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Neuropsychological Assessment > TBI > Flashcards

TBI Flashcards

1
Q

Traumatic Brain Injury

A

Any external mechanical force acting on the brain in which a temporary or permanent dysfunction is the result

Can be open/closed, focal/diffuse

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2
Q

3 initial phases of TBI

A

1) LOC/coma
2) Cognitive/bx abnormalities
3) Memory, sequencing time, inability to learn new info
4) Permanent cognitive sequelae

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3
Q

Timing of phases of TBI

A

LOC or cognitive/bx abnormalities can last a few days to one month post injury

6-12 month period following marked by rapid recovery of cognitive functions and subsequent plateau

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4
Q

Severe TBI

A

Altered/prolonged (>24 hours) loss of consciousness (coma), usually diffuse
Post-traumatic amnesia >7 days

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5
Q

Moderate TBI

A

Positive neuro imaging, skull fracture, intracerebral hemorrhage
Loss of consciousness: 30 min-24 hours
Altered consciousness: >24 hours
Post Traumatic Amnesia: >1 day, >7 days

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6
Q

Mild TBI

A

Negative neuro imaging, concussion, symptoms typically resolve
No loss of consciousness or LOC < 30 minutes
Altered consciousness for a few sec-24 hours
Post-traumatic amnesia 0-1 day
Common features: memory problems, photosensitivity, headache, irritability, cognitive inefficiency

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7
Q

Most common site of brain contusion in TBI

A

Due to bony prominences butting brain tissue in the cranial vaults are anterior temporal lobes and orbitofrontal regions

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8
Q

High rate of false negative errors in TBI may be caused by

A

Use of highly specific sign/symptom (contra lateral neglect)

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9
Q

How does Moderate-Severe TBI differ from anoxic brain injury?

A

Anoxic injury would be marked by slower recovery, poorer outcomes, and visual deficits complicating care/treatment

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10
Q

What might patients played on an SSRI or benzo post-TBI experience?

A
  • Worsened gait/balance
  • Cognitive sedating effects
  • Increased disinhibition
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11
Q

What can single photon emission computed tomography (SPECT) provide?

A

May be used in diagnosis of head injury with no LOC/GSC/other imaging studies are normal

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12
Q

Glascow Coma Scale

A

Used to objectively describe the extent of impaired consciousness in all types of acute medical and trauma patients

Score from 3-15 (3 is worst, 15 is highest)

Ages 5+ (pediatric scale for youngers)

Correlated with mortality

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13
Q

Severe GSC

A

3-8

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14
Q

Moderate GSC

A

9-12

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15
Q

Mild GSC

A

13-15

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16
Q

Barriers with the GSC

A
  • Langauge
  • Hearing/speech
  • intellectual/neurological deficits
  • intubation
  • pharmacological/paralysis
  • orbital/cranial fracture
  • spinal cord damage
  • hypoxia-ischemic encephalopathy after cold exposure
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17
Q

What is a potential problem of the GSC in diagnosis mTBI?

A

Ceiling effect (questions are not difficult enough)

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18
Q

Coma

A

Complete unconsciousness, unable to be awakened, may not respond to sound, touch, pain, unable to communicate/see, unable to follow commands, show emotion, engage in purposeful bx

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19
Q

Vegetative State

A

Still unconscious but may awaken at times
Unresponsive wakefulness syndrome
Brief reaction to sounds, sights, touch
Cry, smile, and facial expressions (reflexes)
Automatically fx still controlled by brain

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20
Q

Minimally conscious state (MCS)

A

Regaining consciousness, some self-awareness
Engage in purposeful bx (inconsistent)
Follow simple commands
Makes intelligible verbalizations
Visually follows people in the room
Functional object use inconsistent

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21
Q

Emerged from MCS

A

Communication consistent
Use of 2 objects in purposeful manner
Yes/no responses
Follow instructions
Perform simple tasks

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22
Q

TBI factors in recommending that a patient not return to work

A

Age (over 50)
Education (less than HS)
Prior work hx (unable pre-injury)
TBI severity (severe)

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23
Q

Severe TBI in pediatrics

A

Children have poorer prognosis (worse with younger ages)
Continued neurobehavioral issues in children depend on age, severity, family resources, and support system

24
Q

In the acute rehabilitation phase (discharge from inpatient to rehab unit), prognosis for functional outcome would depend on

A

the time to follow commands following the injury

25
Q

Important in differentiating moderate and mild TBI

A

PTA and neuro imaging findings to accurately determine the severity of the injury

26
Q

Annual TBI count in the U.S.
Number that result in hospitalization
Number that suffer chronic disability

A

2 million
500,000
80,000

27
Q

Men

A

2x as frequent
4x more likely that TBI will be fatal

28
Q

Bi-modal distribution of TBI

A

Increases from childhood and peaks at 15-25
Falls afterward
Rises again in later states of life

29
Q

Top 4 causes of TBI by percentage

A

50% MVA
21% falls
12% violence
10% sports

30
Q

TBI Risk factors

A

Increased age
Arteriosclerosis
Alcoholism
Premorbid personality
Marital discord
Poor interpersonal relationships
Problems at work/school
Financial instability

31
Q

Mechanism of TBI

A

Mechanical forces applied to the skull is then transmitted to the brain

Damage can be focal or diffuse

32
Q

Intracerebral hemorrhage

A

Bleeding into the brain tissue

33
Q

Ischemic infarct

A

blood supply to part of the brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients

34
Q

Motion from brain inside the skull may lead to

A

Diffuse injury
Stretch/shearing of the axons

35
Q

Secondary processing of TBI

A

Hypoxia (lack of oxygen)
Anemia (lack of blood)
Metabolic abnormalities
Hydrocephalus (build up of CSF in brain ventricles)
Intracranial hypertension
Fat embolism

36
Q

Free radicals

A

Result from the release of excitatory amino acids
Subsequent release of arachidonic acid metabolites
Leads to disruption of neurotransmitters in the synapse

37
Q

Subarachnoid Hemorrhage

A

Bleeding in the space surrounding the brain

Most often occurs when a weaker area in the blood vessel on the surface of the brain bursts and leaks

Blood builds up around the brain and inside the skull, increasing pressure on the brain

Nuchal rigidity

38
Q

Nuchal rigidity

A

Neck stiffness, common symptom of subarachnoid hemorrhage

39
Q

Subdural hematoma

A

Collection of blood forming on the surface of the brain
Blood presses against brain and damages tissue
Can be life-threatening
Can occur in older individuals after minor head injuries
Worsening headache pain within 72 hours, decreased GCS, vomiting, trouble following commands, midline shift, hyper dense crescent-shaped abnormalities on CT

40
Q

Diffuse Axonal Injury

A

Shearing/tearing of the axons
Occurs when brain is injured as it shifts/rotates inside the skull
May cause coma
Often diffuse
Commonly marked by decreased mental efficiency, complex reasoning ability, and ability to perform mental arithmetic

41
Q

Intracranial Pressure

A

Common signs/symptoms:
Heached
Altered mental status (irritability, depressed alertness/attention)
Nausea/vomiting

Likely the cause of decompensation of a patient following TBI within 72 hours of injury

42
Q

Hydrocephalus

A

Abnormal build up of CSF in the ventricles

Causes ventricles to widen and put pressure on brain tissue

Commonly affects the posterior region

Symptoms: headache, nausea, vomiting, cognitive impairment, papilledema (visual), decreased vision

43
Q

Children with early onset hydrocephalus typically perform better on ___ than ____.

A

VIQ (VCI + WMI)
PIQ (PSI + PRI)

44
Q

Normal Pressure Hydrocephalus

A

Abnormal buildup of CSF in ventricles, occurs if the normal flow of CSF in the brain or spinal cord is blocked

Similar to hydrocephalus causing enlargement of the ventricles which put pressure on the brain

Occurs slowly and worsens over time, pressure usually isn’t dangerously high

Classic indications: dementia, mental decline, gait difficulties, urinary incontienence

Primary treatment: shunting

45
Q

Way to distinguish NPH from subcortical dementia

A

Incontinence

46
Q

Congenital Hydrocephalus

A

Extensive accumulation of CSF within the ventricles due to an imbalance between synthesis and absorption of CSF

One of the most common abnormalities of CNS

Most common cause: Lennox-Gastaut Syndrome

47
Q

TBI impact on glutamate pathways

A

CSF increased glutamate

Glutamate antagonists may be beneficial

48
Q

TBI impact on cholinergic neuronal activity

A

Reduction in cholinergic neuronal activity within hippcampal and neocortical areas

Dysfunction of septohippocampal cholinergic pathways, resulting in post-traumatic cognitive and bx deficits

49
Q

TBI impact on ascending biogenic amine pathway

A

Circulating levels of catecholamine (directly correlates with TBI severity)

Increased serotonergic sodium metabolites in CSF

Dysregulation of mesolimbic/mesocortical dopaminergic pathways give rise to manic/hypo manic symptoms

50
Q

Related mood disorders

A

Anxiety, depression, psychoses, apathy

** functioning impairment is related to anxiety/depression, but less so if the imaging is positive

51
Q

Related cognitive problems

A

Delirium, dementia, amnestic disorder, intellectual impairment

Impairment of arousal, attention, concentration, memory, language, exec Fx, memory loss

52
Q

Related behavioral problems

A

Frontal/temporal lobe syndromes, aggressive disorders, personality change

53
Q

Physiological impacts

A

Sleep disturbance, headache, dizziness, fatigue

54
Q

General pharmacological TBI treatment

A

Antiepileptic medications used in inpatient units to manage bx post-severe TBI

Side effect: drowsiness/sedation

55
Q

Mood disorders secondary to TBI

A

Depression/mania most common
Persistent dysphoria (feelings of loss, demoralization, discouragement)
Fatigue, irritability, SI, anhedonia, disinterest, and insomnia (seen in the majority of pts 6-24 months or longer after TBI)
Psychological impairments correlated with severity

Risk factors: poor premorbid Fx, psychiatric hx

Mechanism: disruption of biogenic amine containing neurons as they pass through the basal ganglia or frontal-subcortical white matter

Left dorsolateral frontal and left basal ganglia associated with increased probability of MDD

56
Q

Mood Disorder Treatment Secondary to TBI

A

Antidepressants, psychostiumlants

SSRIs - typically safe, useful for comorbid MDD, mood lability, and impulsivity (no evidence that they treat TBI)

Sertraline and citalopram are preferred based on beneficial effects, limited side effects, and short half-life

Tricyclics and monoamine oxidase inhibitors are not preferred due to anticholinergic side effects and drug/food interactions

Psychostim/some domainergicss can be beneficial

Methylphenidate performs similar to sertraline (and improved neuropsychological performance)

57
Q

Mania/Hypomania

A

Neuropsychological Assessment (9 decks)

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