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Sem 3 Neuro > Case 1 > Flashcards

Case 1 Flashcards

1
Q

During action potential, what happens during upstroke?

A 
Depolarisation of cell. (Becomes more +)
Na+ influx due to increased permeability to Na+. 
Na+ simply diffuse across gradient. 
Activation of (m) gate channels. 
Inhibition of (h) gate channels.
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2
Q

During action potential, how is the impulse propagated?

A

As Na+ channels become more permeable to Na+, Na+ enter cell rapidly.
This causes depolarisation.
Depolarisation causes neighbour Na+ channels to open, and therefore further influx of Na+.
Positive feedback. Unidirectional.

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3
Q

During action potential, what happens at peak?

A 
Once membrane (axon) fully depolarised PNa+ >> PK+.
(h) gate close finally (activated) and (m) gate inactivate. 
Results in inactivation of Na+ channel and activation of K+ channel. 
Na+ entry stops, K+ entry efflux begins. 
Na+/K+ ATP pump begins actively transporting Na+ OUT.
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4
Q

During action potential, what happens during downstroke?

A

Na+/K+ ATP pump actively pumps out Na+ and K+ back in.
K+ channels open
PK+ increases while PNa+ decreases.

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5
Q

How does large diameter of axon affect conduction?

A

Causes an increase of current by increasing cross sectional area.
This decreases electrical resistance, thus quickening conduction.

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6
Q

Characteristic of Aα nerve fibre?

A 
Function: motor proprioception
Diameter: 12-20 um 
Myelinated 
Velocity: 70-120 m/s 
Sensitivity to local anaesthetic: +
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7
Q

Characteristics of Aβ nerve fibre?

A 
Function: touch pressure 
Diameter: 5-12 um 
Myelinated 
Velocity: 30-70 m/s 
Sensitivity to local anaesthetic: ++
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8
Q

Characteristics of Aγ nerve fibre?

A 
Function: muscle spindles 
Diameter: 3-6 um 
Myelinated 
Velocity: 15-30 m/s 
Sensitivity to local anaesthetic: ++
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9
Q

Characteristics of Aδ nerve fibres?

A 
Function: pain, temperature 
Diameter: 2-3 um 
Myelinated 
Velocity: 12-30 m/s 
Sensitivity to local anaesthetic: +++
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10
Q

Characteristics of C nerve fibres?

A 
Function: Pain
Diameter: 0.5-1.2 um 
Non-myelinated 
Velocity: 0.5-2.0 m/s
Sensitivity to local anaesthetic: ++++
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11
Q

What’s the fastest conducting nerve fibre?

A 
Aα 
Motor proprioception 
Myelinated 
12-20 um diameter 
70-120 m/s
Local anaesthetic +
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12
Q

What’s the slowest conducting nerve fibre?

A 
C fibres 
Pain 
0.5-1.2 um diameter 
Non-myelinated 
0.5-2.0 m/s 
Local anaesthetic ++++
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13
Q

How do local anaesthetics work generally?

A

They block Na+ sodium gated ion channels on axon membranes, therefore preventing action potential and impulse propagation.

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14
Q

What are the three germ layers?

A

Ectoderm (neuro-ectoderm), mesoderm and endoderm.

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15
Q

What is gastrulation?

A

Formation of the three different germ layers: ectoderm, mesoderm and endoderm.

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16
Q

Which germ layer is the nervous system derived from?

A

Ectoderm (a.k.a neuro-ectoderm)

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17
Q

What does the ectoderm develop into?

A

Skin

Nervous system

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18
Q

What does the mesoderm develop into?

A

Muscles

Vasculature

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19
Q

What does the endoderm develop into?

A

Internal organs

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20
Q

What induces the ectoderm to become neural tissue?

A

Induction of the neural plate (from ectoderm) requires a signal from the underlying mesoderm.

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21
Q

During human development, which days does neural tube formation happen in?

A

19-23 days

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22
Q

Failure to close the anterior neuropore results in which major congenital defect?

A

Anencephaly

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23
Q

Failure to close the posterior pore results in which major congenital defect?

A

Spina bifida

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24
Q

Neural plate closure results in the formation of what structure?

A

The neural tube.

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25
Q

The neural tube develops into what structure in the human?

A

The spinal cord (and brain anteriorly)

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26
Q

In the neural tube, what morphogen is released from the dorsal side to help pattern the nervous system?

A

BMP (bone morphogenic protein)

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27
Q

In the neural tube, what morphogen is released from the ventral side to help pattern the nervous system?

A

SHH (Sonic Hedgehog)

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28
Q

What do “morphogens” do? And how?

A

They define the identity of different populations of neurones. They do so in a dose-dependant manner.
Concentrations along their gradients therefore determine the cell type.

29
Q

During brain development on the antero-posterior axis: what does the “forebrain” develop into?

A

Telencephalon and Diencephalon

30
Q

During brain development on the antero-posterior axis: what does the “midbrain” develop into?

A

Mesencephalon

31
Q

During brain development on the antero-posterior axis: what does the “hindbrain” develop into?

A

Rhombencephalon (with otic vesicle).

32
Q

During brain development on the antero-posterior axis: what parts do the spinal cord develop into?

A

Cervical, thoracic, lumbar, sacral and coccygeal

33
Q

During brain development on the antero-posterior axis: what do the Telencephalon & Diencephalon develop into respectively?

A

Telencephalon: cerebrum
Diencephalon: thalamus & hypothalamus

34
Q

During brain development on the antero-posterior axis: what does the Mesencephalon develop into?

A

Superior/inferior colliculum and brainstem.

35
Q

During brain development on the antero-posterior axis: what does the rhombencephalon develop into?

A

The brain stem: cerebellum, pons, medulla oblongata.

36
Q

What are the extrinsic diffusible molecules essential for setting up the AP axis? Where are they produced?

A

Morphogens: retinoic acid and FGF produced in the mesoderm

37
Q

What does mutation in Shh cause?

A

Holoprosencephaly (HPE)
holo - combining
prosencephaly - prosencephalon (forebrain telenceph, dienceph)
Aka cyclopia (one eye kind of)
Failure of 2 hemisphere development, NS fails to split down midline

38
Q

What intrinsic mechanisms are superimposed on morphogens during establishment of the AP axis?

A

Homeotic genes

39
Q

What mechanisms pattern the nervous system on the DV and AP axises?

A

Extrinsic mechanisms: morphogens

Intrinsic mechanisms: homeotic genes

40
Q

Steps of neurogenesis?

A

Neural self renewing STEM CELL gives neural early PROGENITOR cell, which gives 3 main neurone types: neurones, oligofendrocyte, astrocyte.

41
Q

What is the significant characteristic of neural progenitor cells in the spinal cord?

A

They are polarised apically. Apical polarity specified by the apical “Par” complex proteins.

42
Q

How do neural progenitor cells proliferate?

A

They divide at the apical surface.
Early stages of development: symmetric proliferative division producing two further progenitor cells. Establishes pool of progenitor cells.
Later stages: Asymmetric divisions where progenitor cell produces one daughter progenitor cell and one differentiated neurone.

43
Q

How is a progenitor cell pool maintained during development of the nervous system and neurone placement?

A

Fine balance between progenitor cell proliferation and differentiation. Asymmetric cell division.

44
Q

How do progenitor neurones differentiate and become “placed” correctly in nervous system?

A

Loss of apical polar complex: by disassembly of the primary cillium complex and centrosome. Results in SHH signals to stop. This allows cells to exit cell cycle and stop differentiation.

45
Q

What morphogen patterns the neural tube and maintains progenitor cells?

A

SHH (maintains proliferation signals)

46
Q

What disease is caused by errors in neurone placement?

A

Periventricular heterotopia.
Seizures, mild intellectual disability. (If severe: brain malformations, microencephaly, developmental delay, abnormal blood vessels)

47
Q

What disease is caused by defects in primary cilia?

A

Ciliopathies e.g. Joubert Syndrome

48
Q

What do “commissural neurones” do?

A

They are projections from the spinal cord to the brain.

49
Q

What is hydrocephalus generally?

A

Build up of CSF inside the ventricles of the brain.

50
Q

What are the different physical consequences of hydrocephalus in babies vs adults?

A

Babies - head enlarges with enlargement of ventricles, compression of developing brain.
Adults - increased inter-cranial pressure with no compliance of skull. So pressure rises very quickly. Breathing centres can compress. (fatal in 8 hours)

51
Q

Lissencephaly?

A

Failure of neurones to STOP migrating (continue to migrate to subarachnoid space).
Brain has no grooves on the outside, large ventricles, smaller than normal.
Results in sever learning disabilities *failure to thrive.

52
Q

Describe difference between Spina Bifida Occulta, Meningomyelocele and Meningocele. Which is worse?

A

Spina bifida occulta - normal skin covering, with hairy patch. Defective bony arch (missing vertebra). Usually incidental finding on X-ray. Not associated with neurological problems.

Meningocele - protrusion of meninges through the gap in the spine. Skin covering is vestigial.

Myelomeningocele/ Meningomyelocele/ myelocele - spinal cord and nerve roots exposed. Condition accompanied by paralysis, numbness of legs & urinary incontinence. *Hyrocephalus & *Arnold Chiari malformation are usually present.

53
Q

What are “banana and lemon signs” and what do they show?

A

They are ultrasound features of the Arnold Chiari malformation in features with spina bifida.
Banana sign - distorted cerebellum
Lemon sign - lemon shaped head resulting from scalloping of frontal bones.

54
Q

What is the difference between Arnold Chiari 1 & 2?

A

1 - foramen magnum is obstructed by the cerebellum
2 - cerebellar tonsils protrude through the foramen magnum and goes down into spinal cord itself.

Both result in blockage of CSF pathway and CSF accumulation.

55
Q

What is the current treatment for hydrocephalus?

A

Surgical shunt of fluid from head into tummy. It maintains the pressure in the head with a valve mechanism.
Prognosis hard to predict, but cerebral cortex is not damaged if hydrocephalus is congenital (on,y brain development is affected).

56
Q

What are the four main differences between ‘brainstem-spinal cord’ development and ‘cerebral cortex’ development?

A

1) Notochord doesn’t control cerebral development.
2) Genes differ
3) Timing difference
4) Fluid system changes

57
Q

Generally, where is CSF made and how?

A

CSF made in the *choroid plexus in the *lateral ventricles.

CSF is *pumped into ventricles against pressure. Uses *energy.

58
Q

How many mL of CSF is produced per min? When does this change/ stop?

A

0.3 mL/min. This is constant throughout life.

59
Q

How does CSF drain?

A

Main site of drainage is the “Superior Sagittal sinus” via *subarachnoid space.
Also drains into *facial lymphatics via the ‘arachnoid pathway’.
Drainage *actively needs energy.

60
Q

What are Radial Glial fibres? What is their relation to CSF?

A

They are neural stem cell “processes”, coming from bottom of cerebral cortex.
They are in direct contact with CSF in the ventricles and subarachnoid space.

61
Q

What role does CSF play in neuronal cell patterning? (CSF signalling pathway)

A

CSF in lateral ventricles stimulate cell proliferation.

CSF in the subarachnoid space involved in the normal migration of cells from the bottom to the top (of cerebral cortex).

62
Q

What is Cortical Heterotopia?

A

Misplaced neural tissue due to damaged CSF signalling pathway.
Characterised by islands of neurones in abnormal locations along their ‘migration routes’ due to problems in the migration process.

63
Q

What is the link between hydrocephalus and the CSF signalling pathway?

A

In the developing brain: When there is a CSF drainage problem, cells on ventricular side stop dividing, so cortex has less migration of cells to the top (results in smaller cortex) and the cortex will not be populated with enough neurones.
This is a development problem and is not technically damaging as cortex is still functional. This can result in neurological deficits.

64
Q

What is the link between CSF, folate and hydrocephalus?

A

1) Folate protein produced by enzymes in CSF (choroid plexus) and not the developing cerebral cortex.
2) In hydrocephalus they found a lack of this folate protein due to obstructed CSF flow. This resulted in arrested development.

65
Q

Why is folic acid prescribed to women who are trying to conceive?

A

Reduces risks of NTD’s such as spina bifida.

66
Q

When should women take folic acid if they are trying to conceive? And how much should they take?

A

400 micrograms BEFORE THEY GET PREGNANT
and during the first 12 weeks of pregnancy (NHS) as spine is developing.
Some women with increased chance of pregnancy NTD’s are advised to take higher dose until 12 weeks (5 milligrams).

67
Q

Should we give “folic acid” supplement after spina bifida effective period?

A

No, it has been shown to increase risk of hydrocephalus.
“Folic acid” is completely artificial.
“Natural folates” like THF and folinic acid showed up to 80% decrease in hydrocephalus during this period, so take instead.

68
Q

How does a genetic folate deficiency result in neurological complications generally later on in life?

A

Folate plays a role in the methylation cycle of DNA.

Folate -> DNA synthesis + methylation purines & pyramidines -> gene expression.

69
Q

What does teratogenic mean?

A

Agent or factor which causes the malformation of an embryo

Sem 3 Neuro (8 decks)

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