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Brain Function and Malfunction > Spinal Cord > Flashcards

Spinal Cord Flashcards

1
Q

Function of spinal cord

A

co-ordinates movement and sensation

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2
Q

Where is the spinal cord found?

A

inside the vertebral column

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3
Q

What does the spinal cord arise from?

A

specialised dorsal ectoderm

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4
Q

Neural tube closure

A

occurs at multiple sites from anterior to posterior neuropore in multiple stages

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5
Q

genes for neural tube closure

A

82 in humans - MTHFR involved in folate metabolism

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6
Q

Primary neurulation

A

day 22-26

neural ectoderm fold and fuse to form neural tube

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7
Q

secondary neurulation

A

tail bid cells condense and form secondary neural tube caudally - coccyx and cauda equina

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8
Q

DRG formation

A

neural folds fuse to form brain and spinal cord

after fusion neural crest cells migrate peripherally to form sensory neurons of DRG

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9
Q

3 layers of the neural tube

A

ventricular - undifferentiated, lining of central canal
mantle - differentiating neurons form grey matter
marginal - nerve fibres - white matter

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10
Q

alar and basal plate

A

alar plate - dorsal - sensory

basal - ventral - motor

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11
Q

where do cells in DRG extend sensory fibres?

A

peripherally and centrally

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12
Q

5 main layers of spinal cord periphery

A

dura mater - tough, fibrous outer layer
epidural space - between dura and vertebra - loose connective tissue
arachnoid mater
subarachnoid space - CSF
pia mater - vascularised, attached to brain and spinal cord

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13
Q

How does the spinal cord transmit information?

A

ascending and descending white matter tracts

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14
Q

How does the spinal cord involve reflex integration?

A

grey matter - spinal reflexes eg knee jerk not initiated voluntarily by the brain

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15
Q

where does human spinal cord end?

A

L1

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16
Q

2 spinal cord enlargements

A

cervical C3-T1
lumbar T11-L2
control of limbs

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17
Q

What is the name for the nerve roots which radiate from L1 to coccyx?

A

cauda equina

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18
Q

How many spinal nerves and what do they contain?

A

31 pairs - sensory and motor

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19
Q

where are sensory nerve bodies located?

A

DRG

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20
Q

cervical plexus

A

C1-5 = neck, head and shoulders

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21
Q

brachial plexus

A

C5-T1 - shoulder and upper limb

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22
Q

lumbar plexus

A

T12-L4 - lower abdomen and lower limb

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23
Q

sacral plexus

A

L4-S4 - legs and feet

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24
Q

central pattern generator

A

produce rhythmic patterns eg walking
fictive motor patterns - motor output in paralysed/isolated spinal cord
alternate muscle extension and flexion

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25
Q

what are CPGs co-ordinated by?

A

propriospinal neuron path

cervical and lumbar enlargements

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26
Q

what is cpg refined by?

A

supraspinal signals - motor cortex

sensory feedback to spinal cord

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27
Q

main problems with NTD

A

neural tissue exposed to amniotic fluid liable to damage and progressive degeneration over time before birth

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28
Q

examples of neural tube defects

A

anencephaly, encephalocele, spina bifida

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29
Q

types of spina bifida

A

occulta, myelomeningocele, meningocele

30
Q

spina bifida stats

A

0.5-2/1000
regional variation
95% no FH

31
Q

What medications can predispose to spina bifida?

A

antidepressants and anticonvulsants

32
Q

surgery for spina bifida

A

in utero or after birth (within 48 hours)

33
Q

what is often (90%) concomitant with spina bifida?

A

hydrocephalus - requirement for a shunt

34
Q

Preventing spina bifida

A

supplement diet with 400mcg folate
fortified foodstuff
inositol (Vit B8)

35
Q

spina bifida and shh

A

shh is responsible for d/v patterning of spinal cord and s present in cilium. Disruptions of signalling can lead to NTD

36
Q

stats for SCI

A

2.5M globally, 50 000 UK age 16-30, males

37
Q

causes for SCI

A

road accidents, sports, violence, alcohol

38
Q

complete SCI

A

45% - total loss of sensation and function below injury level

39
Q

incomplete SCI

A

partial loss of sensation and function below injury level - 55%

40
Q

SCI above C3

A

usually results in death - diaphragm, phrenic nerve

41
Q

4 causes of traumatic primary injury

A

hyperflexion
hyperextension
rotation
vertical/axial compression

42
Q

2 causes of non-traumatic primary injury

A

cord compression eg tumour, reduced blood flow

developmental

43
Q

hyperflexion axial compression

A

eg fall on buttocks - vertebrae forced together and ligaments stretched

44
Q

what is the primary injury?

A

vertebral disc rupture

disc material invades centre of spinal canal and compress cord

45
Q

what can surgery do for primary injury?

A

relieve pressure, restore shape of cord but damage persists

46
Q

where is greatest damage of primary injury?

A

centre - haemorrhage - grey matter more vascular so vulnerable

47
Q

what is the secondary injury?

A

cell death in grey matter

wallerian degeneration in white matter - influx of calcium

48
Q

tracts lost secondary injury

A

ascending above lesion and descending below lesion

49
Q

fibroglial scar components

A

collagen - produce fibroblasts
astrocytes - activated microglia
macrophages

50
Q

microlesion

A

minimally disrupt BBB, axons cannot regenerate

51
Q

contusive lesion

A

meninges intact, astrocytes produce CSPGs, macrophages

52
Q

How are SCI assessed?

A

ASIA scale
A-E
A is complete, always bladder and bower problems

53
Q

Treatment of SCI

A 
immobilise C-spine
CT/MRI/X-ray within 48-72 hours 
test sensory and motor function 
drugs to reduce swelling, maintain bp
surgery - remove bone fragments, clots, disc material
54
Q

What is E on ASIA scale?

A

motor and sensory normal

55
Q

ASIA scale and description

A

A - complete, no sensory or motor below injury through S4-5
B - incomplete. sensory but no motor
C - incomplete - motor below injury and more than half key muscles grade<3
D - same as C but >3
E - normal

56
Q

what ASIA grade are all complete SCI?

A

A

57
Q

What % complete SCI recover significantly?

A

0.9%

58
Q

Complications of SCI

A

pressure sores, infection, DVT, spasticity, autonomic dysreflexia

59
Q

autonomic dysreflexia

A

life threatening increase in bp
injury T5 or higher
irritating stimulus below level of SCI eg full bladder

60
Q

4 main barriers to recovery

A

cell loss
scar is non-permissive for regeneration (fibroblasts, sema 3-A deflect growth, astrocyte CSPG and tenascin)
spared cells in white matter demyelinated
degrading myelin - Nogo-A, MAG

61
Q

6 key things for successful repair

A

damaged nerves must survive or be replaced - prevent secondary injury
surviving neurons must regrow axons despite scar and inhibitory molecules
axons must migrate towards appropriate targets
effective synapses
respond to NT
branching to replace circuitry

62
Q

Different treatments for complete vs incomplete

A 
incomplete = stimulate reorganisation of spared circuitry 
complete = neuron grafts, stimulate regrowth
63
Q

PNS graft

A

permissive PNS environment encouraged CNS axon regrowth

64
Q

Forms of axon growth after SCI

A

new synapse growth and remodelling of new axons
branching and sprouting proximal and distal to lesion
growth through spared tissue
pass through scar

65
Q

Some things that have been used for acute injuries

A

PNS grafts - no evidence of functional recovery
cool injury site
methylprednisolone - stopped in 2013
foetal spinal cord transplants - alone or with molecules inhibit mag/nogo-A, grwoth factors
polymer scaffold seeded with stem cells

66
Q

3 new ways emerging for SCI

A

modulate cAMP levels - overcome MAG inhibition
stem cells
electric fields

67
Q

what direction do axons grow in EF?

A

cathode

68
Q

EF with cathode distal or proximal to lesion

A

distal - prevent die back

proximal - enhance die back

69
Q

acute injury

A

soon after primary injury

70
Q

starting treatment timing

A

acute phase or wait?

acute - hostile, might be better to wait 2 weeks for inflammation and macrophage to stabilise

71
Q

chronic injury treatment

A

Christopher Reeve’s

exercise therapy - repattern cpgs?

Brain Function and Malfunction (7 decks)

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