The primary physician is frequently requested to aid in diagnosis and treatment of children with manifest learning or behavior problems in school. This article is an attempt to clarify the physician's role and to offer some practical suggestions for fulfilling that role with his young patients.
Ideally, the pediatrician should review school progress and adaptation during the child's annual checkup, since early recognition and intervention may prevent serious handicaps from developing. Usually, the child is referred by the school for a neurologic or a psychiatric examination. The parent may be confused or alarmed by the recommendation and may anxiously ask, "What is wrong with my child?" Sometimes a worried or angry parent brings the child because the school threatens to hold him back a grade or to expel him from class. Increasing numbers of parents seek advice about their children because of sensitizarion to the plight of the hyperactive and learning-disabled child from the news media and from preschool teachers or learning-disability specialists who screen children for perceptual deficits and maladaptive behavior.
Since the specific difficulties and reasons for referral are often unclear at the initial visit, it is imperative to obtain complete information from the school personnel detailing their concerns about the child and their expectations of the physician's role in evaluation and treatment. The teacher, principal, guidance counselor, and psychologist may not be sure what they want from a physician. By training, many accept the myth that if "organicity" is suspected as a cause for the child's learning or behavior problems, he must be examined by a neurologist for possible brain damage. Unfortunately, many school systems still require a neurologist or a psychiatrist to certify a child as "neurologically impaired" or "emotionally disturbed" before he can receive special education. Others are now willing to design programs to fit the child's educational needs, special or not, but wisely refer children in whom they suspect an underlying medical or emotional problem. Children are also often referred for medication when they are unmanageable or are inattentive in class.
The pediatrician should become familiar with the educational system in his community, including the educators' tolerance for variation among children, the expectations for academic and social achievement, the viewpoint towards special education, and the availability and methods of special education. The interested physician can educate school personnel regarding his own role; counsel the parents and school as to the nature of a child's problems; aid in treatment of the child with medication, suggest modification of the environment, and refer to other appropriate agencies for counseling or therapy; and join parents in demanding appropriate remediation facilities from the board of education.
Parents and teachers seek a diagnostic label. While labels can be helpful in describing a syndrome or defining a problem, they are unfortunately also used as a comforting, easy explanation or as an entrance pass to or excuse for placement in a special program for children with school difficulties. A label is probably necessary; but in counseling parents and teachers, it is important to clearly state both what it means and what it does not imply.
The most common diagnostic label applied to children referred to child guidance centers for school-related behavioral difficulties is minimal brain dysfunction, or minimal cerebral dysfunction. It covers 5 to 15 per cent of schoolchildren who are described as showing learning disabilities, hyperactivity, or both.1 Minimal brain dysfunction was defined in 1966 by a national task force as descriptive of "children of near average, average, or above average intelligence with certain learning and/or behavioral disabilities ranging from mild to severe which are associated with deviations of function of the central nervous system. These deviations may manifest themselves by various combinations of impairment in perception, conceptualization, language, memory and control of attention, impulse or motor function."2
A 1969 task force amended the definition to exclude children with social, cultural, or emotional difficulties, mental retardation, gross neurologic impairment, or visual or hearing defects and children whose education has been inadequate.3 Most nonmedicai and many medical persons use the term interchangeably with "minimal brain damage" or even "neurologically impaired." Historically, the "brain damage syndrome" was described in children with known brain insults, such as encephalitis or head trauma, who, although of normal intelligence, displayed hyperactivity, emotional lability, impulsiveness, and perceptual dysfunction requiring special education. Some educators still refer to this symptom complex as the "Straussian syndrome," since it was well described by Strauss and his coworkers in the 1940s.4,5 They also described minor neurologic abnormalities in children after the age of 10. Later many children were identified with similar symptoms but without a history or examination compatible with brain damage. The term "dysfunction" was therefore used, usually assuming that the child had acquired damage to areas of the brain that was not extensive enough to produce gross neurologic signs but did produce cognitive, perceptual, and/or coordination disturbances.
There is no evidence that children fitting the task force description of minimal cerebral dysfunction are "brain damaged" or are in any way "neurologically impaired."6 These children form a heterogeneous group in which the behavior is the final common pathway for the expression of diverse causes. Genetic factors may be important. In gathering family histories, it is interesting to find parents who recall that they or a sibling had similar problems with inattentiveness, delay in language acquisition, or dyslexia, frequently persisting in lesser form into adulthood.
Only a few controlled studies have yet appeared to document these impressions.7'9 It is difficult to know in retrospect the exact nature of the child's deficits. Because of the therapeutic effect of amphetamine in children and its role of increasing catecholamines in animal experiments. Wender1,10 has proposed an underlying defect in monamine metabolism. Testing the hypothesis is difficult, since we have no direct means of measuring central nervous system neurotransmitters in human beings.11 It may well be that the entity is not an abnormality at allf but an artificial category describing children with constitutional traits at variance with demands by our society that every child sit quietly for long periods in school and learn to read and write at age six. Just as there is a continuum or bell-shaped curve for intelligence, there is probably a similar variation in activity level and in perceptual and coordination abilities. Werry et al.12 call the syndrome "a biological variant made manifest by the affluent society's insistence on universal literacy and its acquisition in a sedentary position." Schain" points out that "this is quite different from suggesting the presence of a neurological abnormality in a traditional sense of originating from a morbid condition of the nervous system."
Other labels are also used in an attempt to describe the behavior or process without alluding to etiology. It is often assumed to be due to constitutional or genetic factors. The educator uses the term "learning disability," whereas the physician may say it is a "specific learning disability/' "specific or developmental dyslexia," or "dyscalculia." Central processing dysfunction refers to the theory that the child has difficulty receiving, recalling, or integrating the sensory information - i.e., auditory, visual, and haptic - that is necessary for learning. Perceptual dysfunction applies to the same processes. Hyperkinesis and hyperactivity refer to the restless, distractible, inattentive child with labile emotions and low frustration tolerance. Others may be hypokinetic with poor attention spans. The terms "maturational delay" and "developmental lag" may be used in the younger child, since it is difficult to predict whether the child under age seven will be just a "late bloomer" or will manifest marked learning or attention difficulties.
The medical diagnosis of minimal cerebral dysfunction is made by exclusion of all known physical, emotional, and social causes of disruption of behavior and the learning process. This should be the primary concern of the physician during the initial visit. A careful history and physical examination should be carried out to rule out the existence of a debilitating disease or one causing frequent school absences, such as asthma, tonsillitis, or otitis. Malnourishment and metabolic abnormalities - such as hypothyroidism, hyperthyroidism, or inborn errors of metabolism - should be considered. Such frank neurologic syndromes as cerebral palsy, epilepsy, "arrested" hydrocephalus, microcephaly (often associated with mental retardation), neurofibromatosis, and muscular dystrophy must be looked for. Educators often forget that these children are truly neurologically impaired and are more apt than the normal child to exhibit perceptual, cognitive, motor, and attentional deficits.
School phobias, anxiety, depression, and schizophrenia must be considered, but it should be kept in mind that children with hyperkinesis and learning disabilities often develop secondary emotional problems. They can develop a poor image of themselves or a feeling of being rejected by teachers, parents, and peers because of their own apparent stupidity and inability to behave. Too often these children have been labeled "retarded" or "dummy" by peers.
A crowded or chaotic home may predispose to poor school performance. Children who live in crowded apartments are reported to become depressed, listless, and apathetic. The stability of the family and interpersonal relationships can deeply affect a child's behavior. It is also important to assess the expectations of the parents for the child's behavior and academic achievement. They may tolerate aberrant behavior at home, and be uninterested in educational advancement of the child, so the child merely reflects at school the pattern learned at home. The child from a bilingual home may also be at a disadvantage, especially if he is from a poor socioeconomic background.
Recently, chronic lead poisoning has been implicated as a cause of minor degrees of perceptual and cognitive impairment, motor incoordination, and disturbances in attention span.13,14 We now routinely screen for lead intoxication all children referred for school problems.
Once other diagnostic possibilities are eliminated, one can consider the diagnosis of minimal cerebral dysfunction or the separate labels of learning disability and hyperkinesis. The diagnosis is made on the basis of history and psychologic examination. Although the neurologic examination does not show gross or focal deficits, careful attention to the behavioral and cognitive spheres should give clues to the diagnosis.
A careful, complete history is essential and must include present behavioral and achievement data as well as a profile of development. School personnel should provide a description of the child's behavior and his interaction with teachers and peers, results of achievement and psychologic tests, a review of the child's strengths and weaknesses, a description of the classroom and teaching methods, and any other factors they feel may be pertinent. The parents and child should also describe the teacher-child and the teacher-parent relationships and classroom environment.
The physician should inquire into when the behavior or learning disability first appeared and the remedies tried. The origin of school problems of recent onset may be found in an altered school or home environment or interpersonal relationships or, occasionally, in a degenerative illness.
Many potential problems go unrecognized until the child is stressed beyond his capacity. For instance, the child who is barely keeping up reaches the third grade, where his academic inadequacies become glaring. Another child may become overwhelmed and completely disorganized when transferred from a rigidly structured class environment to an open classroom, where children plan their own schedule.
The learning-disabled child usually goes unnoticed until he shows difficulties in learning to read. The first clue to this may be a change in personality or behavior. A child performing within six months of his grade level is not generally considered learning disabled. Myklebust15 states, however, that a child is an underachiever if there is a discrepancy between his actual achievement and his expected level of attainment. A child of superior intelligence who struggles just to stay at grade level may be learning disabled. He can become anxious and withdrawn or overly aggressive if pressured to excel by adults who hold high expectations for him.
The underachiever may have been delayed in acquisition of language, learning his first words after age two and phrases well after age two and a half. His articulation and syntax may still be primitive when he starts kindergarten. Approximately half of learning-disabled children do poorly in tasks demanding verbal and auditory facility as compared with nonverbal skills. The child deserves a complete audio gram to rule out a hearing loss. High-frequency deficits result in loss of consonant recognition.16 Severe deficits are associated with speech disturbance and less severe ones with poor concentration.
Other learning-disabled children may be clumsy, especially in graphomotor and fine hand skills. Poor, labored handwriting may be the only disability, but it can interfere with finishing work on time and the speedy acquisition of other skills. Parents sometimes relate that, compared with peers and siblings, the child was delayed in learning to tie shoes and to ride a bicycle. Further evidence of immaturity in motor control is a delay in establishing bladder control at night. Motor clumsiness and immaturity are not diagnostic of the learning-disabled child, however.
The hyperkinetic or hyperactive child is described by Laufer and Denhoff17 as showing some or all of the following signs: chronic excessive sustained motor activity, short attention span, poor concentration, distractibility, difficulty focusing attention on tasks, shifting frequently from one activity to another, paying more attention to his neighbor's work than to his own, variability and unpredictability of behavior, poor impulse control with inability to delay gratification, poor judgment, emotional lability, and low frustration tolerance. School achievement frequently suffers because of the above traits, but many of the children show perceptual deficits as well. The syndrome is usually recognized in infancy or when the child begins walking, but it may not be apparent until he starts school. The infant maybe irritable and "colicky" and maintain a restless, distractible spirit from the outset. Others are described as happy, placid babies who never stopped moving once they got on their feet. Unlike their siblings, many of these children were difficult to discipline, never profiting from experience. The child whose problem went unrecognized until he started school played happily and securely at home but could not organize his time or attend to tasks long enough to satisfy his teacher in school. Most do not watch television for any length of time, but some are daydreamers who stay mesmerized in front of the TV set for hours. Since the incidence of hyperactivity is higher in males, their identification may depend on the teacher's tolerance for the generally higher activity levels normally found in young boys.
Factors in medical history - such as low birth weight, perinatal anoxia or trauma, head injury with unconsciousness, meningitis, encephalitis, and prolonged febrile seizures - may predispose a child towards a learning disability and/or hyperkinesis, but they are not diagnostic by themselves.
The neurologic examination fails to reveal any evidence of focal or classic neurologic signs, since by definition such findings would exclude children from the syndrome of minimal cerebral dysfunction. The so-called soft signs found in up to 50 per cent of these children also fail to confirm the diagnosis. Schain*1 correctly asserts that few normative data exist; when available, they show that a wide age variation exists for acquisition or loss of these signs.18'19 Motivation and experience in carrying out tasks also affect the results. Soft signs described include clumsiness, choreiform movements, associated or mirror movements, reflex asymmetries, dysdiadochokinesia, ocular apraxia and end-point nystagmus, tremor, finger agnosia, graphesthesia, and extinction to double simultaneous stimulation. These signs are present in the preschool child. When they persist past seven or eight years of age, they may indicate only immaturity of the nervous system. Hart et al.20 recently showed that findings in neurologic examinations of 129 children with poor school achievement and 30 controls bore little relationship to school achievement or intelligence. Vision and hearing deficits should be ruled out, although they do not usually cause poor achievement or hyperactivity.
Examination is not complete without assessing the child's mental status, speech and language, personality, and habits. The child's speech pattern and enunciation should be listened to. Paucity of speech, cluttering speech, and immature or inappropriate syntax should be particularly noted. A so-called shy child may in reality have difficulty in expressing himself verbally. The child's relationship with his parents and with strangers and his behavior in the waiting room as well as in the office should be observed. The hyperactive child frequently remains calm and organized in a nonstressful one-to-one situation, so the diagnosis cannot be made on the basis of office observations. A severely impaired child, however, becomes completely distracted by unfamiliar sights and sounds and sets out on an exploring expedition.
It is wise to conduct a quick screening for the child's academic level of reading, spelling, and arithmetic.21 We have found several children performing at grade level who tested poorly in the school situation. The child should be asked to read a word list and paragraphs for various grade levels and then to write several words from dictation. Children who can read and spell phonetically can be differentiated from those who use sight recognition and those with neither skill. The child's manipulation of a pencil and his penmanship should be observed, and he should be asked to do simple computations both with and without pencil and paper. If the child performs below expected grade level, problems in processing information presented to either the visual or auditory sphere, sequencing information, or recalling information should be sought. Although difficulty in copying geometric figures may be due to poor motor skill, faulty visual perception should be suspected if the child is unable to recall how to reproduce the figures later or fails to notice his copying errors. The child who cannot repeat six numbers forward and four backward by age seven may have difficulty with auditory discrimination, auditory retention, or sequencing in temporal order. This child may also be unable to say the days of the week in order or to follow three commands given at the same time.
Tests for laterality are not helpful. Studies repeatedly show that handedness is not well established until age seven.22 Nor is there a difference in the number of left-handed or ambidexterous children among children who read at grade-school level and those who read two years behind in elementary school. Laterality of the dominant foot or eye is irrelevant. Failure to develop right-left discrimination is more frequent in dyslexic children but is not well established until age nine.18
The routine electroencephalogram cannot be used to make or confirm the diagnosis of minimal cerebral dysfunction. Most studies show that these children have an increased incidence in EEG abnormalities, chiefly background disorganization and mild, diffuse slowing. The same pattern can, however, be found in EEGs of children whose school performance and behavior are within normal limits. Hughes23 compared 214 children of normal intelligence who were underachievers in school with an equal number of controls. Similar EEG abnormalities were found in 41.2 per cent of underachievers and in 29.8 per cent of controls. School officials must be informed of the indications for the EEG and information to be gained from it, because they often request an EEG of every child referred. The main value of the EEG is in diagnosing a seizure disorder and detecting focal cerebral lesions.
According to Paine,24 the indications for an EEG in children with learning disorders include:
"1. Suspicion of petit mal or even merely frequent short episodes of apparent day-dreaming or loss of contact.
"2. Paroxysmal and stereotyped episodes of abnormal behavior, even if consciousness is not lost.
"3. Any suspicion of a progressive or degenerative condition.
"4. Abnormal neurologic signs on examination which suggest a focal lesion or other neurological indications from history or examination."
We also obtain an EEG for the child with a history of unexplained aggressive behavior or rage episodes, looking particularly for temporal lobe abnormalities. Studies using evoked cortical responses may prove of value in the future.25
The most important laboratory data are from the psychologic and educational evaluation, which, ideally, should indicate the child's strengths and weaknesses so that a program of treatment can be outlined. Although the physician should not order specific tests, he should be familiar with them and make sure the test battery covers verbal and nonverbal mental ability (intelligence), academic achievement, cognitive abilities in the area of auditory and visual perceptual skills, expressive and receptive language (spoken, read, and written), fine motor abilities, and social and emotional maturity.
Tests in most common use today include the Wechsler Intelligence Test for Children, which measures both verbal and nonverbal skills; the Bender Visual-Motor Gestalt Test, for testing visual processing and memory; the Wepman Test of Auditory Discrimination; and the Illinois Test of Psycholinguistic Ability, used especially for evaluating language and auditory skills. Since psychologists may not carry out the entire battery, learning-disability specialists frequently complete it and write the "prescription" for the classroom teacher. Speech and language pathologists can help examine the child in whom a language deficit is suspected. If an adequate evaluation is not available at school, the child should be referred to another resource within the community or nearby, such as a university program or private clinic.
Results of the entire evaluation and recommendations should be interpreted clearly to the parents, the educators, and the child.
We agree with Schain'1 that a definite diagnostic term should be used, because "parents are likely to continue to have a nagging concern about the specific nature of the problem" if it is avoided. When the child shows definite evidence of neurologic impairment or of borderline or retarded intelligence, this should be clearly stated. Otherwise the parents should be informed that the child is not retarded and not brain damaged. It is wise to discuss labels used in the community and the ramifications of the term that is used for their child.
Advice on home management is within the scope of the physician. Parental attitudes towards the child often change when they understand the nature of the child's problems. They should drop the role of teacher-parent. By reducing the pressures for academic excellence and discontinuing frustrating evening tutorial sessions, many parents can develop a healthier supportive role with a more relaxed and happier youngster. The hyperkinetic child fares best in a well-ordered, calm, consistent environment where parental expectations for performance bear a realistic relationship to his level of maturity. Psychotherapy is not helpful in treating learning disabilities or hyperkinesis.! It may be a useful adjunct, however, when a child has developed poor selfesteem. Family therapy and counseling may also be important. Programs of behavior modification are becoming available in which the parent is instructed in the practical application of principles of operant conditioning, influencing the child's behavior by rewarding desirable behavior and punishing undesirable behavior.26
The educator plans for the child's optimum education and makes the final decisions for the child's class placement. The physician should describe the child's specific difficulties and needs and point out the responsibility of the school system to meet those needs, if necessary. Resources within the schools vary from group or individual tutoring with a remedial-reading teacher to small classes taught by learning-disability specialists. Some systems employ learningdisability teachers in resource rooms where children spend as much time as necessary during the day apart from their regular classes.
Ideally, instruction should be modified to meet the child's needs, introducing new skills in a structured sequence and often using a multisensory approach.27 Programs of perceptual and motor training - such as those designed by Delacato,28 Frostig,29 and optometrists - are a waste of time and money because they bear little relationship to the academic task and have not been proved of any value in experimentally controlled studies.30 If an adequate educational program is unavailable within the system, parents will need counsel on alternative facilities. The school should be continually pressured to provide for "exceptional children."
Medication should be considered for the hyperactive child only when environmental manipulations have failed. These children do better in a structured, closed-classroom setting. An area where the child can isolate himself to avoid distractions is helpful. Short "work contracts," with ample rewards and individual work with teacher assistants, might keep the child in the educational mainstream. If his problem is moderate to severe, a small special class where he can work in his own "office" and get remedial help can make a dramatic difference in behavior.
The results to be expected from a trial of medication should be carefully explained to the parents. While medication may reduce distractibility and impulsiveness and improve attention span,31-'1- it does not produce learning. Success is unpredictable.33
Anticonvulsant medication can be considered if the child has an EEG pattern consistent with a convulsive disorder even in the absence of clinical seizures. Unapparent petit mal or subclinical seizures can interfere with concentration and attention span. Ethosuximide (Zarontin®), 250 mg. three times a day, is the drug of choice for petit mal (3-per-second spike-and-wave discharges) and diphenylhydantoin (Dilantin®), 5 mg./kg. at bedtime, for other epileptogenic discharges. If the aggressive, irritable child shows a pattern consistent with a lesion or paroxysmal discharges from a temporal lobe, we also treat initially with diphenylhydantoin and, if that is ineffective, primidone (Mysoline®). Use of anticonvulsant drugs should be tapered and then discontinued after six to eight weeks if there is no change in behavior. Their use should be temporarily discontinued at the end of the school year, since improvement might represent a placebo effect.
The most effective drugs for hyperkinesis have been dextroamphetamine and methylphenidate. Occasionally a child will respond to one and not the other. The effect is immediate and short-lived, since the drugs are quickly metabolized. Medication should be started in small amounts in the morning or morning and noon on school days and increased every two to three days until maximum benefit or toxic effects appear. Since the object is improved classroom behavior, a method of evaluation and reporting should be worked out with the parent and teacher. Medication should start with 5 mg. of either drug and be increased by 2.5 to 5 mg. to a maximum of 40 mg. per day of dextroamphetamine and 80 mg. per day of methylphenidate. Side effects include anorexia, insomnia, depression, and crying spells. Use of the drugs can be discontinued during the summer and prolonged vacations and restarted only if the child cannot return to school without them. The average length of treatment is six months to three to five years, and it is usually not necessary after age 11-12.
Little is known regarding the safety of these drugs. Recently Safer and Alien34 reported significant suppression of height and weight in 49 children taking stimulant drugs for more than two years. The effect was dose related and less with methylphenidate than with dextroamphetamine. Growth retardation was less pronounced if drugs were discontinued during the summer and insignificant with 20 mg. or less of methylphenidate.
Phenothiozines (chlorpromazine and thioridazine) are useful in calming extremely hyperactive children in whom stimulants have failed and sometimes in aggressive, acting-out children. They do not improve attention span. Imipramine is a promising drug in the restless child, but control trials are lacking. The report of caffeine as a substitute for stimulant drugs remains unconfirmed.35 The antihistamines occasionally help the young, slightly anxious child, but they are overrated. Dietary therapy directed against hypoglycemia, alterations in vitamin metabolism, or dietary allergies is without proven value.
The few long-term follow-up studies of children with learning disabilities and/or hyperkinesis indicate a guarded prognosis. It is unfair to advise parents that the child will "outgrow it," although we do expect the manifestations to change with maturity. Studies of dyslexic children who have received remedial instruction indicate that, while most become literate, few ever read at an average level.3" Koppitz37 reported that children with an IQ of 85 or less and both visual and auditory perception deficits were likely to require special education until age 21. A poor socioeconomic background also militated against a return to the mainstream.
The hyperkinetic child may become more sedentary during adolescence but still show difficulty adapting behaviorally and socially to the standards of his teachers and peers. Weiss et al.30 followed 64 hyperactive boys for more than four years. At ages 10 to 18, 46 per cent were distractible, 70 per cent were emotionally immature, 30 per cent lacked ambition or an ability to maintain goals, 30 per cent had no steady friends, and 80 per cent performed poorly academically. Cohen et al.39 compared 20 of these adolescent boys with controls and found that they were more impulsive in problem solving and had greater difficulty isolating a sample from a complex background. Denhoff40 cites the studies of Laufer and McCarthy, which followed 60 patients into their third decade who had been treated with amphetamines in childhood. Thirty per cent still showed an abnormal temperament, with mood swings, proneness to anger and violence, and feelings of persecution. Emotional adjustment was poorer in those treated for under two months.
In summary, the pediatrician should become familiar with the problems besetting children within the school and with the educational expectations and methods within the local school system for average and "exceptional children." He should examine the child for medical causes of hyperkinesis and poor learning and be aware of emotional and social factors that may be contributing. He should interpret his findings to the parents and educator and aid them in management by counseling, drug therapy, and referral to appropriate agencies for educational remediation, behavior modification, and/or psychotherapy.
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5. Werner, H., and Strauss, A. A Pathology of figure-background relation in the child. Abnorm. Soc. Psychol. 36(1941), 236.
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7. Hallgren, G. Specific dyslexia ("congenital word-blindness"): A clinical and genetic study. Acta Psychiatr Neurol. Scand. (suppl. 65, 1950). 287 pp.
8. Omenn. G.S. Genetic issues in the syndrome of minimal brain dysfunction. In Walzer, S., and Wolff, P.H (eds.). Minima! Cerebral Dysfunction in Children. New York: Gruñe and Stratton, 1973. pp. 5-17.
9. Mornson, J. R., and Stewart. M. A Evidence for polygenetic inheritance in the hyperactive child syndrome. Am. J. Psychiatry 130 (1973), 791.
10. Wender, P.H. Some speculations concerning a possible biochemical basis of MBD. Ann. N.Y. Acad. Sci. 205 (1973). 18.
11. Coleman, M. Serotonin concentrations in whole blood of hyperactive children. J. Pediatr. 78 (1971), 985.
12. Werry, J. S., el al. Studies on the hyperactive child. VII: Neurological status compared with neurotic and normal children. Am. J. Orthopsychiatry 42 (1972), 441-450.
13. Neidleman, H. L. Lead poisoning in children: Neurologic implications of widespread subclinical intoxication. In Walzet, S.. and Wolff. P.H. (eds.). Minimal Cerebral Dysfunction in Children. New York: Grune and Stratton, 1973. pp. 47-54.
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