" The Journal now offers the first in a series of "Controversies in Pediatrics. Under the able editorial direction of Sydney Gellis, we plan not to "draw out the thread of verbosity" but rather to " present "the staple of the argument, and in so doing we hope to give the reader a look at those aspects of pediatrics that are still areas of debate.—Ed.
The Minimal Brain Barton D.
Schmitt, MD
brain dysfunction (MBD)
Minimal diagnostic synonymously is
Dysfunction Myth
a
term. It is used
with minimal cerebral
dysfunction and minimal brain damage. It implies verification of an organic cause. When a symptom is
attributed to MBD, the symptom is assumed to be secondary to a cerebral structural abnormality resulting from trauma, infection, hypoxia, or other central nervous system (CNS) disease.1 At least 100 clinical manifestations are listed under MBD, includ-
ing dyslexia, dysgraphia, dyscalculia, perception problems, dysarthria, hyperactivity, poor attention span, temper tantrums, aggression, clumsiness, and vague spells. By definition, the children have to be of normal intelligence. The prevalence of the MBD syndrome is allegedly
visual
greater than any other chronic dis-
It has been estimated that 10% to 20% of the total population is affected. The current problem with the MBD ease.
Received for publication Jan 10,1975; accepted March 20. From the Department of Pediatrics, University of Colorado Medical Center, Denver. Reprint requests to Container C230, University of Colorado Medical Center, 4200 E Ninth Ave, Denver, CO 80220 (Dr. Schmitt).
syndrome is that it has become an all\x=req-\ encompassing, wastebasket diagnosis for any child who does not quite conform to society's stereotype of normal children. Learning disorders, hyper-
kinesis, and MBD have come to be used interchangeably. An assumption
exists that the majority of children with hyperactivity or learning prob¬ lems are brain damaged. Almost any behavior problem short of psychosis has been attributed to MBD. Aggres¬ sive children are especially likely to be prejudged as having MBD. Chil¬ dren are labeled as such by school psychologists who find "organicity" on
psychological testing
or even
by
teachers who find certain vague symptoms that they relate to MBD. Labeling troubled children as having MBD has almost become a national
pastime.
The MBD label could not have sur¬ vived if it had not become popular with physicians. If the MBD concept is adhered to, learning disorders and behavior problems can be considered within the medical frame of refer¬ ence. This disease-oriented definition leaves the physician no choice but to assume that he is essential to the diagnosis and management of these problems. Until he can question the very validity of this diagnosis, he is trapped in the ritual of hunting for
the elusive organic factors behind MBD. The main purpose of this re¬ view is to help the practicing pedia¬ trician who is caught in the middle of all the MBD controversy to find a comfortable and effective role for himself. Invalid Criteria Used for Establishing MBD Diagnosis
The type of evidence accepted by different experts as confirmatory of MBD is quite variable. This is not sur¬ prising since no neurological sign or test has yet been proved to differ¬ entiate children with MBD from nor¬ mal children. The medical data dis¬ cussed in the following sections have been frequently abused. Standardiza¬ tions do not exist for most of the data. Reliance on these data has led many MBD. Soft
physicians
to
overdiagnose
Neurological History.—The long-term risks of perinatal problems are especially likely to be over¬ estimated. The history of a long labor or difficult delivery may not be impor¬ tant. Newborn problems of potential importance are severe prematurity, hypoglycemia, meningitis, and a low five-minute Apgar score. Those com¬ plications that are accompanied by neurological manifestations during the newborn period have the highest
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risk. Of
interest, prospective study
large, ten-year
a
the island of Kauai found that serious perinatal difficulties did not correlate with be¬ havior problems or learning problems, except in those subjects with intelli¬ gence quotients below 85.- The major¬ ity of children who failed to function adequately at 10 years of age were environmental casualties rather than reproductive casualties. Once the child is beyond the new¬ born period, any neurological event that does not result in hospitalization is unlikely to be important. Almost every child has struck his head during a fall, and this is not pertinent if there were no acute complications. Important history may include status epilepticus, encephalitis, head injury with prolonged unconsciousness, and lead poisoning. Soft
on
Neurological Signs.—These
ally refer
to fine
or
usu¬
gross motor
deficits of obscure importance. ' Com¬ monly mentioned examples are diver¬ gence of outstretched hands, fine choreiform movements, difficulty maintaining tongue protrusion or lat¬ eral gaze, jerky eye tracking, mirror
movements,
inability to use
a
scissors,
poor handwriting, and a changing Babinski reflex. Anxiety can tran¬ siently cause or accentuate many of the soft neurological signs (eg, hyper¬
by symmetrical deep tendon reflexes). These signs are often not reproducible, and there is a lack of in¬ terest reliability between two exam¬ iners. Hard neurological signs are de¬ tected on the classic neurological examination by testing cranial nerve, cerebellar, extrapyramidal, motor, and simple sensory functions. Hard signs are reproducible and not normal at any age beyond the first year of life. These would include findings such as clonus, tight flexor muscle groups, intention tremor, ataxia, hemiparesis, and cranial nerve palsy. In general, soft neurological signs are not helpful findings. Most of them active
represent transient phenomena and with age. At best they are evidence for neurological immaturity. The point at which they become ab¬ normal is not well standardized. They are so common under age 7 that they should never be considered abnormal
disappear
prior to that age.4-5 Even when they persist beyond age 7, their etiological importance is highly speculative.6 Problems with right-left discrimina¬
tion and mixed cerebral dominance have no correlation with neurological damage or learning problems.7'' One study showed that 9- and 10-year-old learning-disabled children cannot be distinguished from normal-achieving children on the basis of soft neuro¬ logical signs.8 Another study dem¬ onstrated that children with superior intelligence had no advantages in terms of manual dexterity or fine mo¬ tor coordination.10 A third study dem¬ onstrated that the finding of a few soft signs is just as frequent in un¬ derachieves as in a control group.4 Although the presence of numerous soft signs was more frequent in the underachiever group, the number of such signs could not predict which children were having the most diffi¬ culty with schoolwork.1 Some would suggest that the presence of a cluster of soft signs would have more impor¬ tance. However, the number of soft
signs required cause
to prove
is unknown.
an
organic
conclusion, the pediatrician probably should not examine a pa¬ tient for soft neurological signs un¬ less he can validly interpret them. By and large, they lead to additional con¬ In
fusion rather than clarification. Al¬ so, this complicated examination con¬ sumes up to 30 minutes of valuable time that the physician could better use for eliciting other data. Until the real experts have thoroughly studied this subject and straightened out the meaning of soft neurological signs, the pediatrician would be best ad¬ vised not to participate in this contro¬ versial field. If the pediatrician by chance detects a few soft signs in a given child, his best course of action in terms of diagnosis is probably to give the patient a neurological clean bill of health anyway. Certainly, the presence of a few soft signs does not require that one request skull roentgenograms, an electroencephalogram (EEG), or a neurological consultation. Electroencephalogram.—The EEGs have proved to be of limited use in evaluating MBD.41113 Approximately 30% of these children have abnormal
EEGs compared to about 15% in the control groups. However, the findings are in no way specific or diagnostic. The pattern of EEG abnormality does not substantially correlate with neu¬ rological findings in the children. The results of the EEGs also do not influ¬ ence therapy except in a potentially harmful way, that is, when anticonvulsants are given unnecessarily. Gen¬ erally speaking, the mildly abnormal EEG as seen in this disorder is not helpful. In addition, different electroencephalographers demonstrate only a 40% level of agreement in reading the same EEG record.11 If the school personnel request an EEG and no valid indications are present, the physician has every right to refuse to obtain one. Indications for obtaining an EEG would be a his¬ tory that was suspicious for petit mal,
psychomotor epilepsy, a progressive neurological disease, or neurological hard signs suggestive of a focal CNS lesion.
Psychological Tests.—Abnormalities
visual-motor-perceptual tests and verbal-performance discrepancies on intelligence tests have been touted as diagnostic of organicity and hence on
MBD. Less well known is the fact that these same abnormalities are equally characteristic of other groups of children, especially those with psy¬ chiatric disorders.1'1" There is also some overlap between the scores of normal children and those with MBD. In fact, Bender gestalt test errors due to maturational delay are so common that the test is of limited value diagnostically prior to age 8.,; The most commonly used visualmotor-perceptual test in children is the Bender gestalt test. A patient is often referred from a school psycholo¬ gist with the statement, "This test performance is highly suggestive of brain damage." This comment is ex¬ tremely misleading because all the test shows is that the patient has
problems. visual-motor-perceptual These are more likely to be due to normal variation, developmental de¬ lays, cultural deprivation, or reactive disorders than to brain damage. This common misinterpretation of the Ben¬ der gestalt test may relate to the fact that the original observations on the
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response of "brain-damaged" chil¬ dren to the test were obtained from
children whose diagnosis of brain damage rested largely on behavioral criteria.1" A study on 142 soldiers with neurological injuries demonstrated that the Bender gestalt test was not helpful in distinguishing the patients from a control group.1" The Wechsler Intelligence Scale for Children includes both a verbal and a performance score. A greater than 20-point discrepancy between the ver¬ bal and performance scores has been considered diagnostic of brain dam¬ age. However, this is in error because several other conditions are more likely to cause such a finding.-" A high performance-low verbal pattern is most commonly seen in children who come from a verbally deprived envi¬ ronment (eg, inner cities and some rural areas).21 It is also seen in chil¬ dren with auditory-perceptual prob¬ lems or in those who "act out" rather than think (eg, juvenile delinquents). A high verbal-low performance pat¬ tern is commonly seen in neurotics, especially those with obsessive-com¬ pulsive tendencies. It is also seen in children with visual-motor-perceptual problems. Professional people in gen¬ eral rear children with higher verbal scores.-1
danger of these tests is that people (including physicians) consider them totally scientific and place absolute reliance on their inter¬ pretation. Although many psycholo¬ gists realize the limitations of equat¬ ing abnormal test results with pos¬ sible brain damage, the pediatrician The
many
is often unaware of this and may be intimidated by the test findings. A possible solution to this problem is to clarify that organicity is a medical term and that psychologists would do better to determine a child's strengths and weaknesses rather than make gross generalizations about brain dysfunction. In conclu¬ sion, the main value of psychological tests is to help one design a relevant educational plan for a specific child. Their value in determining cause is extremely limited.'--
Diagnostic
Trial
of Stimulants.—
Some have suggested that improve¬ ment of symptoms with administra-
tion of amphetamines is diagnostic for MBD. On the contrary, a rapid and "miraculous" response to stimu¬ lants can also be seen in patients with psychogenic hyperactivity.-;l The im¬ portance in terms of cause is nil. The greatest misuse of these drugs is giv¬ ing them to all problem children on the first visit for a diagnostic trial. Harmful Effects of MBD
Diagnosis
One inescapable fact that must be kept in mind is that the average per¬ son equates MBD with brain damage
despite lengthy explanations regard¬ ing the subtle differences. We must accept the fact that whenever
we la¬ bel a child as having MBD it will fol¬ low that the majority of parents will refer to him or her as brain damaged. It also follows that, if a patient is considered as having something wrong with his brain, it is a serious matter. Harm to the Child.-The MBD diag¬ nosis stigmatizes the child as being defective. It changes the parents' and the school's expectation of him. They may treat the child as one who is unable to learn rather than as an in¬ dividual. As the child begins to view himself this way, the label develops into a self-fulfilling prophecy. The la¬ bel is also very hard to undo. It tends to follow the child from class to class and from school to school. Even if he completely recovers from his disabil¬ ity, his relatives may still refer to him as brain damaged. Attempts to pre¬ dict MBD in infants on very tentative data could be considered extremely harmful.-' A suspected diagnosis of MBD can keep a child from being
adopted.
Harm to the Parents.—The term MBD can connote a hopeless, irre¬ versible diagnosis and can make par¬ ents depressed. Parents will some¬ times blame themselves because of something they did wrong during pregnancy. In addition, parents can become frightened by this diagnosis and they worry needlessly about the possibility of future seizures or intel¬ lectual deterioration. At best, this diagnosis can lead to considerable confusion for parents. Harm to the School.-The MBD con¬ cept can paralyze some schools until a medical evaluation has been com-
pleted. It can make them feel unac¬ countable for coordinating the eval¬ uation and therapy for many of these problems. For the schools that do not have the facilities to evaluate these children, the organic label of MBD permits the schools to shift the re¬ sponsibility for evaluation to the pe¬ diatrician. The MBD label is so well entrenched in some school systems that rules exist that make it manda¬ tory for the child to receive a medical evaluation and an EEG before he is given clearance for special testing or special educational classes. Some neu¬ rologists have found this to be inappropriate.4
Harm to the Physician.—The main disadvantage for the physician in es¬ tablishing the elusive diagnosis of
MBD is the considerable amount of medical time that is wasted. The time expended can delude the physician into thinking he has accomplished something in these cases. It may dis¬ tract him from looking at environ¬ mental factors. In addition, parents may pressure the physician to pre¬ scribe drugs once this diagnosis is made. Harm to the
The MBD
Therapeutic
Process.—
diagnosis commonly leads to overuse of drugs. Drugs may be tried in the preschool child rather than
behavior
modification
tech¬
niques. Drugs may be used in the treatment of the school-age child rather than designing an educational plan. The finality of the MBD diag¬ nosis also results in the failure of some schools to use an aggressive educational approach. This is unfortu¬ nate because even in patients with proved organic brain damage the only modifiable aspects of their condition are the educational problems and the emotional problems. The brain dam¬ age itself often results in a static condition unresponsive to any specif¬ ic therapy. Etiological speculations about diseases that are no longer ac¬ tive are rather irrelevant in terms of
therapy.
Harm to Research.-The MBD diag¬ nosis is made up of many symptoms and many etiological subtypes. Mix¬ ing the subtypes makes the result of any research on such a group uninterpretable. Research requires much
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more
specific diagnoses
Evidence
Against
than MBD.
MBD
Concept
There is no scientific evidence to support the MBD diagnosis. The fol¬ lowing considerations suggest that MBD is an overworked diagnosis. Alleged High Incidence.—It is not logical to believe that over 10% of the population have sustained subtle CNS injuries and are left with an acquired
disability. In some poverty areas, the prevalence of symptoms that could qualify for MBD would include over 50% of the children. This high inci¬ dence points to psychosocial factors rather than organic disorders. Low Incidence in Some Countries.—
On the Isle of Wight, the incidence of hyperactive children was only 0.4%.M The discrepancy in incidence between different countries or communities points to observer bias.1'-" The parent or teacher who is ignorant or intoler¬ ant of the normal behavior of young children may detect excessive num¬ bers with hyperactivity.
Preponderance.—Hyperactiv¬ ity reportedly occurs nine times more frequently in boys than in girls, and the ratio for dyslexia is 10:1. It is again completely illogical to assume that boys are injured that much more commonly than girls. Certain cultures
causal. All of these findings monly seen in children.
Major CNS
ganic cause. Lack of
Clustering
of MBD
Symp¬
toms.—Three studies show a low degree of interrelatedness among hy¬
peractivity, cognitive functioning, and soft neurological signs.23-" The
presence of one of these variables does not predict the presence of oth¬ ers.
Although learning disorders
are
sometimes found in combination with hyperactivity and clumsiness, this is the exception rather than the rule. The finding of soft signs in some pa¬ tients with learning problems or hy¬ peractivity is coincidental rather than
Disease Without MBD
Symptoms.—If MBD is really part of a neurological continuum, the majority of the children with major CNS hand¬ icaps should have symptoms of MBD. However, they do not. The majority
of children who have cerebral palsy or epilepsy, or who have had encephalitis or severe head injury do not have hy¬
peractivity or behavior problems.32-35 Although minor cognitive or percep¬ tual problems are more common in
these children, most of them still have a normal intelligence and learning capacity despite their neurological handicaps. Also, in my experience, most mentally retarded children are
not hyperactive. Absence of Neuropathological Find¬
ings.—No neuropathologist has ever seen the underlying "brain damage" in MBD. This is est
possibly the strong¬ argument against the existence of
an
MBD
entity.
Real Causes Concealed MBD Diagnosis
Male
and certain individuals are less toler¬ ant of the biologically more aggres¬ sive nature of boys. Familial Factors.—Some of the dis¬ orders attributed to MBD can occur in several members of a single family. A polygenetic basis for hyperactivity has been noted.-7 Familial clustering for dyslexia is well known.-'' Again, this argues against an acquired or¬
are com¬
by
People can be vastly different with¬ being diseased or damaged. Often
out
this normal variation is on a heredi¬ tary basis. When one considers the variation among people in physical characteristics, the immense individ¬ ual variation in behavior, emotion, in¬ tellect, and cognitive competency is not surprising.1" The MBD syndrome is not a homogeneous group and would best be looked at in terms of
specific problems, namely, hyper¬ activity, learning problems, behavior problems, and speech problems. Each of these entities has multiple causes. Although it is difficult to make gener¬ alizations about the frequency of each cause, the following estimates are based on my experience: 1.
Hyperactivity
A. Constitutional/genetic, 70% B. Emotional basis, 30% 2. Learning disorders (excluding mental
retardation)
A. Normal variation, 60% B. Cultural deprivation, 30% C. Emotional basis, 10% 3. Behavior problems: psychosocial basis, 99.9% 4. Speech problems (excluding hearing
deficits)
A. Maturational delay/genetic, 90% . Emotional basis, 8% C. Organic, 2%
Hyperactivity usually has its basis in differences in temperament and innate reactivity.17 This has been termed "constitutional hyperactiv¬ ity." There is a strong genetic fac¬ tor.27 Emotional factors are also not uncommon in hyperactivity.''' An or¬ ganic basis can be demonstrated in less than 1% of such children in my experience.1' Learning problems other than men¬ tal retardation are usually the result of normal variation in cognitive abili¬ ties.'3 The process of learning school material is extremely complex and some children are better equipped for it than others. Cultural deprivation and parental neglect are the most common causes of learning problems for children growing up in adverse environments. Since learning re¬ quires considerable self-control and self-confidence, most children with se¬ rious emotional problems will also have learning problems. The fre¬ quency with which organic disease is responsible for learning problems is very low.12 Even in mentally retarded children, a specific organic cause is proved in only 30% of cases. Behavior problems are almost al¬ ways on a psychogenic basis; very few have an organic basis. The most ex¬ treme misuse of the MBD organic la¬ bel is when it is applied to children with misbehavior. If psychosocial fac¬ tors
can
person to anorexia suicide, it is only logical to
drive
nervosa or
a
that they can cause behavior disturbances of lesser magnitude. Speech problems such as delayed speech or poor articulation are usually due to maturational delay.4" Emo¬ tional disorders can also be respon¬ sible (eg, stuttering, elective mut¬ ism). The number of such children with an organic cause for these prob¬ lems is almost negligible once hear¬ ing deficits have been excluded. A speech pathologist is best equipped to deal with the differential diagnosis and therapy of most children with ab¬ normal speech. assume
A Practical
Approach
Once MBD is accepted
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to MBD as a
myth,
the following guidelines may be help¬ ful to the pediatrician in dealing with general symptoms of hyperactivity,
learning problems, Avoid
etc.
Using the Term "MBD".-Con-
fusion regarding MBD can be pre¬ vented only if this label is not used at all. The term "MBD" is simplistic, harmful, and overworked. It is an at¬ tempt to apply a medical diagnosis to a nonmedicai problem. A physician
effectively treat hyperactivity, learning problems, etc, without ever using the term "MBD." It is far bet¬ ter to use labels that describe a prob¬ lem in terms of specific limitations of human functioning. Well-trained edu¬ cators approach learning problems in this fashion and can then proceed to specific treatment strategies. The MBD label tells us nothing about ap¬ propriate therapy. Reconsider MBD Diagnoses.—If the physician is asked to give his opinion on a patient whose condition has pre¬ viously been misdiagnosed as MBD, he has an excellent opportunity to al¬ can
leviate confusion. He can tell the par¬ ents that their child is not mentally retarded or brain damaged. He can remove the MBD label by explaining to the parents that this is a term that previously enjoyed popularity but proved to be imprecise. Most parents are very relieved to learn that their child does not have MBD. He can then apply a more appropriate label for the child's particular problem.
Keep
Medical Evaluation Reason¬
able.—If the patient has not been ex¬ amined by a physician in the past year, one need only do a routine phys¬ ical and neurological examination. Soft neurological signs need not be tested for. These signs have taught us the limitations of our medical diagnostic tools. With this routine approach, the pediatrician can ade¬ quately rule out major neurological disease without referral to a neurolo¬
gist.
Unwarranted diagnostic procedures should be avoided. If the parents or school demand an EEG and it is not indicated, the physician can refuse to order it. The child should not be sent to a psychologist to seek answers to the question about the presence or ab¬ sence of an organic cause. A referral
a psychologist is indicated only when the school and parents do not agree on the child's abilities or when there is a question of mental retarda¬
to
specific learning disability, or emotional problem.22 In these cases the physician should not try to dupli¬ cate the psychologist's skills by trying inexpertly to assess the child's hand¬ writing, geometric design reproduc¬ tions, and reading skills. If time per¬ mits, psychosocial assessment will often yield pertinent information. tion,
a
Prescribe
Drugs Sparingly.—
Most of
the disorders that have previously been labeled as MBD do not require the use of psychotropic drugs.41 They are never indicated for learning prob¬ lems, for no medication has the power to make children smarter. They are needed only in selected patients with hyperactivity.12 They are never indi¬ cated before a behavior modification program has been initiated at home and remedial educational programs have been initiated at school. Drugs
a simplistic approach to an extremely complex problem. It is un¬ fortunate that some physicians have joined the schools in advocating large-scale drugging of noncompliant children. The good physician will re¬
represent
sist pressures from the school to prescribe drugs for children until a complete evaluation is done and envi¬ ronmental factors have been cor¬ rected. Warn Parents About Unwarranted Therapy.—Parents must be warned of the many false-hope merchants who are trying to sell expensive treatment packages for the 20% of preschool and school-age children whom they de¬ scribe as having learning disabilities. They may emphasize relearning mo¬
development through patterning crawling. Body coordination exercises, using laterality training or walking on balance beams, may be tor
and
advocated. There is no evidence that these techniques improve learning. Even some schools have fallen prey to these approaches, since they too would like to find a shortcut to these complex problems. Food allergies have been alleged to be at fault, and hyposensitization treatment has been advocated without verification. So has megavitamin and trace element ther-
apy. Special visual training including muscle exercises, ocular pursuit, and eyeglasses has been advocated for
helping children with reading prob¬ Although these may lead to im¬ provement in eye coordination, they do not lead to improvement in learn¬ ing, reading, or hyperactivity. If the lems.
parents have already become involved with some nonhelpful approach, they may need to discuss with a sympa¬ thetic listener their normal hopes for a
magical
cure.
Endorse School's Plan.—Children with complex problems deserve a
comprehensive,
multidisciplinary
evaluation. Most of it should be done within the school system by special educators, psychologists, and speech therapists. After the child's specific disabilities have been delineated, an appropriate educational and behav¬ ioral treatment program can be de¬ signed." When the school presents its conclusions to the parents, they may not readily accept them for a variety of reasons. If the recommendations are at all reasonable, it is very impor¬ tant that the physician strongly sup¬ port them if the parents should turn to him for advice. Much of the success of any program will depend on the commitment of the family as well as the school. Refer Patient for Specific Therapy If School Cannot Provide It.—In general, the pediatrician is the least impor¬ tant person in designing and provid¬ ing the final treatment program. This is the school's responsibility. If the school does not fulfill its obligations, the physician may need to help the family arrange for comparable ser¬ vices in the community, either pub¬ licly or privately. He needs to be aware of the nearest competent learning disability clinic or private psychologist who can coordinate the diagnosis and management of such
disorders. If the school has not fulfilled its role, it is time for the physician, as well as the family, to complain. He can insist that the school system pro¬ vide an educational program for his patient. Some state laws mandate the schools to provide an appropriate edu¬ cation for all children or risk a law¬ suit. In this way, the physician has
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not
attempted
to evaluate
or
treat
the child in place of the school. In¬ stead, he has taken on the role of child
and, by his position in the community, has influenced the school to better meet the needs of all children; at the least, he has attained prefer¬ ential treatment for his patient. advocate
Give Educational Problems Back to Educational Experts.—The pediatrician has fostered an erroneous expectation that brain damage should be ruled out in all children with school problems. The time has come for us to admit that it is deleterious to automatically fulfill and perpetuate the school's request for extensive neurological evaluation of these children. As phy¬ sicians, we must accept the fact that we are of minor importance in the management of these problems, and that sometimes there is no medical
diagnosis to be made.1213-44 We should impression to the schools that we have special expertise or that special examinations need to
not convey the
be done. The physician has also been ele¬
vated by some parents to an omnip¬ otent level. They expect him to coordinate the multidisciplinary eval¬ uations that pertain to nonmedicai problems. This may be possible for the pediatrician who has special in¬ terest and training in school prob¬ lems. However, the average practic¬ ing pediatrician finds this expanded role unrealistic. It leads to frustration for both him and the patient's family. There are other professionals, usually educators, who are more capable of coordinating the handling of these cases. The physician should focus his energies on those areas where no one
else can do a better job. This is a logical division of labor.
simply
Conclusion
damage" is an in¬ wastebasket diagnosis. Medi¬ valid, cine does not normally permit this de¬ gree of vagueness and imprecision. It is also a harmful diagnosis: it allows us to overlook environmental factors, it labels children in a derogatory way, and it encourages the use of drugs. Even if MBD could be proved to be present in a few patients, this would remain an exercise in futility, since it would not bring forth any specific changes in therapy. It is time to dis¬ card this term. Since physicians in¬ vented the MBD concept, only physi¬ cians can bury it. "Minimal brain
Melvin Weiner, MD, Stephen Cohen, MD, and James McGinnis, MD, reviewed the manuscript.
References 1. Clements SD: Minimal Brain Dysfunction in Children: Terminology and Identification, monograph 3. US Dept of Health, Education and Welfare, National Institute of Neurological Disease and Blindness, 1966. 2. Werner EE, Bierman JM, French FE: The Children of Kauai. Honolulu, University of Hawaii Press, 1971. 3. Lucas A, Rodin E, Simson C: Neurological assessment of children with early school problems. Dev Med Child Neurol 7:145-156, 1965. 4. Hart Z, Rennick PM, Klinge V, et al: A pediatric neurologist's contribution to evaluations of school underachievers. Am J Dis Child 128:319\x=req-\ 323, 1974. 5. Kinsbourne M: School problems. Pediatrics 52:697-710, 1973. 6. Touwen B, Prechtl HF: The Neurological Examination of the Child With Minor Nervous Dysfunction, publication 38. Clinics in Developmental Medicine, London, Spastics International Medical Publications, 1970. 7. Benson DF, Geschwind N: Cerebral dominance and its disturbances. Pediatr Clin North Am 15:759-769, 1968. 8. Benton AL: Right-left discrimination. Pediatr Clin North Am 15:747-758, 1968. 9. Adams RM, Kocsis JJ, Estes RE: Soft neurological signs in learning-disabled children and controls. Am J Dis Child 128:614-618, 1974. 10. Copple PJ, Isom JB: Soft signs and scholastic success. Neurology 18:304, 1968. 11. Capute AJ, Niedermeyer EFL, Richardson F: The electroencephalogram in children with cerebral dysfunction. Pediatrics minimal 41:1104-1114, 1968. 12. Kenny TJ, Clemmens RL: Medical and psychological correlates in children with learning disabilities. J Pediatr 78:273-277, 1971. 13. Kenny TJ, Clemmens RL, Hudson BW, et al: Characteristics of children referred because of hyperactivity. J Pediatr 79:618-622, 1971. 14. Freeman R: Special education and the electroencephalogram: Marriage of convenience. J Special Educ 2:61-73, 1967. 15. Adams J: Clinical neuropsychology and the
study of learning disorders. Pediatr Clin North Am 20:587-598, 1973. 16. Schmitt BD, Martin HP, Camp BW, et al: The hyperactive child. Clin Pediatr 12:154-169, 1973. 17. Weiner IB, Goldberg RW: Psychological testing of children. Pediatr Clin North Am 21:175-186, 1974. 18. Benton AL: Behavioral indices of brain injury in school children. Child Dev 33:199-208, 1962. 19. Mosher DL, Smith JP: The usefulness of two scoring systems for the Bender gestalt test for identifying brain damage. J Consult Psychol 29:530-536, 1965. 20. Schafer R: The Clinical Application of Psychological Tests. New York, International Universities Press Inc, 1948. 21. Anastasi A: Psychological Testing, ed 3. New York, Macmillan Co, 1968. 22. Allmond BW: Psychological testing of children: Review and commentary. Pediatr Clin North Am 21:187-194, 1974. 23. Bradley C: Benzedrine and Dexedrine in the treatment of children's behavior disorders. Pediatrics 5:24-37, 1950. 24. Nichamin SJ: Recognizing minimal cerebral dysfunction in the infant and toddler. Clin Pediatr 11:255-257, 1972. 25. Rutter M, Graham P, Yorke W: A Neuropsychiatric Study in Childhood, publications 35 and 36. Clinics in Developmental Medicine, London, Spastics International Medical Publishers, 1970. 26. Huessy HR, Gendron RM: Prevalence of the so-called hyperkinetic syndrome in public school children of Vermont. Acta Paedopsychiatr 37:243-248, 1970. 27. Morrison JR, Stewart MA: Evidence for polygenetic inheritance in the hyperactive child syndrome. Am J Psychiatry 130:791-792, 1973. 28. Zah\l=a'\lkov\l=a'\M, Vrzal V, Kloboukov\l=a'\E: Genetical investigations in dyslexia. J Med Genet 9:48-52, 1972. 29. Paine RS, Werry JS, Quay HC: A study of minimal cerebral dysfunction. Dev Med Child
Neurol 10:505-520, 1968. 30. Palkes H, Stewart M: Intellectual ability and performances of hyperactive children. Am J Orthopsychiatry 42:35-39, 1972. 31. Werry JS: Studies on the hyperactive child. Arch Gen Psychiatry 19:9-16, 1968. 32. Cruickshank W, Bice H: Personality characteristics, in Cruickshank W (ed): Cerebral Palsy: Its Individual and Community Problems, ed 2. Syracuse, NY, Syracuse University Press, 1966, pp 135-191. 33. Ounsted C: The hyperkinetic syndrome in epileptic children. Lancet 2:303-311, 1955. 34. Gunderman JR, Stamler R: Neuropsychological residuals seven years after acute encephalitis. Clin Pediatr 12:228-230, 1973. 35. Dencker SJ: A follow-up study of 128 closed head injuries in twins using co-twins as controls. Acta Psychiatr Neurol Scand 33(suppl 123):1-125, 1958. 36. Abrams AL: Delayed and irregular maturation versus minimal brain injury. Clin Pediatr 7:344-349, 1968. 37. Werry JS: Development hyperactivity. Pediatr Clin North Am 15:581-599, 1968. 38. Lesser LL: Hyperkinesis in children: Operational approach to management. Clin Pediatr 9:548-552, 1970. 39. Graff M, Scott WE, Stehbens JA: The physician and reading problems. Am J Dis Child 128:516-520, 1974. 40. Ingram TTS: Speech disorders in childhood. Pediatr Clin North Am 15:611-626, 1968. 41. Browder JA: Appropriate use of psychic drugs in school children. Am J Dis Child 124:606\x=req-\ 607, 1972. 42. Freeman RD: The drug treatment of learning disorders: Continuing confusion. J Pediatr 81:112-115, 1972. 43. Clemmens RL, Kenny TJ: Clinical correlates of learning disabilities, minimal brain dysfunction, and hyperactivity. Clin Pediatr 11:311\x=req-\ 313, 1972. 44. Schmitt BD: Responsibility for school problems: An objection to "pediatric globalism." Pediatrics 44:771-773, 1969.
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