Developmental Neuropsychology

1. Developmental Neuropsychology Prepared by: CiciliaEviGradDiplSc., M. Psi

2. Introduction • The process of development does not always run smoothly  it is important to understand the disorders of development  for treatment • Development of neuronal connections  remains unsolved  believed that both genetically determined intrinsic factors and environmentally generated extrinsic factors contribute to the connectivity of the mature NS

3. Intrinsic Factors • Chemospecificity hypothesis by Roger Sperry (1968, 1971): • Neurons become chemically differentiated at early stage of their development  before environmental input is available • Have chemical labels  enable the neurons to recognize their targets  regeneration of neural tissue

4. Extrinsic Factors • Mostly in later stages of development when neuronal connections depend on which connections receive the most environmental stimulation • Plasticity  NS’s capacity to undergo adaptive modification in response to environmental or genetically based disruptions of normal development  ex: how brain reorganize itself after local injury or other external influences

5. Known Causes of Dev Abnormality • Inherited Disorders • Autosomal dominant transmission  transmission via chromosomes other than sex chromosomes requires only one parent gene • Autosomal recessive transmission  requires two genes, one from each parent  ex: PKU that causing mental retardation (intellectual disability) • Sex-linked transmission  any genetic disorders affecting one sex selectively, presumably due to a gene on the sex chromosome • Polygenic inheritance  interaction of several genes and also with environmental factors

6. Contd. • Chromosomal Disorders include a group of defects of the chromosomes as identified by abnormalities of their configuration (karyotype)  due to either environmental or genetic factors • Trisomy  extra chromosomes of three  trisomy 21 or Down Syndrome • Translocation  mismatching of chromosomes pairs or portions of a chromosome • Partial or complete deletion of a chromosome  ex: Turner’s syndrome (missing X chromosome)  impairments in perception of form and space

7. Contd. • Structural Abnormalities  due to disruptions of development  cause death or severe impairments: • Anencephaly  lack of brain development • Microcephaly  very reduced brain development • Prematurity and Low Birth Weight • Prematurity  either a birth weight of less than 2,500 g or birth before 37 weeks of gestation (WHO, 1961)

8. Contd. • Infection • Prenatal  rubella, which is associated with microcephaly, meningoencephalitis and mental retardation • HIV  cognitive impairments on children (not yet developed AIDS) • Hypothesis  also link to development of intelligence, LD and serious psychopathology, incld. schizophrenia  still weak

9. Contd. • Toxin-Related Damage • Fetal Alcohol Syndrome  from alcoholic mothers  characterized by facial malformations, intrauterine growth retardation and neurobehavioral dysfunction (include increased period with eyes open, body tremors, and decreased vigorous body activity( • Lead poisoning  associated with hyperactivity and poor performance in intelligence tests

11. Contd. • Nutritional Disorders • Kwashiorkor  protein-deficient diet • Marasmus  energy-deficient diet • Malnutritional milieu  when nutritional deficiency is being accompanied by other environmental and health-related problems  early sign: low birth weight  influence cognitive abilities • Nutritional deficiencies in adulthood  specific cognitive impairments: Wernicke-Korsakoff syndrome

12. Contd. • Anoxic Episodes  a period of oxygen deprivation, which can result in hypoxic- ischemic encephalopathy • Hypothesis  undiagnosed anoxia in early life may cause subclinical anoxic pathology  neuropsychological impairments, incld LD  received little empirical support • Traumatic Brain Injury  Infants and children are vulnerable to the effects of traumatic brain injury and neurological diseases such as neoplasms and stroke

13. Dev Disorders of Unknown Cause • Learning Disorders • Attention Deficit Disorder • Autism

14. Learning Disorders • An impairment in a specific domain of cognitive, such as: reading, math, or spatial processing  not attributable to general intelligence, lack of opportunity to learn, inadequate home environment, inadequate motivation or a handicapping condition • Presumably due to CNS dysfunction  but often unknown • Dyslexia, dyscalculia and non-verbal LD

15. LD (2) • Dyslexia  specific disorder of reading • Surface dyslexia (phonological reading)  inability to form word-sound correspondences without subjecting the word to phonological analysis  can’t read phonetically irregular words • Phonological dyslexia  can read words by sight, but not on the basis of phonological analysis  unable to read uncommon phonetically regular words or nonsense words  can read all that have entered their sight vocabulary • Deep dyslexia  exemplified by reading jog for run, or bread for cake

16. LD (3) • Cause of dyslexia  several neurologically based causes that interact with non-biologically based causal factors  prove to be the most useful guiding framework for understanding the reading problems confronted by children

17. LD (4) • Dyscalculia  impairment in the ability to perform arithmetic operations, may occur after lesions to the posterior regions of either left or right hemisphere (Grafman et al, 1982) • Language-based dyscalculia  similar to the dyscalculia seen after left-hemisphere lesions  also having problems with spelling and reading, but not with visual or tactual perception • Spatial dyscalculia  right-hemisphere lesion • But, no definitive neuroanatomical causes!

18. LD (5) • Non-Verbal LD  difficulties in areas that are not explicitly verbal, and therefore, less emphasized in the academic environment  heterogeneous, including impairment in the domains of perception, spatial processes and socio-emotional processing • Hypothesis  right-hemisphere dysfunction, possibly including white-matter connections

19. ADD • Behavioral features  distractibility, impulsivity, and restlessness  often diagnosed in children and can extend into adulthood. • Having great difficulty attending to relevant cues and information in their environment  often act as if they are not listening, moving on to other tasks and finish nothing, highly disorganized, difficulty delaying gratifications , hyperactive motor behaviors (not always present), emotional immaturity, shallow social relationships, poor academic/work performance  result in oppositionality

20. ADD (2) • Not a unitary disorder, but a spectrum of disorders with overlapping symptoms • Biological factors in ADD: • Neurotransmitters  decrease in catecholamine and indoleamine activity  often given tricyclic antidepressants • Genetic Factors  no specific gene has been identified  30% higher risk if the parents are ADD themselves

21. ADD (3) • Arousal Theories  has no solid neurobiological evidence • Overarousal  the filter systems in lower brain centers fail to filter stimuli normally – so irrelevant information is not screened out  leads to kind of cognitive shutdown  cause ADD children unable to do selective attention to one particular stimulus • Underarousal  higher brain centers do not receive enough input from lower brain centers  cause distractibility, hyperactivity and risk-taking behaviors

22. ADD (4) • Reward Theories  due to disruption of brain reward centers and/or with other parts of the brain  cause ADD children unable to modify their behaviors, even if they know the consequences • Motivation Theories  dysfunctional in individuals with ADD  cause them unable to stay on-task and to complete tasks that require sustained attention and effort in the absence of ongoing feedback or reward  but, There’s no ADD while playing Nintendo (Barkley)  immediate reinforcement against Reward Theories

23. ADD (5) • Prefrontal cortex  play a critical role in the planning, initiation and regulation of behavior  disturbed in ADD • Disrupt working memory  decrease capacity to profit from experience, to anticipate the consequences of one’s actions, and to use these anticipations to guide future actions

24. Autism • An extremely disabling disorder that almost always begins before age 30 months and lasts a lifetime, though sometimes with improvement • Characterized by: • Severe impairment in verbal and non-verbal communication • Failure to develop social relationships • Stereotyped and repetitive patterns of behavior, interest and activities • Tend not to seek comfort, not looking at their caregivers, do not care if they are hold

25. Autism (2) • Most children with autism are retarded and 75% have an IQ below 50 – however, some are with normal IQ scores • Autistic savant  when autistic child have a special talent or skill in specific area, such as: music, ability to memorize, art or the ability to perform calculations • They lack a theory of mind  a concept or sense that others have mind or consciousness  unable to assume the perspective of others

26. Austism (3) • Asperger’s syndrome  they still able to introspect about their condition and tell others about it • Causes: • Psychogenic theories  autism is not correlated with environment and personality of their parents • Genetic Factors  2%-3% of siblings of autistic persons are themselves autistic • Other factors  rubella, hydrocephalus, perinatal complications, major organic disorders

27. Autism (4) • Conclusions: • no specific brain abnormality or dysfunction that is seen in all causes of autism • Autism is not a homogenous entity, but a group of disorders (Hooper et al., 1993), each of which may be caused by different combinations of genetic factors and brain abnormality occurring early in development (Gillberg, 1992)