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DEVELOPMENT OF NERVOUS SYSTEM

LECTURE BY DR. ANSARI(FOR MBBS SEMESTER –II STUDENTS)

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OBJECTIVES

• NEURAL TUBE DEVELOPMENT AND ITS DERIVATIVES.

• NEURAL CREST CELLS AND ITS DERIVATIVES.• DEVELOPMENT OF MENINGES.• DEVELOPMENTAL ANOMALIES OF NEURAL

TUBE.

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NEURAL TUBE FORMATION

• During III week of development, neurulation is a major change during gastrulation.

• The notochord induce changes on the surface ectoderm, the surface ectoderm thickens multifold and forms neural plate, the forerunner of the future central nervous system.

• Neural plate forms the neural groove, fusion starts at the middle and neural tube is the result.

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Basal lamina/ alar lamina

• The neural tube after fusion will have a dorsal portion and a ventral portion.

• The dorsal portion is called as alar lamina/alar plate.• The ventral portion is basal lamina/plate.• The two laminae are separated by sulcus limitans.• This separation of regions extends from

mesencepalon to spinal cord.• The cells in the alar lamina are sensory, where as

basal lamina cells are motor in function

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The neuropores

• The unfused anterior end of neural tube, is the cranial neural pore/rostral neuropore, it fuses on or before 26 days of development.

• The posterior neuropore/caudal neuropore fuses before the end of 4th week.

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CLOSURE OF ANT.PORE BY 25TH DAY AND POST. PORE BY 27TH DAY

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NEURAL CREST CELLS

• WHEN NEURAL GROOVES UNITES,SOME COLLAR CELLS, CALLED NEURAL CREST CELLS MIGRATES OUT AND SPREAD OUT TO GIVE RISE TO MANY STRUCTURES.

• Spinal ganglia (dorsal root ganglia)• · Ganglia of the autonomic nervous system• · Ganglia of some cranial nerves• · Sheaths of peripheral nerves• · Meninges of brain and spinal cord• · Pigment cells• · Suprarenal medulla• · Skeletal and muscular components in the head19/04/2010

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There are

• 1X1011 neurons in CNS

• MORE NEURONS IN EMBRYO THAN ADULT

• GLIA SERVE AS SUPPORTIVE FUNCTION

• GLIA OUT NUMBER NEURONS; 1X1012 IN CNS

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PRIMARYBRAINVESICLES• The neural tube forms

three primary brain vesicles.

• The primary brain vesicles give rise to five secondary brain vesicles, which give rise to various adult structures.

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SPINAL CORD DEVELOPMENT

• The caudal two third of neural tube forms the spinal cord.

• The tube grows into 3 layers, ventricular zone, intermediate zone and marginal zone. The cells of neural tube called as spongioblast mutiply and changes to neuroblast cells, that on maturation gives rise to neurones.

• The lumen of neural tube becomes the central canal.

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Development of meninges & posterior pituitary

• The dura mater arises from paraxial mesoderm that surrounds the neural tube.

• The pia mater and arachnoid mater arise from neural crest cells.

• The anterior pituitary gland (adenohypophysis) arises from an evagination of the oropharyngeal membrane known as Rathke’s pouch.

• The posterior pituitary gland (neurohypophysis) arises from an evagination of neuroectoderm from the diencephalon.

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Developmental anomalies of neural tube

• Spina bifida as a result of non fusion of caudal neuropore at the end of 4th week of I.U.L.

• Anencephaly, is the failure of the anterior neuropore to close resulting in a failure of brain to develop.

• Neural tube defects can be detected by the presence of alpha-fetoprotein(AFP) in the fetal circulation after the 4th week of development.

• Hydrocephaly, when there is huge collection of CSF in the ventricles of the brain as a result of blockage of ventricular passages.

• Microcephaly is small head resulting from failure of brain to grow normally due to radiation, infection by cytomegalovirus and toxoplasmosis gondii parasites.

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Neural tube defects can be preventedIf folic acid is given during pregnancy

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Migration failure of NCC

• Leads to mega colon, Hirshsprung’s disease.

• A developmental disease where the migration of neural crest cells stops and there is aganglionic segment of colon where there is absence of autonomic ganglionic connections.

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• Congenital disorder of peristalsis of distal bowel caused by absence of parasympathetic ganglion cells in the intramural and submucosal neural plexuses.

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Clinical features of Hirshsprung's disease

• Congenital• 1 in 5000 newborns• Presentation:

– usually first year of life– occasionally adulthood.

• Associated features: – ≈80% male– 10% have Down's syndrome– 5% have other serious neurologic abnormalities sometimes: intestinal atresia– anorectal malformations– familial Symptoms: usually soon after birth: – abdominal gaseous distention– delayed meconium passage– tight anus

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Hirshsprung's DiseaseGanglion cell deficiency results in loss of motility with dilation of the

bowel

proximal to the region of involvement.

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Identify the individual ?

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Alzheimer’s disease

There is an overall shrinkage of brain tissue. The grooves or furrows in the brain, called sulci , are noticeably widened and there is shrinkage of the gyri the well-developed folds of the brain's outer layer.

In addition, the ventricles, or chambers within the brain that contain cerebrospinal fluid, are noticeably enlarged. In the early stages of Alzheimer's disease, short-term memory begins to fade when the cells in the hippocampus, which is part of the limbic system, degenerate.

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• The ability to perform routine tasks also declines.

• As Alzheimer's disease spreads through the cerebral cortex (the outer layer of the brain), judgment declines, emotional outbursts may occur and language is impaired.

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• . As the disease progresses, more nerve cells die, leading to changes in behavior, such as wandering and agitation. In the final stages of the disease, people may lose the ability to recognize faces and communicate; they normally cannot control bodily functions and require constant care.

• On average, the disease lasts for 8 to 10 years, but individuals with Alzheimer’s can live for up to 20 years.

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