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LSB658 > Neurological trauma > Flashcards

Neurological trauma Flashcards

1
Q

List some ways ischaemic reperfusion injury causes secondary damage

A
  • Damaged vasculature and endothelial cell function creates ‘no flow’ problem
  • O2 free radicals
  • Inflammatory response
  • O2 paradox/calcium paradox/pH paradox
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2
Q

Describe how inflammation causes damage

A
  1. ROS and NO derived from inflammatory immune cells can alter cellular proteins and lipids and lead to cell death
  2. Activation of the complement system (after ischaemia) can kill cells by forming pores in the cell membrane leading to cell lysis
  3. Apoptosis inducing receptors are expressed on neurons and glial cells after ischaemia. Attracts dentritic cells, cytotoxic T-cells, and NK cells
  4. Perforin and Granzyme: released by cytotoxic T-cells and NK cells and taken up by damaged neurons and glial cells. Induces apoptosis in the target
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3
Q

Name the three brain meninges

A
  • Dura mater
  • Arachoid
  • Pia mater
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4
Q

Name the two types of penetrating brain injuries

A

Cerebral contusion and cerebral laceration

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5
Q

What is the difference between cerebral contusion and cerebral laceration?

A

Cerebral contusion: membranes are not torn

Cerebral laceration: pia-arachnoid membranes are torn over the site of the injury

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6
Q

What occurs in the brain with repeated brain injury?

A

Brain tissue becomes similar to Alzheimer’s disease brain - accumulation of Tau proteins

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7
Q

List the six events of brain injury

A
  1. Direct blow - tissue damage, direct damage to neurones, may include bleeding
  2. Acute hostile environment in brain - hypoxia, excitotoxicity, local inflammation (death of neurones within minutes)
  3. Swelling - raised ICP
  4. Worsening of hypoxia
  5. Secondary injury (within hours to days)
  6. Recovery phase
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8
Q

How does increased ICP kill neurones?

A

Mechanically (by crushing)

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9
Q

What is cerebral perfusion pressure (CPP)?

A

Gradient that drives perfusion of the brain

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10
Q

Which is normally higher, systemic presssure or intracranial pressure?

A

Systemic

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11
Q

What is the normal physiological result of systemic pressure being higher than intracranial pressure?

A

The brain is continuously perfused

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12
Q

How does increased ICP impact CPP?

A

Decreases CPP as the gradient disappears

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13
Q

Which are generally worse, focal or diffuse brain injuries?

A

Diffuse, though they can be mild

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14
Q

List some general symptoms of acute brain injury

A
  • Headache
  • N+V
  • Fatigue
  • Blurred vision
  • Ears ringing
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15
Q

List some symptoms of severe acute brain injury

A
  • ALOC
  • Motor and balance problems
  • Speech and comprehension problems
  • Behavioural changes
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16
Q

List some symptoms of increasing ICP

A
  • Decreasing LOC
  • Worsening TBI symptoms
  • Pupillary changes
  • Cushing’s triad (bradycardia, bradypnoea, hypertension)
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17
Q

How do flexion injuries (sudden forcible forward movement of the head; whiplash) commonly effect the spinal cord?

A
  • Damages the vertebrae which protrude into the spinal cord, often around C5-C6
  • Spinal ligaments can be torn
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18
Q

How do compression injuries (force transmitted through the head/through the base of the spine/lower limbs) commonly effect the spinal cord?

A
  • Vertebrae (mostly cervical or lower thoracic/lumbar) fracture into pieces
  • Pieces protrude into the spinal canal, damaging the spinal cord
  • Displacement of intervertebral discs which protrude into the spinal canal
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19
Q

How do hyperextension injuries (neck forcibly extended in a backward direction) commonly effect the spinal cord?

A
  • Often little or no damage to the vertebrae
  • Force causes excessive stretching of the spinal cord
20
Q

Injuries to which area of the spinal cord are both the most common and most debilitating?

A

Cervical injuries

21
Q

List some types of acute spinal cord injury (SCI)

A
  • Contusion/compression/concussion
  • Partial lesion
  • Full lesion - transection
22
Q

List some components of primary SCI

A
  • Laceration/contusion/compression
  • Structural disturbances, death of neurones, damage to neural tracts
  • Ischaemia and microvascular damage
  • Excessive extracellular glutamate and other excitatory amino acids released by dead cells leads to further cell death due to excitotoxicity and free radical production
  • Inflammatory response and swelling compresses injury leading to further cell death
23
Q

The anterior spinal artery supplies what area?

A

The anterior 2/3 of spinal cord

24
Q

Two smaller posterolateral spinal arteries supply what area?

A

Posterior 1/3 of the spinal cord

25
Q

List some macroscopic components of secondary SCI degeneration

A
  • Decreased spinal perfusion leads to ischaemia
  • Biochemical cascade causes further damage to a larger region
  • Often results in a rise of injury level
    • e.g. C4/5 acute injury becomes C2/3 chronic injury
26
Q

List some microscopic components of secondary SCI degeneration

A
  • Continued inflammatory immune response
  • Cytokine and interleukin secretion by macrophages and neutrophils (first responders of immune response)
  • Axon demyelination due to oligodendrocyte cell death, reducing neurone ability to function
  • Activated astrocytes migrate to clean up site but form astrocytic scar (an scar can be deleterious to normal function)
27
Q

List four long-term effects of secondary SCI degeneration on the spinal cord

A
  • Loss of cord conduction/synaptic transmission
  • Membrane damage
  • Cytoskeleton damage
  • Structural integrity is compromised
28
Q

How to astrocytes respond to SCI?

A
  • Removal of toxic chemicals (glutamate)
  • Proliferation and secretion of neuroprotective but growth-inhibitory factors
  • Formation of glial (astrocytic) scar
29
Q

How do oligodendrocytes respond to SCI?

A

Massive death due to high glutamate concentrations; myelin production is suppressed

30
Q

How do microglia respond to SCI?

A
  • Initially phagocytosing debris and producing neuroprotective factors
  • Over time become neurotoxic and growth-inhibitory due to constant activation
31
Q

How do Schwann cells respond to SCI?

A
  • Cells de-differentiate to an immature state and lose their myelin sheath
  • Migrate from the periphery into the injury site in the CNS
  • Participate in endogenous repair processes by expression of neurotrophic factors
32
Q

What are the initial systemic effects of SCI on the CVS?

A
  • Increased BP
  • Bradycardia
  • Dysrhythmias
33
Q

What are the subsequent (within minutes) systemic effects of SCI on the CVS?

A
  • Loss of sympathetic activity below lesion
  • Vasodilation
  • Venodilation, reduced venous return
  • Cardiac output falls; BP falls; bradycardia
34
Q

What are the longer term systemic effects of SCI on the CVS?

A
  • Decreased muscle activity
  • Venodilation leading to increased DVT and PE
35
Q

What are the respiratory effects of SCI?

A
  • Lesions above C3 require immediate ventilation
  • Diaphragm function is maintained if lesion is below C5
  • Lesions below C6 affect intercostal and abdominal muscle, resulting in reduced (but partially controlled):
    • Functional residual capacity
    • Forced vital capacity
    • Overall hypoventilation (hypercapnia, hypoxaemia, poor ability to cough/clear secretions)
36
Q

What are the gastrointestinal effects of SCI?

A
  • Paralytic ileus - obstruction of intestine
  • Aspiration, vomiting
  • Gastric distention
  • Potentially fatal
37
Q

What are the effects of SCI on temperature regulation?

A
  • Complete SCI - inability to sweat below level of injury
    • Some quadriplegics cannot sweat above level of injury
  • Result: poikilothermic (temperature varies considerably); susceptible to hypo/hyperthermia
38
Q

Note: regarding the nervous system rather than cognitive function

What are the neurological effects of an SCI lesion within the anterior cord?

A

Corticospinal and spinothalamic tracts; impacts pain and temperature sensation

39
Q

What are the neurological effects of an SCI lesion within the posterior cord?

A

Affects vibration and proprioception (muscle response to stimuli)

40
Q

What are the neurological effects of an SCI hemisection lesion?

A
  • Ipsilateral weakness (on the same side of the body)
  • Contralateral pain and temperature sensation
41
Q

Differentiate between a complete and incomplete functional consequence of SCI

A

Complete - no function (sensation or movement) below the level of injury

Incomplete - partial function below the level of injury

42
Q

List three current treatments regimes that aim to limit secondary degeneration

A
  • Decompression surgery within 24 hours
  • Anti-inflammatory steriods (questionable efficacy)
  • Physiotherapy rehabilitation
43
Q

List some possible chronic problems after suffering SCI

A
  • Respiratory problems
  • Cardiovascular complications
  • Urinary and bowel dysfunction
  • Neurogenic bowel (loss of voluntary control)
  • Neuropathic pain
  • Pressure areas
  • Osteoporosis
44
Q

Autonomic dysreflexia occurs in pts with SCI at which level?

A

T6 and above

45
Q

Autonomic dysreflexia is more common in patients with what two kinds of lesions?

A

Cervical or complete lesions

46
Q

Describe the process of autonomic dysreflexia

A

Strong stimulation below the level of injury generates sympathetic overactivity leading to vasoconstriction below the lesion. Baroreceptors stimulate bradycardia and excessive vasodilation above the lesion. The CNS cannot inhibit the sympathetic response below the injury, resulting in uncontrolled hypertension with bradycardia

47
Q

List the symptoms of autonomic dysreflexia

A
  • Hypertension
  • Bradycardia
  • Pupillary constriction
  • Blurred vision
  • Nasal congestion
  • Flushing and profuse sweating above lesion level
  • Pale/cool skin and piloerection below lesion level

LSB658 (11 decks)

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