Attention Deficit Disorder in Children and Adults

INDEPENDENT STUDY IN PSYCHOLOGY

This paper was written in partial completion of an undergraduate seminar at the Department of Psychology, Trenton State College, Ewing, New Jersey.

Thomas Rue
December 1982.
All rights reserved.

Section One : TAXONOMY

The neuropsychiatric disorder now labeled "Attention Deficit Disorder" has historically born a number of different terms. In times past, a child of normal or above normal intelligence with a behavior and learning disorder might have been described as "brain-damaged," a Strauss child," a victim of the "hyperactive child syndrome" or "minimal cerebral dysfunction," hyperkinetic, "minimally brain damaged," or most recently, a child with "minimal brain dysfunction.'' 1

While much confusion arose from these highly disjunctive categories, most of which imply that damage to the brain is a central causal element, which has never been shown, actual prevalence of ADD in the preadolescent population has been estimated between 5% and 10%. 2

Furthermore, contrary to previous medical opinion, a number of studies have demonstrated that the syndrome persists through adolescence and into adulthood in approximately three-fourths of individuals diagnosed as "hyperactive children." 3

The new term, Attention Deficit Disorder, while eliminating the implication that all such symptoms are the consequence of brain damage, focuses on Just one attribute, attention deficit, which is difficult to quantify. Because of this, Wender has suggested that "we `discover' a short-named 18th-century physician who initially described MBD or something like it and let him (or her) achieve eponymic distinction." 4 Even if such a scientist could not be found, Dr. Wender goes on, "it might not be too immoral to invent one," if for no other reason than to provide a name for this very controversial syndrome which would not imply unsubstantiated causes or homogeneity.

Pointing to taxonomical weaknesses, Langhorne and Loney (1979) 6 found "extreme heterogeneity of behaviors" in victims of ADD, suggesting that the condition be broken down on the basis of aggressive and hyperactive behaviors:

1. Aggressive-Hyperactive

2. Exclusively Aggressive

3. Exclusively Hyperactive Residual State

The distinctions were supported by the Loney, et al. (1978) lows HABIT project (Hyperkinetic/Aggressive Boys in Treatment), a comprehensive longitudinal investigation of the hyperkinetic/MBD/ADD syndrome. 7

Another subgroup of ADD was identified by Theodore S. Fremont (1977) in his Informal Diagnostic Assessment of Children:

Hypoactivity is much less common in the case of MBD, although it is frequently identifiable in clinical settings. It is characterized by a child with very sluggish and delayed motor movements and may strike the examiner as the direct opposite of a hyperactive youngster. These children have sometimes been confused with such labels as withdrawn, depressed, or absorbed in their own private world. 8

When the APA finally published its own set of labels, revising the outdated DSM II, in 1980, they simplified (perhaps too much so) the condition, specifically recognizing only three subgroups:

1. ADD With Hyperactivity (DSM III 314.01)

2. ADD Without Hyperactivity (DSM III 314.00)

3. ADD, Residual Type (DSM III 314.80) 9

When it comes to real people and real cases, however, diagnosis and treatment are seldom so clear-cut. Because ADD children are often the subjects of ridicule, the adult frequently has a poorly defined body image as a part of his/her self-concept. 10 Interacting with this are the actual symptoms of the disorder, sometimes leading to (1) coexistent psychopathology of a more serious nature, or (2) clinical misdiagnoses ranging from schizophrenia, aphasia, dyslexia or dyscalcula, to emotional disturbance or personality disorders, particularly "paranoid" or "passive-aggressive.'' 11 It is not uncommon for ADD victims to develop an adaptive reaction-formation resulting from their obvious lack of organizational skills, sometimes even overcompensating for the organic deficiency, perhaps exhibiting characteristics of the so-called "obsessive-compulsive" personality.

The inexcusable frequency of neuropsychiatric diagnostic error has recently been pointed out by Robert S. Hoffman (1982). In a study of 215 consecutive patients admitted over a 15-month period to a specialized medical-psychiatric inpatient unit, "thorough neuropsychiatric evaluation resulted in a therapeutically important alteration of the referring diagnosis in 41% of the cases! 13 There is little doubt that further reevaluations of this type, on a larger scale, would result in massive deinstitutionalization of long-term mental patients with maladies no more serious than adulthood ADD, or even more condemning of the medical profession, patients whose maladaptive behavioral symptoms are solely the result of toxic reactions to prescription drugs which were unwarranted in the first place.

Along these same lines, considerable research has been conducted by Leopold Bellak and others with respect to a possible familial relationship between incidence of ADD and schizophrenia, demonstrating a high positive correlation between the two among immediate families. 14 Similarly, certain forms of epilepsy 15 and episodal behavioral disorders have also been linked to ADD/MBD, 16 similar symptoms sometimes resulting in clinical confusion and misdiagnosis. If the theses of these and other researchers are correct, a significant portion of chronic mental inpatients are actually victims of Attention Deficit, and with appropriate treatment, could be restored to their places as productive members of society.

Section Two : Etiology

Despite the numerous theories which have been advanced, relatively little has been conclusively determined about the origins and causes of the ADD syndrome. This has long been a basis for criticism by skeptics such as educator John Holt, 17 and a few humanistically oriented clinicians 18 who dispute the validity of a medical model in explaining behavior.

At the other end of the theoretical spectrum are those physicians who would apparently like to see the majority of psychotherapists, analysts, and clinical counselors put out of business. This position is well summarized by the following statement:

In facing the puzzle of mental illness, psychiatric savants of the first half of the twentieth century believed that Freudian theory would provide the answers. However, in the second half of the century, scientific research has uncovered evidence that biological malfunctions are central to mental illness and that much of the by now entrenched psychodynamic theory is irrelevant or even misleading. 19

In contrasting these opposing perspectives, I prefer to take an interactionalist view. While many psychiatric problems, ADD for example, begin as purely perceptual or otherwise organic syndromes, they are frequently exacerbated by phenomenological, interpersonal, and social factors, including the very act of clinical labeling. 20

Dr. Leopost Bellak has published on the subject of subjective perceptions, "distorted" or otherwise, experiences, and environmental phenomena which influence the person who is attention deficit, and how these factors effect the nature of the syndrome. 21

The first predisposer of adulthood ADD is the presence, diagnosed or not, of the condition in childhood. Tautological as it may sound, this is among the central diagnostic criteria listed in DSM III, which states that onset must have been before age seven in order for the label to be appropriate.

Theories of central nervous system (CNS) determinants which have been advanced include ineffective neurotransmission:

Although its etiology is unknown, adoption studies have indicated that there is a hereditary predisposition to ADD. Preliminary investigations in animals and man have suggested that defects in CNS neurotransmitter function, particular dopamine, may play a causal role in the genesis of ADD symptomatology 22

According to this theory, decreased dopamine levels result in inhibition of the reticular activating system, as well as in limbic system dysfunction. Reticutar inhibition, in turn, leads to improper levels of arousal dysfunction of sensory processes. These defects, or decreased functioning, manifest themselves in poor concentration and memory, and other problems of a cognitive nature. RAS inhibition may also act reflexively as an organic defense against the limbic overload described above. 23

As an interesting side note, Wender has suggested a possible relationship between the dopaminic causal elements of Parkinson disease and ADD (in Bellak, 1979, pp. 185-186.)

Since a function of the limbic system is to organize and regulate sensory and emotional input, in concert with higher cerebral centers of conscious thought and behavior processes, instability in this area may lead to sensory overload, mood instability, episodic dyscontrol, violence, or even manic-depressive or schizophrenic psychoses. Failure to stabilize this weakness could lead to spiraling difficulties, increased overload and behavioral outbursts, and further reticular inhibition, perpetuating the cycle. 24

Environmental theories include prenatal brain hypoxia, 25 "genetic and/or embryological damage (perhaps due to such factors as maternal malnutrition during pregnancy), and theories of acquired damage due to impoverished sensory and cognitive during infancy," 26 as well as the effect of certain food additives. 27

In summary, an HEW "Caring About Kids" publication has this to say about the origins of ADD:

The exact origin of the hyperkinetic behavior syndrome is unknown -- no single cause has been established. The disorder has been ascribed to genetic, biological, physiological, social, and environmental factors.

Although there are many theories about the causes, hard evidence is scarce. For example, there is little evidence to support the theory of brain damage as a major cause. Since research has shown that the parents of some hyperkinetic children were themselves hyperkinetic, it may be that certain children inherit a predisposition for hyperkinesis. Other possible causes cited by various investigators include food additives, radiation leaks from television sets or fluorescent lights, lead poisoning, vitamin deficiencies, and complications of pregnancy, including premature birth. Other investigators attribute hyperkinetic behavior to parent-child relationships or to classroom teaching techniques. Others theorize that the disorder develops only from a combination of certain genetic, environmental, or neurological or biochemical contributors. 28

Section Three : DIAGNOSIS

Accurate diagnosis of ADD depends on a variety of measurement instruments and neurological signs. Ordinarily, the clinical interview will reveal such factors as the patient's presenting complaint and/or reason for evaluation (e.g., ineffective job or school performance; hyperactivity; inability to concentrate; etc.), dominant behavioral traits, level of social interaction with peers and with authority, presence or extent of drug and/or alcohol (ab)use, and a variety of other items.

Retrospective questionnaires are also used to determine the subjects' childhood and developmental histories and behavioral traits.

"Hard" neurologic signs having "anatomic localizing value or indicative of] specific lesions... [and] consist of... lateralizing cranial nerve findings, pathologic reflexes, unilateral sensory deficits and movement disorders, and unequivocal abnormal electroencephograms." 29

Research by Dr. Peter Mueller and his associates, under sponsorship of the Temple University Thrombosis Research Center, has also established a relationship between platelet defects, especially in females and prepubescent boys, resulting in increased sensitivity to bruising. One theory for the sex/age distinction is based on testosterone levels, which in post-pubescent males counteracts the platelet secretion deficiency.

* * * Twelve patients with attention deficit disorder who had platelet function studies showed platelet aggregation defects...

This platelet secretion defect, which was reversed by Ritalin™ (methylphenidate) in the six patients who were restudied has not been described for any other medical disorder, said Dr. Mueller of the Princeton (N.J.) Medical Center.

The 12 patients were Dart of a group of 30 patients with attention deficit disorder seen by Dr. Mueller in his practice; 24 bruised easily and had done so for years. * * *

Patients with attention deficit disorder may have membrane release defects in cells other than platelets, such as nerve cells containing neurotransmitter granules. An analogous neurologic membrane release disorder might therefore produce many of the impairments seen in attention deficit disorder, he said.

The therapeutic effect of Ritalin™ in attention deficit disorder may be to facilitate membrane release of neurotransmitters. 30

It should be kept in mind, however, that the absence of any of these so-called "hard" neurologic signs does not in itself rule out the presence of the ADD syndrome, either in children or in adults.

"Soft" neurologic signs, on the other hand, are defined as "signs indicative of nonlocalizing or diffuse dysfunctions." 31 Although such "equivocal" measures as finger approximation, walking a straight line, lateral winking, lateral eye jerking, etc. have been strongly disputed, 32 presence of other "soft" signs remain standard indicators of the presence of ADD.

Wechsler scales have long been used in diagnosis and formulation of"explanatory hypotheses about the nature of hyperactivity and offers direct information for remedial interventions" specifically appropriate for the individual.33 Other tests variously include the Halstesd-Reitan Neuropsychological Battery, Ravens Progressive Matrices, the Bender Visual Motor Gestalt Test, Aphasia Screening, Thematic Apperception Test (TAT), and other standard psychometric devices which measure behavior and cognitive aspects of the person. Personality screening by such instruments as the Minnesota Multiphasic Personality Inventory (MMPI) could also be appropriate, in order to rule out other psychopathology. Typical characteristics of ADD could include any of the following:

a. Disorganization
b. Distractability
c. Perseveration
d. Attention to trivia
e. Figure-ground confusion
f. Impulsivity
g. Disinhibition
h. Hyperactivity
i. Overly-concrete thinking
j. Low attention span 34
k. Emotional lability
l. Poor response to discipline 35
m. Learning difficulties
n. Hypoactivity
o. Interpersonal difficulties
p. Episodic behavioral outbursts 36
q. Low self-image/confidence
r. Poor spatial orientation
s. Uncoordination (gross motor skills) 37

Dr. Leopold Bellak has described the symptomatology of ADD in the following terms:

Pathogenically, MBD usually involves problems of spatial orientation, the development of language, and a low external and internal stimulus barrier. These cortical problems can lead to problems of establishing self-boundaries and coordination, to feelings of perplexity, difficulties with the written and spoken word and abstract conceptualization poor impulse control and defenses, overload by external stimuli, and resulting disorganization. These phenomena in turn cause secondary emotional problems, especially during the school years...

Therapeutically, energizers, together with diphenylhydantoin, at times in combination with lithium are often useful.

Psychotherapy must include education concerning MBD and must deal with the primary and secondary cognitive and emotional aspects of MBD as well as other problems. 38

Part Four : THERAPY

The primary element in the treatment of almost any psychological problem is, first, for the subject to recognize that s/he has the condition, and then to understand the nature of the limitations it places on him/her, and what can be done to extend those limits. The practitioner's initial task, then, before drug therapy is even begun, is to educate the patient with respect to the nature of ADD.

The diagnosis and handling of MBD is indeed bound to increase rather than ease the problems of doctor and patient alike, to begin with because the diagnosis is by nature presumptive and therefore easy to minimize or disregard...

Patients should be helped to recognize cognitive and physical limitations, not in order to excuse them, but so as to become more objective about them and apply themselves to a treatment plan that requires remedial learning and better emotional adaption. Patients should be impressed with the treaters' determination not to allow them to deny their difficulties in exchange for their help, love, and respect... 39

Once the patient is aware of the organic limitations inherent to the syndrome, Dr. L. Eugene Arnold suggests "cultivating the placebo effect." In his words, "One of the therapeutic qualities that medication shares with other interventions is that of the placebo effect -- changing negative expectations to positive expectations end placebo benefit by specific, concrete, honest descriptions of the expected benefits." 40

Dr. Arnold goes on to say that the patient should be informed of the typical side-effects of the medication. In the case of psychostimulants, s/he should expect to lose appetite, possibly become irritable and depressed for a while, and possibly have trouble sleeping. Possession of this information not only makes the unpleasant aspects of the treatment more acceptable, Arnold says, but "it also tends to make them reinforcers of the positive expectations. When the predicted side effects occur, they confirm the credibility of the doctor who also predicted the benefits: 'The medicine is working just like the doctor said it would.'"

While opinions may vary as to the ethics and honesty of Arnold's procedure as described above, the placebo effect is doubtless an element of the efficacy of drug therapy.

Which particular drug to use will depend largely on the individual, but numerous double-blind trials have conclusively demonstrated the efficacy of amphetamines and other stimulants. 41

Although concern has been expressed that children treated with such agents would develop later drug-abuse pattern, 42 justify this fear. 43

In order to further prevent the misuse of "controlled dangerous substances" such as Ritalin™ (TM), Dexedrine (TM), and other amphetamines and sympathomimetic amines, in the State of New Jersey the Board of Medical Examiners issued a Ruling in 1979 which outlawed the prescription or dispensation of any such drugs, except:

1. For the treatment of:

i. narcolepsy;

ii. hyperkinesis;

iii. drug-induced brain dysfunction;

iv. epilepsy;

v. depression shown to be refractory to other therapeutic modalities; or
2. For the differential diagnostic psychiatric evaluation of depression; or
3. for the clinical investigation of the effects of such drugs.

In view of these controls and of the drugs' efficacy, at least on a short-term basis, added to the fact that there are no known lasting side-effects to any of the traditional stimulants, perhaps with the exception of Tegretol™ (TM) (carbamazpine), 45 such therapy is certainly warranted in some, if not most, cases of ADD.

One remaining question, however, involves whether psychostimulant therapy is effective over a long period. although the ethical problem of constructing a methodologically acceptable control group (maintaining a patient on a placebo or a nonresponder on meditation for months or years) prevents rigorous analysis, studies indicate that stimulants' efficacy does not decline over years of use. For this reason, it has been found that stimulant therapy may be continued from childhood, through adolescence, and into adulthood, without any harmful results.

Not only is the belief that ADD disappears when adolescence occurs, according to numerous researchers, false; but again contrary to popular belief, stimulant medication retains its "paradoxical effect" for ADD adults. 46

With respect to duration of treatment, Arnold says: "In most cases the period of drug therapy should not be considered indefinite. It would ordinarily be considered a temporary facilitation of the individual's ability to make use of other resources in adapting and compensating. 47

Based on the studies cited here and elsewhere, it seems that psychostimulants deserve an integral part in the treatment of ADD, along with educational measures, and possibly some behavior modification techniques.

If the attention deficit child or adult is assisted in overcoming his or her difficulty, or at least made aware of its presence, the individual has a very good change of leading a normal, well-adapted life. To illustrate, Dr. Peter S. Mueller, whose work has been cited herein, himself a victim of the syndrome, gave the following response to Who's Who In America when asked for "some thoughts on my life:"

For some, a hyperactive learning disorder is a curse that hobbles them throughout life; but, for others, including myself, this disorder has become a somewhat uncomfortable and bewildering spur for lifelong compulsive puzzle-solving. This bittersweet mandate has produced the original, serendipitous, and occasionally disconcerting ideas which have marked my life. 48

Like most things in life, ADD is what the person makes it, and limits him or her only to the extent that s/he is willing. Drug therapy, however, by correcting a basic organic deficiency, frees the individual to expend energy in other important areas of personal growth.

Footnotes

1. Bennett A. Shaywitz, MD: Davis J. Cohen, MD; and. Sally E. Shaywitz, MD: "New Diagnostic Terminology for Minimal Brain Dysfunction," Journal of Pediatrics, Vol. 95, No. 5, part 1, November 1979, pp. 734-736.

2. David R. Wood, MD; Frederick W. Reimberr, MD; Paul H. Wender MD; and Glen E. Johnson, MD: "Diagnosis and Treatment of Minimal Brain Dysfunction in Adults," Archives of General Psychiatry, Vol. 35, December 1976, pp. 1453-1460.

3. Paul H. Wender, MD: "The Concept of Adult Minimal Brain Dysfunction," in Psychiatric Aspects of Minimal Brain Dysfunction in Adults, Leopold Bellak, ed.: Grune & Stratton, Inc., New York, 1979, pp. 1-12. (Cf. W. Mendelson & N. Stweart: "Hyperactive Children as Adolescents: A Followup Study," Journal of Nervous Mental Disorders 153:273-279, 1971, in which 77% had difficulty with concentration; 71% continued to be overactive; and 74% were impulsive.)

4. Ibid., p. 2.

5. Loc. cit., ADD was portrayed at least as early as 1845 in "Fidgety Philip" (Struwwelpeter, Literanseag Anstalt, Frankfort, Germany). See Mary Carpenter: "Hyperkinesia Said to Persist in Adulthood," Medical Tribune, Vol. 21, No. 36 (12 November 1980), pp. 1, 12.

6. John E. Langhorne, Jr., PhD, and Jan Loney PhD: "A Four-Fold Model for Subgrouping the Hyperkinetic/MBD Syndrome," Child Psychiatry and Human Development, Vol. 9, No. 5, 1979, Human Sciences Press, pp. 153-159.

7. Jan Loney, PhD; Robert J. Prinz, EdS; Joel Mishala, MD; and Jesse Joad, MD: "Hyperkinetic/Aggressive Boys in Treatment: Predictors of Clinical Response to Methylphenidate," American Journal of Psychiatry, Vol. 135, No. 12, Dec. 1975, pp. 1487-1491.

8. Theodore S. Fremont, EdD; David M. Selfart, EdD; and John H. Nilson, EdD: Informal Diagnostic Assessment of Children, Charles C. Thomas, publisher, SprLngfield, Ill., 1977, p. 76.

9. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Washington, PC, APA, 1980, pp. 4l-45.

10. Leopold Bellak, MD: "Psychiatric States in Adults With Minimal Brain Dysfunction," Psychiatric Annual, Vol. 7, Mo. 11, November 1977, pp. 575-58Q (581). (Cf. Bellak, 1979, op. cit., pp. 73-101.)

11. Loc. cit.

12. "Link Brain Dysfunction, Obsessive Compusive Disorder in Children," Clinical Psychiatry News, Vo. 10, RIo. 11, November 1982, pp. 1, 27. (See also DSM III 301.40. )

11. Robert S. Hoffman, MD: "Diagnostic Errors in the Evaluation of Behavioral Disorders," Journal of the American Medical Association, Vol 248, No. 8, 27 August 1982, pp. 964-967, end editorial comment on p. 977.

11. See, for example, Leopold Bellak and Edward Charles: "Schizophrenic Syndrome Related to Minimal Brain Dysfunction: A Possible Neurologic Subgroup," Schizophrenia Bulletin, Vol. 5, No. 3, 1979, pp. 480-489.

15. David Beor, MD: "The Significance of Behavioral Change in Temporal Lobe Epilepsy," McLean Hospital Journal, June 1977, pp. 9-21, and David C. Taylor: "Epileptic Experience, Schizophrenic and the Temporal Lobe," Ibid., pp. 22-58.

16. Russell R. Monroe: "Episodic Behavioral Disorders: An Unclassified Syndrome" in American Handbook of Psychiatry, Vol III, chapter 11, Basic Books, Inc. 1977, pp. 237-254.

17. John Holt: "Quackery," The New York Review of Books, 15 August 1970.

18. Edward T. Ladd, "Pills for Classroom Peace?," Saturday Review, 21 November 1970.

19. Paul H. Wander, MD and Donald F. Klein, MD: "The Promise of Biological Psychiatry," Psychology Today, February 1981, pp. 25-41 (26).

20. Sheryl Young; Bob Algozzine; and Rex Schmid: "The Effect of Assigned Attributes and Labels on Children's Peer Acceptance Ratings," Education and Training of the Mentally Retarded, December 1979, pp. 257-261.

21. Bellak (1977), op. cit.

22. Peter S. Mueller, MD; Kazuo Keike, MD; A Koneti Rao, MD; George Christine, PsyD; and Holm Holmsen, PhD: "A Platelet Secretion Defect in Attention Deficit Disorder," presented at meetings of the American Psychosomatic Association, Cambridge, Mass, March 1980; and the 8th International Congress on Thrombosis and Haemostasis, Toronto, Ontario, July 1980, published by Thrombosis Research Center, Temple University, Philadelphia.

2A. Loc. cit.

25. H. A. Handford: "Brain Hymonia, MD, and Schizophrenia," American Journal of Psychiatry, Vol. 152, pp. 192-194, 1975 (cited in Bellak, 1977, op. cit.)

26. Thorne Shipley, PhD: "Intersensory Evoked Cortical Responses in Learning Disability of Diffuse Origin (So-Called Hyperactivity and/or the Minimum [sic] Brain Dysfunction Syndrome)" in Sensory Integration in Children, Charles C. Thomas, publisher, Springfield, Ill., 1980, pp. 72-75.

27. National Institute of Allergy & Infectious Disease, and National Institute of Child Health & Human Development (cosponsors): "Consensus Conference: nefined Diets and Childhood Hyperactivity," Journal of the American Medical Association, Vol. 248, No. 3, 16 July 1982, pp. 290-292.

28. U. S. Dept. of Health, Education & Welfare; Public Health Service; Alcohol, Drug Abuse, and Mental Health Administration; Nationa1 Institute of Mental Health: Caring About Kids: Helping the Hyperactive Child, U.S. Government Printing Office, Washington, D. C. 1978, pp. 3-4.

29. Gary J. Tucker: "Sensorimotor Disturbances in Psychotics, 1979, op. cit., pp. 127-136 (129).

30. International Medical News Service, "Platelet Abnormality Identified in Attention Deficit Disorder is Reversed by Ritalin™," March 1980.

31. Tucker, in Bellak (1979), loc. cit.

32. Randall N. Foster, MD; Lionel Margolin, MD; Charles Alexander; Oscar Benitez; and Fred Carr: "Equivocal Neurological Signs, Child Development, and Learned Behavior," Child Psychiatry and Human Development, Vo. 9, No 1, Fall 1978, pp. 28-32.

55. Richard S. Milich, PhD and Jan Loney, PhD: "The Factor ComFosition of the WISC for Hyperkinetic/MBD Males," Journa1 of Learning Disabilities, Vo. 12, No. 8, August 1979, pp. 67-71 (68).

3A. Claudette Stock, MA: MBD Child: Some Clinical Manifestations; Definitions; Descriptions and Remediation Approaches; Pruett Publishing Co., Boulder, Colo., 1969, pp. 14-31.

35. Jonathan O. Cole, MD: "Drug Therapy of Adult MBD," McLean Hospital Journal, Vol. 3, No. 1, 1978, pp. 37-46 (37).

36. Paul H. Wander, MD: Minimal Brain Dysfunction in Children, Wiley-Interscience, Inc., New York, 1971.

37. Bellak (1977), op. cit., p. 581.

38. Bellak & Charles (1979), op. cit., p. 1 (abstract).

39. Peter Hartocollis: "MBD in Young Adults," in Bellak (1979), op. cit., pp. 103-111 (111).

40. L. Eugene Arnold: "Medicating Adults With MBD," in Bellak (1979), op. cit., pp. 177-184 (181).

41. Mottimer D. Cross, MD: "A Comparison of Dextro-Amphetamine and Racimic-Amphetamine in the Treatment of the Hyperkinetic Syndrome or Minimal Brain Dysfunction," Diseases of the Nervous System, January 1976, pp. 14-16.

James A. Lewis, MD and Rosemarie Young, MD: "Deanol and Methylphenidate and Hyperactivity: Fffects on Teacher Behavior," Science, Vol. 208, 13 June 1980, pp. 1280-1282.

Timothy M. Rivinus, MD: "Psychiatric Effects of the Anticonvulssnt Regimens," Journal of Clinical Psychopharmacology, Vol. 2, No. 3, pp. 165-192 (174-175).

42. Ladd (1970), op. cit.

43. Leah Beck, Mr; William S. Longford, MD; Mary MacKay, Mr; and Grace Stun, MSW: "Childhood Chemotherapy and Later Drug Abuse and Growth Curve: A Follow-up Study of 30 Adolescents," American Journal of Psychiatry, Vol. 123, No. 4, April 1975, pp. 436-458.

44. State of New Jersey, Department of Law and Public Safety, Division of Consumer Affairs, Board of Medical Examiners, "Rule on the Uses of Amphetamines and Sympathomimeticamines - Effective March 21, 1979."

45. Personal communication, Anne L. Kruger, PhD to Dr. Sidney A. Wolfe, Health Research Group, Washington, DC: Kendell Park, NJ, December 1982, (9 pp. with attachments) charging that "There have already been at least one and perhaps two actual suicides attributable to "toxic" reactions to Tegretol™ (TM), A Ciba-Geify, Inc. product.

46. Virginia Snodgrass Cowart: "Stimulant Therapy for Attention Disorders," Journal of the American Medical Association, Vol. 248, No. 5, pp. 279-287 (284).

47. Arnold, in Bellak (1979), op. cit., p. 183.

48. Peter S. Mueller, MD: "Thoughts on My Life," a one-paragraph holographic mss., 15 October 1981, submitted for publication in Who's Who in America, Marquis Who's Who, Inc., Chicago, 42d ed. (1982-1983).

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