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Lecture 1 Flashcards

1
Q

The three main characteristics of ABI are:

A

Non-congenital, rapid onset, non-progressive

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2
Q

T/F

In a closed-head injury, the skull has been perforated.

A

False

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3
Q

Head injuries encompass damage to what?

A

Skull, muscles & nerves of the face, skin over the skull

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4
Q

Head injuries and traumatic brain injuries fall under the umbrella of __________.

A

Acquired brain injury

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5
Q

The opposite of a closed-head injury is _________

A

An open-head injury

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6
Q

The major cause of TBI from 0-1 years is ______.

A

Violence

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7
Q

The major cause of TBI from 1-5 years is _____.

A

Falls

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8
Q

The major cause of TBI from 5-15 years is:

A

Bicycles and sporting injuries

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9
Q

The major cause of TBI from 15-60 years is:

A

Motor vehicle accidents

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10
Q

The major cause of TBI from age 60+ is:

A

Falls

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11
Q

In general, what is the incidence of TBI?

A

100-200 per 100,000 people

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12
Q

T/F

Mild head injury is over-reported.

A

False – 80% of mild head injury cases are unreported in Ontario

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13
Q

For how long do most people experience a loss of consciousness in TBI cases?

A

< 1 hour

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14
Q

Describe the criteria for mild TBI.

A

< 24 hours post-traumatic amnesia, coma <30 minutes, Glasgow Coma Scale after coma 13-15

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15
Q

Describe the criteria for moderate TBI.

A

1-7 days post-traumatic amnesia, GCS 9-12

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16
Q

Describe the criteria for severe TBI.

A

> 7 days post-traumatic amnesia, GCS 3-8

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17
Q

T/F

The incidence of TBI is greater than that of multiple sclerosis, spinal cord injuries, HIV/AIDS and breast cancer.

A

True

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18
Q

List risk factors for TBI.

A
  • Age
  • sex
  • SES
  • substance abuse/criminal record/known to social services
  • pre-existing learning disorder
  • psychiatric illness
  • prior brain injury
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19
Q

2/3 of brain injuries occur during what age?

A

Less than 30 years old – peaks are 15-24 for males and 15-19 for females

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20
Q

T/F

Females are more likely to die from TBI than males.

A

False – males are more likely to die from TBI than females

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21
Q

T/F

A lower SES is a risk factor for ABI.

A

True

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22
Q

Injury variables that can affect TBI recovery are:

A

Diffuse vs focal, secondary injuries, severity

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23
Q

An individual’s pre-injury characteristics that can affect TBI recovery are:

A

Education/intelligence, personality/motivation, psychosocial functioning, occupational status

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24
Q

Environmental influences that can impact TBI recovery are:

A

Family, support structure, culture

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25
Besides injury variables, pre-injury characteristics and environmental influences, other variables that impact TBI recovery are:
Time, rehab resources
26
3 impairments that predict poor long-term outcomes are:
Ineffective personal skills, frontal lobe dysfunction, compromised learning skills
27
State the terms that can be used to describe how TBI occurs.
- penetrating (depressed, perforating, penetrating) - closed: focal and diffuse (contact, aka non-acceleration – hematomas; acceleration – coup, rotational) - metabolic cascade - gliosis
28
State the terms that describe when TBI can occur.
Primary | Secondary
29
State the terms that describe where TBI can occur.
Focal | Diffuse
30
T/F | The effects of penetrating TBI are largely focal.
True
31
What is the difference between penetrating and perforating?
Penetrating – object goes into the cranium and stays there | Perforating – object goes into the cranium and leaves
32
T/F | Closed-head injuries are much more common than open-head injuries.
True
33
In closed head injuries, the ___ is damaged while the _____ remains intact.
Brain | Skull
34
What occurs at the point of contact in non-accelerational closed-head TBI?
Contusions, which reflect localized bruising/lacerations and can lead to subdural hematomas
35
Describe subdural hematomas.
- Primary focal injury but often part of diffuse effect - can cause structural changes - slow bleeding between dura mater and brain that is venous in origin - brain is intact, but blood causes damage through increased intracranial pressure - can be resolved through shunt/drilling a hole
36
T/F Recovery in a subdural hematoma, which is venous in origin, is better than recovery in an extradural hematoma, which is arterial in origin.
False – the arterial bleeding in extradural hematomas increases morbidity, but it can be detected and treated more readily. Subdural hematomas can go undetected, leading to death.
37
What is the effect of an untreated extradural (epidural) hematoma?
Ventricles are pushes aside, leading to hypoxia and increased intracranial pressure
38
Acceleration-based closed-head injuries can be classified as ____ and _______.
Coup/contrecoup (linear velocity) and rotational (angular velocity)
39
Explain the mechanism for acceleration-based closed-head injuries occurring at linear velocity.
- head accelerates quickly while slower-moving brain hits skull back and forth until the brain reaches a standstill - leads to focal lesions at site of initial contact (coup) and at exact opposite side (contrecoup) - there is bleeding inside the brain
40
How are diffuse axonal injuries (DAI) caused?
White matter fibers are compressed, stretched and rotated by the force of the injury.
41
When can the effects of DAI develop?
- Within 1 hour of the injury; develop up to 72 hours | - secondary deterioration of axons can occur weeks and months following injury
42
What are the effects of DAI in the brain?
- transient disruption of action potentials - enlargement and swelling of axons - structural and irrevocable damage leading to micro-lesions of white matter tracts and shearing at white-grey matter junction
43
The ________ is consistently vulnerable to DAI.
Corpus callosum
44
_________ is an indicator of DAI, and _________ is an imaging tool that can be used to detect DAI.
Petechial hemorrhage | Diffusion tensor imaging
45
Rotational (angular velocity) closed-head injuries can lead to:
DAI, hemorrhage, cranial nerve trauma
46
The 5 steps of a metabolic cascade are:
Excitotoxicity, hypoperfusion, oxidation, hyperglycolysis, dysregulation and metabolic depression
47
Describe the excitotoxicity step of the metabolic cascade.
- massive increase in glutamate leads to excitotoxicity and hypergylcolysis - areas with NMDA receptors (e.g. medial temporal lobe, hippocampus) are especially susceptible to glutamate surges
48
Describe the hypoperfusion step of the metabolic cascade.
-increase in extracellular calcium can increase vasoconstriction, which accounts for the reduction in CBF and may activate destructive lipases and proteases
49
Describe the oxidation step of the metabolic cascade.
-production of reactive forms of oxygen species cause damage via the induction of lipid and oxygen oxidation
50
Describe the hyperglycolysis step of the metabolic cascade.
-increased levels of K+ results in metabolic stress and hyperglycolysis
51
Describe the dysregulation/metabolic depression step of the metabolic cascade.
- loss of autoregulation, as seen by hyperglycolysis lasting up to 1 week following injury - reduction of CBF - hyperglycolysis is followed by a period of metabolic depression and reduction in glucose use (hypoglycolysis) that lasts up to 10 days in experimental TBI - decrease in protein synthesis and oxidative metabolism
52
Describe gliosis.
Glial cells (e.g. phagocytes) migrate to the site of damage and eliminate non-functioning tissue.
53
Primary focal effects of TBI are:
Coup/contrecoup, hematoma, contusion
54
Primary diffuse effects of TBI are:
DAI
55
Secondary diffuse effects of TBI are:
Edema, anoxia/hypoxia, increased ICP, seizures
56
Secondary focal and diffuse effects of TBI are:
Ischemia, metabolic cascade, gliosis
57
How do coup/contrecoup injuries affect the frontal lobe?
There are bony protuberances on the fossa of the anterior inferior frontal lobes and temporal lobes, which make these regions become badly injured through the linear acceleration of the brain in the skull. The orbitoprefrontal cortex is especially susceptible because it sits on top of the prominences.
58
What are the roles of executive function?
- regulate/integrate cognitive and behavioural functioning - goal-setting (formulation) - goal-directed behaviour (initiation) - insight (monitoring, self-awareness, self-correction, metacognition) - problem-solving - abstract reasoning - planning, organization, sequencing - regulation of behaviour and emotion (inhibition/disinhibition)
59
Acquired psychiatric symptoms that can result from frontal lobe dysfunction include:
OCD, mania, paranoia, impatience, impulsivity, being argumentative, irritability, depression, anxiousness, immaturity
60
Changes associated with orbitofrontal damage include:
Poor social judgement, impulsivity, disinhibition, lack of concern for others, euphoria, sexual disinhibition, restlessness, lability, talkativeness, pseudopsychopathic personality, irritability, distractibility, loss of control of anger
61
Changes associated with dorsolateral prefrontal damage include:
Reduced initiation, apathy, lack of drive, lack of emotion, decreased anticipation, impoverished discourse, concrete thinking, perseveration, slowness, difficulty forming and shifting mental sets, decreased mental flexibility, motor sequencing difficulty
62
Deficits associated with left prefrontal damage include:
Increased personal concern, depression, decrease initiation, decreased verbal fluency, reduced language output
63
Deficits associated with right prefrontal damage include:
Unawareness, inability to read social cues, inability to produce appropriate nonverbal communication, decreased comprehension of prosody and indirect meanings, inattention to context, increased anxiety

Neuro (11 decks)

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