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Neurodegenerative > TBI & SCI > Flashcards

TBI & SCI Flashcards

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

A

20mmHg

22
Q

Severe brain swelling ICP

A

30mmHg

23
Q

Monroe Kellie doctrine

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

A

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

25
Q

Key events in TBI: secondary injury - Neurochemical injury

A

Excessive production of free radicals
Excessive release of excitatory neurotransmitters
Alterations in glucose metabolism
Decreased cerebral blood flow
Neuro inflammation

26
Q

Key events in TBI: late/delayed injury

A

White matter degeneration and cerebral atrophy
Postraumatic hydrocephalus
Post traumatic seizures

27
Q

Secondary injury - Neuroinflammation

A

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
Q

AD and TBI comparison - MRI

A

Both have accentuated gyri
Both have neuronal atrophy

29
Q

Diffuse axonal injury (DAI)

A

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
Q

Chronic traumatic encephalopathy (CTE)

A

Progressive and degenerative brain condition that has been linked to repeated head injuries and repeated concussion
Aka dementia puglistica and punch drunk syndrome

31
Q

Chronic traumatic encephalopathy (CTE): symptoms

A

Begins gradually - years after initial trauma(s)
Memory loss
Confusion
Impaired judgement
Impulsive control problems
Aggression
Depression
Parkinsonism
Progressive dementia

32
Q

Molecular/cellular changes found in CTE

A

Abnormal tau accumulation and neurofibrillary tangles
Microgliosis, astroiosis
Brain atrophy
Englarged ventricles
Abnormalities in TBL-43 (frontotemporal dementia and ALS)

33
Q

Woodpeckers

A

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
Q

Spinal cord injury (SCI) facts

A

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
Q

Spinal cord anatomy

A

Cervical 1-8
Thoracic 1-12
Lumbar 1-5
Sacral 1-5
Coccygeal 1

36
Q

What information is carried in which tract

A

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
Q

Paraplegia versus quadriplegia

A

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
Q

Priorities for recovered function amongst SCI patients

A

Arm/ hand function highest priority for quadriplegics

Sexual function highest priority for paraplegics

39
Q

SCI - partial lesions

A

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
Q

ASIA (American spinal injuries association)

A

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
Q

Spinal shock

A

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
Q

SCI and TBI - comparisons of initial injury

A

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
Q

SCI - impact of injury

A

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
Q

CNS injury - spinal cord, astrocytes and glial scar

A

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
Q

GFAP as a stain

A

Injury dark
Area around bright

46
Q

Mechanism of Inflammatory cells in SCI

A

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
Q

Wallerian degeneration in PNS

A

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
Q

Wallerian degeneration in adult CNS

A

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
Q

Damaged neurons - chromatolysis

A

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
Q

Spinal cord injury and traumatic brain injury - issues for repair and recovery

A

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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