Neuronal Development Dr. Donald Allen. Development of the Brain Begins on day 28 Vesicles Flexures.

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Presentation transcript:

Neuronal Development Dr. Donald Allen

Development of the Brain Begins on day 28 Vesicles Flexures

Three Primary Vesicles Develop during 4 th week Prosencephalon Mesencephalon Rhombencephalon

Two Flexures Cervical Flexure Cephalic flexure

Five Secondary Vesicles Develop by 5 th week Derived from primary vesicles

Five Secondary Vesicles Prosencephalon – Mesencephalon Rhombencephalon –

Adult neuroanatomy terms The terms used are strictly used only to describe parts of the brain during development Some of these terms are used (probably incorrectly) to describe structures in the adult brain –Telencephalon –Diencephalon –Mesencephalon

Table 5-1, page 88 Telecephalon –Cerebral hemispheres –Basal ganglia Diencephalon –Thalamus, hypothalamus Mesencephalon –Midbrain

Pontine flexure Does not persist in adulthood As flexure forms, the walls of neural tube split apart

Further Development of Telencephalon Page 89, Figure 5-8 The cerebral hemispheres expand so that they cover the diencephalon The hemispheres become C-shaped The insula region does not grow as fast, and it becomes covered by the frontal and temporal lobes Surface folds to produce gyri and sulci

Processes of Development Cell migration Growth cone Neuronal death Axonal retraction Muscle fiber types Myelination Growing into deficit

Cell migration Neurons that divide are located next to the ventricles Where is the gray matter (soma) in the cerebral cortex? Neurons will either migrate by: –Sending out processes –Follow radial glia Neurons differentiate once they reach their location Location can determine differentiation

Growth cone When neurons migrate or send out a process Growth cone – process –Samples environment Moves toward attractants Moves away from other chemicals –When growth cone reaches its target Vesicles are produced Synapse forms

Neuronal death The nervous system tends to overproduce neurons, which then compete for a limited number of targets Neurons which do not make connections with other neurons or are not active tend to die Motor neurons in spinal cord

Axonal retraction During innervation of muscles Initially more than one motor neuron innervates each muscle fiber During development, axons retract so that only one motor neuron innervates each muscle fiber

Muscle fiber types Muscle fibers can be slow-twitch or fast twitch The muscle fiber type is dependent on the nerves, not the muscle If we change the nerve, we can change the muscle fiber type

Myelination Begins 4 th fetal month Most myelination completed by end of third year of life Myelination occurs at different rates in different systems –Lower motor neurons – by 1 month –Projections from motor cortex to spinal cord – 2 years (Babinski reflex)

Growing into Deficit There may be neurological problems that may not be immediately noticed These impairments will become observed as the impaired systems become functional For example, balance or lower extremity impairments may not be observed until a child begins to try to stand and walk

Brain Development Postpartum At birth, 400 grams Increases in brain weight –Myelination –Number of processes –First 3 years, 3-fold increase in weight –Brain growth then slows down –11 years old – 1400 grams ( )

Brain weight with age and gender Brain weight fairly constant till 50’s, then slow decline in overall weight Men: larger brain by weight Women: larger brain by weight of brain/weight of body

Critical Periods Times during development that are crucial for normal development and outcomes Occur when –Neurons are dividing –Neurons competing for connections Motor neurons :: number of limbs Examples in humans –Vision –Language

Disorders of Development Neural tube disorders –A neuropore does not close correctly Normal development depends on cells making contact with the proper types of other cells Usual structures may not develop, or may develop incorrectly

Caudal Neuropore Failure to close – spina bifida –Vertebrae do not form normally –Associated with inadequate folic acid intake by mother –Several types (page 92) Dr. Emmel in Systems Screening I

Rostral Neuropore Failure to close –Failure of forebrain to develop correctly Often brainstem is present –Skull does not form over incomplete brain –Most fetuses die before birth Otherwise, usually die within a week of birth

Arnold-Chiari Syndrome Developmental abnormality of hindbrain Two types

Arnold-Chiari Type I Herniation of cerebellar tonsils through the foramen magnum Medulla and pons often small Often have no symptoms –Often begin in adolescence and early adulthood Headache induced by coughing, sneezing, straining Possible hydrocephalus (block CSF flow) Cranial nerve dysfunction

Arnold-Chiari Type I - Treatment If deficits are stable, no treatment If deficits are progressing, the bone that is compressing the hind brain can be removed

Arnold-Chiari Type II Signs present in infancy Usually associated with meningomyelocele Malformation of brainstem and cerebellum –Extend through foramen magnum

Arnold-Chiari Type II Progressive hydrocephaly Paralysis of sternocleidomastoid muscles Deafness Weakness in lateral eye movements Weakness in facial muscles

Fetal Alcohol or Cocaine Exposure Fetus exposed in utero Fetal Alcohol Syndrome

Fetal Cocaine Exposure Effect depends on stage of development Disrupts neuronal proliferation Interferes with neurodevelopmental processes Effects more subtle than those of alcohol Also affected by low socioeconomic status, use of other illegal drugs, smoking, poor maternal nutrition, and STD

Cerebral Palsy Non-progressive and permanent Injury to developing brain –Prenatal, postnatal, or at time of birth Defined by motor and postural impairments, though may also have sensory and cognitive impairments Growing into deficit is common

Types of Cerebral Palsy Spastic Athetoid Ataxic Mixed

Spastic Cerebral Palsy Damaged neurons next to ventricles –Axons of neurons in cerebral cortex Toe Walking Scissor gait

Athetoid Cerebral Palsy Damage in basal ganglia Slow, writhing movements of extremities and/or trunk

Ataxic Cerebral Palsy Damage to cerebellum Lack of coordination Weakness Shaking movements (tremor) during movements

Mixed Cerebral Palsy Combination of above types of cerebral palsy