8. Development of the Brain Flashcards

1
Q
  1. What is the process of the formation of neural tube?
A

Gastrulation- Week 3

formation of primitive streek in caudal region of embryo and at rostral end = primitive node (with groove and pit)

cells from epiblast migrate, prolif, run into, force down, interact with signals, become germ layers

mesoderm–> notochordal process

notochord–> induces formation of NEURAL plate by sonic hedgehog

neural plate invaginates= neural fold; space= neural groove; tube rounds up making neural tube!

rostral and caudal neuropore close at day 25, 27 respecively

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2
Q

What is primary vs. secondary neuralation? when does it occur?

A

Primary neuralation (around day 22-27) gives rise to brain all way to down to lumbar SC

Secondary neuralation (days 20-42) has caudal eminence that will attach to primary neural tube to form sacral and coccyx regions of spinal cord

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3
Q

What does neuroectoderm give rise to in terms of cells? mesodermal cells?

A

NE–> neurons, protoplasmic astrocyte, fibrous astrocyte, oligos, ependymal cells and choroid plexus

mesoderm–> mesenchymal cell makes microglial cells (technically derived from blood monocytes)

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4
Q
  1. What are the regions of the neural tube that become the CNS?
A

brain: cranial to fourth somites (mesoderm)

spinal cord: caudal to fourth pair of simites

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5
Q

3.1 What arises from primary brain vesicles?

A

Prosencephalon–> forebrain

Mesencephalon–> midbrain

Rhombencephalon–> hindbrain

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6
Q

In what week do the forebrain and hindbrain divide? into what?

A

5th week

Prosencephalon–> telencephalon and diencephalon

rhombencephalon–> metencephalon and myelencephalon

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7
Q

3.2 What arises from secondary brain vesicles?

A

Telencephalon–> cerebral hemisphere (cortex, subcortical white matter and internal capsule, olfactory bulb and tract, basal ganglia, amygdala, hippocampus)

diencephalon–> thalamus, hypothalalmus, epithalalmus, eye

mesencephalon– midbrain (cerebral peduncles, superior/inferior colliculi, 2 CNs for each eye)

metencephalon–> pons and cerebellum

myelencephalon–> medulla (olive and pyramid)

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8
Q

What ventricles come from the secondary vesicles and hallow tube?

A

telencephalon–> lateral ventricle

diencephalon–> third ventricle

mesencephalon–> cerebral aqueduct

bw metencephaln and myelencephalon–> 4th ventricle

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9
Q
  1. What are the different brain flexures? and what divisions do they establish? which persists?
A

Cervical flexure (week 5): demarcates hindbrain from spinal cord

Pontine flexure (later): divides hindbrain into caudal myelencephalon and rostral metencephalon

cephalic (mesencephalic flexure): bend bw midbrain and forebrain(diencephelon); PERSISTS

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10
Q

When does basal ganglia and cortical structure develop?

A

bw weeks 6-32

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11
Q

What is Holoprosencephaly (HPE)? what are the clinical features?

A

results from incomplete separation of cerebral hemispheres (from prosencephalon)

most associated with facial abnormalities (cleft lip, one nose, probiscus, cyclopia)

reduction of forntonasal prominence

Other features: microcephaly (small head), micropthalmia (small eyes), intellectual disability or developmental delay, epilepsy, hydrocephalus, dystonia, movement disorder, autonomic dysfunction, and hypothalamic/pituitary dysfunction

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12
Q

What are the causes of holoprosencephaly?

A

genetic + environmental factors, maternal diabetes, teratogens (alcohol)

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13
Q
  1. How is the pituitary gland formed?
A

First arch ectoderm (surface) gives rise to roof of mouth (by stomodeum), anterior lobe of pituitary gland, and hypophysial diverticulum (Rathkes pouch)

Posterior lobe of pituitary gland from NE and it is coming from the diencephalic floor and the neurohypophysial diverticulum

How: portion of diencephalon by infundibulum and then rathkes pouch migrates up to this area and will fuse, making anterior lobe (surface ecto) and posterior lobe (NE)

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14
Q
  1. What is the significance of the alar and basal plates as it relates to afferents and efferents? what separates them
A

Two subdivisions within neural tube= alar and basal plate

ALAR plate–> dorsal horn, sensory/aff neurons that stay contained within CNS

BASAL plate–> motor neurons; will leave to go out to skeletal muscle; will also give rise to preganglionic autonomics

separating them= sulcus limitans

right in center= central canal

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15
Q

11.2 What are the three zones of the spinal cord and examples of cells found in each?

A
  1. Ventricular zone (right next to central canal/ventricle)–> stem cells giving rise to neurons (ependymal blasts–> ependymal cells and choroid plexus
  2. Intermediate zone (mantle layer)–> migration of neurons into these areas (neurons, astrocytes, microglia); GRAY matter
  3. Marginal zone–> WHITE matter, axon tracts, and oligos to myelinate axons
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16
Q

How is the alar and basal plate pattern maintained in the brainstem? what changes?

A

Alar plate will form dorsal horn (sensory) and basal plate will form ventral horn (motor)

except for when have pontine flexure- bend roof of 4th ventricles; have sensory laterally and motor more towards midline (can see in pons and medulla)

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17
Q

Describe the organization in the medulla and pons after the 4th ventricle moves laterally:

A

GSE (motor nuclei) are going to be closest to midline = CN 3,4, 6, and 12

GVE= just lateral to GSE

SVE= lateral to GVE (PAs; 5, 7, 9, 10)

sulcus limitans

GVA and SVA lateral to sulcus limitans

SSA and GSA = most lateral

18
Q

How do you know youre in the upper/lower midbrain?

A

upper midbrain: see superior colliculus

lower midbrain: exactly same but pickup trochlear nucleus at same plane as inferior colliculus

19
Q

What is cerebral palsy and its types?

A

can occur by many factors and extra fluid in ventricles

SPASTIC- damage adjacent to ventricles (corticospinal tract)

DYSKINETIC= damage to basal ganglion (athetoid, dyskinetic) and VL thalamus (dyskinetic)

ATAXIC: damage to cerebellum

mixed

20
Q

What is Syringomyelia and what is it associated with?

A

excess fluid in central canal; form cerynx (found in C2-T9 mostly)

can go higher or lower

highy associated with CHIARI TYPE 1 malformation

due to trauma, viral infections, idiopathic

21
Q

What would it look like if someone had the various cerebral palsys?

A

spastic- toe walking scissor gait

athetoid- slow writhing movements of extremities and/or trunk

ataxic- incoordination, weakness and shaking during voluntary movement

mixed

could also have hemiplegia, quadriplegia, diplegia (lower limb more) classification

22
Q
  1. 1 What is Arnold Chiari Type 1?
A

deformity of hindbrain, herniation of cerebellar tonsils through foramen magnum

usually no symptoms (head and neck pain, lower CNs- tongue, facial muscles, lateral eye movements, decreased hearing, dizziness, coordinating movements)

23
Q
  1. 2 What is Arnold-Chiari type 2?
A

herniation of medulla and cerebellum through foramen magnum

hydrocephalus almost always (bc AQUADUCTAL STENOSIS)

lower CN problems (head and neck pain, lower CNs- tongue, facial muscles, lateral eye movements, decreased hearing, dizziness, paralysis of SCM, coordinating movements)

Associated almost always with meningocomyocele/spina bifida

24
Q

17.3 When does Arnold Chiari type 1 occur vs. type 2?

A

Type 1- late adolescence to adulthood

Type 2- infancy or childhood

25
Q

17.4 How is the Arnold Chiari type 2 diagnosed?

A

can be made in utero by fetal MRI; demonstrates lumbar myelomeningocele and cerebral chiari 2 malformations

26
Q

What is the Dandy Walker Malformation?

A

large posterior fossa cyst continuous with 4th ventricle

hypoplasia of cerebellum, with partial/absence of vermis

atresia of foramina of luschka and magendia (which causes dilation of cyst in 3rd, lateral, and 4th ventricles)

associated with other abnormalities

27
Q

What is hydranencephaly?

A

unknown cause (maybe obstruction of blood flow to areas supplied by ICA)

absences of cerebral hemispheres or represented by membranous sacs with dispersed tissue

brainstem intact

excessive head growth after birth

little to no cognitive development

28
Q

What is hydranencephaly?

A

unknown cause (maybe obstruction of blood flow to areas supplied by ICA)

absences of cerebral hemispheres or represented by membranous sacs with dispersed tissue

brainstem intact

excessive head growth after birth

little to no cognitive development

29
Q

What is the cytodifferentiation that occurs in the neuroepithelium of the cerebrum and cerebellum?

A

newer parts of brain have 6 laminae, and older parts have 3

sensory areas have LARGE laminae 4

motor areas have LARGE laminae 5

inside OUT sequence

30
Q

What is the inside out sequence of cytodifferentiation of the cerebrum?

A

first neurons are produced from the VENTRICULAR zone–> form superficial layer= preplate–> axons from these neurons and form INTERMEDIATE zone

next neurons to be born migrate into Middle of preplaet and divide into: marginal zone, cortical plate, and subplate

early neurons of cortical plate will form deep layers (laminae 5 and 6) of finished cortex

later born neurons migrate RADIALLY up radial glia from ventricular zone across intermediate zone and sbuplate through earlier layers of 5 and 6 –> established laminae 4–> 3 –> 2

31
Q

What is Lissencephaly or Agyria (smooth brain)?

A

incomplete or failure of neuronal migration during 12-24 weeks (no bumps/grooves)

characterized by: microcephaly, ventriculomegaly, wide sylvian fissures and mimimial operculum of insula, complete or partial agenesis of corpus callosum

infants typically have apnea, poor feeding, or abnormal muscle tone

patients later develop seizures, mental retardation, and mild spastic quadriplegia

32
Q

What is Microcephaly?

A

SIGN not diagnosis

2 major mechanisms: abnormal or lack of brain development during neurogenesis; injury or insult to previously normal brain

can be genetic, prenatal or perinatal brain injury (if mom has cytomegalovirus, rubella, toxoplasm gondii), craniosyntosis (premature fusion of sutures), postnatal brain injury, unknown

33
Q
  1. What is the cytodifferentiation of the cerebellum?
A

Ventricular zone–> PC layer and deep cerebellar nuclei

external germination center migrate over PF and deep cerebellar nuclei

external germination center cells will then migrate back in and form the granular layer

Cerebellum complete (NE!!)

34
Q

Where does the spinal cord end in newborns and adults? where should do lumbar puncture?

A

Newborn: L2/L3

Adult: L1/L2

lumbar puncture BELOW (L3/L4 or L4/L5)

35
Q

What gives rise to spinal ganglion cells and sensory neurons in periphery?

A

NC cells (touch, pain, temp cells)

36
Q
  1. What cells contribute to the PNS?
A

NC and ectodermal placode form PNS (preganglionic= NE, postganglionic = NC)

cells that develop from NC = neurons of DRG, sensory gangia of CNs, schwann cells, sympathetic ganglia (ciliac, otic, etc.)

37
Q

When does myelination occur and by what cells?

A

forms during late fetal period–> continues into first postnatal year

CNS: oligos (start in lower brain stem–> older tracts FIRST!!); 6th mo–> puberty

PNS: Schwann (motor roots BEFORE sensory roots); 4th month

38
Q
  1. What are the types of spina bifida? what is it caused by?
A

failure of closure of CAUDAL neuropore (vertebral arches)

spina bifida occulta (tuft of hair)

meningocele (CSF cyst like protrusion)

meningomyelocele (cyst with meninges and neuro tube in cyst

myelocele/myeloschiasis (no cyst, but spinal cord exposed)

folic acid CAN PREVENT

39
Q

What is anencephaly (meroanencephaly)?

A

failure of closure of ROSTRAL neuropore; didnt close at all

40
Q

What is an encephalocele?

A

timing of closure of ROSTRAL neuropore was off ( can be with or without brain tissue)