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Embryological Development of CNS Department of Anatomy and Histology Faculty of Medicine Brawijaya University 1 SKDI 2012 • KELAINAN KONGENITAL SISTEM SARAF HYDROCEPHALUS SPINA BIFIDA CEREBRAL PALSY 2 3 Tingkat Kemampuan 1: Lulusan dokter mampu mengenali dan menjelaskan gambaran klinik penyakit, dan mengetahui cara yang paling tepat untuk mendapatkan informasi lebih lanjut mengenai penyakit tersebut, selanjutnya menentukan rujukan yang paling tepat bagi pasien. Lulusan dokter juga mampu menindaklanjuti sesudah kembali dari rujukan. Tingkat Kemampuan 2: Lulusan dokter mampu membuat diagnosis klinik terhadap penyakit tersebut dan menentukan rujukan yang paling tepat bagi penanganan pasien selanjutnya. Lulusan dokter juga mampu menindaklanjuti sesudah kembali dari rujukan. 4 ILUSTRASI KASUS • Dokter…anak saya lahir normal, kenapa lama kelamaan kepalanya membesar? • Penyebabnya apa dokter? • Bisa sembuh dokter? • Kalau dioperasi, dia bisa jadi anak normal ? 5 ILUSTRASI KASUS • Dari hasil USG tampak penonjolan berisi kista pada bagian posterior janin.. • Kemungkinan spina bifida • Apa itu dokter?? • Penyebabnya apa dokter? • Bisa dioperasi dokter? • Anaknya bisa normal dokter? 6 ILUSTRASI KASUS • Anak saya umur 3 tahun belum bisa jalan…normalkah dokter? • Kalau merangkak juga gerakannya aneh.. • Pernah kejang-kejang.. • Kalau makan, sepertinya ia juga sulit menelan… • Dokter :????? 7 MARI BELAJAR TUMBUH KEMBANG CNS 8 A little flashback.... 9 ASAL USUL Zygote (fertilized egg) • Produced from combination of male and female parent chromosomes • Mitotic Division Begins • New Cells called Blastomeres which form a Morula Two-cell Stage Four-cell Stage Morula ~3 days 10 ASAL USUL Blastocyst • Embryoblast • Blastocyst • Trophoblast 11 ASAL USUL Blastocyst Uterine stroma Trophoblast cells Embryoblast Blastocyst cavity 12 The first week ASAL USUL 13 The second week: Bilaminar Embryo ASAL USUL Embryo has two primary layers: Epiblast & Hypoblast Cytotrophoblast Amniotic Cavity Epiblast Hypoblast Primary Yolk Sac Exocoelomic Membrane 14 ASAL USUL Gastrulation …. caused by a proliferation of epiblast cells 15 Third week: Trilaminar Embryo Develops ASAL USUL 16 Third week: Trilaminar Embryo Develops ASAL USUL • Embryo Trilaminar: three layers between amniotic cavity and yolk sac – Ectoderm – future covering (skin, nails, hair, but also CNS) – Mesoderm – future muscles, bones, heart – Endoderm – future digestive tract 17 Third week: Trilaminar Embryo Develops Presomite Embryo – 18 days Cut edge of amnion Neural plate Primitive pit Primitive streak (mesoderm) Neurulation formation of the neural plate18 and neural tube Third week: Trilaminar Embryo Develops • Primitive Streak Forms dorsally • Forms neural tube, notochord (cartilaginous rod, future spine) and neural crest cells • Notochord : mesoderm origin 19 Presomite Embryo – 20 days Cut edge of amnion Neural groove Somite Primitive streak 20 Early Highlights • Day 18 - Neural plate invaginates (encloses) to form neural groove • Day 22 - Neural Tube Forms – Becomes brain and spinal cord • About the same time, Neural Crest Forms – Becomes cranial and spinal nerve ganglia 21 Neural Tube • • • • • • Cranial 2/3 will form brain Caudal 1/3 will form spinal cord Day 25 - Cranial opening closes Day 27 - Caudal end closes Problems cause neural tube defects The walls of the neural tube thicken to form the brain and the spinal cord • The neural canal forms the ventricular system of the brain and the central canal of the spinal cord 22 LAYERS OF EARLY NEURAL TUBE 1. Ventricular zone : ependymocyte, choroid plexus cells 2. Intermediate zone: neuroblast, glioblast 3. Marginal zone : glioblast 23 Human Embryo – 22 days Neural fold Optic placode Somite Cut edge of amnion 24 Human Embryo – 23 days Cranial neuropore Pericardial bulge Caudal neuropore 25 • Brain has 3 sections • = Primary brain vesicles Prosencephalon/ forebrain Mesencephalon/ midbrain Rhombencephalon/ hindbrain 26 Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Embryology of the brain • The secondary brain vesicles grow rapidly, especially the telencephalon, which overlaps the diencephalon • Telencephalon = lateral ventricles + cerebrum • Diencephalon = third ventricle + thalamus + hypothalamus • Mesencephalon = cerebral aqueduct + midbrain • Metencephalon = fourth ventricle + pons + cerebellum • Myelencephalon = fourth ventricle + medulla oblongata Neural Crest Development • Cranial neural crest cells • Trunk neural crest cells 1. from somite 6 to the most caudal somites and 1. There is a remarkable migrate relationship between 2. Trunk neural crest cells differentiate into the the origin of cranial following structures: neural crest cells from a. Melanocytes the rhombencephalon b. Schwann cells (hindbrain) and their c. Chromaffin cells of adrenal medulla final migration into d. Dorsal root ganglia pharyngeal arches 2. The rhombencephalon is e. Sympathetic chain ganglia f. Prevertebral sympathetic ganglia divided into eight g. Enteric parasympathetic ganglia of the gut segments called (Meissner and Auerbach; CN X) rhombomeres (R1–R8). 29 h. Abdominal/pelvic cavity parasympathetic ganglia. Maturation of CNS • At birth, all neurons you will ever have present. – Only a few exceptions (neurons involved w smell) • Process of myelination signals onset of mature function – Slow process • Partially completed completed by age 7 • Axons and dendrites not until teens • Some areas continue to age 70 • Some cells have programmed cell death (Apoptosis) 30 Neuron structure Classification of neurons Structural classification based on number of processes coming off of the cell body: 33 Histological Differentiation • Nerve cell : neuroblast • Glial cells : glialblast – Astrocytes : – Oligodendroglial cell : myelin sheaths – Microglial cells : appears in CNS • Neural Crest Cells sensory ganglia of the spinal cord 34 Myelination • Short Gaps (Nodes of Ranvier) on Axons – Speed up neural activity • In CNS, formed by Oligodendrocytes • In PNS, formed by Neurilemmal or Schwann cells 35 Seven Steps of CNS Development 1. Production of initial neurons and glial cells 2. Migration of cells to definitive location 3. Selective gathering of cells to functional group 4. Cytodifferentiation (axon, dendrite, synaptic patterns) 5. Selective death of some cells in groups 6. Outgrowth of axons to specific target cells and establishment of connections 7. Elimination of certain connections and functional stabilization of others 36 Abnormal Development Neural Tube Defect : Abnormal closure of the neural folds in 3rd and 4th weeks of development • Anencephaly – Cerebral Hemispheres reduced or missing • Spina Bifida – Spina Bifida Occulta : • defect in the vertebrae arches, does not involve neural tissue, lumbosacral region – Spina Bifida Cystica : • Neural tissue and/or meningens through defect in the vertebral arches and skin cysticlike sac 37 38 Anencephalic Newborn 39 40 Cranium Bifida 41 Other Developmental Conditions • Hydrocephaly – Enlarged head, brain atrophy mental deficiency – Excessive production of CSF or obstruction of drainage pathways 42 Congenital Hydrocephalus • 1 dari 1000 bayi lahir hidup menderita kelainan ini • insidens congenital hydrocephalus adalah 0,12-2,5 tiap kelahiran. • Gen X-linked, L1CAM, adalah satu-satunya gen yang diketahui berkaitan dengan perkembangan congenital hydrocephalus pada manusia. • Mutasi pada gen tersebut mengakibatkan banyak kasus hydrocephalus X-linked. • Kelainan genetic jenis autosomal-recessive juga diketahui dapat mengakibatkan hydrocephalus pada manusia 43 Primary Cilia Dyskinesia • Infertilitas pd pria • Anosmia • Polycistic kidney 44 45 Causes of hydrocephalus 46 Cerebral Palsy • brain injury or malformation • Impairments resulting from cerebral palsy range in severity, usually in correlation with the degree of injury to the brain. • The primary effect of cerebral palsy is impairment of : – – – – – – – muscle tone, gross and fine motor functions, balance, control, reflexes, posture. Oral motor dysfunction, such as swallowing and feeding difficulties, speech impairment, and poor muscle tone in the face, – Associative conditions, such as sensory impairment, seizures, and learning disabilities that are not a result of the same brain injury, occur frequently with cerebral palsy. 47 signs and symptoms CP • developmental delay. • (+) abnormal muscle tone, unusual posture, persistent infant reflexes • not readily visible at birth, except in some severe cases, and may appear within the first three to five years of life as the brain and child develop. • delivery was traumatic/ Risk factor +observe carefully 48 Cause of CP • Periventricular Leukomalacia (PVL) – BRAIN INJURY –DAMAGE TO THE WHITE MATTER BRAIN TISSUE : cell apoptosis • BRAIN MALFORMATION OR ABNORMAL BRAIN DEVELOPMENT Cerebral Dysgenesis • LACK OF OXYGEN TO THE BRAIN OR ASPHYXIA Hypoxic-Ischemic Encephalopathy, or HIE, or Intrapartum Asphyxia • BRAIN HEMORRHAGE Intracranial Hemorrhage, or IVH 49 50 Cemungudh ! 51