week 4: neurobiology: spinal cord injury Flashcards

1
Q

most spinal cord injuries in UK and USA caused by

A

traffic accident
falls

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2
Q

spinal cord injuries age and gender stats

A

80%+ males
average age: 41
no valid explanation

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3
Q

quadriplegia

A

injury affects lower and upper limbs

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4
Q

paraplegia

A

injury affects lower limbs only

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5
Q

impact of SCI lesion

A

neurotic death of neurons
severs axons
vascular injury may occur (extravasation of blood)
blood brain barrier may break
release of excitatory amino acids

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6
Q

if blood brain barrier breaks,

A

leucocytes invasion and release of toxic cytokines

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7
Q

release of excitatory amino acids causes

A

massive increase in Ca2+
causes excitotoxicity
further damage to cells that may have survived intitial trauma

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8
Q

secondary injury

A

-can continue to grow for months
-Wallerian degeneration
-triggers second invasion of inflammatory cells
-activated macrophages and microglial invasion
-astrocytes proliferate and hypertrophy: glia limitans (scar)

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9
Q

Wallerian degeneration

A

process occurs when axons are severed
axons will die back to soma

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10
Q

glia scar

A

structure that forms around region to try to mend and protect area
forms several weeks after initial injury
formed by astrocytes
proliferation of astrocytes needed
form scar around region to prevent further damage and to restore barrier between blood and spinal cord
produce inhibitory molecules, chemical and physical barrier to regrowth (of axons?)

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11
Q

ectopic sprouting

A

sprouting of axons
abnormal growth
causes abnormal reflexes
can cause hyper-reflexia and spasticity
reorganisation of nociceptors
reorganization of autonomic circuits

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12
Q

what can reorgnisation of nociceptors cause

A

chronic pain syndrome

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13
Q

what can reorganisation of autonomic circuits cause

A

autonomic dysreflexia
dysregulation of autonomic reflexes e.g controlling blood pressure
many of these reflexes are vital for survival

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14
Q

spinal shock

A

occurs immediatly after injury
complete lack of reflexes
areflexia or hypo-reflexia and flaccid paralysis

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15
Q

weeks after spinal injury

A

return of segmental reflexes and hyper-reflexia

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16
Q

months after spinal injury

A

spastic paralysis:
large spasms and clonus

17
Q

plasticity

A

structural, physiological, chemical change in CNS

18
Q

what do denervation and axotomies result in

A

reorganisation of networks above and below lesion

19
Q

limited capacity of CNS to repair itself due to:

A
  1. limited neurogenisis
  2. spontaneous failure of CNS axon regeneration
  3. limited endogenous repair
  4. insufficient compensatory plasticity
20
Q

what can we do to help repair

A
  1. reduce secondary damage
  2. enhance growth potential
  3. eliminate obstacles
  4. facilitate synaptic reconnectivity
21
Q

approved pharmacological treatments to help gain function after spinal cord injuries

A

none

22
Q

locomotor training

A

based on principle of neuroplasticity
designed to improve movement and mobility
take advantage of functioning circuits
lumbar spinal cord possesses all necessary circuitry to produce rhythmic coordinated alternating locomotor behaviors