1st Shifting Lec 01

NeuroScience

NEUROEMBRYOLOGY
Formation of the Neural Tube and Neural Crest

3rd Week  formation of endoderm, mesoderm and ectoderm • Notochord

b. Secondary Neurolation  day 20 to 42  formation of
coccygeal segment Caudal Eminence

sacral and cord from

  

stimulates ectoderm to thicken secretes cell adhesion molecules

Induction – proper development of structure is dependent on proper development of neighboring structures Neurolation

becomes the neural plate and neural groove (from neural plate) of which both will function as one due to adhesion molecules  becomes nucleus pulposus in adults as its remnants • Neural groove and neural fold formation

Disorders of Primary (Dysraphic Defects)

a. Anterior Neuropore Closure Defects 1. Meroanencephaly / Anencephaly 2. Incomplete development of brain and calvaria 3. Abnormal Facies 4. Mircocephaly Note: Role of folic acid supplements is for prevention

• Neurolations a. Primary Neurolation formation of Neural Crest (becomes the PNS) *Neural Crest Derivatives: a. Schwann Cells b. Cranial Nerve Ganglion c. Dorsal Root Ganglion d. Autonomic Ganglion e. Chromaffin Cells of Adrenal Medulla f. Pia and Arachnoid of meninges g. Melanocytes

b. Posterior

formation of Neural Tube (CNS) *Neural Tube Derivatives: a. Rostral 2/3 (Anterior Neuropore) – brain b. Caudal 1/3 (Posterior Neuropore) – spinal cord but up to lumbar only * Note: The anterior neuropore closes first duu to shorter travel distance at day 24 while the posterior part closes at day 26

Neuropore Closure Defects (Myeloschisis) 1. Sipina Bifida Oculta – defect in vertebral arch fusion -region of occurrence is seen with tufts of hairs 2. Spina Bifida Cystica a. Meningocoele – no nerve tissue protrusion b. Meningomyelocele – involves nerve tissue protrusion 3. Myelorachischisis

Disorder of Secondary (Myelodysplasia)

Neurolation


caudal eminence involvement neural tube malformation

accompanied by unusual skin pigmentation, unusual hair growth, superficial capillaries and prominent dimple

1. Tethered Cord Syndrome

1 -VRVM

between forbrain and midbrain -AKA “cephalic flexure” 3. Alar Plate – Dorsal Gray Horn d.conus medullaris and filum terminale are abnormally fixed (immobilized) NeuroScience • • • Ventricular zone – becomes ependymal calls as remnants Marginal zone – an acellular zone due to it only contains processes . Alar Plate Derivative (Sensory Function) TRANSVERSE DIFFERENTIATION NEURAL TUBE OF PRIMITIVE    Gracile Nuclei Cuneate Nuclei Descending Nucleus of V Solitarius Nuclei (IX and X)  2 -VRVM . X. Cervical – between hindbrain and spinal cord 2.becomes ventral gray horn and lateral horn • 4th Week formation of three Primary Vesicles 1.becomes the white mater Intermediate zone (mantle layer)  Alar plate (posterolateral part) – for sensory function becomes the dorsal gray horn Basal plate ( ventrolateral part) – for motor function . When they do.1st Shifting Lec 01 . Forebrain ( Prosencephalon) 2. Pontine – demarcates metencephalon and myelencephalon 4. hence. Telencephalic – between telencephalon and diencephalon  *Sulcus limitans – demarcates alar plate and basal plate *Basal plate and Alar plate later become NUCLEI Spinal Cord Derivatives a. Neural Cavity – Spinal Cord b. Hindbrain (Rhombencephalon) • •  5th Week formation of Secondary Vesicles that originated from the primary vesicles) Secondary Caviti Derivative Wall Vesicles es Cerebral Lateral Telencephal Hemisph Ventric on Forebrain ere le (Prosencepha Third lon) Diencephalo Thalami Ventric n le Cerebr Midbrain Mesencepha al (Mesencephal --lon Aqued on) uct Upper Pons part of Metencepha and 4th lon Cerebell ventric um Hindbrain le (Rhombencep Lower halon) part of Myelenceph Medulla 4th alon ventric le • formation of Flexures 1. XI and XII 1.conformations are dorso-ventral in proximal 1/3 and medio-lateral in late 2/3 • formation of cranial nerves IX. Marginal Zone – White Mater Guide for Innervation • • Fibronectin molecules and Laminin – matrix Integrins – for recognition *Spinal nerves develop connections by having integrins in their processes where these search for laminins and fibronectins found in connective tissues. Basal Plate – Ventral and Lateral Gray Horn e. Ventricular Zone – Ependymal Cells c. Midbrain. they reach end target organs Development of Medulla (Myelencephalon) . Midbrain ( Mesencephalon) 3.

Basal Plate Derivative (Motor Function) . Alar Plate Derivative Function) (Sensory Dorsal Motor Nucleus of X Neural Canal / Cavity Central Canal / IV Ventricle     Inferior Colliculus Superior Colliculus Substantia Nigra Red Nucleus .auditory .R.  Hypoglossal Nuclei Ambiguus Nuclei – tongue – deglutition • formation of cranial nerves III and IV 1.H in formation diencephalon of • Prosencephalization – sequence of events telencephalon and Development of Cerebellum Metencephalon) from rhombic lip conformation is still jn lateral form (from medio- • formation of an additional zone: External Germinal (Granular Layer) Zone from Marginal Zone . Alar Plate Derivative (Sensory Function) . HSV *Holoproncephaly – failure of prosencephalon to undergo cleavage Development of Telencephalon   Granule Cells Stellate Cells Basket Cells • formation of Primitive Tube  formation of cortical plate between the marginal zone and intermediate zone formation of sub-plate beneath the cortical plate  • Intermediate Zone becomes internal granular layer. VI. VII and VIII 1.1st Shifting Lec 01  Vestibular / Cochlear Nuclei Inferior Olivary Nuclei Basal Plate Derivative (Motor Function) -efferent in nature hence. Rubella. Basal Plate Derivative (Motor Function)   Oculomotor Nucleus (III) – superior Trochlear Nucleus oblique eye muscle (IV)   Pontine Nuclei 2. Others. Neural Cavity Derivative: Sylvian (*Cerebral) Aqueduct 2.in medio-lateral conformation Abduccens nuclei – lateral rectus of eye muscles  Facial nuclei Development of Forebrain (Prosencephalon) • develops  at 2nd month of gestation simultaneous with formation of facial structures from mesoderm • follows an development INSIDE OUT pattern to of CNS Motor Nucleus of Trigeminal muscles of mastication(V) 3. CMV.    3.O.  Development of Thalami (Diencephalon) • largely derived from Alar Plate 3 -VRVM .C.visual Development of Pons (from Metencephalon) • formation of cranial nerves V.neurons migrate inward to form: *Inside out pattern is where the first cell to develop is found inside *TORCH – Toxoplasmosis. “motor” NeuroScience Development of Midbrain (Mesencephalon) conformation is reverted to dorsoventral form  2.in lateral conformation  Rhombic Lip (Cerebellum) Sensory Nucleus of Trigeminal face only (V)  Mesencephalic Nucleus of V 3. Neural Canal / Cavity  IV Ventricle  – • Inf=ections may predispose abnormalities – T. neurons migrate outward to form Deep Cerebellar Nuclei and Purkinje cells.

Less gyrus.Affects leukodystrophies. Therefore. Synaptogenesis – requires right cues from target cell (synaptic stabilization) • establishment of an orderly map of the sensory world in the Thalamic Nuclei ( Retinotopic and Tonotopic mapping)  • gives rise to:  Epithalamus  Thalamus – establishes orderly map of the sensory world (retinotopic mapping. phenylketonuria as well as nutrition (malnutrition) *New borns are having reflexes because myelination is not yet complete •   Cellular Events in Brain Development Parameters in brain organization • • density of neurons (which are about 100 billion) pattern of axon and dendrite branching 4 -VRVM . tonotopic mapping)  Hypothalamus  *Outside first sequence is when the first cell to develop will be placed outside. less neurons. Development of Cerebral Cortex • follows INSIDE OUT pattern • formation of cortical plate at interface of marginal zone and intermediate zone • formation Mechanism of Plasticity – alteration in selective neuronal cell death. Overproduction of neurons and apoptosis role of nerve growth factors and fibroblast growth factors in interrupting apoptosis b. axon simplification and retention of transient axonal branches and synapses that would otherwise be lost *An infant is more resistant to brain damage due to hypoxia because brain can still reclaim neurons that are programmed to die by mechanism of plasticity. therefore mental defect. • Marginal Zone – gives rise to 1st Layer of Cerebral cortex • Cortical Plate – 2nd to 6th layer • Sub-plate and Intermediate Zone – gives rise to sub-cortical white matter Gross Abnormalities Development of Cortical  • • • Lissencephaly – failure of gyri to forming smooth surface of cerebral cortex Pachygyria – large gyri Microgyria – small gyri Schizencephaly – abnormal patterns of sulci and gyri with unilateral or bilateral clefts in cerebral hemispheres *A gyrus is like an inverted villi for increasing surface area. *Likewise. It usually starts at age of 3 but varies from region to region. Synaptic Development . it too increases the availability of neuronal space for neuronal development.1st Shifting Lec 01 • development occurs in OUTSIDE FIRST sequence NeuroScience • pattern of synaptic contacts – occurs throughout life a. Critical Period – time period when these types of plastic changes cease to occur. Axonal Outgrowth – growth can reach distant targets through tropic factors c. neuronal apoptosis starts at age 3 because the cessation of mechanism of plasticity.peaks from birth to first year .parallels cellular development and migration Myelination .starts at 6 months to life .

: Obliteration of Aqueductal Stenosis arachnoid villi 5 -VRVM .1st Shifting Lec 01 NeuroScience Ventricular System Abnormalities Obstructive Non-Obstructive Hydrocephalus Hydrocephalus Non-Communicating Communicating Due to blockage in Due to abnormalities of the ventricular system the subarachnoid space ie.: Congenital ie.