Diovol Forte AntacidlAntiflatulent COMPOSITION DIOVOL FORTE SUSPENSION Each 5 ml contains: Aluminum hydroxide equivalent to dried 300mg gel Magnesium hydroxide.300mg Simethicone.40 mg pH:7.5-8.5 ACTION Both aluminum and magnesium hydroxides are non-systemic antacids. They neutralize gastric contents but do not tend to cause systemic alkalosis. Simethicone is an inert compound with antifoaming action which helps dispel gas trapped in mucoid foam in the stomach and bowel. "In vitro" studies show that DIOVOL FORTE Suspension has a duration of buffering action of more thin 90 minutes within an optimum pH of 3.0 to 5.0. The ingredients are not absorbed into the bloodstream to any extent. Excretion is via the feces. INDICATIONS DIOVOL FORTE is indicated whenever an antacid-antiflatulent agent might bring relief of symptoms, as, for example, in the symptomatic treatment of peptic ulcer, g.i. hyperacidity, heartburn and g.i. distress and discomfort caused by gas retention. CONTRAINDICATIONS In patients severely debilitated or suffering from renal impairment. In cases of distention due to complete or partial intestinal obstruction. PRECAUTIONS Because DIOVOL FORTE interferes with the absorption of tetracycline, concomitant use should be avoided. Protect Suspension from freezing. ADVERSE REACTIONS None repQrted. POISON CONTROL No cases of poison with DIOVOL have been reported. Symptoms of Overdosaqe: In the presence of renal insufficiency, accumulation of magnesium in the circulation may cause ONS depression. Prolonged use may lead to phosphorus deficiency in the presence of a low phosphorus diet. Treatment of Overdosage: Symptomatic. DOSAGE AND ADMINISTRATION One to four teaspoonsful 3 times daily 20 to 60 minutes after meals or as required for relief. SUPPLY Suspension: Bottles of 341 ml

*H.R.R

the need to ensure that they were protected from these risks. At each stage in this sequential process, programs were refined progressively to meet the needs of the changing situation. The medical profession has met each new challenge as it has arisen by providing the basic scientific information required to authenticate the need for more modern programs. The evidence now accumulating that so many disease processes are environmental in origin poses a still greater challenge for the profession in both research and practical patient care. Incorporation of counselling in regard to productive lifestyles is now becoming a key component of the patient-physician relationship. Since prevention of disease is

always more effective and desirable than its treatment, this challenge may in the long run turn out to be the most important. Nowhere is the need more apparent than in the matter of smoking and disease. Active support by the medical profession for the objectives of the National Education Week on Smoking would therefore seem reasonable and worthy of encouragement. NORMAN C. DELARUE, MD Canadian Medical Association representative Canadian Council on Smoking and Health

References 1. Canadian Trends in Smoking Related Diseases: Lung Cancer Mortality, tech rep ser no 3, research bureau, nonmedical use of drugs directorate, health protection branch, Health and welfare Canada, Ottawa, July 1976

Electroconvulsive therapy today Throughout medical history physical measures such as bleeding, purging, water therapy and surgical procedures have been used to treat mental disorders. Some, such as suffocating the mad ideas by ducking,1 have died by attrition, while others (insulin coma therapy, for example) have been dispatched following trials of treatment. The only persistent and commonly used physical "procedure" remaining in psychiatry is convulsive therapy. Synonyms for this treatment are shock therapy, electroshock and electroconvulsive therapy (ECT) or electroshock therapy (EST) since convulsions are usually induced by electricity rather than the older methods of injection or inhalation. Originally the reasoning behind such treatment was based on the observation that epilepsy and schizophrenia were rarely seen together; epileptic fits therefore somehow prevented psychotic illnesses. This proved to be a false observation but it encouraged clinicians to induce fits in schizophrenic patients, eventually in 1938 by means of electricity.2 The apparent success of the treatment led, in the 1940s and 1950s, to its extravagant use and it became prescribed for almost all psychiatric disorders. In time, though, clinical sense prevailed and efforts have been directed towards determining the symptoms and illnesses most responsive to this treatment.

8 CMA JOURNAL/JANUARY 7, 1978/VOL. 118

Carney, Roth and Garside3 showed that some of the features of severe affective disorders, such as weight loss, motor retardation, pyknic build, early morning wakening and a short history of illness, were related to the best outcome at follow-up. Mendels4 found a family history of depression and somatic delusions also to have a good prognosis.. At present, ECT is prescribed mostly for manic-depressive or bipolar and unipolar affective disorders and, to a lesser extent, for the schizoaffective and catatonic forms of schizophrenia. While ECT is not generally used to treat the thought disorder and perceptual abnormalities of schizophrenia, it is sometimes used as a last resort. Indeed, one follow-up study suggested that schizophrenic patients treated with ECT did at least as well as those receiving drug therapy.3 Persons with neurotic, personality and addictive disorders should not receive ECT. The effectiveness of ECT has been examined in many controlled trials,6 and this treatment is now used to shorten the illness episode rather than act as a prophylactic agent. As a result of the use of ECT and antidepressant drugs there has been an extraordinary change in the natural history of the affective disorders. A trial carried out by the Medical Research Council showed that ECT seemed especially effective for depression in women, was more effective and faster acting than

some antidepressant drugs and shortened the hospital stay.7 Formerly the average duration of an attack of mania or depression was 6 months or more, most patients had more than one episode and there was a substantial hospital mortality due to suicide and cardiovascular and intercurrent diseases.8 Although the importance of ECT in reducing the suicide rate is unknown,9 recently it was shown that the general death rate was lower among persons with affective disorders treated with ECT than among similar persons not receiving adequate antidepressant treatment.10 ECT is now akin to a minor operation, with the very low mortality and morbidity associated with such a procedure. After providing written consent the patient fasts overnight and is given in the treatment room a short-acting anesthetic agent (for example, sodium thiopental administered intravenously) and a neuromuscular blocking agent (for example, succinylcholine). The patient is well ventilated before and after the seizure, which is induced when an electrical current is passed for a fraction of a second. In the recovery room the patient usually awakens within 10 minutes and is ambulant in 30 minutes. Treatment for both inpatients and outpatients is given three times a week. The only absolute contraindications to ECT are brain tumour, recent cerebrovascular accident and recent myocardial infarction. The cerebral effect of ECT remains conjectural but the idea that the treatment merely blocks out unpleasant memories has been discarded. Ottosson11'12 argued, from a psychophysiologic perspective, that electrical seizures have a specific effect on depression and specific effects on the central nervous system since ECT is better than any other treatment for endogenous depression. The antidepressant effect of ECT is better than any other of its effects (e.g., antipsychotic and antimanic) and it is not bound to or dependent on an "organic.. effect. Ottosson believed that the antidepressant effect, which is seizure-related, and the memory disturbance, which is seizure- and current-related, are not associated. Furthermore, he argued that there is no memory disturbance from antidepressant drugs and no antidepressant effect from other memory disturbing agents. The antidepressant effect, then, is thought to involve the hypothalamic area, and the memory disturbance (diminished retention) the hippocampal-mammillary system. The electroencephalogram after ECT shows bilateral synchronous slow waves that may involve brain stem structures. Since these waves do not appear with antidepressant drug therapy, they are

regarded as side effects of the treatment. The improvements in sleep, appetite, weight, menstruation and libido after ECT reinforce the idea that this treatment affects the diencephalic centres. Kety,13 arguing from a neurochemical perspective, suggested that the treatment produces changes in cerebral protein synthesis or biogenic amine concentrations, and that this process takes place over time. Antidepressant drugs, which are alleged to influence brain metabolism of biogenic amines, take several weeks to have an effect. Accordingly, for ECT treatments to be effective they may have to be given over several weeks. Efforts have been made to maximize the benefits and reduce the unpleasant effects. Several treatments a day, socalled regressive ECT, produce an acute organic brain syndrome and is to be avoided. Multiple monitored ECT14 - that is, inducing several fits at one time with forced oxygenation and electroencephalographic and electrocardiographic monitoring - is a procedure that is practised in parts of the United States and is still under review. It is not clear whether the central nervous system processes involved in the treatment of depression can be accelerated. The memory complications have been approached by modifying the electrical current and the position of the electrodes. The least amount of electrical energy should be used to induce a fit and this is achieved by varying the duration and intensity of the stimulus. For a reduction in the amount of electrical energy but sufficient stimulation the current should be in a pulse wave-form. Some manufacturers have recently introduced this facility in their machines. Sine-wave stimulus and the so-called glissando technique are now outmoded. Unilateral ECT, given to the nondominant hemisphere, was introduced almost 20 years ago by Lancaster, Steinert and Frost,15 and increasingly sophisticated studies have shown it to be as effective as bilateral ECT but with much less memory loss.16 Retrograde amnesia is produced by ECT, and memory consolidation is affected, but Squire and Chace17 have demonstrated from follow-up study that this is more of a subjective than an objective problem for patients. The evidence demonstrating permanent brain damage due to ECT is lacking. What evidence has been put forward has been based on animal work and current strengths far greater than are used in clinical practice. A recent study on cerebral atrophy and chronic schizophrenia,18 indeed, showed that, in contrast to patients treated with ECT, those untreated tended to have enlarged ventricles. Despite better understanding of ECT

and improved techniques, this treatment has become increasingly criticized by the lay public and action groups. By frying calves' brains with electrical currents in supermarkets, action groups have hoped to make the public antagonistic towards ECT, although these groups do not seem to have the same concern about cardioversion. Movies such as "One Flew Over the Cuckoo's Nest" have shown ECT as it was given 20 years ago and have helped to disseminate ill-founded propaganda. Legislation involving the use of ECT has been made much tighter in several American states and in Alberta. ECT has stood the test of time during the past 40 years, however, and is one of the best treatments in medicine if given appropriately. In a variety of Toronto hospitals we have found that it has been prescribed for about 6% of the total psychiatric inpatient population and about 20% of the inpatients with affective disorders (unpublished data, 1977). ECT has an established place in the management of affective disorders, particularly when the patient is agitated, physically run down or suicidal, or fails to respond to antidepressant drug therapy. It has an important place in the management of affective disorders in the elderly, owing to the relative safety of the procedure compared with the cardiotoxic risks of tricyclic antidepressant drugs.19 The future use of ECT will be based on increased knowledge of the psychobiologic aspects of the affective disorders. Clinicians should concentrate on the optimal use of ECT rather than be distracted by polemics about whether the treatment is barbaric or harmful. M.R. EAsrwooD, MD, FRCP[C], FRC PSYCH S. STIASNY, B SC, MBA Measurement in psychological medicine section Clarke Institute of Psychiatry Toronto, Ont. References I. VAN HELMONT F: quoted by HUNTER R, MACALPINE I (eds): 300 Years of Psychiatry,

1535-1860, London, Oxford U Pr, 1963, p 254 2. CERLETTI U, Bmts L: L'elletroshock. Arch

Gen Neurol Psichiatr Psicoanal 19: 266, 1938

3. CARNEY MW, ROTH M, GARSIDE RF: The diagnosis of depressive syndromes and the prediction of E.C.T. response. Br J Psychiatry

111: 659, 1965 4. MENDELS J: Electroconvulsive therapy and depression. III. A method for prognosis. Ibid. p 687 5. MAY PRA, TUMA AH, YALE C, et al: Schizo-

phrenia - follow-up study of results of treatment. 11. Hospital stay over two to five years.

Arch Gen Psychiatry 33: 481, 1976 6. BLACHLY PH (ed): Some controlled studies on convulsive therapy. Convulsive Ther Bull 1:

3, 1976 7. Clinical trial of the treatment of depressive illness. Report to the Medical Research Council by its clinical psychiatry committee. Br Med 1 1: 881, 1965

8. MAYER-GROSS VV, SLATER E, ROTH M (eds):

Clinical Psychiatry, 3rd ed, London, Baillihre, 1969 9. EAsrwooo MR. PEACOCKE J: Seasonal patterns of suicide, depression and electroconvulsive therapy. Br J Psychiatry 129: 472,

1976

10. AVERY D, WINOKUR G: Mortality in depressed patients treated with electroconvulsive therapy and antidepressants. Arch Gen Psy-

chiatry 33: 1029, 1976

CMA JOURNAL/JANUARY 7, 1978/VOL. 118 9

(beclomethasone 11. Orrossot'i JO: Psychological theories of ECT: a review. Psychological or physiological theories of ECT. mt J Psychiatry 5: 170, 1968 12. Idem: in Psychobiology of Convulsive Therapy, FINK M, Ks'r. S. MCGAUGH 3, et al (eds), New York, Halsted Pr, 1974, p 19 13. KETY SS: Effects of repeated electroconvulsive shock on brain catecholamines. Ibid. p 231 14. BLACHLY PH (ed): Multiple monitored ECT: (MMECT). Convulsive Therapy Bulleiin with Tardive Dyskinesia Notes 1: 23, 1976

15. LANCASTER NP, STEINERT RR, FROST I: Unilateral electro-convulsive therapy. I Ment Sci 104: 221, 1958 16. D'ELIA G, RAOTMA H: Ts unilateral ECT less effective than bilateral ECT? Br I Psychiatry 126: 83, 1975 17. SQUIRE LR, CHACE PM: Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 32: 1557, 1975 18. CRow TJ, JOHNSTONE EC: Cerebral atrophy and cognitive impairment in chronic schizophrenia (C). Lancet 1: 357, 1977 19. MoIR DC, CROOKS J, SAWYER P, et al: Car-

diotoxicity of tricycic antidepressants. Br I Pharmacol 44: 371P, 1972

Medical education in Afghanistan It is difficult sometimes for a physician with a background in North American medicine to appreciate fully the priorities in health care delivery necessary in developing nations. The need for, and yet the fiscal impracticality of, such a basic necessity as a potable water supply for all the citizens of such countries, so recognized by the 1976 United Nations Habitat Conference in Vancouver, exemplifies the widespread deficiencies in health care in these countries and underlines the small offerings that most Canadian physicians are prepared, by experience, to give these nations. At the same time, because of, or coincident with, these deficiencies in basic public health measures, illnesses that can better be managed with the help of sophisticated clinical skills do occur. It is because of this that many Canadian physicians offer their clinical or teaching skills to programs established by various organizations operating throughout the world. In the Islamic Republic of Afghanistan, a land-locked country in central Asia (population, approximately 15 million) the size of Alberta, Care! Medico established in 1961 a postgraduate teaching program in medicine and surgery. The permanent team now includes five Canadians: two physicians, a surgeon and two nurses. With an expenditure of less than $200 000 per year plus donated supplies and skills, a clinical service for medicine and surgery has developed that is probably the best in the country, and it trains most physicians in these specialties. There have been 25 graduates from the postgraduate training program in surgery and 30 graduates from the program in medicine. Of these graduates 22 now are serving in provincial hospitals.1 Comparable service and teaching units in pediatrics and ophthalmology are supervised by a team from India and the international Afghan Mission (a Christian organization), re-

spectively. The Care/Medico teaching program depends to a large degree on visiting specialists from Europe, Australia and North America, more than 200 of whom have participated since 1965. The trainees are English-speaking graduates from the two medical schools in Afghanistan, chosen by the Ministry of Health and assigned to the programs on the basis of their rank in competitive examinations. Both medical schools now have exclusively Afghan faculty. The newest school, at Ningrahar University in Jalalabad, initially had the help of American faculty members. The older school, at Kabul University, was founded in 1932 with the help of a Turkish medical mission. From 1947 to 1963, French teachers were prominent in the faculty and many of the present Afghan faculty were trained in France. From 1938 to 1974, 1195 physicians graduated from Kabul University and in 1975 the 1st-year class in medicine totalled 210 students. It is estimated that there are 1600 physicians in the country, 170 of whom are women, and that 400 to 500 live in the city of Kabul. There is little or no immigration of physicians into the country and permission for them to leave the country for even brief visits is difficult to obtain, especially if their compulsory military service has not been completed. Hence, under present conditions the development of medical and surgical skills in Afghan graduates depends on the teaching teams now resident in the country and, to a large degree, upon visiting volunteer teachers. Adaptation to the limited patient-care resources and support services available in Afghanistan is difficult and extremely challenging. Infectious diseases such as tuberculosis, hepatitis, gastrointestinal infections, malaria and trachoma are very common. It has been estimated that the mortality in the first 5 years of life outside Kabul approaches 85%.

10 CMA JOURNAL/JANUARY 7, 1978/VOL. 118

Beconase Nasal Spray Prescribing information indications and clinical uses Beconase is indicated for the treatment of perennial and seasonal allergic rhinitis unresponsive to conventional treatment. Contraindications Active or quiescent tuberculosis or untreated fungal, bacterial and viral infections. Children under six years of age. Warnings In patients previously on high doses of systemic steroids, transfer to Beconase may cause withdrawal symptoms such as tiredness, aches and pains, and depression. In severe cases adrenal insufficiency may occur, necessitating the temporary resumption of systemic steroids. The safety of Beconase in pregnancy has not been established. If used, the expected benefits should be weighed against the potential hazard to the fetus, particularly during the first trimester of pregnancy. Precautions The replacement of a systemic steroid with Beconase has to be gradual and carefully supervised by the physician. The guidelines under "Administration" should be followed in all such cases. Unnecessary administration of drugs during pregnancy is undesirable. Corticosteroids may mask some signs of infection and new infections may appear. A decreased resistance to localized infection has been observed during corticosteroid therapy. During long-term therapy, pituitary-adrenal function and hematological status should be periodically assessed. Fluorocarbon propellants may be hazardous if they are deliberately abused. Inhalation of high concentrations of aerosol sprays has brought about cardiovascular toxic effects, and even death, especially under conditions of hypoxia. However, evidence attests to the relative safety of aerosols when used intranasally and with adequate ventilation. There is an enhanced effect of corticosteroids on patients with hypothyroidism and in those with cirrhosis. Acetylsalicylic acid should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. Patients should be advised to inform subsequent physicians of the prior use of corticosteroids. During Beconase therapy, the possibility of atrophic rhinitis and/or pharyngeal candidiasis should be kept in mind. Adverse reactions No major side effects attributable to Beconase have been reported. Occasional sneezing attacks have followed immediately after the use of the intranasal aerosol. A few patients have complained of burning sensation and irritation in the nose after Beconase nasal inhalation. When patients are transferred to Beconase from a systemic steroid, allergic conditions such as asthma or eczema may be unmasked.

Dosage and administration The usual dosage for

patients of all ages who received no previous systemic steroid is one application (50 mcg of beclomethasone dipropionate) into each nostril three to four times daily. Maximum daily dose should not exceed twenty applications in adults and ten applications in children. If Beclovent is used concurrently, the maximum dose of each aerosol is ten applications in adults and five applications in children. Beconase should not be used under six years of age. Since the effect of Beconase depends on its regular use, patients must be instructed to take the nasal inhalations at regular intervals and not, as with other nasal sprays, as they feel necessary. They should also be instructed in thecorrect method, which is to blow the nose, then insert the nozzle firmly into the nostril, compress the opposite nostril and acuate the aerosol while inspiring through the nose, with the mouth closed. In the presence of excessive nasal mucus secretion or edema of the nasal mucosa, the drug may fail to reach the site of action. In such cases it is advisable to use a nasal vasoconstrictor for two or three days prior to Beconase. Careful attention must be given to patients previously treated for prolonged periods with systemic corticosteroids when transferred to Beconase. Initially, Beconase and the systemic corticosteroid must be given concomitantly, while the dose of the latter is gradually decreased. The usual rate of withdrawal of the systemic steroid is the equivalent of 2.5 mg of prednisone every four days if the patient is under close supervision. If continuous supervision is not feasible, the withdrawal of the systemic steroid should be slower, approximately 2.5 mg of predriisone (or equivalent) every ten days. If withdrawal symptoms appear, the previous dose of the systemic steroid should be resumed for a week before further decrease is attempted. Dosage form Beconase is a metered-dose aerosol, delivering 50 micrograms of beclomethasone dipropionate with each depression of the valve. There are two hundred doses in a container. Official product monograph on request.

Allen & Hanburys A Glaxo Canada Ltd. Company Toronto, Canada