Dezv Sistem Nervos

7/28/2019 Dezv Sistem Nervos

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Neural Development &

Developmental Disorder


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Between 4 weeks and 9 months the brain

undergoes rapid development


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Development of the Brain

Stages of neuroanatomical development

1. Zygote stage: Begins upon fertilization of the ovum

and ends with the formation of the embryonic disc

at approximately 14 days after conception.

Conception involves 2 sets of 22 chromosomes, and

one set of sex chromosomes. Total of 23 pairs of

chromosomes (XX= female, XY= male)


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Egg and sperm each

contribute a complete

single set of chromosomes.

This includes 22

chromosomes plus the 23

sex chromosome (X or Y)

Mitosis proceeds normally

from the first cell division


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From Conception to 8-14 days


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2. Embryonic Stage (2 weeks8 weeks):

Begins at the full formation of embryonic disc.

Ectoderm: forms nervous system (brain),

fingernails, hair, and skin. Changes:

1. Thickens in the middle (neural plate)2. Groove starts to form (neural groove)

3. Groove closes to form tube (neural tube)

a. At the top of canal is neural crest,forms PNS


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Simplified View of Neural Plate Formation


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Formation of the Neural Plate with the

thickening of Ectoderm


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Formation of the Brain, Spinal Cord and PNS

(Neuroectoderm)


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Neuroectoderm forms when foundation for the

three main structures has been developed:

1. 3 swellingsa. Hindbrain

b. Midbrain

c. Forebrain2. Closed Neural Tube becomes spinal cord

central canal and ventricles of the brain.

Spina bifidaNeural Tube Defect (NTD) -

spinal cord doesnt close, often linked to

mental retardation

**NTDs can be discovered in utero **


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Ectoderm to Neuroectoderm: 20 days to 30 days(note the formation of the spinal nerves at 30 days and the three swellings

that make up the hindbrain, midbrain and forebrain)


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3. Fetal Period: Eight weeks to Birth (38 weeks)


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Foundation for the entire CNS is set

6 stages of CNS development complete the

prenatal process


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(a) Mitosis and Neurogenesis

Mitosis (cell division) orNeurogenesis in the ventricular zone, One celldivision can lead to a daughter cell, will divide again forming an immatureneuron


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(b) Migration

Migration: cells move from VZ to their destination; this migration is aided by glial

cells, abnormal migration found in a number of disorders. Filopodia (next slides, also)

assist in finding location after leaving radial glial cells. Abnormalities in migration

have been found in the CNS of people with learning disabilities, schizophrenia and

autism

vz = ventricular zone


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Forebrain Development


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Growth Cones & Filopodia

Photomicrograph of growth cone & filopodia


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(c) DifferentiationThe process which gives rise to specific neurons

and glial cells

(d) SynaptogenesisNeuronal maturation

1. Elongation of axons (w/growth cones)

2. Establish terminals

3. Elongation of dendrites

4. Expression of NT

Neurotrophic factorsstimulate cell growth,i.e. nerve growth, factor helps neuron to mature.


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(e) Cell Death

Apoptosisactive cell death during development

(f) Synaptic Rearrangement


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Active Cell Death40%-50% neuronal lossoccurs during the first 2 years of life, and it

occurs on a different scale in adolescence(hormone related, final pruning)

1. Essential because many cells are

unconnected and useless2. Dysfunction in apoptosis is seen in post-

mortem brains of children with autism(particularly problems in cerebellum,

midbrain, & hippocampus); insufficienthooking up of neurons


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Post-natal brain development

1. At birth the brain weighs 25% of the full adult

brain2. By the age of 6 it increases to 95%

a. Increase is due to myelination, synapticdevelopment, neuronal maturation, glial cell

growthb. At birth the brain is myelinated through thethalamus

c. Myelination is in part based on experience (thepremature baby will have substantially moremyelin than that of the full term baby)


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Cellular Development of the

Postnatal Brain

Cells of the Cerebral Cortex


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Cells of the

Cerebellum


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Critical Periods:

Rapid changes in a system of an organism, if

interrupted will result in permanent &irreversible problems

Prenatal Critical Periods: these involve structural

abnormalities (see next slide, brown bars)Postnatal Critical Periods: this varies with the

function.Examples:

Uncorrected strabismus permanently impairs depth perception. Binocular vision

begins within weeks after birth and ceilings between 1 and 3 weeks of age.

Linguistic features (e.g., bilateral neural communication between left and right

hemispheres) develop between ages 1 and 2, suggesting a critical period for

language. Interference prevents the full acquisition of adult linguistic features.


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Brain Cells can Continue to

Develop in Abnormal WaysEarly

Childhood

Adulthood


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Experience can Modify Brain Cell

Connections


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How experience affects development

1. Experience-expectant plastic changes: CNS

changes that rely on experiences during criticalperiods for specific synapses to develop. Theprimary sensory cortices require sensorystimulation for normal development, otherwise

long lasting impairments occur (e.g., strabismusand depth perception impairment).

2. Experience-dependent plastic changes: uniqueexperiences that occur during critical periods

that affect brain development (e.g., musicaltraining affects the sensorimotor cortex for

playing and primary auditory cortex forlistening).


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Normal Plasticity or Apoptosis causes

rearrangement of cells

N l D ti d t N i


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Neuronal Degeneration due to Necrosis

(cell damage due to to injury)Note subsequent damage

to other neurons, across

or transneural loss


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Rearrangement following Necrosis:

Collateral Sprouting


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Normal DevelopmentOverall Brain Development Between

Birth and 21 years old.

Age

Temporal Lobes or Language Areas


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Temporal Lobes or Language Areas,

Birth - 21

Age

Ages 1-2 interhemispheric(myelin and neurons)

connections increase

Ages 2-12 marked dendritic

arborization in speech areas,occurs in waves

Ages13-17 may have a

large environmental

component (e.g. education,socialization) in addition to

effects of puberty on brain

development.


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Parietal Areas, Birth - 21

Age

Birth to 3 years rapid

growth as child interacts

with world. Corresponds

with visuospatial andvisuosensorimotor skills.

Continued steady growth

in waves, corresponding

with changes in temporallobe.


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Limbic System for Emotions/Attachment,

Birth - 21

Age

Includes the hippocampus,

which develops by 1year,

but is not fully connected

with other brain areas forstable episodic memories

(autobiographical). This

occurs beginning around

age 4.

Increase during

adolescence reflects shift

from family to peer and

pair bonding.


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Frontal Lobes for Behavioral Control,

Birth - 21

Age

This includes motor cortex in

cephalocaudal(head before

arms/truck before legs) and

proximodistal (head/trunk/armsbefore hand/fingers; or gross motor

before fine motor) by age 9.

Executive Functions (planning,

shifting, inhibiting, emotionalregulation) in prefrontal cortex.

Judgment in social settings for

ambiguous situations established

by age 14.


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Disorders of Development

CongenitalBirth Defects

CongenitalTeratogenic AgentsTrisomy Disorders

Williams Syndrome

Autism


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Teratogens

Agents that cause congenital malformations

during critical periods, and subtle 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.

C iti l P i d D f t S hi h l


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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 21st Chromosome


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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 canhappen at the

first cell division


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Non-disjunction of

the 21st

chromosome cab

occur after the first

cell divisionresulting 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 andfixed flexion of fingers

CNS: severe mental

retardation, neural tube

defect, ocularabnormalities

Respiratory: apnea

Cardiovascular problems

Gastrointestinal and

genitourinary 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 7

th

ChromosomeFeatures:

1 in 20,000 births

Neurodevelopmental delays,

cognitive deficits, LD,

ADHD

Overly friendly, social

Extremely empathic

Low muscle tone

Extremely sensitive hearing


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Specific Brain Areas

Affected:

Amygdala activates more

for threatening scenes and

very little for threatening

faces. This accounts for

absence of anxiety in

interpersonal interactions

(no fear, hence over-

friendliness).

Normal Control Williams Syndrome

Amygdala


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Additional CNS Features in

Williams Syndrome Normal frontal & temporal lobes Reduction in parietal and occipital lobes

Decrease in white matter affecting connection

between frontal lobe and amygdala (except formedial-prefrontal connection, which is linked toempathy and the only structure still wellconnected to the amygdala)

Link to Chromosome 7 (next slide) suggestsinvolvement in parietal, occipital, and/or whitematter in CNS

Elastin protein, made only during the prenatal period, is absent and causes vascular problems


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Genetic Abnormalityof Chromosome 7:

21 genes missing

p , y g p p , p

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 social

interaction and

communication.

Age of onset: typicallybetween 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 thesuperior 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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