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Neuropsychology > Test #3 > Flashcards

Test #3 Flashcards

1
Q

Malingering

A

intentional production of false or grossly exaggerated physical or psychological symptoms motivated by external incentives (work, criminal, money)

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2
Q

How is malingering distinct from somatoform disorder?

A

the physical symptoms are not intentionally feigned or produced and the incentive is not psychological

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3
Q

How is malingering distinct from factitious disorder?

A

the symptoms are not performed to assume the sick role, though behaviors are intentional

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4
Q

Definitional difficulties for malingering

A
  • Somatoform/Factitious definitions do not target cognitive symptoms
  • Definition requires judgment about internal states
  • Determining relative weight of external incentive and sick role (external incentives must be absent)
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5
Q

Criteria for definite malingering

A
  • presence of substantial external incentive
  • evidence of negative response bias
  • behaviors are not due to psychiatric, neurological, or developmental factors
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6
Q

Criteria for probable malingering

A
  • presence of substantial external incentive
  • two or more types of evidence from testing (excluding negative response bias)–or one from testing and one from self-report
  • behaviors are not due to psychiatric, neurological or developmental factors
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7
Q

Cogniform Disorder

A
  • cognitive complaints/ test performance is rare for the level of brain injury
  • delayed onset of excessive cognitive complaints
  • inconsistencies across scores/ repeated evaluations
  • evidence of suboptimal effort
  • condition: inconsistencies between performance in evaluation and other areas of life
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8
Q

Risk factors for extended recovery times following mild TBI

A
  • premorbid psychiatric history
  • severity of self-reported symptoms
  • involvement in compensation seeking
  • physical comorbidities
  • concurrent PTSD/pain
  • lower education
  • income/ level of employment
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9
Q

incidence estimates of cogniform disorder/ extended recovery times for mTBI

A

1-50%

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10
Q

Malingering Designs: Simulation

A
  • analogue design in which subjects are given instructions to feign, then are compared to normal and brain injured groups
  • generalizability concerns.
  • motivation/preparation of participants
  • simulation malingering paradox
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11
Q

Simulation malingering paradox

A

ask people to comply with instructions to study people who don’t comply with instructions

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12
Q

Malingering Designs: Differential prevalence designs

A
  • high & low base rate groups
  • allow determination of average responses
  • maybe good malingerers are still getting by
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13
Q

Malingering Designs: known group designs

A
  • used when you have an identified group of malingerers
  • how are they identified?
  • maybe good malingerers are still getting by
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14
Q

Malingering Detection Strategies

A

Symptom validity testing

  • Word Choice Effort Form (Wechsler)
  • forced choice paradigm (ex. left vs right hand)
  • TOMM
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15
Q

TOMM scores

A

45 questionable, 42-43 basically never seen, expect near 50

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16
Q

Gold standard for Malingering Detection Strategies

A

below chance

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17
Q

Rey 15-item test

A
  • used to detect malingering
  • is a poor measure
  • 1,2,3, I, II,III,A,B, C,a,b,c, triangle, circle, square
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18
Q

Problems with Malingering Detection Strategies

A
  • floor effect
  • poor sensitivity (not catching fakers)
  • poor specificity (identifying people who aren’t faking as fakers)
  • ethics
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19
Q

Floor effects & the Rey 15-item test

A
  • cut off is 7-9 items

- pattern of response failure

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20
Q

Floor effects and Malingering Detection Strategies

A

even people with known, moderate to severe injuries obtain correct scores

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21
Q

key component of a malingering measure

A

they should look more difficult than they are

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22
Q

Malingering: Embedded measures

A
  • WAIS-IV
  • CVLT-II
  • Rarely Missed Index
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23
Q

WAIS-IV & Malingering

A

-low digit span (age corrected score

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24
Q

CVLT-II and Malingering

A
  • low recognition
  • low delayed forced choice
  • sensitivity questionable for other CVLT scores
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25
Q

Rarely missed index & malingering

A

-WMS recognition items examined for frequency of misses

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26
Q

Performance curve

A

How does an individual’s pattern of responding change

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27
Q

what way to examine performance curve

A

response latencies

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28
Q

Response Latencies

A

examine the rate of change in response latencies in relation to task difficulty

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29
Q

Measure of response latency

A

dot counting task

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30
Q

dot counting task

A
  • 25 dots on a page randomly spaced around –> count dots as fast as you can!
  • does not work at all
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31
Q

Performance curve in malingerers

A
  • tend to have a flatter slope with increasing complexity

- tend to respond more slowly to easy items and more quickly to difficult items than controls

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32
Q

Selecting a cognitive malingering measure

A
  • Ease of use
  • length of administration
  • credibility of rationale
  • apparent difficulty of measure
  • coaching issues
  • how easy is it to “beat” the test
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33
Q

Sample Malingering Measure (Reid’s)

A

-7 categories for possible difference, which range from easy to hard

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34
Q

what did the Sample Malingering Measure (Reid’s) take into consideration?

A
  • floor effect
  • missing easy categories while getting hard categories correct
  • people should be faster on easy problems compared to hard problems adding total time spent on those problems
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35
Q

what principles did the Sample Malingering Measure (Reid’s) utilize?

A
  • inconsistency within category
  • symptom validity (e.g. total response time)
  • total response time slope
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36
Q

Test Development the Sample Malingering Measure (Reid’s)

A
  • developed cut scores to distinguish between malingerers and effortful test takers
  • cut scores were not different between TBI & Controls
  • made a decision tree
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37
Q

Malingering: Atypical Presentation

A
  • unusual presentation (e.g. choosing up/down when told to choose left/right)
  • not clinically validated (because they don’t occur frequently)
  • autobiographical memory (hard for people to forget this stuff)
  • primacy (recency) effect
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38
Q

Summary of malingering assessment

A
  1. use specific malingering measures
  2. evaluate patterns of performance on clinical measures
  3. look for unusual test patterns
  4. inconsistency of test scores within/across situations
  5. independent confirmation of abilities
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39
Q

cerebrovascular accident/ stroke basic info

A
  • third leading cause of death in US
  • incidence: 167,000 fatalities/ 700,000 cases
  • death rates of declined in recent years
  • more common in men
  • women account for more than 1/2 deaths
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40
Q

risk factors for CVA

A
  • hypertension
  • increasing age
  • tobacco use
  • diabetes
  • cholesterol
  • cerebrovascular disease
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41
Q

Stroke

A

-a sudden loss of brain function caused by a blockage or rupture of a blood vessel to the brain, characterized by loss of muscular control, diminution or loss of sensation or consciousness, dizziness, slurred speech, or other symptoms that vary with the extent and severity of the damage to the brain

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42
Q

Transient Ischemic Attacks

A
  • last less than 24 hours, often only minutes

- 50% resolve within 60 minutes

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43
Q

Two types of stroke

A
  • Ischemic

- Hemorrhagic

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44
Q

Ischemic Stroke

A
  • blockage of blood supply
  • most common (88%)
  • 4-5 minutes of blood stoppage is irreversible
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45
Q

Ischemic attack: causes

A
  • build up of fat deposits on artery walls with fibrous tissue
  • infarction occurs due to growth of blood particles and tissue overgrowth (embolism 20%)
  • sudden blocking of an artery by clot or foreign material
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46
Q

Can you die from an Ischemic Stroke?

A

Yes; 9% fatal within 30 days, Thrombus (60-70%)

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47
Q

Hemorrhagic Stroke

A

-blood leaks from artery directly into brain

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48
Q

can you die from a hemorrhagic stroke?

A

37% fatal in 30 days

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49
Q

how dies hemorrhagic differ from ischemic?

A
  • less lateralizing than ischemic

- more recovery than ischemic due to greater initial impairment

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50
Q

What happens to brain as a result of a hemorrhagic stroke?

A
  • results in mass effects (can fix by relieving pressure)

- blood toxicity (can damage neurons but they can possibly recover)

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51
Q

what is the most common cause of a hemorrhagic stroke?

A

aneurysm

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52
Q

which is worse: hemorrhagic or ischemic stroke?

A

hemorrhagic stroke has a larger chance of fatality but you’re more likely to recover

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53
Q

aneurysm

A

a protrusion in a blood vessel that causes a weakness

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54
Q

what dictates the damage from a stroke?

A
  • location in the brain

- severity depends on the size of the vessel blocked/ruptured

55
Q

where is stroke most likely to happen?

A

middle cerebral artery

56
Q

occlusion

A

block

57
Q

impact of block in middle cerebral artery

A
  • most common
  • motor function (contralateral side)
  • sensory functioning (somatosensory cortex)
  • language (left side)
  • upper limb difficulties
58
Q

what are left sided strokes associated with?

A
  • greater deficits
  • verbal (VIQ) deficits
  • some PIQ deficits
59
Q

what are right sided strokes associated with?

A
  • decreased pragmatics
  • more anosagnosia (lack of insight of impairment)
  • disinhibition/ confabulation
  • PIQ deficits
60
Q

impact of block in Anterior cerebral artery

A
  • lower limb difficulties
  • similar to middle cerebral artery
  • only 2% are solely ACA
61
Q

what side is most associated with memory deficits after a stroke?

A

bilateral

62
Q

infarcts

A

a small localized area of dead tissue resulting from failure of blood supply.

63
Q

impact of block in posterior cerebral artery

A
  • visual involvement
  • blindness
  • facial recognition problems
  • reading problems
  • more pure sensory symptoms possible
  • memory
64
Q

Vascular Dementia

A
  • second leading cause of dementia (12-20% of dementia cases)
  • must have evidence of being due to a stroke
65
Q

risk factors for vascular dementia

A
  • older age
  • hypertension
  • cardiac disease
  • previous transient ischemic attack/stroke
66
Q

Vascular disease & AD

A
  • significant vascular disease is present in 15-20% of patients with AD
  • criteria overlap in diagnosis
67
Q

How can you determine if dementia is likely due to vascular causes or not?

A

use the Hachinski Ischemic Score scale

68
Q

Hachinski Ischemic Score

A
  • more useful than differentiating between VaD and AD than combined disorders
  • immediate & delayed often less impaired in VaD than AD
  • structure & cuing can facilitate recall
  • emotional lability and affective disorder can be greater in VaD
69
Q

CVA and depression

A
  • adjustment vs neurochemistry
  • both? structural changes initially followed by frustration
  • difficult to diagnose
70
Q

prevalence of CVA and depression

A

25-80%

71
Q

Depression assessment in CVA

A
  • need background
  • multimodal (family, staff, patient)
  • left vs right lore
72
Q

left vs right lore in depression in CVA

A
  • language confounds this–> may be more frustrating with left sided stroke bc of language impairment
  • emotional processes between the two
73
Q

white matter hyperintensities

A
  • lesions are located in the deep white matter

- often seen together with vessels affected by small vessel disease

74
Q

what causes white matter hyperintensities?

A

-affected vessels (small vessel disease) are presumed to induce the lesions in deep white matter through chronic hypoperfusion of the white matter and disruption of the blood-brain barrier, leading to chronic leakage of plasma into the white matter

75
Q

hypoperfusion

A

inadequate supply of blood to an organ or extremity

76
Q

Prevalence of White matter hyperintensities

A
  • increased rate of recognition with increased technology
  • prevalence: 11-21% (64 y.o.); 94% (82 y.o.)
  • initially difficult to identify clinical corelates
  • subsequent research has found increased risk of stroke (3.1) and dementia (1.9)
  • associations between cognitive dysfunction, especially processing speed and executive functioning
77
Q

Differential diagnosis of dementia

A 
D ementia
A lzheimers
M etabolic abnormalities
N eurologic (e.g. stroke)
I nfection
T rauma
78
Q

Dementia: mild cognitive impairment

A
  • an individual’s report of his or her own memory problems, preferably confirmed by another person
  • measurable, greater-than-normal memory impairment detected with standard memory assessment tests
  • normal general thinking and reasoning skills
  • Normal ability to perform daily activities
  • Transitional phase b/w normal aging & AD?
79
Q

why is mild cognitive impairment important?

A

About 39% of people diagnosed with MCI progress to dementia

80
Q

Major neurocognitive disorder: Domains

A
  • complex attention
  • executive function
  • learning and memory
  • language
  • perceptual
  • social cognition
81
Q

complex attention

A

patient has increased difficulty in environments with multiple stimuli (TV, radio, conversation). Has difficulty holding new information in mind (recalling phone numbers, or addresses just given or reporting what was just said).

82
Q

executive function

A

: patient is not able to perform complex projects. Needs to rely on others to plan instrumental activities of daily living or make decisions.

83
Q

learning and memory

A

patient repeats self in conversation, often within the same conversation. Cannot keep track of short list of items when shopping or of plans for the day. Requires frequent reminders to orient task in hand.

84
Q

language

A

patient has significant difficulties with expressive or receptive language. Often uses general terms such as “ that thing” and “you know what I mean”. With severe impairment may not even recall names of closer friends and family.

85
Q

social cognition

A

patient may change changes in behavior ( shows insensitivity to social standards). Makes decisions without regard to safety. Patient usually has little insight into these changes.

86
Q

perceptual

A

Has significant difficulties with previously familiar activities (using tools, driving motor vehicle) , navigating in familiar environments.

87
Q

AD

A

-Most common dementing illness (~60% of all dementia cases in western Europe and North America)
-Prevalence
– Age 60 to 64: 1%
– Age 65 to 84: 5% to 10%
– > Age 85: 35% to 50%

88
Q

AD Risk Factors

A

-Age
-Family History of AD increases risk
–(75% of cases occur in families w/out history of AD)
–Up to 50% of family members in genetic risk group may develop the disease (multiple genetic markers)
–Early onset increases genetic risk
-Females at higher risk
-Lower education at higher risk

89
Q

criteria for possible AD

A
  • dementia established by clinical examination and documented by the Mini-Mental Test; Blessed Dementia Scale, or some similar examination, and confirmed by neuropsychological tests;
  • deficits in two or more areas of cognition;
  • progressive worsening of memory and other cognitive functions;
  • no disturbance of consciousness;
  • onset between ages 40 and 90, most often after age 65; and
  • absence of systemic disorders or other brain diseases that in and of themselves could account for the progressive deficits in memory and cognition
90
Q

criteria for probable AD

A
  • progressive deterioration of specific cognitive functions such as language (aphasia), motor skills (apraxia), and perceptions (agnosia);
  • impaired activities of daily living and altered patterns of behavior;
  • family history of similar disorders, particularly if confirmed neuropathologically; and
  • laboratory results of:
  • normal lumbar puncture as evaluated by standard techniques,
  • normal pattern or non-specific changes in EEG, such as increased slow-wave activity, and
  • evidence of cerebral atrophy on CT with progression documented by serial observation
91
Q

Pathology of AD: Tangles

A
  • Definitive D(x) based on neuropathology
  • Neurofibrillary tangles
  • Tau proteins contribute to microtubule development
  • In AD, Tau proteins aggregate into filaments
  • Early in course pathology focused in medial temporal lobe structures
  • Parietal then frontal more involved as disease progresses
92
Q

Pathology of AD: Plaques

A
  • Amyloid plaques
  • Between nerve cells (neurons) in the brain
  • Amyloid is a general term for protein fragments that the body produces normally
  • In a healthy brain, these protein fragments are broken down and eliminated
  • In Alzheimer’s disease, the fragments accumulate to form hard, insoluble plaques
  • The small clumps may block cell-to-cell signaling at synapses
  • They may also activate immune system cells that trigger inflammation and devour disabled cells
93
Q

pathology of AD: loss of subcortical neurons in

A
  • Nucleus Basalis of Meynert (cholinergic system)
  • Raphe nucleus (serotonin)
  • Locus Coeruleus (noradrenergic system)
  • Pronounced Cortical Atrophy w/ enlarged ventricles and widened sulci
94
Q

Stage I/II (pre clinical AD)

A
  • Changes limited to entorhinal & transentorhinal regions
  • (can be seen in people as young as 30)
95
Q

stage III/IV (early AD)

A
  • Severe involvement of transentorhinal , moderate changes in hippocampus,
  • Mild changes in cortical association areas
96
Q

stage V/VI (clinical AD)

A
  • Cortical association areas severely involved;

- only primary sensory and motor areas spared

97
Q

impaired delayed memory: AD

A
  • Difficulty remembering recent history
  • Not facilitated by external structure
  • Deficits in consolidation/storage
  • Remote memory not as good as it appears
98
Q

impaired naming: AD

A
  • Struggle to find words
  • Formal testing may be necessary
  • Deficit in semantic memory primarily
99
Q

attention and executive functions: AD

A
  • Less pronounced/consistent than deficits in memory
  • More obvious on more demanding tasks (Trails A versus Trails B)
  • Unawareness of deficits
100
Q

verbal deficits: AD

A

Deficits more pronounced on naming, word fluency

101
Q

visuospatial deficits: AD

A

Deficits more pronounced in visuospatial skills

102
Q

global deficits: AD

A
  • Combined deficits

- (up to 60% of cases combined)

103
Q

early versus late onset (before 65)

A
  • Early 5-10% of cases
  • More likely genetic component
  • Tends to have more rapid progression
104
Q

Early in the course of AD

A
  • Loss of interest in activities
  • Increase in inactivity/watching TV
  • Increase in agitation
  • Nearly 90% of pt’s with AD engage in behaviors suggestive of psychopathology
  • Apathy/Agitation occur in nearly 50%
  • Irritability/Disinhibition in nearly 35%
  • Depression variable (0% to 80%)
  • Suspiciousness
105
Q

vascular dementia

A

-Second leading cause of dementia (12% to 20% of dementia cases)
-Criteria similar to AD, must be evidence of being due to stroke
-Risk factors
–Older age, HTN, Cardiac disease, previous TIA/stroke
-Sig. vascular disease present in 15% to 20% of pts w/ AD

106
Q

normal pressure hydrocephalus

A

Production of CSF in brain ventricles exceeds absorption
–Enlarged ventricles, reduced blood flow to periventricular white matter
-Can be secondary to Head trauma, hemorrhage, CNS infection
-Estimates of 2% to 12% of dementia cases involve NPH

107
Q

characteristics of normal pressure hydrocephalus

A
  • Abnormal, wide-based gait
  • Urinary Incontinence
  • Cognitive Changes
  • Apathy, lack of spontaneity, mental slowing, perseverative responding
108
Q

Lewy Body dementia

A
  • Lewy bodies aggregates of protein that develop inside nerve cells
  • Spherical mass displaces other cell components
  • Subcortical characteritic of Parkinson’s disease
  • Cortical characterized in dementia
  • Account for 10% to 30% of all dementias
109
Q

Lewy body dementia: Symptoms

A
  • Fluctuating cognition with great variations in attention and alertness from day to day and hour to hour
  • Recurrent visual hallucinations (seen in 25% to 75% of people with DLB)
  • Motor features of PD
110
Q

Frontotemporal dementia

A
  • Includes primary progressive aphasia, semantic dementia, frontal dementia, Pick’s disease
  • Degeneration of frontal lobes as well as temporal lobes
  • Neurofibrillary tangles underlie FTD
  • Onset between 40 and 65
  • 6.7 per 100,000
111
Q

frontotemporal dementia: Symptoms

A
  • Initial signs personality changes
  • behavioral lethargy or disinhibition, inappropriate jocularity
  • Executive function deficits
  • Compulsive behavior
  • Memory deficits less severe than in AD
  • Hallucinations rare
112
Q

pseudodementia

A
  • Synonyms: Dementia syndrome of depression, depression-related cognitive dysfunction
  • Depression vs. underlying cortical pathology
  • Clarfield (2003) Meta-analysis
  • potential reversible causes seen in 9% of cases
  • Actually reversed in 0.6% of cases
113
Q

features of delirium

A
  • Acute onset (hours/days) and a fluctuating course
  • Inattention or distraction
  • Disorganized thinking or a altered level of consciousness
  • Not better accounted for by dementia
  • Evidence
114
Q

factors to consider for delirium

A 
D   Dementia
   E   Electrolyte disorders
   L   Lung, liver, heart, kidney, brain
   I    Infection
   R   Rx Drugs
   I    Injury, Pain, Stress
   U   Unfamiliar enviroment
   M   Metobolic
115
Q

non-pharmacologic management of delirum

A
  • Optimize environment
  • Personal belonging – photographs
  • Quiet
  • Sitter/company
116
Q

pharmacologic management of delirium

A

Neuroleptics may be needed if the patient is having distressing hallucinations/delusions or
the patient is very agitated
-High potency with low anticholinergic activity
-Low dose
-Haloperidol or risperdone
-Benzodiazepine if delirium is secondary to benzo or alcohol withdrawal

117
Q

prevalence of TBI

A

-500,000 to 1.9 million per year
-Peak ages:
–14 to 24
–0 to 5
–Elderly
-Causes
–14 to 24 MVA
–Other age groups generally falls

118
Q

characteristics of concussion/TBI

A

-Reversible traumatic paralysis of function that is always immediate
-Effects of concussion last for seconds to prolonged coma
-Change in momentum provides optimal conditions
–Particularly rotational forces

119
Q

immediate impact of concussion

A
  • Loss of consciousness, suppression of reflexes, transient arrest of respiration, momentary drop in BP, followed by subsequent rise in BP
  • Typically periods of retrograde and anterograde amnesia
  • More severe correlated with worse outcome
120
Q

susceptible brain regions

A
  • Brain stem (upper reticular formation)
  • Frontal Pole (–tend to hit things head on)
  • Temporal Pole
  • Coup & contra coup (brain jiggles can send out waves that fuck up other parts of the brain)
  • Shearing forces (cell injury/deathà shaking neurons; damaging myelin)
121
Q

behavioral/cognitive alterations: TBI

A

-Mental speed reduced (shearing)
-Attention difficulty
–Switching, divided attention, selective attention
-Memory
–Consistent with FL injury
–Source memory
–Decreased attention
-Executive functions

122
Q

Course of recovery: TBI

A

-0 to 6 months “fastest” recovery (first “few” months)
-6 to 12 recovery slows
-12 mo. on – more behavioral compensation (skills, strategies, ways to approach tasks)
-Behavioral deficits central to long term deficits
–Initiation, planning, organizing thoughts, self-control

123
Q

Mild TBI (initial, uncomplicated) criteria

A

-Criteria

–LOC

124
Q

common symptoms of post concussion syndrome

A

– Fatigue, dizziness, poor concentration, memory problems, headache, irritability, malaise, mood swings, insomnia

125
Q

mTBI course

A 
-One Month
  –Measurable differences b/t TBI & Controls on speed of processing/demanding tasks
-Three Months
  –Differences equivocal
-6 to 12 months
  –Symptoms at base rates
126
Q

mTBI paradox

A
  • Ambiguous, uncertain nature of deficits increases attention to these deficits
  • This attention may unintentionally contribute to persistence
127
Q

TBI symptoms base rates

A
  • 90% of healthy sample report experiencing somatic symptom over previous week Kellner & Sheffield (1972)
  • Headaches (49%)
  • Tiredness (47%)
  • Muscle Pains & aches (42%)
  • Irritability (32%)
128
Q

MMPI-2 symptoms base rates TBI

A
  • 34% females, 25% males endorsed “I feel tired most of the time
  • 20% endorse “I have few or no pains” in negative direction
  • 37% endorse “I forget where I leave things”
129
Q

mTBI dx rates

A

-Meares et al (2008)
–mTBI group compared to control group of non-TBI trauma pts
–43.3% of mTBI met PCS criteria
–43.5% of control met PCS criteria
-Factors associated with PCS
-Female, higher IQ, oral SDMT (similar to coding to the WAIS), acute stress, pre-injury psychiatric history (best predictor)

130
Q

mTBI and the military

A

-2525 Soldiers surveyed 3 – 4 months after return from deployment
-4.9 % reported LOC, 10.3% reported injury w/ altered mental status (AMS), 17.2% other injuries.
-Proportion meeting PTSD Criteria:
–LOC group, 43.9%; AMS, 27.3%, other: 16.2%, no injury control, 9.1%
-Controlling for PTSD, removed all relationships b/t TBI and health symptoms (except headache)

131
Q

Ponsford TBI study

A
  • 123 mTBI, 100 trauma controls
  • Cognitive, Depression, Anxiety, PCS symptoms
  • 1 week, mTBI predicted PCS
  • 3 months, pre-injury physical & psychiatric but not mTBI predicted persistent symptoms
  • Cognitive predictors not significant (ImPACT) ever
  • See Military Guidelines on PCS
132
Q

Broglio multiple concussions

A
  • 19 HS students, 20 concussions
  • Measured hit intensity data (helmet data)
  • No relationships between symptoms or cognitive change scores and any of the impact measures
  • Individual differences in cell structure, function, cranial and vascular morphology may explain the lack of a relationship
  • What are we measuring with regard to biomechanics and cognitive/behavioral symptoms?
133
Q

Chronic Traumatic Encephalopathy

A
  • Neurodegenerative processes associated with CNS trauma
  • CTE is tau protein aggregation disorder characterized by neurofibrillary tangles throughout the brain in the absence of ß-amyloid deposits (as would be seen in AD)
  • CTE associated with history of concussion, but causal link not confirmed
134
Q

Evidence of deficits in absence of evidence of deficits: TBI

A

–Measures
–Head Impact Telemetry (HIT)
–Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT)
–fMRI
–Participants
–11 jv/varsity HS football players (screened from 24)
–Two apriori categories
–No dx concussion/no neurological changes
–Dx’s concussion/associated neurological changes
–Found a third category after matching for collision characteristics
–No dx of concussion/neurological changes equivalent to concussion group
–Results
–4/8 control participants showed deficits in visual working memory similar to concussed group
–Significant decrease in fMRI activation in DLPFC during visual working memory task
–Non-concussed group showed significantly more collision events.
–For combined groups, number of collision events correlated with fMRI task

Neuropsychology (7 decks)

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