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Neurodegenerative diseases > Traumatic brain injury > Flashcards

Traumatic brain injury Flashcards

1
Q

how many severe brain injuries occur per year in the UK?

A

10000 - 20000

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2
Q

what groups are most at risk for traumatic brain injury?

A

15-24 year old males & over 80 year olds

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3
Q

what are some common causes of TBI?

A
  • Motor vehicle accidents
  • cycling accidents
  • sports injuries (boxing, American football, rugby)
  • violence
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4
Q

wearing a helmet can reduce TBI risk up to…

A

…88%

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5
Q

what are the potential effects of head injury?

3 categories

A
  • Behaviour and personality changes – Anxiety, depression, loss of motivation, difficulty controlling anger, and impulsivity (frontal cortex)
  • Cognitive Impairment – Problems with memory, attention and concentration, low tolerance for noisy or stressful environments, loss of insight and initiative (hippocampus entorhinal cortex)
  • Motor & Sensory deficits changes – Loss of coordination, muscle rigidity, epilepsy, difficulty speaking, sight/smell/taste loss, fatigue, sexual problems, paralysis (motor cortex)
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6
Q

what is the main diagnosis method for traumatic brain injury?

A

Glasgow Coma Scale (GCS)

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7
Q

what is the Glascow Coma Scale (GCS)?

A

GCS is an clinical indicator of head injury severity.
* Monitors changes in consciousness
* Monitors motor response, verbal response and eye opening
Scores immediately and 24 hrs post-injury correlate with degree of long term impairment
Scoring ranges from 1 (no response) to maximum 4-6 (normal)

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8
Q

what do GCS scores mean?

A
  • <8 is a severe head injury (coma)
  • 9-12 is a moderate head injury
  • > 12 is a mild head injury
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9
Q

what levels are there to the motor repsonses in the GCS?

A

best motor response - 6 obeying commands, 5 localising to pain, 4 withdrawing to pain, 3 flexor response to pain, 2 extensor response to pain, 1 no response to pain

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10
Q

what levels are there to the verbal repsonses in the GCS?

A

best verbal response - 5 oriented (time place person), 4 confused conversation, 3 inappropriate speech, 2 incomprehensible sounds, 1 none

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11
Q

what levels are there to the eye opening repsonses in the GCS?

A

4 spontaneous, 3 in response to speech, 2 in response to pain, 1 none

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12
Q

what is a open/penetrating injury?

A

When an object goes through the skull and enters the brain.
There is an obvious external wound

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13
Q

what is a closed head injury?

A

A trauma causes the brain to be violently shaken inside of the skull, such as a blast injury. No visible wound. No obvious external signs

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14
Q

what is a crush injury?

A

When the head is sandwiched between two hard objects.

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15
Q

what is a Coup injury?

A

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

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16
Q

what is a Contrecoup injury?

A

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

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17
Q

what are the three layers of the meniges in the brain that protect it from trauma?

A

The delicate inner layer is the pia mater. The middle layer is the arachnoid, a web-like structure filled with fluid that cushions the brain. The tough outer layer is called the dura mater

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18
Q

what other froces occur in the brain at the time of the TBI that cause damage?

A

in addition to the shaking back and forth that occurs with the intial blow there are also rotational forces that occur, with shearing and twisting

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19
Q

what damage occurs with a contrecoup injury?

A
  • contusion
  • swelling
  • blood clots
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20
Q

what is whiplash?

A

Hyperextension of the neck, followed by hyperflexion. Major area of damage done to anterior longitudinal ligament, but vertebrae can also become dislocated and/or fractured

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21
Q

what is hyperextension of the neck?

what happens dring whiplash?

A

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

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22
Q

what is hyperflexion of the neck?

what happens during whiplash?

A

Head recoils forward and stops. Occipital lobe strikes back of skull.

23
Q

what are contusions?

A

(bruising of brain on impact, damage to blood vessels)

24
Q

what damage occurs in the primary injury (at the time of impact)?

A
  • skull fracture
  • contusions
  • haemorrhage
  • haematoma
  • diffuse axonal injury (DAI)
  • concussion
25
Q

what is a haemorrhage?

A

bleeding from ruptured blood vessels

26
Q

what is a haematoma?

A

localised pooling of blood (from ruptured blood vessels)

27
Q

what damage occurs in the secondary injury?
in terms of intracranial events
6
| over hours days and weeks after impact

A
  • brain swelling, cerebral oedema, hydrocephalus
  • increased intracranial pressure
  • intracranial haemorrhages, traumatic haematomas, infections
  • blood flow changes and metabolic changes
  • epilepsy
  • hypoxia-ischaemia

all leading to atrophy of brain tissue and wide ranging symptoms

28
Q

what is hydrocephalus?

A

a build-up of fluid in the brain.

29
Q

what are the differences in the brain of someone with TBi vs a control brain of the same age?

A

Atrophy of the tissues - visibly gyri are more pronounced
Ventricles are vastly larger -

30
Q

what is the Monroe Kellie Doctrine?

A

The Monro-Kellie doctrine or hypothesis states that the sum of volumes of brain, cerebrospinal fluid (CSF) and intracerebral blood is constant. An increase in one should cause a reciprocal decrease in either one or both of the remaining two. (An increase in one component results in the compression of another)

31
Q

what percentage volumes do the 3 components in the Monroe Kellie doctrine make up?

A
  • Brain: 80% of total volume, tissues and interstitial fluid
  • Blood: 10% of total volume = venous and arterial
  • Cerebrospinal fluid: 10% of total volume
  • V intracranial = V brain + V blood + V CSF
32
Q

using the principle of the Monroe Kellie homeostasis what would happen if there was a growing mass in the brain

A

A mass (tumour) would cause a disruption to the system – there would be a release of more fluid to compensate for the additional mass. (compensated state in disease normal ICP)
If the mass increases past a point where the brain cant compensate you get an increase in ICP that can’t be rectified so surgical intervention is needed. (decompensated state in disease high ICP)

33
Q

what happens/how does the body compensate when there is some increase in ICP?
(specific vessels)

A

venous volume can decrease through increased release of venous blood into the jugular veins.
CSF volume can decrease through increased release of CSF through the foramen magnum into the spinal canal.

34
Q

what happens when there is a large intracranial mass in the brain increase?

ICP

A

The intracranial mass is much larger, beyond the pressure-buffering capacity of venous blood and CSF; there is a net rise in ICP.

venous volume can decrease through increased release of venous blood into the jugular veins. CSF volume can decrease through increased release of CSF through the foramen magnum into the spinal canal.

35
Q

what potential treatments are available for TBI?

A
  • Medically induced coma
  • Brain diuretic (reduce fluid/water)
  • Placement of shunt
  • Craniectomy (partial skull removal)
36
Q

what damage occurs in the secondary ijury after the primary TBI injury?
in terms of neurochemistry

A
  • Excessive production of free radicals
  • Excessive release of excitatory neurotransmitters
  • Alterations in glucose metabolism
  • Decreased cerebral blood flow
  • Neuroinflammation
37
Q

what damage occurs in the late/delayed injury months to years after TBI?

A
  • White matter degeneration and cerebral atrophy
  • Posttraumatic hydrocephalus
  • Posttraumatic seizures
38
Q

what damage occurs in the secondary injury of a TBI?
in terms of neuroinflammation

A
  • Activation of microglia, astrocytes, neurons
  • Activation and recruitment of macrophages
  • Microglia secrete pro-inflammatory modulators to degrade BBB, release cytokines (in response to DAMPs/damage-associated molecular patterns)
39
Q

whats the role of astrocytes in TBI?

A

Following CNS trauma, reactive astrocytes proliferate and dynamically intertwine to form a barrier that isolates inflammatory cells into numerous clusters, effectively containing an otherwise harmful inflammatory response to the site of injury

40
Q

whats the role of oligodendrocytes in TBI?

A
41
Q

whats the role of microglia in TBI?

A
42
Q

describe the immune reponse in the brain that occurs following TBI

A
43
Q

compare the neuropathology of the brain of a 14 year old with severe TBI and the brain of an 86 year old with probable alzheimers

A

both see atrophy shown by more pronounced gyri as well as larger ventricles

44
Q

what is Diffuse axonal injury (DAI)?

A

the shearing (tearing) of the brain’s long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull.

45
Q

whats the role of beta amyloid precursor protein in TBI?

A

BAPP is produced by neurons in response to injury (DAI)
it accumulates at points of axonal damge (constriction/transection)
some axons have multiple swellings (beaded appearance) which may persist for years resulting in a dysfunctional axon

46
Q

in what autoimmune disease do you see axonal injury similar to DAI?

A

Multiple sclerosis

47
Q

what is chronic traumatic encephalopathy (CTE)?

A

CTE is a progressive and degenerative brain condition that has been linked to repeated head injuries and repeated concussions.
Also known as ‘dementia puglistica’ or ‘punch-drunk syndrome’

48
Q

what are the symptoms of chromic traumatic encephalopathy?

A
  • Begins gradually, years after initial trauma(s)
  • Over time Memory loss, confusion, impaired judgment, impulsive control problems, aggression, depression, suicidality, parkinsonism, progressive dementia
    (can appear as personality changes)
49
Q

what condition has been linked to repeated hits in sports like american football or boxing?

A

Chronic traumatic encephalopathy CTE

50
Q

how is CTE different from TBI?

A

CTE has a much slower progression than TBI occuring after repeated hits

51
Q

what molecular and cellular changes found in CTE are similar to hallmarks of neurodegenerative diseases?

A
  • Abnormal Tau accumulation (and neurofibrillary tangles)
  • Microgliosis, astrogliosis
  • Brain atrophy (both gray and white matter) (stages 3-4)
  • Enlarged ventricles
  • Abnormalities in TDP-43 (phosphorylated 43kDa TAR binding protein; prominent in frontotemporal dementia and ALS)
52
Q

what is hypoperfusion?

A

(shock) is the inadequate delivery of vital oxygen and nutrients to body tissues, which left unchecked will result in organ system failure and death
Chronic brain hypoperfusion is not a disease but a sign that cerebral perfusion is functioning improperly

53
Q

what is hyperperfusion?

A

The prefix “hyper” means increased or excessive, and “perfusion” refers to the passage of blood through a blood vessel. Cerebral hyperperfusion is defined as a greater than 100 percent increase in blood flow through the carotid artery compared with baseline

Neurodegenerative diseases (9 decks)

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