Neurological trauma

Question 1

List some ways ischaemic reperfusion injury causes secondary damage

Answer 1

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

Question 2

Describe how inflammation causes damage

Answer 2

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

Question 3

Name the three brain meninges

Answer 3

• Dura mater
• Arachoid
• Pia mater

Question 4

Name the two types of penetrating brain injuries

Answer 4

Cerebral contusion and cerebral laceration

Question 5

What is the difference between cerebral contusion and cerebral laceration?

Answer 5

Cerebral contusion: membranes are not torn

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

Question 6

What occurs in the brain with repeated brain injury?

Answer 6

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

Question 7

List the six events of brain injury

Answer 7

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

Question 8

How does increased ICP kill neurones?

Answer 8

Mechanically (by crushing)

Question 9

What is cerebral perfusion pressure (CPP)?

Answer 9

Gradient that drives perfusion of the brain

Question 10

Which is normally higher, systemic presssure or intracranial pressure?

Answer 10

Systemic

Question 11

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

Answer 11

The brain is continuously perfused

Question 12

How does increased ICP impact CPP?

Answer 12

Decreases CPP as the gradient disappears

Question 13

Which are generally worse, focal or diffuse brain injuries?

Answer 13

Diffuse, though they can be mild

Question 14

List some general symptoms of acute brain injury

Answer 14

• Headache
• N+V
• Fatigue
• Blurred vision
• Ears ringing

Question 15

List some symptoms of severe acute brain injury

Answer 15

• ALOC
• Motor and balance problems
• Speech and comprehension problems
• Behavioural changes

Question 16

List some symptoms of increasing ICP

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

• 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

Question 19

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

Answer 19

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

Question 20

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

Answer 20

Cervical injuries

Question 21

List some types of acute spinal cord injury (SCI)

Answer 21

• Contusion/compression/concussion
• Partial lesion
• Full lesion - transection

Question 22

List some components of primary SCI

Answer 22

• 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

Question 23

The anterior spinal artery supplies what area?

Answer 23

The anterior 2/3 of spinal cord

Question 24

Two smaller posterolateral spinal arteries supply what area?

Answer 24

Posterior 1/3 of the spinal cord

Question 25

List some macroscopic components of secondary SCI degeneration

Answer 25

* 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

Question 26

List some microscopic components of secondary SCI degeneration

Answer 26

* 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)

Question 27

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

Answer 27

* Loss of cord conduction/synaptic transmission * Membrane damage * Cytoskeleton damage * Structural integrity is compromised

Question 28

How to astrocytes respond to SCI?

Answer 28

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

Question 29

How do oligodendrocytes respond to SCI?

Answer 29

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

Question 30

How do microglia respond to SCI?

Answer 30

* Initially phagocytosing debris and producing neuroprotective factors * Over time become neurotoxic and growth-inhibitory due to constant activation

Question 31

How do Schwann cells respond to SCI?

Answer 31

* 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

Question 32

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

Answer 32

* Increased BP * Bradycardia * Dysrhythmias

Question 33

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

Answer 33

* Loss of sympathetic activity below lesion * Vasodilation * Venodilation, reduced venous return * Cardiac output falls; BP falls; bradycardia

Question 34

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

Answer 34

* Decreased muscle activity * Venodilation leading to increased DVT and PE

Question 35

What are the respiratory effects of SCI?

Answer 35

* 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)

Question 36

What are the gastrointestinal effects of SCI?

Answer 36

* Paralytic ileus - obstruction of intestine * Aspiration, vomiting * Gastric distention * Potentially fatal

Question 37

What are the effects of SCI on temperature regulation?

Answer 37

* 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

Question 38

# Note: regarding the nervous system rather than cognitive function What are the neurological effects of an SCI lesion within the anterior cord?

Answer 38

Corticospinal and spinothalamic tracts; impacts pain and temperature sensation

Question 39

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

Answer 39

Affects vibration and proprioception (muscle response to stimuli)

Question 40

What are the neurological effects of an SCI hemisection lesion?

Answer 40

* Ipsilateral weakness (on the same side of the body) * Contralateral pain and temperature sensation

Question 41

Differentiate between a complete and incomplete functional consequence of SCI

Answer 41

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

Question 42

List three current treatments regimes that aim to limit secondary degeneration

Answer 42

* Decompression surgery within 24 hours * Anti-inflammatory steriods (questionable efficacy) * Physiotherapy rehabilitation

Question 43

List some possible chronic problems after suffering SCI

Answer 43

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

Question 44

Autonomic dysreflexia occurs in pts with SCI at which level?

Answer 44

T6 and above

Question 45

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

Answer 45

Cervical or complete lesions

Question 46

Describe the process of autonomic dysreflexia

Answer 46

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

Question 47

List the symptoms of autonomic dysreflexia

Answer 47

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