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TBI & SCI Flashcards

(50 cards)

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1
Q

Traumatic brain injury facts

A

Acute trauma to head and brain with or without skull fracture
10000-20000 severe traumatic brain injuries per year
Men 2x more likely
15-24 yrs old and over 80s most at risk

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2
Q

Common causes of TBI

A

Motor vehicle accidents
Cycling (helmet reduces 88% chance)
Sports injuries
Violence
Falls and accidents

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3
Q

Potential effects of head injury

A

Behaviour and personality changes - anxiety, depression, loss of motivation, difficulty controlling anger, impulsivity
Cognitive impairment- problems with memory, attention, concentration. Low tolerance for noise or stressful environments, loss of insight and initiative
Motor and sensory deficit changes- loss of coordination, muscle rigidity, epilepsy, speech issues, sight/smell/taste loss, fatigue, sexual problems, paralysis

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4
Q

Glasgow coma scale (GCS) - TBI diagnosis

A

Monitors changes in consciousness
Monitors motor response, verbal response and eye opening
Score ranges from 1 to 4-6
<8 is a severe head injury (coma)
9-12 moderate head injury
>12 mild head injury

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5
Q

Traumatic brain injury: closed injury

A

Trauma cause brain to be violently shaken inside of skull eg blast injury. No visible wound

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6
Q

Traumatic brain injury: open/penetrating injury

A

Object goes through the skull and enters brain

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7
Q

Traumatic brain injury: crush

A

Head is sandwiched between two hard objects

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8
Q

Traumatic brain injury: coup

A

Primary injury cause when the head stops suddenly and the brain rushes forward. Brain incurs a primary impact injury at the site of skull stroke as well as surrounding tissue

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9
Q

Traumatic brain injury: counter coup

A

Secondary injury caused when brain bounces off the primary surface of impact and goes on to impact the opposite side of the skull. Brain incurs focal area of damage as well as damage to nearby surrounding tissue

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10
Q

Traumatic brain injury: coup and contrecoup forces

A

Rotational forces - shearing and twisting
Coup - blow
Countrecoup - contusion, swelling, blood clots

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11
Q

Whiplash injury, TBI and cervical vertebrae

A

Hyperextension of the neck followed by hyperflexion
Major area of damage done to anterior longitudinal ligament
Vertebrae can become dislocated and/or fractured

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12
Q

Whiplash: hyper extension

A

Sudden backwards acceleration of skull. Once skull stops moving, the frontal lobe strikes the front of skull

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13
Q

Whiplash: Hyperflexion

A

Head recoils forward and stops
Occipital lobe strikes back of skull

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14
Q

Key events in TBI: primary

A

Skull fracture (open)
Contusions (bruising, damage to blood vessels)
Haemorrhage (bleeding from raptured blood vessels)
Haematoma (localised pooling of blood)
Diffuse axonal injury (DAI) (damage to axons through the brain)
Concussion (temporary - neuronal dysfunction)

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15
Q

Key events in TBI: secondary

A

Intracranial - evolves over hrs, days, week after impact
Brain swelling, cerebral oedema, hydrocephalus
Increased intracranial pressure
Intercranial haemorrhages, traumatic haematomas, infections
Blood flow changed and metabolic changes
Epilepsy
Hypoxia-ischaemia (reduced o2 to brain)

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16
Q

What can haemotoma lead to?

A

Increased intracranial pressure and shifting of brain tissue so increased pressure in brain tissue

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17
Q

What do all the key events in TBI lead to?

A

Atrophy of brain tissue and wide ranging symptoms

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18
Q

Neuropathology of TBI

A

Atrophy and increased ventricles
(Seen through T1 weighted MRI)

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19
Q

TBI - intracranial pressure (ICP)

A

Cerebral perfusion pressure = mean arterial pressure - intracranial pressure
CPP should not fall below 70mmHg - risk of hypoxia and ischaemia

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20
Q

Normal ICP

A

7-15mmHg

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21
Q

Drowsy and confused patients ICP

22
Q

Severe brain swelling ICP

23
Q

Monroe Kellie doctrine

Study These Flashcards
A

V intracranial = V brain + V blood + V CSF

Brain = 80%
Blood = 10%
CSF = 10%
Increase in one results compression of others

24
Q

ICP: homeostasis and treatments

Study These Flashcards
A

Diuretic
Medically induced coma
Placement of shunt
Craniectomy (partial skull removal)

25
Key events in TBI: secondary injury - Neurochemical injury
Excessive production of free radicals Excessive release of excitatory neurotransmitters Alterations in glucose metabolism Decreased cerebral blood flow Neuro inflammation
26
Key events in TBI: late/delayed injury
White matter degeneration and cerebral atrophy Postraumatic hydrocephalus Post traumatic seizures
27
Secondary injury - Neuroinflammation
Activation of microglia, astrocytes, neurons Activation and recruitment of macrophages Microglia secrete pro inflammatory modulators- degrade BBB and release cytokines in response to DAMPs Astrocytes - up regulate extracellular matrix to wall off areas of lesion Oligodendrocytes - violin that sits around lesion but don’t do much after
28
AD and TBI comparison - MRI
Both have accentuated gyri Both have neuronal atrophy
29
Diffuse axonal injury (DAI)
Injury to axon - twist and tear BAPP is produced by neurones in response to injury Accumulates at points of damage (construction/transection) Some axons have multiple swellings (beaded appearance) may persists for years Axonal transport stopped Severe white matter degeneration and atrophy of corpus callosum
30
Chronic traumatic encephalopathy (CTE)
Progressive and degenerative brain condition that has been linked to repeated head injuries and repeated concussion Aka dementia puglistica and punch drunk syndrome
31
Chronic traumatic encephalopathy (CTE): symptoms
Begins gradually - years after initial trauma(s) Memory loss Confusion Impaired judgement Impulsive control problems Aggression Depression Parkinsonism Progressive dementia
32
Molecular/cellular changes found in CTE
Abnormal tau accumulation and neurofibrillary tangles Microgliosis, astroiosis Brain atrophy Englarged ventricles Abnormalities in TBL-43 (frontotemporal dementia and ALS)
33
Woodpeckers
Less CSF Tongue has a bone to act as a spring - dampens force on brain Recent evidence shows that smaller brain size allows larger concussion threshold
34
Spinal cord injury (SCI) facts
1000-2000 new cases in uk a year 42 avarage age at injury (20s and old) Males more likely Pneumonia and septicaemia - common cause of death of SCI patient
35
Spinal cord anatomy
Cervical 1-8 Thoracic 1-12 Lumbar 1-5 Sacral 1-5 Coccygeal 1
36
What information is carried in which tract
Lateral corticospinal tract - motor control (motor descending tracts) Posterior columns - vibration, light touch, proprioception (sensory ascending tracts) Anterior spinothalamic tract - pain and temperature (sensory ascending tracts)
37
Paraplegia versus quadriplegia
Quadriplegic - no longer control any of limbs (C4 and C6 injury) Paraplegia - don’t have use of legs but have arms (T6 and L1)
38
Priorities for recovered function amongst SCI patients
Arm/ hand function highest priority for quadriplegics Sexual function highest priority for paraplegics
39
SCI - partial lesions
brown sequard syndrome of spinal cord - Same side as lesion UMN weakness, loss of position and vibration Side of opposite lesion loss of pain and temp Central cord syndrome - Lesion interrupts fibres crossing to enter spinothalamic tracts (stretch reflex, autonomic function)
40
ASIA (American spinal injuries association)
A (complete injury) -E (normal) levels Determines sensory lvls for right and left Motor levels for right and left Single neurological lvl - lowest spinal level that is normal on both sides Injury complete or incomplete
41
Spinal shock
State of temporary loss of function in spinal cord (often lasts a day can be up to month) (replaced by spastic paralysis after spinal shock) Flaccid paralysis below the lesion Loss of tendon reflexes Impaired sympathetic outflow to vesicular smooth muscle can cause decreased blood pressure (high cervical injury) Absent sphincter reflexes and tone
42
SCI and TBI - comparisons of initial injury
Lesions - contusion, necrosis, apoptosis, hemorehage, oedema, breakdown of BBB, swelling, excitotoxicity, DAI, hyperthermia, inflammation Loss of function - local vs global Acute versus chronic (primary vs secondary)
43
SCI - impact of injury
Acute injury, lesion spread, chronic injury Contusion injury - lesion in centre and tissue responding for days becoming bigger. After week has a hole with debris, 2 weeks to month - strong capsule as fluid filled
44
CNS injury - spinal cord, astrocytes and glial scar
Astrocytes become reactive - become hypertrophic, secrete chondroitin sulfate proteoglycans (CSPGs), increase expression of normal molecules eg glial fibrillation acidic protein (GFAP) Result = glial scar Glial scar + myelin debris = area which growing axon cannot get through
45
GFAP as a stain
Injury dark Area around bright
46
Mechanism of Inflammatory cells in SCI
Flood lesion and release pro inflammatory cytokines so affect neuronal viability Diffusable inflammatory mediators (nitrous oxide) affect neuronal excitably Axons/neurons die or degenerate
47
Wallerian degeneration in PNS
Axon becomes fragmented at injury site Myelin debris released and Schwann cells become reactive Macrophages recruited and both clear debris Schwann a cells for regeneration tubes (bands of bungner), axons sprout and regrowth through tube
48
Wallerian degeneration in adult CNS
Injury Microglia and astrocytes activated Macrophages begin to remove debris Myelin debris not fully removed Oligodendrocytes survive Glial scar firmed. Cell body undergoes chromatolysis and synaptic terminal retract Axons attempt to sprout but regeneration fails due to persistent myelin debris and glial scar
49
Damaged neurons - chromatolysis
Nissl substance stains RE and poly ribosomes - no axon present Neurones undergoing chromatolysis have a displacement of nucleus, Nissl substance only at cell body periphery Neurones usually undergo apoptosis
50
Spinal cord injury and traumatic brain injury - issues for repair and recovery
Major biomedical problem and increasing in frequency Prevention better than cure Prevent secondary damage, anti inflammatory response, increase neuro protection, increase axon protection Repair damage?

Neurodegenerative (8 decks)

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