Transcript Developmental Neuropsychology

Developmental
Neuropsychology
Prepared by:
Cicilia Evi GradDiplSc., M. Psi
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
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
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
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
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
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)
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
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
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
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
Dev Disorders of Unknown Cause
• Learning Disorders
• Attention Deficit Disorder
• Autism
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
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
LD (3)
• Cause of dyslexia  several neurologically
based causes that interact with nonbiologically based causal factors  prove to
be the most useful guiding framework for
understanding the reading problems
confronted by children
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!
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
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
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
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
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
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
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
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
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
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)