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Sem 3 > neuroembryology/case 1 > Flashcards

neuroembryology/case 1 Flashcards

1
Q

what is neurulation?

A

process of formation of the NS during neural plate formation: folding and closure of neural plate

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2
Q

what is circulatory formation?

A

formation of synapse and connections between neurones and muscle cells

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3
Q

what is the difference between the brainstem/spinal cord and cerebral cortex development?

A

brainstem/spinal cord are hard wired whereas the cerebral cortex is plastic:

  1. notochord does not control the development of forebrain
  2. genetics:
    - Hox gene for brainstem/spinal cord
    - EMX and Otx for forebrain
  3. timing
  4. fluid system
    - brainstem/spinal cord don’t produce CSF
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4
Q

What are the 4 steps of the development of the NS

A
  1. induction of the neural plate
  2. patterning of the CNS
  3. neurogenesis (neuronal differentiation)
  4. wiring of the brain to establish functional neuronal circuits
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5
Q

Which stem cell develops into the NS?

A

ectoderm

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6
Q

When does induction of the neural tube start?

A

3rd-4th week

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7
Q

What happens with the induction of the neural tube?

A
  • dorsal midline ectoderm undergoes thickening –> neural plate
  • lateral margins become elevated to become neural folds and middle depression –> neural groove
  • neural folds become opposed –> neural tube
  • cells from neural folds becomes separate and form neural crest
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8
Q

when does the anterior neuropore close and what happens if there is failure to close?

A

day 25

anencephaly

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9
Q

when does the posterior neuropore close and what happens if there is failure to close?

A

day 28

spina bifida

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10
Q 
which part of the neural tube do the 
1. rostal part
2. caudal part
3. central cavity
4. neural crest
become?
A
  1. brain
  2. spinal cord
  3. central canal of spinal cord and ventricles of the brain
  4. sensor ganglia of spinal, cranial nerves and autonomic ganglia
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11
Q

what is a morphogen?

A

signalling molecule (secreted proteins) that acts directly on cells to produce specific cellular responses depending on its local concentration (dose dependent)

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12
Q

What is the dorsoventral axis set up by?

A

cross dose-dependent gradient of morphogens:

  • ventral region (floor plate): secretion of SHH (by notochord)
  • dorsal region (roof plate): secretion of BMP initially and TGF-beta proteins (transforming growth factor beta)
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13
Q

What is the sulcus limitans?

A

longitudinal groove that appears on the lateral wall of the embryonic spinal cord and caudal part of the brain (in spinal cord separates alar and basal plates

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14
Q

what is the alar plate?

A

dorsal cell groupings: predominant sensory functions

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15
Q

what is the basal plate?

A

ventral cell groupings: predominant motor functions

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16
Q

What are the cell groupings within the alar plates?

A

from dorsal to ventral:

  • special somatic afferent
  • general somatic afferent
  • special visceral afferent
  • general visceral afferent
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17
Q

What are the cell groupings within the basal plates?

A

from dorsal to ventral:

  • general visceral efferent
  • brachial efferent
  • somatic efferent
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18
Q

What does SHH stand for?

A

Sonic hedgehog

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19
Q

What does BMP stand for?

A

Bone morphogenic protein

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20
Q

What is the anteroposterior axis set up by?

A

expressed by SGF gradient (secretory growth factor):
-FGFs (fibroblast growth factor) expressed in gradient from posterior end
-retinoic acid: expressed from anterior end
+ homeotic genes

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21
Q

By when do the 3 primary brain vesicles develop?

A

5th week

22
Q

By when do the 5 secondly brain vesicles develop?

A

7th week

23
Q

What are the three primary brain vesicles?

A
  • prosencephalon (forebrain)
  • mesencephalon (midbrain)
  • rhombencephalon (hindbrain)
24
Q

What are the five secondary brain vesicles?

A
  • telencephalon (cerebral hemisphere)
  • diencephalon (thalamus)
  • mesencephalon (midbrain)
  • metencephalon (pons, cerebellum)
  • myelencephalon (medulla oblongata)
25
Q

What are the flexures of the neuraxis?

A
  • midbrain/cephalic flexure: junction of forebrain to midbrain
  • cervical flexure: between brain and spinal cord
  • pontine flexure: between mesencephalon and myelencephalon
26
Q

What causes the splitting of the two hemispheres of the brain?

A

SHH

27
Q

What are the characteristics of neuroprogenitor cells?

A
  • polarised (at apical surface due to apical complex)

- proliferate by diving at apical surface (symmetric proliferative

28
Q

what does wiring of the NS?

A

functional circuits to respond to stimulus

29
Q

what are pioneer neurons?

A

an axon that lays down growing paths for the other axons of the same neuron to follow

30
Q

What radar do pioneer neurons follow?

A

the SHH radar (from ventral to dorsal and from posterior to anterior): neurons move from dorsal to frontal regions and then move up towards brain: the neutrons are first attracted then repulsed by SHH

31
Q

What are causes for neurodevelopment defect?

A
  • genetic
  • metabolic/immune disorders
  • environmental
  • accidents (trauma/infections)
32
Q

axons form synapses through molecular and activity dependent mechanisms, what happens to neurons that do not form synapses?

A

dynamic process of elimination: refine the circuit

33
Q

What are the three most common of neural tube defects?

A

spina bifida
anencephaly
chiari malformations

34
Q

What are the three type of spina bifida?

A
  • spina bifida occulta
  • meningocele
  • myelomeningocele
35
Q

What are the characteristics of spina bifida occulta? (symptoms, pathophysiology, treatment)

A
  • “hidden”: frequently no symptoms, small patch of hair, dimple, darker-coloured skin or selling in the skin over affected vertebrae due to growth factors
  • small opening in the vertebrae of spinal cord but no damage to the spinal cord itself
  • no treatment needed
36
Q

What are the characteristics of meningocele? (symptoms, pathophysiology, treatment)

A
  • rarest type
  • spine is open and meningocele (sac) comes through containing meninges and spinal fluid: cord is not affected
  • surgery
  • mild disabilities
37
Q

What are the characteristics of myelomeningocele? (symptoms, pathophysiology, treatment)

A
  • open spina bifida: meninges and nerves are out
  • danger of infections
  • can lead to leg paralysis, difficulty in urination and bowel movement (sensory and motor neurone affected) + leg and foot deformities
  • hydrocephalus due to Arnold Chiari 2 malformation (cerebellum and brainstem tissue slip down into foramen magnum) + collection of too much CSF in brain, can’t drain normally causing pressure to build up leading to seizures, problems with NS or mental retardation
  • treatment: prenatal/postnatal surgery, urinary cauterisation, wheelchair or crutches, shunts for hydrocephalus (to drain fluid)
38
Q

What is the aetiology of spina bifida?

A
  • genetic and environmental
  • 30% of neural tube defects are sensitive to folate acid: 1st trimester vey important (until W4)
  • ectoderm form ridges that become neural tube: fails to close properly; absence of vertebral arches due to failure of mesoderm to organise over region of defect
39
Q

What are risk factors for spina bifida?

A

-obesity
-poorly controlled diabetes
-antiseizure medicine
-folic acid (B9) deficiency
-low SES
-low parity
(more educated women are less likely to have spina bifida but women that work have higher chance of having a baby with spina bifida)

40
Q

How do you diagnose spina bifida?

A
  • at 16-18 weeks: increase AFP (alpha fetoprotein) in mothers serum (leakage of APF into amniotic fluid due to missing skin around foetus spine)
  • HCG, inhibiting A, oestriol (blood tests)
  • ultrasound: lemon test (anencephaly detectable at week 12 and SB at week 16-20
  • amniocentesis (AFP and assay of neuronal acetylcholinesterase)
41
Q

What is the Lemon/Banana sign?

A
  • ultrasound features of the Arnold Chiari malformations in foetuses with open neural tube defects
  • banana sign: shape of cerebellum (caudal displacement)
  • lemon sign: lemon shaped head (scalloping of frontal bone)
42
Q

What are the different types of Arnold-Chiari malformations?

A
  1. type 1: acquired (symptoms: headaches)
  2. type 2: associated with lumbrosacral myelomeningocele (clinical features: paralysis below spinal defect)
  3. type 3: downwards displacement of cerebellum into posterior encephalocele (extremely rare and generally incompatible with life)
  4. type 4:cerebellar hypoplasia
43
Q

What is the Arnold-Chari malformation?

A
  • congenital disorders: distortion of base of skull and protrusion of the lower brainstem and parts of cerebellum through foramen magnum
  • may be associated with hydrocephalus and springomyelia (cyst formation in spinal cord)
44
Q

what are the different cranial markers for spinal bifida?

A
  • lemon sign
  • ventriculomegaly
  • microcephaly (smaller head than normal)
  • obliteration of the cisterna magna with an absent cerebellum
  • abnormal anterior curvature of the cerebellum
45
Q

What is the epidemiology of neural tube defects?

A

1:500 global

46
Q

What is the difference between anencephaly (1), encephalocele (2)?

A
  1. absence of a major portion of the brain, skull and scalp

2. sac-like protrusions of the brain and the membranes that cover it through openings in the skull

47
Q

what does teratogenicity mean?

A

property of producing congenital malformations

48
Q

How do anti epileptic drugs cause teratogenicity?

A

causes malabsorption of folic acid in the intestine

49
Q

What does folic acid do?

A

(DNA synthesis/repair
cell division
neurodevelopment)
-folic acid is converted to THF (tetrahydrofolate) which plays a role in transfer of 1-carbon units to essential substrates involved in synthesis of DNA and RNA

50
Q

What is the notochord?

A
  • required for patterning surrounding tissues (signal secreted by notochord is SHH)
  • mechanical influence of the folding in early embryo
51
Q

how are neuroblasts generated?

A

asymmetrical devision: (one daughter cell becomes post-mitotic neuroblast and the other re-enters the cell cycle)

Sem 3 (20 decks)

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