Hyperkinesis revisited

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PEDIATRICS Vol. 61 No. 2 February 1978 319 COMMENTARIES

Hyperkinesis

revisited

Four decades after Bradley’s introduction of amphetamines for the treatment of childhood behavior disorders1 and two decades after the

confirmation of his clinical observations by

placebo-controlled trials, there is an ongoing debate about the effectiveness of stimulants, the indications for their use, whether hyperkinetic behavior disorder is a syndrome, and what

infer-ences can be made about its cause. The paradigm of the double-blind trial was correct as far as it went, but it has become evident that it did not go far enough; that is, there is no reason to doubt the repeated demonstration of symptomatic benefit

in the four to eight weeks of experimental studies, but investigators were slow to appreciate the long-term nature of the clinical problem. It had been widely assumed that, because clinicians had observed an age-related deciease in the

overactiv-ity, the principal therapeutic task was to help the child through the years prior to adolescence.

Furthermore, since attention span did increase

during drug treatment in the short run, it was expected that this would be reflected in better learning over the long run. Systematic follow-up studies have dashed those fond hopes. Though overactivity does diminish with age, it remains a problem for some youngsters; worse than that, cumulative school failure, behavior problems, and low self-esteem are serious problems for more.2’3 Clearly, stimulants are not enough and it remains unclear what is.

At the same time, the diagnosis of hyperkinesis

has become all too fashionable and the prescrip-tion of drugs almost a reflex response by the

harrassed practitioner. Because there are no pathognomonic laboratory findings and because

the behaviors in question differ more in quantity than in quality from normal behaviors, the very existence of hyperkinesis as a medical disorder has

been criticized as but another example of the “medicalization of deviance.”4

It is in this climate that the articles by Miller and by O’Leary and Peiham in this issue (pages

217 and 211) take on particular significance. The

first makes the case that the condition is overdiag-nosed, argues that it is an emotional disorder

rather than a result of brain dysfunction, and

reports poor outcome despite therapeutic efforts.

The second describes a behavior modification program that yields short-term symptomatic

results fully as good as those obtained with stimulants, yet without the risk of drug toxicity. The two articles are by no means in full agree-ment and a few words of commentary may be in order from a reviewer who recommended the publication of both, despite his reservations about each.

Dr. Miller demonstrates that clinical acumen in pediatric practice, when combined with syste-matic review of accumulated experience, can make a significant contribution to our

under-standing. Almost 12% of the children in his

practice had been “diagnosed” by a teacher, a psychologist, or another physician as overactive, but in only a quarter of these (or just under 3% of his patient population) was the diagnosis warranted. Some might demur that we have only his judgment to rely on for the distinction between true and false cases. I disagree. Because the children were and remained his patients, he was able to follow their course; if he erred, the

error would come home to roost. (This is in sharp

contrast with the experience of the consultant [like myself] who renders an opinion without either the opportunity or the necessity to live with the consequences of that opinion.)

In Miller’s experience, the families of the true

hyperactive patients were characterized by

concealed anger, an unwillingness to acknowl-edge their role in the genesis of the problem, a

refusal to follow through on psychological

inves-tigations, and a pattern of going from agency to agency without telling one that another was at work. Over a follow-up interval of six years, he

reports an outcome even more forbidding than the earlier accounts. His article adds valuable

data to existing information on the nature and the

course of the syndrome.

I am less persuaded by his contention that hyperkinesis is an “emotional problem” and that it overlaps with “childhood depression.” While I

agree that the customary attribution of

hyperki-nesis to “minimal brain dysfunction” is far too facile, I do not see much to be gained by relabeling it as an emotional disorder which is generally held to mean psychogenic and/or

psychodynamic. Both labels betray an either/or

view of the nature-nurture question. Whether we call the intrinsic factor “temperament,” “devel-opmental lag,” or even “cerebral dysfunction,” it

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320 HYPERKINESIS REVISITED

seems clear that some predispositions intrinsic to

the child interact with particular features of the social environment to give rise to the deviant behavior that makes a given child a patient and not the siblings. Indeed, several studies have shown a greater frequency of minor physical

anomalies (which arise early in intrauterine

devel-opment) in hyperkinetic children, both those in a normal nursery and those referred for treatment.6 Little is added by calling overactivity a

“depres-sive equivalent.” The family histories of

hyperki-netic children do not show the expected excess of depressed members7; to argue from drug effects

(

more precisely, from drug labeLs) is of dubious legitimacy. Similar “logic” has been used to term

enuresis a depressive equivalent on the ground

that tricyclic antidepressants are effective (though only in the short run) in its treatment. By extension, the bell and pad that work so much better for enuretics than tricyclics must have an even more powerful “antidepressant” mode of action. The line of argument is simply irrelevant. Both the stimulants and the tricyclics have too wide a range of pharmacologic actions to allow us to infer the crucial site of action in one disorder on the basis of what may seem to be true in

another.

O’Leary and Peiham do not contest the exis-tence of the syndrome nor do they deny the short-term efficacy of stimulants. Rather, they are concerned with establishing that a

nonpharmaco-logical treatment, behavior modification, brings about the same benefits without the attendant

risks. They make a persuasive case. Having first

shown that stimulant drugs did in fact produce a

significant decrease in directly observable tar-geted behaviors in their patients, they were

successful in introducing behavioral means for bringing about equivalent gains. What merits

emphasis in their study is the use of behavioral methods carefully tailored to the characteristics

of the individual child. An additional virtue of

their approach is the extent to which parents and teachers become cotherapists, thus confronting directly the problem of parental uninvolvement which Miller has highlighted. Of course, the

sample is small and selected; one is uncertain how many of the families in Miller’s practice would

have invested the effort required of the partici-pants in the Stony Brook trial.

The O’Leary and Peiham study, like the other

reports of behavior modification in the literature,

suffers from the very same restrictions that proved so serious a flaw in the drug studies, namely, a focus on symptoms, a time-limited

(

four-month) course, and a failure to measure

academic progress directly. Critics of behavior modification have questioned whether children

learn more than to sit still and keep quiet,

whether the results generalize into other

situa-tions, and whether they are durable after the

training program is discontinued.8’9 These are all important issues that must await longer-term studies. For the moment, the evidence is persua-sive that behavior modification, intelligently applied, can reduce symptoms that are disruptive in the classroom and at home. There ought to be a considerable benefit to the child who no longer suffers social disapprobation. But “ought to be” is not the same as “is”; the data have yet to be provided. The cost (and consequent lack of

avail-ability) of behavior therapy in many communities

remains a problem for the practitioner who wishes to prescribe it; and, like all therapies, it

requires motivation to ensure cooperation, no

small difficulty in many families.

Amid the controversies and uncertainties, what clinical posture is appropriate for the pediatri-cian? The evidence on the long-term course of children with hyperkinetic behavior syndrome indicates clearly that this is not a transient

developmental disturbance nor a matter of child-hood exuberance. It warrants continuing pedi-atric concern and surveillance akin to that provided in epilepsy or obesity. Parents require support, guidance on the management of a diffi-cult child, and counseling to deal with complex

family feelings. Remedial education must be

viewed as the central component in care. Behavior modification and/or stimulant drugs can be useful adjuvants in treatment but do not

suffice in themselves.’0 There is at least initial

evidence from a one-year follow-up that a combined (“multimodal”) treatment approach can be effective in mitigating academic failure,

delinquent behavior, and psychological malad-justment (J.H. Satterfield et al., unpublished data).

In the continuing search for a better under-standing of the nature of the problem, and for more effective ways of managing it, pediatricians are urged, as James Miller has done, to put pen to paper and share their clinical experience with their colleagues.

LEON EISENBERG, M.D.

Children’s Hospital Medical Center

300 Longwood Avenue Boston, MA 02115

REFERENCES

1. Bradley C: The behavior of children receiving benze-dnne. Am I Psychiatry 94:577, 1937.

2. Weiss G, Minde K, Werry JS, et al: Studies on the

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PEDIATRICS Vol. 61 No. 2 February 1978 321

hyperactive child: VIII. Five year follow-up. Arch

Get, Psychiatry 24:409, 1971.

3. Mendelson W, Johnson N, Stewart MA: Hyperactive

children as teenagers: A follow-up study. I Nerv

Ment Die 153:273, 1971.

4. Eisenberg L: Psychiatry and society: A sociobiologic synthesis. N Engl I Med 296:903, 1977.

5. Waldrop M, Pedersen F, Bell R: Minor physical anom-alies and behavior in preschool children. Child Dee

39:391, 1968.

6. Rapoport JL, Quinn P0, Lamprecht F: Minor physical

anomalies and plasma dopamine-beta-hydroxylase in hyperactive boys. Am I Psychiatry 131:386,

1974.

7. Stewart MA, Morrison JR: Affective disorder among the relatives of hyperactive children. I Child Psychol

Psychiatry 14:209, 1973.

8. Winet RA, Wikler RC: Current behavior modification

in the classroom: Be still, be quiet, be docile. IAppl

Behav Anal 5:499, 1972.

9. Sherman JA, Bushell D: Behavior modification as an educational technique, in Horowitz FD (ed):

Review of Child Development Research 4. Chicago, University of Chicago Press, 1975, pp 409-462. 10. Eisenberg L: The clinical use of stimulant drugs in

children. Pediatrics 49:709, 1972.

Use of pneumococcal

vaccine

in children

A 14-type pneumococcal polysaccharide vac-cine has been licensed for use in the United States (Pneumovax, Merck & Co., Inc.). Although there are more than 80 immunologically distinct capsular types of pneumococci, the strains incor-porated into the vaccine have been responsible for approximately 80% of the cases of serious pneumococcal disease in the United States in

recent years. The vaccine should be of value for

selected children at risk for severe or

life-threat-ening disease due to the pneumococcus.

Pneumococcal vaccines have been used since the turn of the century. In 1914, Sir Almroth Wright0 and colleagues reported favorable results of a whole cell vaccine administered to gold

miners in South Africa. ‘ Subsequently, Francis

and Tillett2 and Finland and co-workers3 explored

#{176}Wrightwas the director of the Inoculation Department at St. Mary’s Hospital in London and a good friend of George Bernard Shaw. Shaw used Sir Almroth as the model for the leading character, Sir Colenso Ridgeon, in The Doctor’s

Dilemma. The play was published in 191 1 and is remarkably contemporary in discussions of medical ethics, use of vaccines, and the role of humoral and cellular factors in immunity.

the immunogenicity of type-specific pneumo-coccal polysaccharides. These investigations led to development of vaccines prepared from purified polysaccharide materials. In 1945,

MacLeod et al.4 reported the efficacy of a

four-type polysaccharide vaccine in prevention of type-specific pneumonia in military personnel. The success of this study stimulated preparation of two vaccines for the civilian population soon

after the end of the war. With the introduction of

penicillin, however, physicians showed little interest in the vaccines. Because of limited use, the vaccines were withdrawn from the market by the manufacturer.

In recent years, Austrian has advocated the need for a pneumococcal vaccine in populations at risk for severe disease due to this organism. Following Sir Almroth Wright’s lead, Austrian returned to South Africa and demonstrated in a

series of clinical trials the efficacy of multitype

vaccines in prevention of pneumococcal pneumo-nia. Radiologically confirmed pneumococcal pneumonia caused by types present in the vaccine was reduced by more than 80%. In one trial using a tridecavalent vaccine, an 82% reduction occurred in cases of pneumococcal bacteremic infection caused by types in the vaccine; ten cases occurred among 3,957 vaccinees and 1 17 cases

occurred in 8,035 controls. Dr. Austrian estimates

that more than a half million people have received a pneumococcal vaccine in the past 60

years. However, there is no estimate of how many

of the recipients of vaccine have been children. The currently licensed pneumoccal vaccine contains purified polysaccharide antigens of the 14 types of pneumococcus most frequently asso-ciated with disease in adults and children. These

types are 1, 2, 3, 4, 6 (6A), 9 (9N), 12 (12F), 14, 19

(19F), 23 (23F), 25, 51 (7F), and 56 (18C). (The capsular designations are listed by the American

system of typing with the Danish types listed in

parentheses.) A 0.5-ml dose contains 50 tg of each poiysaccharide type dissolved in isotonic saline solution containing 0.25% phenol as a preserva-tive and is administered subcutaneously or intra-muscularly. The vaccine is well tolerated. Chil-dren who received the vaccine had some pain, erythema, and induration at the site of injection and a small number had a minimal elevation in temperature. No significant reactions have been noted in children.’

Each antigen produces a satisfactory, indepen-dent antibody response in the majority of adults, and protection against infection develops in about two weeks. In adults, persistence of antibody was demonstrated to persist at half the peak titer for

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1978;61;319

Pediatrics

Leon Eisenberg