Embryology of brain


Published on

Published in: Health & Medicine, Technology
1 Comment
No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • The CNS appears at the beginning of the third week as a slipper-shaped plate of thickened ectoderm, the neural plate, in the middorsal region in front of the primitive node. Its lateral edges soon elevate to form the neural folds.
  • With further development, the neural folds continue to elevate, approach each other in the midline, and finally fuse, forming the neural tube.
  • Fusion begins in the cervical region and proceeds in cephalic and caudal directions. Closure of cranial neuroporeproceeds cranially from the initial closure site in the cervical region and from a site in the forebrain that forms later. This later site proceeds cranially, close to the rostral most region of the neural tube, and caudally to meet advancing closure from the cervical site. Final closure of cranial neuroporeoccurs at 18-20 somite stage (25th day). Closure of caudal neuroporeoccurs approx. 2 days later (day 27)
  • Primary brain vesicles (prosenephalon, mesencephalon, rhombencephalon) are formed during the 4th week of development. Secondary brain vesicles (telencephalon, diencephalon, mesencephalon, metencephalon, myelenephalon) are formed during the 5th week of development. Mesencephalon is considered as the most primitive brain vesicle
  • At the cervical and mesencephalic (cranial) flexures, the bends are ventrally directed while that of the pontine flexure is dorsally directed.
  • Cerebral aqueduct may become very narrowed and otherwise known as the aqueduct of Sylvius
  • Matrix layer/ependymal/germinal layer- nerve cells, glial cells & more germinal cells producedMantle layer- developing nerve cells & glial cellsMarginal layer- no nerve cells; reticulum of glial cells into which developing nerve cells grow
  • Dorsal view of mesencephalon and rhombencephalon (8-week embryo) (4-month embryo)SEM of mouse embryo at slightly younger stage than A, showing the cerebellarprimordium (arrow) extending to the 4th ventricle (V); Mesencephalon (M)High magnification of the cerebellar region in C
  • Dorsal view of mesencephalon and rhombencephalon (8-week embryo) (4-month embryo)SEM of mouse embryo at slightly younger stage than A, showing the cerebellarprimordium (arrow) extending to the 4th ventricle (V); Mesencephalon (M)High magnification of the cerebellar region in C
  • During further development, a number of cells formed by the neuroepithelium migrate to the surface of the cerebellum to form the external granular layer. Cells of this layer retain their ability to divide and form a proliferative zone on the surface of the cerebellum
  • Dorsal view of mesencephalon and rhombencephalon (8-week embryo) (4-month embryo)SEM of mouse embryo at slightly younger stage than A, showing the cerebellarprimordium (arrow) extending to the 4th ventricle (V); Mesencephalon (M)High magnification of the cerebellar region in C
  • Red nucleus= nucleus ruber- receives fibers from cerebellum
  • Embryology of brain

    1. 1. saRavanan
    2. 2. The human brain is the most complex mass of protoplasm on earth-perhapsWhat’s on your mind? even in our galaxy.-Marian C. Diamond and Arnold B. Scheibel
    4. 4. Formation of the neural groove, neural tube and neural crest
    5. 5. A. Dorsal view of human embryo (approx. day 22) B. (approx. day 23) C. SEM of mouse embryo at stage similar to that of A.
    6. 6. Lateral views of the fetal brain, from 10 to 40 weeks of gestational age.
    7. 7. RHOMBENCEPHALON• Consists of the myelencephalon, the most caudal of the brain vesicles, and the metencephalon, which extends from the pontine flexure to the rhombencephalic isthmus
    8. 8. Myelencephalon• Gives rise to medulla oblongata• Differs from spinal cord: its lateral walls are everted A. Dorsal view of the floor of the 4th ventricle in a 6-week embryo B-C. Myelencephalon at different stages of development
    9. 9. Lateral view of the brain vesicles in an 8-week embryo
    10. 10. Metencephalon• The metencephalon, similar to the myelencephalon, is characterized by basal and alar plates.• Two new components form: – (a) the cerebellum, a coordination center for posture and movement, – (b) the pons, the pathway for nerve fibers between the spinal cord and the cerebral and cerebellar cortices.
    11. 11. Transverse section through the caudal part of metencephalon
    12. 12. CEREBELLUM
    13. 13. A. 8 weeks (approx. 30 mm) B. 12 weeks (70 mm) C. 13 weeks D. 15 weeks.
    14. 14. • In the sixth month of development, the external granular layer gives rise to various cell types.• These cells migrate toward the differentiating Purkinje cells and give rise to granule cells.• Basket and stellate cells are produced by proliferating cells in the cerebellar white matter.
    15. 15. CEREBELLAR MALFORMATIONS AND MALFUNCTIONS• Hypoplasias- under development• Dysplasias- abnormal tissue development• Heterotopias- misplaced cells• Schizophrenia- related to early defects in neuronal migration, the expression of neurotransmitter receptors, or myelination• Ataxia- disruption of coordination; result from degeneration of cerebellum
    16. 16. • Trisomy 13- vermis is hypoplastic and neurons are heterotopically located in the white matter• Cerebellar dysplasia- usually of the vermis; characteristic of Trisomy 18• Trisomy 21 (Down Syndrome)- may involve abnormalities of the Purkinje and granule cell layers• Chromosome deletion syndromes: – 5p-(cri du chat), 13q-, 4p-
    17. 17. • Friedriech ataxia- autosomal recessive; affects the dorsal root ganglia, spinal cord, cerebellum; progressive disorder• Other autosomal recessive cerebellar ataxia syndromes: Ataxia- telanglectasia, Marinesco- Sjogren syndrome, Gillespie syndrome, Joubert syndrome, congenital disorders of glycosylation• Olivopontocerebellar atophy- caused by deficiency in the excitatory neurotransmitter glutamate, resulting from deficiency in glutamate hydrogenase
    18. 18. • Cerebrospinal ataxia syndromes: – Many are caused by unstable CAG trinucleotide repeat tracts within the coding region of genes – CAG codes for glutamine; polyglutamine disorders occur when tract of glutamine residues reaches the disease-causing threshold. – Genetic anticipation can cause the worsening of the disease in successive generations
    19. 19. PONS Pons is formed by proliferation of cell and fiber tracts on ventral side of metencephalon
    21. 21. proSENCEPHALON• The prosencephalon consists of the: – telencephalon, which forms the cerebral hemispheres, and the – diencephalon, which forms the optic cup and stalk, pituitary, thalamus, hypothalamus, and epiphysis.
    22. 22. Diencephalon
    23. 23. Roof Plate and Epiphysis
    24. 24. Alar Plate, Thalamus, and Hypothalamus
    25. 25. Hypophysis or Pituitary Gland
    26. 26. Hypophyseal Defects• Occasionally a small portion of Rathke’s pouch persists in the roof of the pharynx as a pharyngeal hypophysis.• Craniopharyngiomas arise from remnants of Rathke’s pouch.
    27. 27. Telencephalon
    28. 28. Cerebral Hemispheres
    29. 29. • Development of gyri and sulci on the lateral surface of the cerebral hemisphere.• A. 7 months. B. 9 months.
    30. 30. Cortex Development• The cerebral cortex develops from the pallium which has two regions: – (a) the paleopallium, or archipallium – (b) the neopallium
    31. 31. Commissures
    32. 32. Congenital Malformations of Cerebral Cortex• Classical lissencephaly (incidence: 1/100,000 live births)– Results from incomplete neuronal migration to the cerebral cortex during the 3rd and 4th months of gestation– Pachygyria (broad, thick gyri), Agyria (lack of gyri), heterotopia (cells in aberrant positions), enlarged ventricles, corpus callosum malformations– Newborns appear normal but sometimes have apnea, poor feeding, or abnormal muscle tone– Patients later develop seizures, profound mental retardation, mild spastic quadriplegia
    33. 33. • Subcortical Band Heterotopia– Believed to result from aberrant migration of differentiating neuroepithelial cells– Patients have bilateral circumferential and symmetric ribbons of gray matter located just beneath the cortex and separated from it by thin band of white matter -> double cortex syndrome– Seizures, mild mental retardation, behavioral anomalies often present in infancy– Intelligence can be normal and seizures may begin later in life– X-linked lissencephaly and SBH
    34. 34. Genes related to lissencephaly and SBH• LIS1- encodes a protein that functions as a regulatory subunit of platelet activating factor acetylhydrolase, which degrades platelet activating factor and involved in microtubule dynamics• Doublecortin- highly expressed in fetal neurons and their precursors during cortical development; protein associated with microtubules
    35. 35. • Kallman syndrome – characterized by anosmia (loss of sense of smell) or hyposmia (diminished sense of smell) and hypogonadism. – X-linked form caused by KAL1, which encodes an extracellular matrix glycoprotein called ANOSMIN-1
    37. 37. “Biology gives you a brain.Life turns it into a mind.” ― Jeffrey Eugenides, Middlesex