Retardation in Young Children: A Developmental Study of Cognitive Deficit

The most recent literature estimates an incidence of mild MR at This is consistent with a recent study using a national survey of 46, households in the United States that found the prevalence of MR in the noninstitutionalized population to be 7. MR has been found to occur more frequently in boys with a male to female ratio of 1. Mild MR tends to be familial or polygenic compared with severe MR, which tends to be sporadic. Severe MR has no socioeconomic, racial or geographic predilection. A survey of physicians referring patients with MR to subspecialists has shown that a high priority is given to determining the cause of MR Determining such etiology can be useful in counselling families about prognosis, recurrence risks and preferred modes of available therapy.

Malnutrition is probably the most common cause of mild MR worldwide, in conjunction with sociocultural deprivation and other problems related to poverty This suggests that in a significant proportion of children, mild MR is associated with growing up in a deprived environment. Stromme and Hagberg 14 studied children with MR derived from a population-based series of 30, children born between and in Norway. Monogenic and chromosomal disorders were more frequent in the severe MR group, whereas, less specific deficits were associated with mild MR.

Prenatal factors were implicated more often than perinatal or postnatal factors combined. Noteworthy, a study conducted in Atlanta, Georgia, of children born in the mids revealed that low birth weight was associated with a two-to fourfold increased risk for MR Despite substantial changes in neonatal management in the interim, the smallest infants are still at increased risk for developing mild and severe MR. Finally, a recent longitudinal follow-up study of very low birth weight infants those weighing less than g born between and found that they had lower mean IQs than controls.

Down syndrome is the most common with an incidence of one in to live births Some conditions occur predominantly in boys eg, Fragile X and Coffin Lowry 18 , In a Norwegian population-based series, X-linked recessive conditions occurred in six of 63 9. Other conditions, such as Rett syndrome, occur predominantly in girls Angelman syndrome was found to account for 1.

About one-third of individuals with Noonan syndrome have a mild intellectual disability with an average IQ 10 points below that of unaffected family members The literature on the prevalence of FAS is far from consistent. The occurrence of FAS can range from 0.

People with FAS can have IQs from well within the normal range to the severely mentally retarded range. On average, individuals with the full syndrome have mild MR with IQ scores in the 60s Physical anomalies can be slight or quite striking. Table 3 presents the clinical features of FAS Learning difficulties, poor attention, hyperactivity and adaptive functioning problems that grow more significant as the child matures have also been described with FAS. It is well recognized that children who have been exposed to alcohol antenatally may be at risk for the primary and secondary disabilities associated with antenatal alcohol exposure even if the physical phenotype is normal.

For this and other reasons, different groups have attempted to create accurate, reproducible tools for diagnosing FAS and related conditions. One such approach is the University of Washington 4-digit diagnostic code This approach attempts to score the magnitude of expression of four key features growth deficiency, facial phenotype, brain dysfunction and gestational alcohol exposure in a reproducible manner.

The end result is 22 possible unique clinical diagnoses ranging from FAS, alcohol exposed to no cognitive, behavioural or sentinel physical findings detected, no alcohol exposure. These specific diagnoses can then be better used for educational planning, advocacy, reporting and research. MR is also associated with a number of disorders.

Cerebral palsy is a static disorder of motor function that occurs as a result of injury or abnormal morphogenesis of the motor region of the immature developing brain. Sensory impairments visual and hearing , psychiatric disorders and language deficits are also common among individuals with MR. Further, the co-occurrence of these disorders tends to increase with the severity of retardation. Central nervous system malformations are present in some patients with MR This can include neural tube defects and hydrocephalus. In a study of 60 patients with MR, 10 Neuronal migrational disorders, such as lissencephaly, and defects of cortical organization, such as polymicrogyria and schizencephaly, often present with MR along with other features, such as seizures, spasticity and microcephaly.

Other neurological conditions to be considered include neuromuscular disorders and neurocutaneous syndromes, such as tuberous sclerosis TS and neurofibromatosis type 1 NF One-third of patients with Duchenne muscular dystrophy can have mild to moderate MR The degree of intellectual dysfunction ranges from very mild to severe.

Individuals whose seizures continue after treatment and those with a large number of cortical tubers have a much greater likelihood of mental disability. Autism is a neurobehavioural syndrome characterized by pervasive and severe deficits in verbal and nonverbal communication and social skills, and includes the presence of abnormal repetitive and stereotyped behaviours. It has been widely documented that the majority of individuals with autism also have MR.

There is a higher incidence of autism in boys, with one study 33 of 97 children finding It has also been established that, on average, the mean IQ scores of groups of girls with autism are slightly lower than for groups of boys with autism 34 , Further, in the very severe and profound ranges of retardation, the sex ratio of males to females has been found to shift from 4. This suggests that there is an excess of girls with autism in the severe range of MR Visual-spatial abilities are usually better in autistic individuals, often resulting in a higher Performance IQ score than Verbal IQ score and, hence, an uneven cognitive profile.

While certain behavioural and cognitive features may be over-represented in all patients with MR, it is important to know that specific behavioural patterns may be associated with certain genetic syndromes. Specific molecular or molecular cytogenetic tests exist for these and many other genetic syndromes associated with recognizable behavioural phenotypes.

In addition to the above disorders, studies have reported significant psychiatric morbidity in individuals with MR. Psychiatric disorders such as depression including bipolar affective disorder , psychosis and anxiety disorders including obsessive compulsive disorder and phobias were noted. Behavioural problems were also reported to be prominent in another study. They included problems in feeding, elimination, sleeping, hyperkinesis, hypokinesis, stereotyped behaviours, self-injurious behaviour and licking.

Further, these behaviours were closely associated with cognitive development level Other presentations may include congenital hypotonia, seizures, feeding problems, or other symptoms associated with CNS malformations. Milder forms of MR may not be picked up until the school years.

Impairments in adaptive functioning, rather than low IQ, are the usual presenting features. Lack of communication skills may predispose to disruptive and aggressive behaviours. Therefore, careful attention to the rate of development in separate developmental streams in children is very important. The history, including pre-, peri-and postnatal features, could assist in determining an etiology.

The use of prescribed medications and other drugs during pregnancy should be closely reviewed. Consumption of an average daily alcohol volume of one or more drinks during pregnancy has been associated with an increased risk of FAS and related disorders A rash or fever during the pregnancy should raise the possibility of a congenital infection. Recurrent unexplained illness, seizures or loss of psychomotor skills raise the possibility of a metabolic disorder.

Childhood human immunodeficiency virus-related encephalopathy may also present with unexplained illnesses and global impairment of cognitive and social functioning Gathering a careful family history is essential in the etiological search of MR. When MR is suspected, the child should always have a complete physical examination. A thorough physical examination helped to determine a diagnosis in 22 of patients Such an examination should incorporate a review of growth parameters including head circumference and the skin looking at neurocutaneous stigmata, abnormal pigmentation and dermatoglyphics 29 , Dysmorphic features looking especially at the face, hands and feet and genitalia can be suggestive of aneuploidy.

This is particularly the case if there is reduced family resemblance. Finally, a detailed neurological examination should always be performed. Clinical photographs may be useful to document and follow findings. A behavioural phenotype may be apparent after observing cognitive, language and social skills during the consultation. Audiological assessment and an ophthalmological review can supplement the initial clinical examination. Information from other sources eg, past health records, teacher reports may also be of help.

Obviously, the need for referral depends on the comfort and competency of the primary practitioner to take the history outlined above and elicit the appropriate clinical findings. Access to and familiarity with the investigations, which are outlined below, will also play a role in the decision of whether to refer.

A number of recent reports have highlighted the beneficial role played by subspecialist involvement be it by a neurologist, geneticist or developmental paediatrician in the diagnosis and management of MR 47 , There is no universally accepted approach to the etiological work-up of developmental delay and MR A consensus conference using available literature and expert opinion sponsored by the American College of Medical Genetics in attempted to identify some consensus recommendations and is summarized in Table 4 Selective laboratory testing in most patients should include a karyotype at the band level, especially if the diagnosis is not apparent.

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Chromosomal abnormalities are one of the most common causes of MR The severity of MR and presence of congenital anomalies has been thought to increase the yield of abnormality Such microdeletion syndromes represent cytogenetic alterations not observed in a routine karyotype. These probes should be considered when clinically indicated Table 2. It is important to remember that if FISH testing is ordered, you must specify which disorder is under consideration. It should be considered in both boys and girls with unexplained MR, especially in the presence of a positive family history, or a suggestive physical or psychiatric phenotype It has been argued that screening for Fragile X in all patients with idiopathic MR would result in the detection in 0.

There is debate, however, about whether Fragile X screening can be refined with screening checklists 47 , Neuroimaging should be considered in patients without a known diagnosis especially in the presence of focal neurological abnormalities, cranial contour abnormalities, macrocephaly, or microcephaly Shevell et al 48 found that imaging studies performed for a specific indication eg, microcephaly were more than three times as likely to result in an etiological yield than when done on a screening basis.

The magnetic resonance imaging MRI scan is superior to the computed tomography CT scan because it provides more accurate images of the structures of the posterior fossa and of maturational differences in the brain including myelination. A higher rate of abnormality detected by MRI compared with CT has been observed in the literature There is also lack of exposure to ionizing radiation.

The CT scan is useful, however, for conditions associated with intracranial calcifications and suspected craniosynostosis. Neuroimaging is not required in known syndromes unless there are additional neurological signs not consistent with the diagnosis. Careful analysis of brain neuroimaging, combined with a detailed history and physical examination, enables clinicians to establish etiological links and insights into the developmental brain problems associated with MR. Recent investigations have reported that high intensity lesions on T2-weighted images and hyperintense lesions on T1-weighted images could be disease specific abnormalities for NF-1 Although the significance of such lesions and their relationship to clinical features such as MR has not been established, this is an example of how imaging techniques are shedding new insights into conditions associated with MR It remains controversial, however, whether neuroimaging is indicated in all cases of NF It has been argued that routine metabolic screening should be abandoned because of its low yield in the work-up of MR Endocrine and metabolic causes of MR accounted for only 0.

This figure is in agreement with a recent Australian study that showed the diagnostic yield of urine amino and organic acid screening tests to be 1. The authors of this study 55 argue that despite the low diagnostic yield, these investigations should still be strongly considered. It is argued that the expense of these investigations is outweighed by the early diagnosis of inborn errors of metabolism. Such benefits include early therapeutic intervention, assisting couples in making reproductive decisions and the potential reduced costs to society with respect to the long term supervised care that affected individuals may require as adults.

Certainly, if the clinical picture suggests such a cause eg, growth failure, hypoglycemia or acidosis , then metabolic studies are mandatory Table 5. Such a screen would include screening the urine amino acids, organic acids, complex and simple sugars and mucopolysaccharides and blood plasma amino acids, serum lactate and serum ammonia.

In addition, other metabolic investigations that may be considered depending on the scenario could include very long chain fatty acids, serum 7-dehydrocholesterol and total cholesterol, thyroid function studies, lactate to pyruvate ratios and cerebral spinal fluid studies lactate, amino acids and glucose. A creatinine phosphokinase may be fruitful in boys in the preschool years presenting with developmental delay, particularly, if there are concerns about gross motor skills given the association of MR with some forms of muscular dystrophy such as Duchenne.

Congenital infection accounted for 0. Serology, however, is not useful in diagnosing such infections beyond the newborn period. Battaglia et al 45 found a relatively high diagnostic yield 8. Seizures often coexist with Rett and Angelman syndromes. For this reason, new technologies are being developed. At present, one exciting new test modality is the ability to screen for subtelomeric chromosome deletions. The telomeres are the gene-rich ends of the chromosomes. While these tests are not yet widely available, these and other tests should become more accessible on a clinical basis within the next few years.

It remains to be seen whether specific checklists may help triage which patients should be studied using these techniques It should be noted that most of the studies cited were performed by subspecialists eg, neurologists, developmental paediatricians or geneticists. Therefore, general paediatricians may be unlikely to undertake such investigations. However, it is useful for them to be aware of the above tests and procedures so that they can refer patients who may be appropriate. While some studies of investigations of MR in children have been retrospective chart reviews 45 , 47 , there have also been some prospective studies conducted All these studies have confirmed that the most important aspect of any evaluation remains a thorough history and physical examination This was the case in the study by Shevell et al 48 where physicians did not follow a specified template, but rather used their own discretion when ordering tests.

However, this makes it difficult to generalize the yield of such tests to all populations It has been suggested that a multisite, protocol-driven study would be of value in obtaining a degree of uniformity in investigations carried out and hence allow some estimation of the yield of the investigations outlined above. The aims of paediatric management are to provide support to people with MR and their families and to assist them in creating personally satisfying lives Table 4. It is vital that the practitioner not fail to diagnose specific syndromes or treatable genetic conditions.

Patients with MR, along with their families, benefit from a directed clinical and laboratory evaluation aimed at establishing etiology, as outlined in the preceding paragraphs. This in turn provides a focus for education about the diagnosis and counselling about prognosis. Paediatricians must be aware, however, that most causes of MR are not treatable directly. Nevertheless, accurate diagnosis may aid in genetic counselling, and alleviate parental guilt.

More importantly, even if an etiological diagnosis cannot be made, the provision of sound advice and emotional support from both the primary physician and sometimes from other parents through support groups can assist in planning for future needs. While few details of the consultation in which a diagnosis or lack thereof will be remembered in later years, the way in which this information is conveyed may well be. Key components leading to increased satisfaction in this study included a sympathetic and approachable manner, combined with direct and clear communication.

A range of emotions and reactions from the parents is possible, ranging from wanting to be left alone to having questions answered immediately Research has demonstrated that parents wish to be given as much information as early as possible and to be treated as the people primarily responsible for their child Physicians can learn directly from parents and people with MR about the best way to communicate a diagnosis of MR. A summary of key components involved in informing parents about a diagnosis of MR are presented in Table 7.

Recurrence risks, where appropriate, and guidelines for management, such as referral to appropriate services for therapy, education, financial and other support services should be addressed Provision of accurate recurrence risk counselling depends on identifying the correct underlying diagnosis. If a specific diagnosis is reached, then the possibility for carrier testing or prenatal diagnosis may exist.

In addition, the child with MR should personally receive recurrence risk counselling in adolescence or adulthood when appropriate. It is important that the practitioner has an intricate knowledge of community resources for the family.

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Services will vary from province to province and may involve both government and subsidized agencies. Services for children of different ages may also be provided by different government departments. For the family of a child with MR, this array of services may be confusing. Obviously each family will have their own particular needs for their child but the United Nations has listed a number of services that governments should provide This includes provisions discussed elsewhere including information, counselling and consumer or parent support groups.

Other important services include financial assistance, equipment at low cost , recreation or community access facilitation and, ultimately, vocational training. Respite care often with other families has been found to be an important resource for families of children with MR, particularly if the primary caregiver has some underlying distress Further, it has been found to reduce the incidence of child maltreatment The medical practitioner also plays a crucial role in managing medical problems, such as those related to nutrition, epilepsy and spasticity.

Anticipatory guidance on expected medical complications is also of benefit to the patient and family. There are now some excellent resources to help physicians and other healthcare professionals manage their patients who present with common syndromes. One such example is the textbook Management of Genetic Syndromes The number of medical conditions associated with MR that are completely treatable by medical means is small.

The prototypical example is phenylketonuria PKU. The profound MR and autistic features associated with untreated PKU can now be completely prevented by dietary manipulation. It is for this reason that newborn screening programs for PKU exist in virtually every jurisdiction. It is now recognized that treatment for PKU should continue life-long to prevent subtle effects on IQ and performance. It is also well known that women with a known history of PKU, or with a previously undiagnosed case of hyperphenylalaninemia, are at significant risk for having children with MR.

For this reason, strict management is needed during pregnancy. In other disorders associated with MR, specific therapies may help at least modify behavioural symptoms. The autosomal recessive disorder Smith-Lemli-Opitz SLO syndrome is caused by an inborn error of cholesterol metabolism. Replacement therapy with high doses of cholesterol is associated with improved growth in patients with SLO.

We have made a proposal for such a classification Table 2 incorporating the "Cognitive domains". Global developmental delay GDD and intellectual disability previously known as mental retardation. Cognitive deficits in children may affect all domains of cognitive functions including motor and executive functions. The causes of GDD are diverse, and usually an underlying causative pathology is identifiable in most cases [].

Intellectual disability is also heterogonous group of disorders where the cognitive deficit is global. Intellectual disability is defined as the significant limitation in intellectual functioning and adaptive behavior which covers every day social and practical skills. The disability commences before the age of 18 years.

Intellectual disability has a diverse etiology and varying severity. Causes of global development delay and intellectual disability include genetic disorders, inborn errors of metabolism, endocrine disorders, developmental and degenerative disorders of the central nervous system, demyelinating disorders, intrauterine infections, hypoxic ischemic insults, prematurity, birth trauma and exposure to drugs and toxins.

Numerical abnormalities of sex chromosomes e.

A rational approach to the child with mental retardation for the paediatrician

XXX are sometimes associated with cognitive impairment. Structural chromosomal abnormalities include deletions, insertions, inversions and translocatios. Cytogenetically invisible deletions like interstitial microdeletions and subtelomeric deletions can also produce psychomotor retardation and behavioral problems. Specific language Impairment SLI is defined as an unexpected persistent impairment in language ability despite adequate opportunity and intelligence, in the absence of explanatory medical conditions.

SLI is further classified according to the sub domain or modality of impairment into development articulation disorder, specific speech articulation disorders, developmental expressive language disorder, developmental receptive language disorder, developmental mixed receptive expressive disorder and acquired aphasia with epilepsy ICD, DSM-IV-TR.

The exact etiology of SLI is not fully sorted out and attributed to heterogeneous causes. There is a significant contribution of genetic factors. Over the past few years there have been several investigations to unravel the genetic factors associated with language impairment. Specific disorders of scholastic skills are best examples of cognitive deficits affecting specific domains.

These include specific disorders of reading Dyslexia , writing Dysgraphia , arithmetic ability Dyscalculia , non-verbal learning disability and Gerstman syndrome. Four candidate genes in 6pp22 region have recently been identified, with the results indicating that a disturbance in neuronal migration could lead to the symptoms associated with dyslexia [42]. Autism Spectrum Disorder ASD , also known as Pervasive Developmental Disorder PDD , is a complex neurodevelopmental disorder characterized by impairments in social interaction and communication, restricted repertoire of interests and stereotyped activities [].

It is often diagnosed before the age of four, and is at least four times more frequent in males than females. One of the salient features of ASD is the striking etiological, clinical and genetic heterogeneity. In the past few decades, an alarming increase in the prevalence of ASD has been observed in different countries worldwide.

Genetic basis of ASD: Multiple domains of cognitive functions are affected in ASD. SNPs, which are single base alterations in a DNA sequence, are responsible for much of the genetic variation in the human genome. Genetic association studies can be used to examine whether a particular genetic variant is associated with the disorder. Since most of the associated SNPs are located in the non-translated portions of the genome, their functional impact cannot be determined. However, several functional SNPs, leading to a defective protein, have also been identified in the exonic regions of autistic individuals.

Despite the diversity, ASD patients exhibit similar behavioral and neuronal conditions, although differing in severities and co-morbidities. This commonality of neurological phenotypes suggests that the susceptible genes may act through a limited set of pathways [46]. Several studies have suggested a role for the genes involved in synaptic assembly, such as the synaptic cell adhesion molecules CAMs , ion channels, neurotransmitter receptors, and the scaffolding and cytoskeletal proteins that work harmoniously to provide synaptic structural integrity and functionality [47].

The concept of copy number variations CNVs as a possible genetic contributor to the development of ASD emerged ever since the publication of first CNV based study on autism families [48]. Since then, multiple large studies have been performed using different platforms to examine different cohorts. Several novel or rare CNVs, both de novo and inherited, were identified, especially affecting regions like 1q21, 5p De novo events were often more deleterious than inherited variations. The reported CNVs in autism are often enriched in genes with important functions in the nervous system like post synaptic translational regulation, neuronal cell adhesion, neuronal activity modulation and excitatory and inhibitory function imbalance [51].

Functional impact of CNVs were recently been investigated by studying the expression profile of genes within the rare de novo CNVs [52]. Genes which are involved in neural-related pathways were found to be mis-expressed. Over the past three years, several independent groups have conducted whole exome sequencing using non-overlapping ASD samples [], using trio families, showed that de novo point mutations are overwhelmingly paternal in origin.

Such a paternal bias in de novo point mutations has also been reported by Battaglia et al. Several novel genes were identified through these studies as playing a role in liability for ASD. These results further highlight the extreme genetic heterogeneity of ASD, while pointing towards a relatively small number of implicated biological pathways. Many of these de novo mutations identified disrupted genes in neural development and plasticity, chromatin related proteins involved in transcriptional regulation, especially during prenatal brain development [60].

Attention deficit hyperactivity disorders ADHD Hyperkinetic Disorder in ICD is another group of neurobehavioral disorders where the cognitive deficit extends into more than one cognitive domain-attention, executive function, language and learning. Though considered as a childhood disorder, ADHD can extend into adulthood, and can cause lifelong effects on cognitive and social functioning [63,64]. There are certain structured assessment tools with internationally accepted diagnostic criteria DSM IV that can make accurate diagnosis to reliable level. The etiology and pathology of ADHD is poorly understood.

ADHD is a complex disorder influenced by genetic and environmental factors. It is a highly heritable disorder. The number of children with cognitive deficits is escalating.

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Cognitive deficits may be developmental or acquired, occurring in all ages and in both sexes due to heterogeneous causes. The causes include prenatal and perinatal insults, malnutrition, genetic disorders, infectious diseases e. Given a world population of approximately 6. Individuals with cognitive deficits experience significant limitations in both intellectual functioning and in adaptive behavior, which adversely affects daily social and practical skills.

Even though many of these cognitive disorders have a genetic basis there are preventable measures at various levels from conception to early period of development. The scientific basis of carrier state and temporal relation of disease manifestation provide us themes to develop working models for prevention or amelioration of the severity of the disease. The theory of developmental origin of Health and disease DOHaD can be used as building block for developing treatment strategies for several genetically determined diseases.

A rational approach to the child with mental retardation for the paediatrician

As development is a continuum, supplementation of growth factors can be remedial to many disabling conditions. Children with intellectual disability or Global developmental delay should have a comprehensive evaluation to establish the etiology of the disability. This is illustrated in Figure 2. A specific etiological diagnosis offers the opportunity to discuss treatment, prognosis and advise against genetic recurrence.

A diagnosis can also avoid unnecessary testing and evaluation and costly repeated investigations and can lead to opportunities for improved health and functional outcome. The key elements of diagnostic evaluation are: Medical and developmental history, antenatal, natal and perinatal history 3-generation family history and Pedigree charting, Dysmorphologic examination, Neurologic evaluation and judicious use of laboratory and neuroimaging technique. A multidisciplinary team approach is the one globally advocated for the management of children or adults with cognitive deficits.

In the case of children special emphasis is on planning of educational intervention. The proposed Multidisciplinary team includes,. Specific guidelines and protocols are utilized to detect infant hearing impairment, visual impairment and global developmental delay. Specific screening for inborn errors of metabolism, endocrine dysfunction, and genetic tests are also being carried out. Delineation of deficits and identification of the nature of deficits and its extent.

Descriptions of numerous screening tests appropriate for pediatric office use are available at the Developmental-Behavioral Pediatrics Online Community. Instruments include the following child development inventories,. Comprises mental, motor, and behavior rating scales. Possibly the preferred test to determine IQ in those aged years. Appropriate for children aged 2. A comprehensive evaluation is required to establish the etiology of intellectual disability or global developmental delay.

The key elements of evaluation includes medical and developmental history, antenatal, natal and perinatal history, pedigree charting, dysmorphologic examination, neurologic evaluation, and genetic test. Since the use of karyotyping to first identify trisomy 21 in , genetic testing has evolved tremendously. Fragile-X testing still continues to be recommended for the initial evaluation of intellectual disability or global developmental delay. Chromosome microarray, which has replaced the standard karyotyping and fluorescent in situ hybridization subtelomere tests, has now become a first line test for the evaluation of intellectual disability.

Advances in genetic research now permit genome-wide discovery of chromosomal copy-number changes and single-nucleotide changes in patients with intellectual disabilities using technological advances such as microarraybased comparative genomic hybridization array CGH , single nucleotide polymorphism SNP genotyping arrays, and massive parallel sequencing also called next generation sequencing.

This has opened up new possibilities for the evaluation of individuals with intellectual disabilities or global developmental delays who have previously eluded a genetic diagnosis [37,50,]. Recent guidelines of American Academy of Pediatrics AAP on genetic testing in children warrant pediatrician's awareness of the newest genetic screening modalities. Assimilation and integration of data by specialists in a conference setting offers the most specific and accurate diagnosis. Differential diagnoses are lengthy for children with cognitive deficits and include the following,.

The scientific awareness and resources for prevention are limited in majority of the developing countries. Therefore, the challenge for this century is to encourage community leaders and government officials to take upon prevention of cognitive impairment as the highest priority for society. In the United States, the number of child behavior and development specialists, including child psychologists, behavioral-developmental pediatricians, and child psychiatrists, is approximately 8, Compare this with Uganda, where, in , there were two child psychologists, no child psychiatrists, and no behavioral-developmental pediatricians for a population of 10 million children.

In Saudi Arabia, there is just one behavioral pediatrician. In Laos and Afghanistan, there are no child psychologists, child psychiatrists, or behavioral pediatricians, and no special education programs. This is the norm in several developing countries where there is little recognition that some diseases, which affect children in the early years of life, may have long-term negative impacts in terms of brain function.

Thus, while number of children with cognitive limitations is increasing, they have little access to professional expertise. All possible measures should be taken through judicious planning of the investigations so that the best possible etiology and pathology can be arrived at.

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Each member of the team should view the case as a whole and generate a constructive approach for remediation and rehabilitation. Cooperation with schools and other agencies involved. Obtaining signed releases of information and regularly scheduled perhaps annually or more often if needed routine conferences. Identification and management of concurrent illness, seizure disorders, or physical etiology of cognitive impairment in a medical setting. In the case of mental retardation, a combination of appropriate school placement with a high level of slow-paced appropriate material working towards specific goals, good behavioral management, and strategies at home is the most helpful intervention.

Parents should be able to access educational and social service resources within the school setting. Common behavioral problems, including oppositional behavior or social skills deficits, may be referred to a mental health professional skilled in working with such patients. Children who have speech and language delays and other learning disabilities require an educational plan that not only sets goals each year, but also meets these goals. If the fully implemented and supportive academic approach turns out to be problematic by middle school, serious consideration should be given to prevocational and vocational training in high school.

Theories on cognitive processing, based on neurobiological experimental paradigms on adult lesion model, may not be fully applicable to the developing cognitive functions of a child. Knowledge of the neurobiological basis of cognitive processing is influenced greatly by advances in contemporary sciences including, Computer Science, Genetics, Developmental Neurobiology, Neurochemistry, Neurophysics, Neuroradiology, and Nanotechnology. Therefore, a multidisciplinary team approach consisting of Neurologists, Pediatricians, Clinical Psychologists, Speech Language Pathologists, Physiotherapists, Occupational Therapists, Clinical Linguists, Special Educators, Geneticists, Biochemists, Neuroradiologists, and Computer experts is essential to develop a multisectoral protocol for the comprehensive management of cognitive impairments in children.

All Published work is licensed under a Creative Commons Attribution 4. Cognitive Deficits and Behavioral Disorders in Children: Visit for more related articles at Annals of Behavioural Science. Cognitive Development in Children Different stages of cognitive development, along with influencing factors and cognitive defects are shown in Figure 1. Theory What it means? Cognitive Dissonance Festinger, Fundamentally motivational in nature. It is a post-structuralist psychological theory that construes learning as an interpretive, recursive, on-linear building process by active learners interacting with their surrounding physical and social world.

Social Learning theory Bandura Most human behavior is learned observationally through modeling: Social learning theory explains human behavior in terms of continuous reciprocal interaction between cognitive, behavioral and environmental influences Observation through modeled behavior therapy technique Appropriate attitude and emotional reaction behavioral modification 4. Social Development theory Vigotsky, Explains social influence on cognitive development. Learning is a universal aspect of the process of developing culturally organized, specific human psychological function.

The theory portrays multilevel agreement oriented conversation among participants supported by modeling facilities, suitable communication and action interface, and hence, applied epistemology. Conversation exchange and discussion general, educational 6. This is achieved through the presentation of reinforcements: According to the theory of operant conditioning, learning is controlled by an association between a particular behavior and its consequences. Appropriate reinforcement and punishment to a particular behavior 7.

Conditions of Learning Gagne There are different types and levels of learning of which, the major categories are verbal information, intellectual skills, cognitive strategies, motor skills and attitudes. The theory is mainly focused on intellectual skills which can be organized in a hierarchy based on its complexity. Delivering apt instructions for each activity Sequential learning 8. He expounded adult learning based on 6 assumptions, 1 the need to know, 2 self-concept, 3 adult learner experience, 4 the readiness to learn, 5 orientation to learning, and 6 motivation.

The core part of adult learning is from their experience. Pennington BF, Bennetto L. Toward a neuropsychology of mental retardation. Handbook of Mental Retardation and Development. Cambridge University Press; Genetic perspectives on mental retardation. Richardson SA, Koller H. Causes and Consequences of Mental Retardation. Harvard University Press; The prevalence of mental retardation: Dev Med Child Neurol. Epidemiology and prevalence of psychopathology in people with mental retardation. J Consult Clin Psychol. DSM-IV disorders in children with borderline to moderate intellectual disability.

Conduct disorder and cognitive functioning: Childhood mental ability and dementia. Relation between intelligence and psychopathology among preschoolers. J Clin Child Psychol. Mental health disorders among individuals with mental retardation: Emotional disturbances in mentally retarded children. Prevalence of dual diagnosis in community-based day programs in the Chicago metropolitan area. Rutter M, Graham P. Epidemiology of psychiatric disorder. Education, Health and Behavior.

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Isle of Wight Studies, — Developmental ecology through space and time: Examining Lives in Context: Perspectives on the Ecology of Human Development. American Psychological Association; On the definition and classification of mental retardation. Am J Ment Defic. Zetlin A, Murtaugh M. Whatever happened to those with borderline IQs? Maternal and neonatal risk factors for mental retardation: Like mother, like child: Self-sufficiency at ages 27 to 33 years: The Collaborative Perinatal Project: A scaled version of the General Health Questionnaire. Alcohol screening questionnaires in women: Houghton Mifflin Co; Emotional and behavioral problems in children and adolescents with and without intellectual disability.

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Lawrence Erlbaum Associates; Support Center Support Center. Please review our privacy policy. Lived with both parents. Less than 6 family moves. Maternal education less than high school. Not living with both parents at age 7. Family instability 6 or more moves. Inadequate family interaction score of 25 or above.