a short attention span.the most com¬ mon symptoms of hyperactivity.may also signal insufficient stimulation. Children who receive little personal at¬ tention from ...
The hyperactive child A number of those who have been con¬ cerned with the emotional health of children and families have stressed the contribution the child makes through his inborn behaviour patterns to diffi¬ culties that develop between him and his environment. For example, Thomas,
Chess and coworkers1'2 have found that specific temperamental traits of very young children are reasonably good predictors of later adjustment to developmental demands made by peer in¬ teraction, school and early adolescence. The use of diagnostic terms such as hyperactivity or minimal brain dysfunc¬ tion, or both, supports this view. These terms
suggest a condition, present early
in life, that is possibly related to some type of brain damage and hence rather resistant to traditional environmental manipulation. The recent publicity about the efficacy of certain drugs in the treatment of hyperactivity and other behaviour disorders in children has underscored pharmacologic management of troubled children, which has placed behaviour problems in a more tradi¬ tional medical context. In fact, an in¬ creasing number of children presenting with various behaviour disorders are now treated with stimulant drugs by pediatricians and general practitioners. This is a laudable development, for the family physician should be concerned with both the physical and emotional aspects of a child and his family. Yet all too often these practitioners see be¬ haviour. disorders as conditions that can be alleviated by medication, often given in an arbitrary dose without regular supervision, together with superficial reassurance to the family. This ap¬ proach denies some essential steps necessary for the treatment of any child at odds with his environment. Physicians are well trained to obtain histories about physical symptoms from their patients and are aware of the pitfalls of this approach. A developmental or behavioural history, however, re¬ quires different precautions. Parents are generally reliable when they de¬ scribe the child's present behavioural symptoms in the home, but they are poor in recalling past events and quite inaccurate when asked to specify perinatal events on which basis the diagno¬ sis of hyperactivity is often made.3 They often also do not know how the child behaves in school. Hence, any psychologic history should include in¬ formation, preferably from the teacher of the child, asking specifically about problems in attention and learning, peer relationships, aggressivity and overt shyness. (Children who do well in school
but poorly at home or vice versa should generally not be treated with psychopharmacologic drugs because their problem is most likely purely psycho¬ logic.) The majority of children who have difficulties with the world around them are not primarily hyperactive but are reacting to an environment that does not provide them with the necessary ingredients for their development. An understanding of these developmental needs can only be gained when we as¬ sess the total life-space of a child, which includes school, family and the child himself. For example, general aimless overactivity, impulsiveness and a short attention span.the most com¬ mon symptoms of hyperactivity.may also signal insufficient stimulation. Children who receive little personal at¬
tention from their environment and
get much of their entertainment from
watching television are often bored and become restless, impulsive and aggressive. These children most often need people whom they can trust, ra¬ ther than drugs. Children under the age of 5 years, regardless of activity level, should only in very exceptional circumstances receive stimulants, for they are usually very amenable to en¬
vironmental
of titrating medication against symptom relief is to begin with 10 to 20% of the maximum dose of the drug of choice and increase the dose by the same amount each day until the target symp¬ toms (e.g. hyperactivity, impulsivity and a short attention span) are controlled. Once this is achieved without undue side effects, remedial help in school and counselling of the family may be initiated. If possible all medication should be discontinued or at least de¬ creased during weekends and holidays. This prevents possible habituation and permits maximum symptom control with minimum drug dosage. There is one final area of concern. Some children who seem genuinely hy¬ peractive do not respond to stimulant medication. Weiss compared children who had received long-term drug treat¬ ment with those who had been on med¬ ication for less than 4 months. The majority of children in the latter group either had not responded to the drug or had side effects necessitating discon¬ tinuation. This raises the question as to what extent hyperactivity is indeed a homogeneous symptom related to uni¬ form cerebral dysfunction. An increas¬ ing number of investigators believe that there are various forms of hyperactivity, only some of which will respond to sti¬ mulant medication. Conners5 has iden¬ tified certain subgroups of hyperactive children with the help of extensive psy¬ chologic tests, whereas others6 have used special electroencephalographic techniques to predict drug reactors. The problem all these approaches share is their need for a technologic approach. This makes them of little use to the
manipulation. important treatment for any truly hyperactive child consists of the relationships offered him by his environment. The main purpose of any drug is to enable a child to use these relationships more effectively. The behavioural changes induced by drugs make it easier for us to teach a youngster a skill such as reading and qualities such as compassion and respect practising physician. How then can we solve the dilemma for others' rights that he needs to cope with his world, for he can now sit and of potentially overprescribing stimulants listen to us and is not out of his chair to a vast segment of our population? We must first of all agree on the speci¬ or the classroom every 2 minutes. In this issue of the Journal (page 159) fic symptoms that constitute the "hy¬ Weiss and her colleagues show convin- peractivity".and a recent unpublished cingly that medication alone, even if study has shown that pediatricians and given for several years, does not bring teachers in a good-sized Canadian city about a basic change in the behaviour reached virtually no agreement on any of hyperactive children. This confirms symptom of hyperactivity. Teachers stressed the short attention span and previous work of the same group.4 The maintenance dose of any psy¬ restlessness of the children; physicians chiatric drug must be determined with thought learning problems and intel¬ great caution. The majority of hyper¬ lectual immaturity were the most con¬ active children respond to rather low sistent symptoms of the group. We must turn away from outcome doses of methylphenidate (5 to 10 mg/ day) or an appropriate equivalent. There studies that give us the percentages of is no evidence whatsoever that daily children whose condition was improved doses exceeding 50 mg of methylpheni¬ or unimproved by treatment with a date (or 25 mg of dextroamphetamine specific drug over a certain period and or 150 mg of chlorpromazine) will help begin to observe more closely hyperac¬ those children who have not responded tive children in their natural interacto less. The most advantageous method tions with peers and adults. This will The most
130 CMA JOURNAL/JANUARY 25, 1975/VOL. 112
allow us to specify much more accurately the effect a hyperactive child, receiving medication or not, has on his environment; it is to be hoped that it will also help us to bring about a "good fit" between the child and his world, a fit that will serve his needs to develop and provide him with a future he can look forward to.
KLAUS K. MINDS, MD, ntcp[c] Department of psychiatry
The Hospital for Sick Children, Toronto, Ont.
J Psychiatry 110: hyperactive child. factors associated Child Neurol 10:
651, 1964 VI. Prenatal and paranatal with hyperactivity. Dev Med 355, 1968
3. MINDS K, WEBB G, SYKES D: Studies on the
4. MINDE K, WEISS G, MENDELSON N: A 5-year
References I. THOMAS A, CHESS 5, BIRCH HG: Temperament
and Behaviour Disorders in Children. New York, NYU Pr, 1968 Temperamental characteristics in infancy and later development of behavioural disorders. Br
2. RUTTER M, BIRCH HG, THOMAS A, et al:
follow-up study of 91 hyperactive school dren. I Acad Child Psychiatry 11: 595, 5. CONNERS KC: Psychological assessment of dren with minimal brain dysfunction. NY Acad Sci 205: 283, 1973
chil1972 chilAnn
6. SATTERFIELD JH, Lsssut LI, SAUL RE, et al:
EEG aspects in the diagnosis and treatment of minimal brain dysfunction. Ibid, p 274
Antihistamines and gastric acid secretion To the chagrin of therapists, the conventional antihistamine drugs fail to inhibit histamine-stimulated gastric acid secretion and are therefore of no value in the treatment of peptic ulcers. They also fail to antagonize the action of histamine in increasing heart rate and in inhibiting contractions of the rat uterus. It is believed that they act only on certain receptors now known as H1-receptors. The other receptors, refractory to conventional antihistamines, have been termed H2-receptors, and some antihistamine drugs act as competitors at the IL-receptor sites. Among these agents, metiamide, with good oral activity, has aroused interest. Details of pharmacology and toxicology of metiamide have been described at a recent symposium1 on 112-histamine receptor antagonists and by Brimblecombe, Duncan and Parsons.2 And in this issue of the Journal (page 203) Badley discusses the role of histamine H2-receptor antagonists in the medical management of acid-pepsin disease. Metiamide inhibits gastric acid secretion; almost certainly it acts as an antagonist at IL-receptors. Studies in human volunteers confirmed that metiamide was effective, when given either intravenously or into the intestine by nasogastric tube, in inhibiting maximum gastric acid secretion induced by infusing histamine. The effect on pepsin concentration was marginal *but inhibi-
tion of acid secretion and total acid output was significant. Mainardi and colleagues3 have studied 17 patients with duodenal ulcers; they reported details of basal and peptonemeal-stimulated gastric acid secretion. Single oral doses of 100, 200 or 300 mg of metiamide, as well as placebo, were used to study acid secretion. All the patients were males; they had uncomplicated duodenal ulcers and the level of acid secretion decreased significantly after institution of therapy. Basal acid secretion decreased by 80% after 200 or 300 mg, and stimulated acid secretion decreased by over 80% after 300 mg. The latter type of inhibition correlated better with peak blood concentrations of the drug than with the ingested dose. Inhibition persisted for 2 hours in both types of study. (Other observers have suggested inhibition continues for even longer.) Although this drug might represent an interesting approach to the treatment of peptic ulcer, there is one potential danger: a communication from Smith, Kline and French has reported transient agranulocytosis in two patients on chronic therapy, and Brimblecombe's group2 noted the same side effect in dogs, although the agranulocytosis found in one animal was readily and repeatedly reversible on withdrawal of metiamide treatment. A witty editorial by Ingelfinger sum-
marizes the present position, as a follow-up to a commentary by Code.5 Code was excited at hearing of the discovery of H2-histamine receptors and agents that could inhibit gastric secretion by blocking them. As Ingelfinger rightly points out, many doctors and patients were equally jubilant because they were weary of the present unsatisfactory regimens for the treatment of duodenal ulcer. So stagnant, wrote Ingelfinger, is the art of duodenal ulcer care that any development holding promise of a new approach is eagerly grasped; this has been the reason for the temporary and quite illogical enthusiasm for certain bizarre therapies in the past. Until metiamide has been more fully investigated for its long-term effects on the bone marrow we must restrain our jubilation at finding at last a remedy that may truly help those who suffer from peptic ulcer. References 1. Hoon CJ, SIMKINS MA (eds): International Symposium on Histamine H2-Receptor Antagonists. Weiwyn Garden City, England; Smith, Kline and French, 1973 2. BRIMBLECOMBE RW, DUNCAN WAM, PARSONS
ME: Pharmacology and toxicology of metiamide, a histamine He-receptor antagonist. S Afr Med J 48: 2253, 1974
3. MAINARDI M, MAXWELL V, STURDEVANT RAL,
et al: Metiamide, an Ha-receptor blocker, as inhibitor of basal and meal-stimulated gastric acid secretion in patients with duodenal ulcer. N Engi J Med 291: 373, 1974 4. INOELFINGEIt FJ: Unrefined antihistamine lode (editorial). Ibid, p 413 5. Coia CF: New antagonists excite an old histamine prospector (editorial). N Engi I Med 290: 738, 1974
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