If You Were Retarded
Identification and Evaluation of Mental Retardation
Am Fam Physician. 2000 February 15;61(4):1059-1067.
Encounter related patient data handout on mental retardation, written by the authors of this article.
Article Sections
- Abstruse
- Prevalence
- Etiology
- Illustrative Case
- Diagnosis
- Evaluation and Referrals
- References
Mental retardation in immature children is often missed by clinicians. The condition is present in ii to 3 percent of the population, either as an isolated finding or as role of a syndrome or broader disorder. Causes of mental retardation are numerous and include genetic and environmental factors. In at least 30 to 50 percent of cases, physicians are unable to decide etiology despite thorough evaluation. Diagnosis is highly dependent on a comprehensive personal and family medical history, a complete concrete examination and a careful developmental cess of the kid. These will guide appropriate evaluations and referrals to provide genetic counseling, resource for the family and early on intervention programs for the kid. The family physician is encouraged to proceed regular follow-up visits with the child to facilitate a smoothen transition to adolescence and young adulthood.
The diagnosis of mental retardation in young children is often missed. The three most mutual errors fabricated by clinicians who overlook the possibility of mental retardation are (i) concluding that a child does non "await" retarded, (2) assuming that a child who is ambulatory is unlikely to be retarded and, (3) if retardation is actually considered, final that it is not possible to test immature children.i
Prevalence
- Abstract
- Prevalence
- Etiology
- Illustrative Case
- Diagnosis
- Evaluation and Referrals
- References
Mental retardation is nowadays in most 2 to 3 percent of the population. It tin can exist defined as cognitive ability that is markedly below average level and a decreased ability to adapt to one's surround. The onset of the status occurs during the developmental flow, i.e., gestation through age 18 years.
Mental retardation comprises v full general categories: deadline, mild, moderate, severe and profound. Categories are based on scores obtained through utilize of age-standardized tests of cognitive ability (Table 1).ii Mental retardation may occur as part of a syndrome or broader disorder but is most ordinarily an isolated finding.
TABLE one.
Developmental Characteristics Related to Level of Mental Retardation (DSM-IV Criteria)
| Mild retardation | Moderate retardation | Severe retardation | Profound retardation |
|---|---|---|---|
| 75% to 90% of all cases of retardation | ~x% to 25% of all cases of retardation | ~10% to 25% of all cases of retardation | ~10% to 25% of all cases of retardation |
| Function at i half to two thirds of CA (IQ: fifty to seventy) | Function at one tertiary to one half of CA (IQ: 35 to 49) | Function at one 5th to one third of CA (IQ: xx to 34) | Part at < one 5th of CA (IQ: < xx) |
| Tedious in all areas | Noticeable delays, specially in speech | Marked and obvious delays; may walk tardily | Marked delays in all areas |
| May take no unusual physical signs | May accept some unusual physical signs | Little or no advice skills but may have some understanding of speech and testify some response | Congenital abnormalities oft nowadays |
| Can larn applied skills | Tin larn simple communication | May be taught daily routines and repetitive activities | Need close supervision |
| Useful reading and math skills up to grades iii to 6 level | Can acquire elementary health and safety habits | May be trained in simple self-care | Often need bellboy intendance |
| Tin arrange socially | Tin can participate in simple activities and self-care | Need direction and supervision | May answer to regular physical activity and social stimulation |
| Can acquire vocational skills for self-maintenance | Can perform tasks in sheltered conditions | — | Not capable of self-care |
| Integrated into general society | Can travel solitary to familiar places | — | — |
The inclusion of concurrent related limitations in two or more adaptive skill areas was added to the definition of mental retardation in 1992 by the American Association on Mental Retardation.3 Because standardized testing in very young children is less predictive of future cerebral outcome, the term "developmental delay" has been used to characterize the developmental status of children under age three.
Etiology
- Abstract
- Prevalence
- Etiology
- Illustrative Case
- Diagnosis
- Evaluation and Referrals
- References
A number of environmental, genetic or multiple factors tin can cause mental retardation. Unfortunately, in approximately xxx to 50 percentage of cases, the etiology is not identified even afterward thorough diagnostic evaluation.4,5 Some persons have a congenital malformation of the brain; others had impairment to the brain at a disquisitional period in pre- or postnatal development. Caused causes of retardation include near-drowning, traumatic brain injury and central nervous system malignancy.
Prenatal causes of mental retardation include congenital infections such every bit cytomegalovirus, toxoplasmosis, herpes, syphilis, rubella and human immunodeficiency virus; prolonged maternal fever in the kickoff trimester; exposure to anticonvulsants or alcohol; and untreated maternal phenylketonuria (PKU). Complications of prematurity, especially in extremely depression-nascence-weight infants, or postnatal exposure to atomic number 82 can too cause mental retardation.half-dozen
Metabolic disorders are another possible crusade of mental retardation. In some cases (e.g., PKU, hypothyroidism), retardation is preventable with early handling. Other disorders (e.thou., mucopolysaccharidosis, sphingolipidoses) are less responsive to early intervention. Molecular medicine has made it possible to diagnose a number of conditions referred to every bit mitochondrial prison cell diseases.vii
A number of single-cistron disorders effect in mental retardation. Many of these are associated with singular or dysmorphic physical characteristics. Such conditions include fragile X syndrome, neurofibromatosis, tuberous sclerosis, Noonan's syndrome and Cornelia de Lange's syndrome. A complete listing of syndromes associated with mental retardation is beyond the telescopic of this article, and the reader is referred to the reference listing.8,9
As many equally ane fourth of persons with mental retardation accept a detectable chromosome abnormality. Children with Down syndrome (trisomy 21) usually accept highly recognizable concrete characteristics, but features associated with other chromosomal abnormalities, such as Klinefelter'southward syndrome (47,XXY), may not exist as obvious to family members or the doctor. Other children may have a small deletion or duplication of a particular chromosome that is rarely reported; thus, the phenotype is still undetermined. Some chromosomal abnormalities are inherited from a parent but virtually occur de novo. Many previously described clinical syndromes take been found to take an associated chromosomal aberration (eastward.g., DiGeorge, Prader-Willi, Angelman and Williams syndromes).
The following case report highlights the importance of early diagnosis, in planning therapy for the child and in providing family unit planning information to the parents.
Illustrative Instance
- Abstract
- Prevalence
- Etiology
- Illustrative Case
- Diagnosis
- Evaluation and Referrals
- References
A 16-month-old male child was referred for developmental assessment because he was not yet talking.
He was born to a 30-yr-erstwhile woman, gravida two, para 2, living children 2. He was delivered at term by cesarean department with no prenatal, labor or postnatal complications. He was slightly blue at birth and required oxygen. Female parent and babe went home in ii days, and no other newborn problems were noted. Birth weight was 3.2 kg (vii lb, 1 oz). The infant was breast-fed for most 12 months. Solid foods were added at 10 months, only some difficulty was noted with chewing. The boy rolled over at 3 to 4 months, sat without support at seven months and crawled at 7 to eight months. He began to walk at 16 months but nonetheless did not talk. The mother first became concerned about lack of speech when the child was 13 months onetime. The remainder of the medical history, the review of systems and the family history were noncontributory.
At 16 months, the kid's meridian and weight were less than the 5th percentile; head circumference was at the 25th percentile. The child was pleasant, alert, agile and cooperative. No vocalisation of any kind was noted during the test. Physical findings included a slightly prominent forehead with a depressed wide nasal bridge and a apartment nose. The midface appeared depressed; the child's confront closely resembled his mother'due south. The only other aberrant finding was a small left testis. The boy could represent a few seconds without support and was able to have a few steps. His muscle tone was mildly low but within the reference range.
The physician's impressions included the post-obit: midface hypoplasia, minor stature, rule out hearing loss, speech communication and language delays and global developmental delay, hypoplastic left testicle, incoordinated swallowing, rule out genetic syndrome related to hypoplastic facial features, developmental delay, small stature and familial resemblance.
In the pediatric genetics dysmorphology clinic, the above dysmorphic features were confirmed. He also had distinctive blepharophimosis, ptosis, epicanthal folds, altered palmar creases and hyperextensibility of the fingers and knees. Ohdo blepharophimosis syndrome was diagnosed, based on a London Dysmorphology Database search. Chromosomal status was 46,XY.
At 17 months' chronologic age, his developmental quotient was 61, with most filibuster occurring in speech, which was at the five-month level. Motor skills were at the xi- to 12-month level. He was evaluated past subspecialists who addressed his various problems. Initial hearing assessment revealed moderate hearing loss. The child was referred to an early intervention program.
Subsequent follow-upwards at 52 months of age revealed that the male child still had difficulty with feedings and was not yet toilet trained. His cognitive skills were at approximately a 27-month level, and genetic follow-up confirmed Ohdo blepharophimosis syndrome. The female parent had subsequently given nascency to a 2d child with the same syndrome.
Diagnosis
- Abstract
- Prevalence
- Etiology
- Illustrative Instance
- Diagnosis
- Evaluation and Referrals
- References
The physician must take a high index of suspicion to consider the diagnosis of mental retardation in any child. Some helpful clues include delayed speech, dysmorphic features (small-scale anomalies), hypotonia generally or of the extremities, general inability to do things for self and, not to the lowest degree, expressed business organisation by the parents.
The first and virtually important step in the diagnosis of mental retardation is to obtain a comprehensive patient and family history. Previous gynecologic and obstetric history may reveal infertility or fetal loss. Cess of maternal health condition during pregnancy with the involved child should include questions regarding utilise of tobacco, booze and drugs (prescribed and illicit); lifestyle or other risks for sexually transmitted diseases; weight gain or loss; signs of infection; serious illness or injury; and surgery or hospitalization.
To constitute a knowledgeable baseline history of the child, the physician should obtain data regarding length of pregnancy, premature onset of labor or rupture of the membranes, duration and form of labor, type of commitment and any complications. Apgar scores at one and (especially) five minutes should exist reviewed, and birth weight, length and head circumference measurements obtained and plotted on advisable growth charts. The parents should be asked about whatever illnesses, feeding or sleeping difficulties in the newborn menstruum and problems with sucking or swallowing, every bit well as the baby'southward general disposition. Extremes in infant temperament are often the beginning clue to an atypical class in child development.
The systems review of the child should be complete, with special attention to growth issues, history of seizures, lethargy and episodic vomiting. A developmental screen should be used at all well-child visits to obtain information about the timing of the kid'southward developmental milestones, any concerns past parents or caregivers and comparison of the child'southward developmental rate and blueprint with those of siblings. Specific questions most the kid's electric current developmental abilities should be asked at each visit.
The Revised Denver Prescreening Developmental Questionnaire10 is a useful screening tool that parents can readily complete to help determine the need for farther evaluation with the time-honored Denver Developmental Screening Examination.11,12 Another practical and reliable tool with which to monitor evolution in infants is the Kansas Infant Development Screen.13 The findings can be recorded and plotted only equally with somatic growth charts and shared with parents. Other developmental screening tests are also bachelor.
Delays in speech development are common and may become more obvious when contrasted with the speech development of a sibling. Enquiry should be made regarding concerns most hearing and vision. One cannot overemphasize the importance of addressing concerns voiced by a parent well-nigh a child'southward evolution, behavior and learning, considering these expressed concerns accurately target the bulk of children with developmental problems.
Information should be obtained almost the family unit, parents' occupations and educational achievements, educational and developmental condition of siblings, role of the patient in the family, discipline of the children and identity of the child'due south caregiver when the parents are not home. Family history of fetal loss, mental retardation, severe learning problems, congenital abnormalities and unexplained childhood deaths, too equally other serious illnesses in start- and second-degree family members, should be elicited.
A consummate physical examination can brainstorm with a review of growth curves since birth, if these are available. The head circumference should continue to be plotted. The examination should be thorough, with special attention to physical findings that are compatible with any chance factors obtained from the history.
The child should be examined closely for dysmorphic features or minor abnormalities, such as unusual eyebrow pattern, eyes that are widely or closely spaced, low-set ears or abnormal palmar crease patterns. Pocket-size abnormalities are defined equally defects that have unusual morphologic features without serious medical implications or untoward cosmetic appearance.8 Most minor abnormalities involve the face, ears, hands or feet, and are readily recognized fifty-fifty on cursory test.14 The presence of three or more than minor abnormalities in newborns is correlated with a xc percent frequency of coexistent major abnormalities,15 suggesting close clan with morphogenesis in utero. Thus, minor abnormalities may provide clues to developmental problems of possible prenatal origin.
Evaluation of the head, face, eyes, ears and mouth must include general cess of visual acuity and hearing. Examination of the breast, eye, spine, abdomen, genitalia, extremities, muscles and neurologic reflexes can reveal abnormalities that may be associated with retardation. Table ii highlights five common syndromes or problems associated with retardation.
TABLE ii.
Common Syndromes Associated with Mental Retardation
| Diagnosis | Incidence | Etiology, including inheritance | Clinical manifestations and early recognition | Associated conditions | Diagnostic evaluation* | Prognosis | Special considerations |
|---|---|---|---|---|---|---|---|
| Down syndrome | one in 600 to 800 births | Results from extra copy of chromosome 21, usually a sporadic event; 2% of cases may be inherited from a balanced translocation carrier parent | Hypotonia; flat facial profile; upslanting palpebral fissures; pocket-size ears; in-curving fifth fingers; single transverse palmar creases | Wearisome growth; congenital heart defect; thyroid dysfunction; developmental delay, especially spoken language | Chromosome analysis in all patients; chromosome assay of parents if translocation is found; pediatric cardiology evaluation with echocardiogram by 6 weeks of age | Cognitive limitations, with well-nigh in mild to moderate MR range; decreased life expectancy tin be associated with built eye defect, especially if not recognized in early on infancy | Except in cases where parent has a translocation, risk for recurrence is i% |
| Fetal alcohol syndrome | 0.05 to 3 in one,000 children diagnosed annually in United States | Alcohol consumption by female parent during pregnancy | Diagnosis tin be made at birth, based on history, baby's facial features (medial epicanthal folds, wide nasal span, small upturned nose, long philtrum, narrow or broad upper lip), low nascence measurements | May include retardation, behavior bug, ADHD, seizures, autism | Skillful history and physical examination imperative; history of maternal drinking, pre- and postnatal growth retardation, dysmorphic facial features, CNS involvement; no laboratory tests bachelor | Varies; growth may amend during adolescence and facial features may soften, but behaviors may crusade serious problems | Many of these children are adopted; FAS and fetal alcohol effects (usually developmental and behavioral problems) are totally preventable |
| Delicate Ten syndrome | 1 in ii,000 to 3,000 male person live births; females may also exist afflicted | Abnormality in FMR-1 gene located on Ten chromosome; inherited in X-linked mode so males are more severely affected | Macrocephaly; large ears; enlarged testicles after puberty; hyperextensible fingers | Autism/autistic- like behaviors; developmental delay, specially speech; awkwardness; mitral valve prolapse | DNA testing for fragile X mutation (chromosome testing for delicate X misses upwardly to vii% of cases); mothers of affected boys are obligate carriers of the gene | Normal life expectancy; balmy to profound MR | Females usually less severely affected than males; up to l% of females with mutation accept MR or educational difficulties; adventure for recurrence is 50% |
| [ corrected] Velocardiofacial syndrome | 1 in 700 live births | Deletion of chromosome 22; normally de novo but may exist inherited in an autosomal dominant mode | Cleft palate; congenital heart defect; spoken language filibuster; elongated face with almond-shaped optics; wide nose with hypoplastic alae nasi; small ears; slender, hyperextensible fingers | Learning disabilities ± mild MR; psychiatric disorder in 10% | High-resolution chromosome analysis with chromosome painting (FISH) to observe chromosome 22 deletion; parents should also exist tested | Normal life expectancy unless astringent heart defect (eastward.g., truncus arteriosus, interrupted aortic arch) is present | Risk for recurrence as high equally fifty%, depending on family history |
| Unknown cause of MR | xxx to fifty% of all cases of MR | Variable; diagnosis may evolve over time, so repeated evaluations may be helpful | Nonspecific cluster of minor malformations; delayed milestones, especially language development | Behavioral phenotype may as well aid diagnosis as course evolves | Cytogenetic studies; encephalon imaging; metabolic studies | Will vary considerably based on etiology (if it can be established) and/or severity | Diagnostic techniques that may help in diagnosis are constantly being refined |
Evaluation and Referrals
- Abstract
- Prevalence
- Etiology
- Illustrative Case
- Diagnosis
- Evaluation and Referrals
- References
Findings from the history and physical examination of the child volition help determine which diagnostic tests and referrals are appropriate for further cess. The physician needs to explain to the parents what these findings are and the reasons for further evaluation. The laboratory and radiographic assessment of individual children should be based on clinical presentation (Table three).16
TABLE iii.
Suggested Indications for Tests When Mental Retardation Is Unexplained
| Magnetic resonance imaging of the brain |
| Cerebral palsy or motor asymmetry |
| Abnormal caput size or shape |
| Craniofacial malformation |
| Loss or plateau of developmental skills |
| Multiple somatic anomalies |
| Neurocutaneous findings |
| Seizures |
| IQ < l |
| Cytogenetic studies |
| Microcephaly |
| Multiple (fifty-fifty pocket-size) somatic anomalies |
| Family history of mental retardation |
| Family unit history of fetal loss |
| IQ < 50 |
| Skin pigment anomalies (mosaicism) |
| Suspected face-to-face gene syndromes (due east.one thousand., Prader-Willi, Angelman, Smith-Magenis) |
| Metabolic studies |
| Episodic airsickness or languor |
| Poor growth |
| Seizures |
| Unusual torso odors |
| Somatic bear witness of storage disease |
| Loss or plateau of developmental skills |
| Movement disorder(choreoathetosis, dystonia, ataxia) |
| Sensory loss (especially retinal abnormality) |
| Acquired cutaneous disorders |
This initial sharing of information with parents is an extremely important step and volition probably ready the phase for the future physician-family unit-patient relationship. Ample fourth dimension should be scheduled to talk over the findings and to allow for questions, which will be numerous. The family unit should exist encouraged to write a list of questions for further communication with the physician. The clinician should clarify the term "developmental filibuster," considering parents ofttimes misinterpret this as meaning the child has the ability to take hold of upwardly.
It is best to seek other opinions as soon as mental retardation is suspected rather than adopting a "look-and-run across" approach. The Individuals with Disabilities Instruction Act (1997)17 provides for developmental assessment of children older than three years in every school district. For children younger than iii, similar baby-toddler assessment and early intervention resources are available, usually through local wellness departments, school districts or regional assessment centers. (The responsible agency varies in each state.)
Referral may be made to a third-level child development unit that can provide interdisciplinary evaluations (developmental pediatrics, genetics, neurology, ophthalmology) as well as functional assessments (occupational and concrete therapy, speech/language pathology, audiology, psychology). Families volition usually welcome such a referral and comprehensive evaluation, especially if the mental retardation is unexplained. Evaluations by a nutritionist and a kid psychiatrist may too exist appropriate for some patients.
The family doc should wait complete information on the findings from this type of team evaluation. The family should expect to be referred dorsum to their local community for ongoing primary intendance and, in some instances, subspecialty care. Data well-nigh early intervention resources in the local community should be shared with the family, and appropriate support services should be identified.
If the kid with mental retardation has a head circumference that falls beneath the 5th percentile (microcephaly) or above the 95th percentile (macrocephaly), a magnetic resonance imaging scan of the brain should be considered. This is usually preferable to computed tomographic scanning because of the enhanced visualization of developmental abnormalities of the cerebral cortex, such as pachygyria, polymicrogyria and schizencephaly. These disorders reflect an abnormality during the outset 25 weeks of gestation in the early on migration of the neurons into the normally half-dozen-layered cortex.
A consultation with a medical geneticist/dysmorphologist is invaluable. This would include a review of a iii-generation pedigree and records of pertinent relatives, evaluation for subtle dysmorphic features and assessment for a pattern to the patient's presenting characteristics.
Most mentally retarded patients who visit a genetics role undergo chromosome analysis. While this testing could be done by the referring physician, in that location are different levels of test quality, and it is usually best performed by a adept cytogenetics laboratory associated with a university hospital or children's infirmary. This allows for ease in interpretation of the results to the patient'south family unit in the event an abnormality is constitute. DNA testing for fragile X syndrome should be done instead of cytogenetic testing, which can miss upwardly to vii percent of those who are affected.18 Metabolic testing in the absenteeism of a history suggestive of metabolic disease is probably of little value.4
Diagnosis may require several periodic visits to a geneticist, because a phenotype may evolve slowly, and new syndromes are constantly being reported. The importance of making a diagnosis in a child with mental retardation cannot be overemphasized. An accurate diagnosis allows for anticipatory guidance for the patient, recurrence gamble information and genetic counseling for the parents, and opportunities for the family to become involved in specific support groups. An uncertain diagnosis should exist conveyed as such; no diagnosis is preferable to an incorrect 1.
Inside a given family, the risk of recurrence of mental retardation in future siblings or other relatives of the patient depends on the specific diagnosis. The recurrence chance for mental retardation cannot be given to the family until a diagnosis has been made, although a general discussion with a geneticist may be of benefit. The family physician is a valuable resources in periodically reviewing the recurrence run a risk for the family unit.
Practise guidelines for master intendance of children with sure weather (Down's syndrome, fragile 10 syndrome) are also bachelor,19–21 as are special somatic growth charts for some syndromes. There are also guidelines for the management of adults with mental retardation who have been deinstitutionalized.22 Tabular array iv lists Net resource that may exist valuable to the family md.
TABLE 4.
Internet and Computer Resources on Mental Retardation for Family Physicians
All physicians who care for children with mental retardation or developmental disabilities should remember that these patients quickly outgrow their childhoods. As they become adolescents and young adults, almost of them will demand professional intervention to help them become their own advocates in the health care organisation. Families should be supported as they encourage independent functioning on the part of their adolescent or immature-adult son or daughter.23 Problems relating to sexuality, family planning, custodial care, estate planning and guardianship are highly of import but are across the scope of this article.
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REFERENCES
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8. Jones KL, Smith DW. Smith'southward recognizable patterns of human malformation. fifth ed. Philadelphia: Saunders, 1997.
ix. Baraitser G, Winter RM. London dysmorphology database [CD-ROM]. New York: Oxford University Press, 1996. Retrieved June 1999, from Www: http://www.personal.monash.edu.au/~hofman/medcd/GEN1.htm.
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12. Frankenburg WK, Dodds JB, eds. Denver developmental screening test II. Denver: Denver Developmental Materials, 1990.
xiii. Holmes GE, Hassanein RS. The KIDS nautical chart. A simple, reliable infant development screening tool. Am J Dis Child. 1982;136:997–1001.
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15. Marden PM, Smith DW, McDonald MJ. Built anomalies in the newborn infant, including minor variations. J Pediatr. 1964;64:357–71.
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17. The Individuals with Disabilities Teaching Human action. Retrieved July 1999, from Globe Wide Web: http://www.ed.gov/offices/OSERS/Idea/train.html.
18. Rousseau F, Heitz D, Tarleton J, MacPherson J, Malmgren H, Dahl North, et al. A multicenter study on genotype-phenotype correlations in the delicate Ten syndrome, using direct diagnosis with probe StB12.3: the first 2,253 cases. Am J Hum Genet. 1994;55:225–37.
xix. Health supervision for children with Down's syndrome. American Academy of Pediatrics Committee on Genetics. Pediatrics. 1994;93:855–9.
20. Health supervision for children with fragile X syndrome. American University of Pediatrics Committeeon Genetics. Pediatrics. 1996;98(2 pt 1):297–300.
21. Hayes A, Batshaw Thou. Down's syndrome. Pediatr Clin North Am. 1993;40:523–35.
22. Tyler CV Jr, Bourguet C. Main care of adults with mental retardation. J Fam Pract. 1997;445487–94.
23. Lollar DJ, Reinoehl JK, Leverette AT, Martin JC, Posid VA. Facilitating and assessing progress toward independence: SPARX. Z Kinderchir. 1989;44suppl 118–20.
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