disorders of development-lecture
TRANSCRIPT
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Disorders of Development
CongenitalBirth Defects
CongenitalTeratogenic Agents
Trisomy Disorders
Williams Syndrome
Autism.
Dr Saim Ali Soomro.MBBS,MCCM.
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Birth Defects occur during Critical Periods
in Development
1. Defects during Zygote are aborted;
2. Defects in the remaining prenatal period
are irreversible;
3. Critical Periods: a time of rapid change in
the development of the organism (i.e., system
or structure) and if interrupted will result in
permanent congenital abnormalities.
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Sensitive periods in development
1. Occur prenatally and less irreversible
2. Interference will disrupt growth; may
result in subtle dysfunctions
3. Continues into post-natal periodTeratogens
- Agents that cause congenital
malformations in critical periods, andsubtle alterations in the brain during
sensitive periods
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Critical Period Defect:
Cleft Palate Irreversible congenital
abnormality affecting acritical period (palate
development) during theembryonic and early fetalstages
May affect pituitarygrowth as the palate and
anterior pituitary arederived from the sameembryonic tissue.
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Critical Period Defect:
Anencephaly (absence of brain)
Failure for the brain to grow
beyond the rhombencephalon.
Neonate failed to survive.
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Critical Period Defect: Schizencephaly
Developmental of the brain affected during the fetal period
(i.e., growth of the forebrain). Cells either failed to migrate
or ventricular region failed to close.
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Teratogens
Agents that cause
congenital
malformations
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Fetal Alcohol Syndrome
Features: Growth retardation, neurodevelopmental abnormalities (fine motor
skills, LD, behavior disorders, and mental retardation in 50%). Facial
dysmorphia during embryonic period (week 4-8), CNS problems during the fetal
period (migration problems, smaller dendrites, few neurons in brain regions)
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Genetic Conditions:
Chromosomal Abnormalities Trisomy 21 (Downs Syndrome)
Trisomy of other chromosomes
Edwards Syndrome (Trisomy 18)
Pataus Syndrome (Trisomy 13)
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Trisomy 21: Downs Syndrome
Non-disjunction of the 21stChromosome
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Anatomical Dysmorphia & Risk (Increase withMaternal Age)
Just 1%-
20%
graphed
here
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How does Trisomy21 happen?
First, normal
development
In normal
development
mitosis proceeds
normally from the
first cell division
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In Downs
Syndrome, non-
disjunction of
the 21st
chromosome can
happen at the
first cell division
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Non-disjunction of
the 21st
chromosome cab
occur after the first
cell division
resulting in a
mosaic form of
Downs Syndrome
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Faulty distribution
can occur in the egg
or sperm when the
mother or father is acarrier.
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Trisomy 18Edwards Syndrome
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Some Features of Edwards Syndrome
Facial: microcephaly, low set
malformed ears
Skeletal: webbed neck,
overlapping of fingers and
fixed flexion of fingers
CNS: severe mental
retardation, neural tube
defect, ocularabnormalities
Respiratory: apnea
Cardiovascular problems
Gastrointestinal andgenitourinary problems
Life Span: death by 12-24months (very few reach
adulthood)
Incidence: 0.2/1000 births
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Trisomy 13: Pataus Syndrome
Features:
0.1/1000 births
Spina bifida & cleft palate
CNS: underdevelopment offrontal lobe (fails todivide) and corpuscallosum
Profound Mental RetardationExtra fingers and toes, deaf
Life Span: 82% die in thefirst month, 5-10% die infirst year.
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Williams SyndromePartial Deletion of
the 7th
ChromosomeFeatures:
1 in 20,000 births
Neurodevelopmental delays,cognitive deficits, LD,
ADHD
Overly friendly, social
Extremely empathicLow muscle tone
Extremely sensitive hearing
B i A Aff d
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Brain Areas Affected:
Amygdala activates more
for threatening scenes and
very little for threateningfaces. This accounts for
absence of anxiety in
interpersonal interactions
(no fear, hence over
friendliness).
Also, abnormal activity in
frontal lobe and a
disconnect with the
amygdala (except for
medial-prefrontal which is
linked to empathy and the
only structure still
connected to the amygdala)
Normal Control Williams Syndrome
Amygdala
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Genetic Abnormality
of Chromosome 7:
21 genes missing
Elastin protein, made only during the prenatal period, is absent and causes vascular problems
during life; the missing elastin gene is use to identify the 21 missing genes in Williams Syndrome.
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Autism
A neurodegenerative
disorder characterized by
impairment in socialinteraction and
communication.
Age of onset: typically
between ages 2 and 4
(sometimes earlier)
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Symptoms
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Theories for Etiology and CNS Problems
Genetic alterations
Prenatal exposure to
toxins and/or viruses Maternal and fetal
immune interactions
Vaccination with
mercury base
Amygdala less active andarea is smaller
Hippocampus is smaller
Frontal areas (medialprefrontal region) lessactive
Less activity in the
superior temporal sulcus(involved in understandingothers)
Larger & heavier brainsuggests apoptosis failure
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Microglia Activation in Autism
(white matter of the cerebellum)
Microglial cells
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Brain Areas Affected in Autism: Fusiform Face
Area (FFA), Amygdala, Left Frontal Lobe, Left
Temporal Lobe, and Cerebellum
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References for Photos
(slides 5,6,9,11,16,18,19,22-25)
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