. Restrictions exist in many countries, but these vary considerably-for example, even amongst the United States of America.’ Unfortunately, there is good evidence from several countries that many currently ineligible people with epilepsy are driving. This evidence is based on: 1. A shortfall of people declaring epilepsy when applying for a licence compared with the expected figures derived from known figures of incidence and prevalence.2,3 2. A mismatch between referrals to an EEG department for THERE
are
from
35.
Levine AS. Corticotropin releasing factor, grooming and ingestive Life Sci 1982; 31: 1459-64 Stuckey JA, Gibbs J. Lateral hypothalamic injection of bombesin decreases food intake
Morley JE, behavior
36
Brain Res Bull 1982; 8: 617-21 Levine AS, Prasad C. Histidyl-proline diketopiperazine decreases food intake in rats. Brain Res 1981; 210: 475-78. 38 Hoebel BG, Hernandez L, McLean S, et al. Catecholamines, enkephalin and neurotensin in feeding and reward. In: Hoebel BG, Novin D, eds. The neural basis of feeding and reward. Brunswick, Massachusetts: Haer Institute, 1982: 465-78. 39. Della-Fera MA, Baile CA. Cerebral ventricular injections Of CCK-octapeptide and feed intake: the importance of continuous injection Physiol Behav 1980; 24: 1133-38. 40 Liebowitz SF. Neurochemical systems of the hypothalamus in control of feeding and drinking behavior and water electrolyte excretion. In: Morgane P, Panksepp J, eds. Handbook of the hypothalamus, vol 3. New York: Marcel-Dekker, 1980: 299-437. 41. Blundell JE. Serotonin and feeding. In: Esmon WB, ed. Serotonin in health and disease, vol 5, Clinical applications New York. Spectrum, 1979: 403-50. 42. Paul SM, Hulihan-Giblin B, Skolnick P. (+)-Amphetamine binding to rat hypothalamus: relation to anorexic potency of phenylethylamines. Science 1982; 218: 487-90. 43. Pollard H, Lorens C, Schwartz JC, Gras C, Dray F Localization of opiate receptors and enkephalins in the rat striatum in relationship with the nigrostriatal dopaminergic system. Brain Res 1978; 151: 392-98 44. Urwyler S, Tabakoff B. Stimulation of dopamine synthesis and release by morphine and D-ala-d-leu-enkephalin in the mouse striatum in vivo Life Sci 1981; 28: 2277-86. 45. Cooper SJ. Benzodiazepines as appetite enhancing compounds Appetite 1980; 1: 7-19. 46. Grandison S, Guidotti A. Stimulation of food intake by muscimol and beta endorphin. Neuropharmacology 1977; 16: 533-36 47. Morley JE, Levine AS, Kneip J Muscimol induced feeding: a model to study the hypothalamic regulation of appetite. Life Sci 1981; 29: 1213-18. 48 Mrosovsky N, Powley TL Set points for body weight and fat. Behav Biol 1977; 20: 205-23. 49. Wirtshafter D, Davis JD. Set points, settling points and the control of body weight. Physiol Behav 1977; 19: 75-78. 50. Armstrong S, Coleman G, Singer A. Food and water deprivation: changes in rat feeding, drinking, activity and body weight. Neurosci Biobehav Rev 1980; 4: 378-402. 51 Levine AS, Morley JE The effect of prostaglandins (PGE2and PGF2&agr;) on food intake in rats Pharmacol Biochem Behav 1981, 15: 735-38. 52. Porte D Jr, Woods SC. Regulation of food intake and body weight by insulin. Diabetologia 1981; 20: 274-80. 53. Morley JE, Levine AS, Murray SS, Kneip J, Grace M. Peptidergic regulation of stressinduced eating. Am JPhysiol 1982; 243: R159-63 54 Panksepp J, Bishop J, Rossi J. Neurohormonal and endocrine control of feeding. Psychoendocrinology 1979; 4: 89-106. in rats
37.
Morley JE,
402
epilepsy and the numbers of these patients subsequently found from licensing-authority records to hold a driving licence.5 An estimate that 9 out of 10 people with epilepsy applying for a licence concealed their epilepsy. 3. A comparison between information given about epilepsy at examination for military service in the Netherlands and subsequent driving-licence applications. Of those with a history of epilepsy at military examination, only 9% of those who by 5 years later had obtained a licence had declared their epilepsy when applying for the licence.6 4. Inquiries about driving, with promised confidence, of people with epilepsy in the community. 19 of 62 subjects (31070), currently ineligible to hold a licence7 under British regulations, admitted that they were driving. In Great Britain "an applicant for a licence suffering from epilepsy shall satisfy the conditions that: definite
(a) he shall have been free from any epileptic attack during the immediately preceding the date when the licence is to have effect; or (b) in the case of an applicant who has had such attacks whilst asleep during that period, he shall have had such attacks only whilst asleep during a period of at least three years immediately preceding the date when the licence is to have effect; and (c) the driving ofa vehicle by him in pursuance of8 the licence is not likely to be a source of danger to the public". two years
Prominently printed on each British driving licence is the "You are required by law to inform DVLC (Drivers and Vehicle Licensing Centre), Swansea, at once if you have any disability which is or may become likely to affect your
three o’clock in the morning. Assuming he has had no more seizures, when may he drive? (c) An engineer of 40 had ten grand mal seizures between the ages of 10 to 22, when his medication was changed to phenytoin, 400 mg daily; he has had no more seizures since. He holds a current driving licence. He is admitted to hospital for a minor surgical procedure, and the house surgeon finds that his serum phenytoin is 100 mol/1 (25 ug/ml) (upper limit of "therapeutic range" 72 J.lmol/l [18g/ml]). Despite there being no evidence of clinical toxicity, he reduces the dosage to 200 mg daily. Ten days later the engineer has a grand mal seizure whilst awake. He immediately goes back to taking 400 mg of phenytoin a day, and consults you four weeks later, having had no further seizures, and when his serum phenytoin is 100 mol/1 (25 g/m1). Assuming he has had no more seizures, when may he drive? (d) A woman of 45 is treated for depression with amitriptyline. Three weeks after starting this treatment she has two grand mal seizures in the space of three days, one whilst asleep, and one whilst awake. Physical examination and investigations revealed no structural abnormalities of the brain. You see her in outpatients one month after the second seizure. She has stopped the amitriptyline. Assuming she has no more seizures, when may she drive? (e) A municipal gardener of 37 has had epilepsy characterised by daily myoclonic jerks and weekly grand mal seizures from the age of 10. Five years ago he was put on sodium valproate, since when he has had no generalised seizures, but he continues to
sentence
fitness as a driver, unless you do not expect it to last for more than three months". The onus is therefore on the licence holder who has experienced a seizure to report it. Doctors may be presumed to have a duty to inform their patients of the diagnosis of epilepsy, or at least that the patient has a relevant disability, and to remind patients of the need to inform the DVLC, and their insurance company.9 When the DVLC is notified, it will usually obtain information from the patient’s family doctor, and sometimes a report from hospital doctors as well, before deciding on that patient’s eligibility to hold a driving licence. A small panel of neurologists and neurosurgeons advises the DVLC about general principles, and members of this panel are consulted about specific doubtful cases. The DVLC may recommend revocation of the licence, or grant a licence for a limited period. A licence to drive a private car may be allowed, but not a heavy goods or public service vehicle. If the patient is not satisfied, he has the right of appeal to a magistrate’s court. We have become increasingly aware of the number of "grey" areas into which some patients fall, of inconsistent advice given by colleagues, and of our inability to predict the DVLC’s rulings. In an attempt to identify the areas of confusion, we have investigated current practice and
understanding among neurologists. METHODS
We sent
to
all 233 clinical members of the Association of British
Neurologists 23 short case-histories, of which these are examples: (a) An insurance salesman aged 19 had his first grand mal seizure whilst awake at the office two months ago. Assuming he has had no more seizures, when may he drive? (b) A managing director has had epilepsy for many years, characterised by grand mal seizures whilst awake but which have now been controlled with phenytoin for over ten years. He holds a current driving licence renewed annually. He consults you with his wife who tells you that on four occasions in the past six months her husband had grand mal seizures whilst asleep at
Fig. I-Neurologists’ understanding of Driving Licence Regulations. Intervals refer to time when patients may resume driving, assuming no further seizures.
403
correspondence to neurologists and patients by the DVLC that patients may drive one year after a single seizure-advice that does not occur in the regulations-is illogical in the face
Fig. 2-Influence of abnormal EEG on advice given by neurologists about driving. have
myoclonic jerks within an hour of awakening or whilst nodding off to sleep. This is now his only symptom. (i) His EEG is now normal; when may he drive? (ii) His EEG continues to show 3 Hz spike-and-wave activity; when may he drive? As well as being asked when they thought the subject of each casehistory could become eligible to hold a driving licence under the regulations then currentl° (when the seizure-free period required was three years), the neurologists were asked to indicate their understanding of the regulations without referring to them. They were also asked when they would prefer each of these hypothetical patients to be allowed to drive, if this interval were different from
what they thought the
regulations required. RESULTS
130 neurologists replied, a response rate of 56%. Figs. 1 and 2 show the very considerable variation in their understanding of the regulations amongst neurologists. Similar variations occurred in the responses not shown here (these and the other case-histories sent out can be obtained from the authors). Although the neurologists were asked to express any preferences for duration of restriction they seemed satisfied with what they thought the regulations required. However, as the figures show, there were wide differences of opinion among neurologists and discrepancies between their interpretation of, and the apparent intent of, the regulations. 8, 10 DISCUSSION
Certain areas of confusion are obvious. The first seizure (fig. la).-After a first grand mal seizure, 12% of neurologists would allow the patient to continue driving, 27% would advise against this for one year after the seizure, and 28% for three years after the seizure. The regulations offer no comment about a first seizure. Current epidemiological definitions of epilepsy require "more than one non-febrile’ seizure". 7,11 One seizure is therefore not considered sufficient to justify a diagnosis of epilepsy. However, one study reported that the cumulative risks of recurrence after a first seizure are 16% after one year, 21% after two years, and 27% after three years. 12 In another study the recurrence rate was 15% in the first year and a further 20% in the second.13 The criteria for inclusion in these two studies were not identical. The advice often given in
of this evidence. The role of investigations.-Guidance proffered to us by the DVLC in respect of individual cases often refers to the normality or otherwise of investigations, a matter which is not mentioned in the regulations. Although Hauser and his colleagues’2 reported that seizures were more likely to recur in patients with generalised spike-and-wave abnormalities in the EEG, this is an unusual abnormality to find in those with epilepsy who are of an age to drive. Hauser et al. found no difference in recurrence rate between those with normal EEGs and those showing a focal abnormality. Although many British neurologists do not arrange an EEG after a first seizure, fig. 2 shows that some do take the EEG into account in other circumstances when advising about driving. Seizures precipitated by specific circumstances.-Is a single seizure precipitated by a tricyclic antidepressant epileptic or not? Fig. ld shows the wide range of interpretation by neurologists. What should be done if seizures recur on altering dosage of anticonvulsant drugs after a long seizurefree period? A strict interpretation of the new regulations would prevent driving for two years after a seizure that occurred soon after stopping or reducing anticonvulsant drugs. Fig. Ic shows that many neurologists took a more realistic line. We are informed that the DVLC will now allow a probationary period of 12 months after a single seizure if the patient has previously had five seizure-free years off anticonvulsants. This concession is not generally known because it has not been publicised; as neurologists interested in epilepsy, we discovered it only by chance. Sleep Mr.—Gibberd’ presented the cumulative risk of having a daytime seizure after a period of having seizures only whilst asleep, and the regulations are presumably meant to reflect this information. However, the wording of the regulations about epileptic attacks whilst asleep remains confusing. Take the situation of a single nocturnal attack occurring after a period of many years’ remission of seizures whilst awake. Can the patient drive now on the basis that the only attack he has had in the past three years has been whilst asleep; or can he drive in two years if he has no further attacks; or does he have to establish a new three-year history of asleeponly attacks? The old regulations were interpreted by the neurologists in either of two ways, nearly a third of all neurologists suggesting that the patient could continue
driving (fig. lb). In the absence of any published advice from the DVLC, doctors turn to quasi-official pamphlets such as that published by the Medical Commission on Accident Prevention.l5 The advice proffered seems to us to be often misleading, and to reflect only the views of the authors. It is, however, often interpreted as "the official view". It has been argued that since a doctor’s only obligation is to inform the patient of his duty to report his disability to the DVLC, he does not need to know what the regulations are, but patients naturally ask their doctors what they expect the DVLC’s ruling will be. It is churlish to refuse to reply, inadequate to plead ignorance, and positively harmful to give an inaccurate
reply. We believe that the situation could easily be improved by better communication. The advisory panel might usefully send all neurologists and neurosurgeons-if not all doctorsnotes of guidance about particular circumstances that we have discovered give rise to doubt. Difficult cases could still
404 to hospital. We have determined the frequency and of readmission to a modern geriatric medical unit to identify the problems and define the changes required in
be referred to the advisory panel, but the numbers would surely be reduced, and advice throughout the country would become more consistent. Above all, there is need for further studies of the risks of recurrence of seizures under various circumstances, so that the guidance given by the DVLC and its advisory panel may be more firmly based on fact.
people
Correspondence should be addressed to P. H., Department of Neurological Sciences, Royal Free Hospital, Pond Street, London NW3.
Details of all admissions, discharges, and deaths occurring in the four wards (one male; three female) of an 84-bedded geriatric medical unit at St Francis’ Hospital were analysed retrospectively each week during the year ending April 2, 1982. The age, sex, marital status, and nature of home support were noted for each patient. Case records were used to identify those who had been discharged from any hospital during the preceding twelve months, and the interval between discharge and readmission was noted. The reasons for readmission were determined (by H. G.) from information obtained from the patients, the hospital records, and individual medical, nursing, and remedial staff. Patients’ relatives and neighbours were also interviewed at the hospital when it was considered they could contribute helpful details. The patients were divided into two classes; class A patients had not been admitted to hospital during the preceding twelve months, and class B patients had been readmitted following discharge from a hospital in the King’s Health District at some time during the preceding twelve months. Thereclasses were compared to identify significant differences and to determine whether and how readmission could have been prevented. The readmitted patients were allocated to one of five groups according to the principal reason for readmission: group 1, unavoidable clinical deterioration; group 2, inadequate medical management; group 3, noncompliance of patient; group 4, social problems; and group 5, inadequate rehabilitation. Patients readmitted within two weeks of their previous discharge were studied separately. The frequency of readmission was also measured for each quarter to assess the effects of seasonal variations. The cumulative rate of readmission was determined for each group of patients. Statistical comparisons were made using the standard error of the difference between two means.
REFERENCES 1. Hormio A. Does
epilepsy mean higher susceptibility to traffic accidents? Acta Psychiatry Scand 1961; 150: suppl. 210-12. 2. Waller JA. Chronic medical conditions and traffic safety: review of the California experience. N Engl J Med 1965; 273: 1413-20. 3. Millengen KS. Epilepsy and driving. Proc Aust Assoc Neurol 1976; 13: 67-72. 4. Epilepsy International. Report of the Committee on Driving Licence Regulations in various countries (1980). Unpublished report. 5. Maxwell RDH, Leyshon GE. Epilepsy and driving. Br Med J 1971; 3: 12-15. 6. van der Lugt PJM. Is an application form useful to select patients with epilepsy who may drive? Epilepsia 1975; 16: 743-46. 7. Hopkins AP, Scambler G. How doctors deal with epilepsy. Lancet 1977; i: 183-86. 8. Statutory instrument 1982 no. 423. Road Traffic Act. Motor Vehicles (Driving Licences) (Amendment) (no. 3) Regulations (United Kingdom) 1982. 9. Editorial. Lancet 1980; i: 401. 10. Statutory instrument 1981 no. 952. Road Traffic Act. Motor Vehicles (Driving Licences) Regulations (United Kingdom) 1981. 11. Hauser BH, Kurland LT. The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967. Epilepsia 1975; 16: 1-68. 12. Hauser WA, Anderson VE, Loewnson RB, McRoberts S. Seizure recurrence after a first unprovoked seizure. 1982; 307: 522-28. 13. Cleland PG, Mosquera I, Steward WP, Foster JB. Prognosis of isolated seizures in adult life Br Med 1981; 283: 1364. J 14. Gibberd FB, Bateson MC. Sleep epilepsy, its pattern and prognosis. Br Med J 1974; ii: 403-07. 15. Medical Aspects of Fitness to Drive, 3rd ed. London: Medical Commission on Accident Prevention, 1976.
N Engl J Med
Hospital Practice CAN READMISSIONS TO A GERIATRIC MEDICAL UNIT BE PREVENTED?
HELEN GRAHAM
causes
patient care. PATIENTS AND METHODS
RESULTS
BRIAN LIVESLEY 617
Dulwich, London SE22 0SQ, and Department of Clinical Gerontology, St Francis’ Hospital, London SE22 8DF
Summary
During the year ending April 2, 1982, 153 patients readmitted to a geriatric
medical unit within twelve months of their previous discharge from any hospital in the district accounted for 24·8% of the 617 patients admitted. Readmission of the 153 patients was due to unavoidable clinical deterioration (32%), inadequate medical management (21%), non-compliance of patient (20·2%), social problems (18·3%), or inadequate rehabilitation (8·5%). Readmission could have been
prevented in 73 (47·7%) patients. These figures emphasise the importance of greater medical interest in the problems of the aged and support the need for a higher consultant/bed ratio in geriatric medical units to allow more effective management of patients aged 75 years and over. INTRODUCTION
DURING the past
decade, high-turnover geriatric medical
units have been increasing bed usage but despite this, the occupancy of non-maternity hospital beds by patients aged 75 years and over rose from 33% in 1973 to 39% in 1978. By the end of the century, however, the population aged 75 years and over will increase by 20%2 and place an even greater demand on the whole hospital service. One feature of this increasing demand is an apparently high rate of readmission of old
patients (220 men, 397 women; aged 59-101 years) admitted during the year. 464 patients (class A) were admitted for the first time and 153patients (class B) (24. 8% of all admissions; 56 men and 97 women) were readmitted. 106 patients had been discharged from the geriatric medical unit and 47 from non-geriatric wards. The period in which readmission was most likely to occur was two weeks after discharge; 43 of the 153 readmissions occurred within two weeks. The 49 patients (26 men and 23 women) in group 1 were admitted because of unavoidable clinical deterioration (a new medical event in 18, deterioration of an existing disorder in 19, and for terminal care in 12 patients who died from carcinoma or intractable disease within three weeks). 32 patients (10 men, 22 women; group 2) were admitted because of inadequate clinical management. In 17 the disorder was incompletely defined or controlled (e.g., Parkinson’s disease, falls). 6 patients had been discharged unwell (3 had exacerbation of existing bronchitis and 3 postoperative complications) and 2 with side-effects of drugs. In 2 cases drugs ordered by the consultant were not instituted by the junior medical staff and in a further 2 significant radiological evidence of bronchus carcinoma was overlooked. In 3 cases the general practitioner persistently refused to attend the patient. Of the 31 patients in group 3 (5 men, 26 women) 18 refused residential home or community services, 9 did not comply with therapy, and 4 discharged themselves from hospital. were