disorders of development-lecture

8/10/2019 Disorders of Development-lecture

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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)

http://images.google.com/imgres?imgurl=http://www.hallym.or.kr/~kdcp/cytogenetics/cytogen-

ds.files/c6_cleft_lip.jpg&imgrefurl=http://www.hallym.or.kr/~kdcp/cytogenetics/cytogen-

ds.htm&h=483&w=316&sz=61&tbnid=9z1GFXy5kykJ:&tbnh=126&tbnw=82&hl=en&start=61&prev=/images%3Fq%3DWilliams%2BSyndrome%26start%3D60%26svnu

m%3D10%26hl%3Den%26lr%3D%26client%3Dfirefox-a%26rls%3Dorg.mozilla:en-US:official_s%26sa%3DN

http://images.google.com/imgres?imgurl=http://cas.bellarmine.edu/tietjen/HumanBioogy/Finished%2520Images/gen12.gif&imgrefurl=http://cas.bellarmine.edu/tietjen/Hu

manBioogy/bills_developmental_abnormalities.htm&h=383&w=400&sz=117&tbnid=KbFuC4QsI4sJ:&tbnh=114&tbnw=120&hl=en&start=3&prev=/images%3Fq%3DEdw

ard%2527s%2BSyndrome%26svnum%3D10%26hl%3Den%26lr%3D%26client%3Dfirefox-a%26rls%3Dorg.mozilla:en-US:official_s%26sa%3DG

http://images.google.com/imgres?imgurl=http://www.cmu.edu/cmnews/extra/extra_art/Just_Fig1.jpg&imgrefurl=http://www.cmu.edu/cmnews/extra/extra_art/&h=421&w=

150&sz=25&tbnid=0aXX65rnVysJ:&tbnh=122&tbnw=43&hl=en&start=189&prev=/images%3Fq%3Dautism%2Bbrain%26start%3D180%26svnum%3D10%26hl%3Den

%26lr%3D%26client%3Dfirefox-a%26rls%3Dorg.mozilla:en-US:official%26sa%3DN

http://www.altcorp.com/DentalInformation/autismcytokines.htm

http://www.neuro.jhmi.edu/neuroimmunopath/Microglia%20pictures/5_lg.jpg

http://images.google.com/imgres?imgurl=http://www.fetalalcohol.com/images/face-thm.gif&imgrefurl=http://www.fetalalcohol.com/what-is-

fase.htm&h=260&w=304&sz=16&tbnid=RpmOv4g5G04J:&tbnh=95&tbnw=112&hl=en&start=6&prev=/images%3Fq%3DFetal%2BAlcohol%2BSy

ndrome%26svnum%3D10%26hl%3Den%26lr%3D%26client%3Dfirefox-a%26rls%3Dorg.mozilla:en-US:official_s%26sa%3DG

http://images.google.com/imgres?imgurl=http://www.infobiogen.fr/services/chromcancer/IntroItems/Images/tri21FaceEng.gif&imgrefurl=http://www

.infobiogen.fr/services/chromcancer/IntroItems/PolyTri21Eng.html&h=429&w=463&sz=50&tbnid=XGXbYU9uVcYJ:&tbnh=115&tbnw=125&hl=en&start=1&prev=/images%3Fq%3DTrisomy%2B21%2Bface%26svnum%3D10%26hl%3Den%26lr%3D%26client%3Dfirefox-

a%26rls%3Dorg.mozilla:en-US:official_s%26sa%3DG
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disorders of development-lecture

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