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Neuropsychology > Disorders > Flashcards

Disorders Flashcards

1
Q

What does damage to the Cortico-Spinal Tract produce?

A

-HEMIPLEGIA aka limb paralysis on contralateral side of body.

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2
Q

What is Hemiplegia?

A
  • limb paralysis on contralateral side of body.
  • Increased muscle tone.
  • hyperreflexia (babinski reflex)
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3
Q

What is the Babiniski Reflex?

If seen in adults what can it implicate?

A
  • Fanning of toes
  • Usually seen in babies

Seen in adults when there is damage to the cortico-spinal tract

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4
Q

What are the functions of Cortico-Spinal Tract?

A

Precise movements of fingers, toes, arms, and legs

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5
Q

What are the functions of the Cortico-Bulbar Tract?

A

Precise movement of face, eyes, and mouth

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6
Q

What does damage to Cortico-Bulbar Tract produce?

How does damage affect smiling?

A

-Loss of voluntary facial movements

Person can’t smile on command (volitional) but can smile spontaneously.

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7
Q

What is the General Function of the the Basal Ganglia Motor System?

A

Functions in very early initiation of movement

“Turning thought into action”

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8
Q

What are disorders are associated with the Basal Ganglia?

A
  • Huntington’s Disorder
  • Parkinson’s Disorder
  • Tourette’s Syndrome
  • Tardive Dyskinesia
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9
Q

What are Huntington’s Disorder Causes?

A

EXCESS Dopamine due to defective receptors

  • Genetic (chromosome #4) , rare, and progressive disorder
  • Atrophy of Caudate & Putamen (seen in CAT Scan)

Fatal, No cure. Treatment: Tranquilizer (reduce concentration of dopamine).

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10
Q

What are Motor, Cognitive, and Emotional Symptoms of Huntington’s Disease?

A

MOTOR:

  • Motor slowing
  • CHOREIFORM movements (uncontrolled aimless jerky limb movements)
  • Normal voluntary movements become impossible

COGNITIVE:

  • Subcortical Dementia
  • Apathy

EMOTIONAL:

  • Depression
  • Mania or Paranoid Psychosis
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11
Q

Parkinson’s Disorder Cause

A

Too Little Dopamine due to degeneration of substantia nigra
-Loss of dopamine producing neurons.

Caused by exposure to CO2, toxins, metal, drugs, head traumas, viruses, “idiopathic”, genetic

No cure and can be treated with L-DOPA (dosage dependent)

PET Scan: Decrease of dopamine activation in caudate and putamen.
-If ask the person to smile they can (volitional) but they can’t spontaneously smile.

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12
Q

Parkinson’s Motor Symptoms

A
  • Resting Tremor
  • COGWHEEL RIGIDITY
  • Impaired posture and gait
  • Shuffle walk
  • Akinesia (diminished movement)
  • Bradykinesia (slowed movement)
  • MASKLIKE FACE
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13
Q

Parkinson’s Cognitive and Emotional Symptoms

A
  • Subcortical Dementia
  • Impoverished feelings and emotions (flat voice tone)

-Depression

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14
Q

Tourette’s Syndrome

A
  • Hypersensitivity to dopamine receptors in caudate
  • spectrum disorder
  • Uncontrollable Tics and vocalizations
  • Echolalia
  • Involuntary Swearing
  • OCD and ADHD symptoms

Childhood onset, peaks at age of 10 and diminishes towards adulthood

Treated with TMS

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15
Q

Tardive Dyskinesia

A

Side effect of antipsychotic drugs
Symptoms: Involuntary movement of face, mouth, head, and tongue. Dystonia

Incurable symptoms, can lead to permanent damage

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16
Q

General Cerebellar Damage Symptoms

A
  • Intention tremor
  • Decomposition of movement (Mr.Roboto)
  • Ballistic movements miss target
  • Impaired new motor learning
  • Cognitive Impairments in procedural learning, coordination of attention and arousal, cognitive “timing”
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17
Q

Vestibulo-cerebellum

A

Input: Vestibular Nuclei

Damage: Impairment of balance and posture

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18
Q

Spino-cerebellum

A

Input: Spinal Cord
Damage: Uncoordination of skilled movements

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19
Q

Cerebro-cerebellum

A

Input: Motor and Association Cortex
Damage: Impaired Motor Learning and Procedural Learning.

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20
Q

Association Cortex

A

Damages lead to “motor plan” impairments.

Apraxia

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21
Q

Apraxia (in general)

A

UNILATERAL LESION usually but BILATERAL IMPAIRMENT
-Impairment carrying out voluntary skilled movements.

  • Motor strength and coordination intact
  • cannot link gestures to coherent act.
  • performing whole body movements to command intact.
  • Imitation of movements impaired, but better than to verbal command.
  • Manipulates actual objects appropriately
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22
Q

Oral Apraxia

A

INFERIOR FRONTAL LESION

-causes difficulty manipulating objects using facial muscles.

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23
Q

Limb Apraxia

A

LEFT PARIETAL TEMPORAL LESION

- apraxia manifests in limb movements on both the right and left even if lesion is only on the right.

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24
Q

Blind Sight

A

These people deny sight but in “blind” field they can:

  • Localize position of stimulus
  • Judge if stimulus is moving
  • Make appropriate hand gestures when reaching for object.

This may be due to connections from the superior colliculus (SC).

-DTI shows that the pathway from the SC to the visual cortex (association areas) is still intact.

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25
Q

Agnosia

A

This is a modality-specific recognition disorder.

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26
Q

Apperceptive Agnosia

Perceptual Dysfunction

A

Normal Acuity but appear functionally blind
They can’t:
- match, recognize, copy, or discriminate simple visual stimuli.
-Impaired object recognition.
-difficulty perceiving overall form
-may try to recognize objects by individual features but are thrown off by stray marks. (A heart and a slash through it.)

Motion or manual tracing can aid recognition.

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27
Q

Apperceptive Agnosia Lesion

Perceptual Dysfunction

A
  • Diffuse BILATERAL OCCIPITAL

- RIGHT hemisphere LATERAL OCCIPITAL TEMPORAL

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28
Q

Smiultagnosia

Perceptual Dysfunction

A

Normal visual fields but act blind

  • Can only perceive one object at a time.
  • Counting objects is difficult.
  • Can’t read text (only see one word at a time).
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29
Q

Dorsal Simultagnosia Lesion

Perceptual Dysfunction

A

ACT BLIND ALL THE TIME

  • can’t see more than 1 object (abnormal limit on visual attention).
  • BILATERAL PARIETAL-OCCIPITAL DAMAGE
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30
Q

Visual Object Agnosia

Memory Access Dysfunction

A

Vision is intact but…

  • impaired at naming objects, pictures, and demonstrating their use.
  • can’t sort objects by category
  • They can recognize faces, and describe shapes/parts of objects. They can also recognize objects via smell, touch or sound and they can correctly copy objects.

They can perceive the objects but can’t access memory of what they do.

-Characteristic motions of objects, seeing object in a familiar context can help them recognize the objects.

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31
Q

Visual Object Agnosia Lesion

Memory Access Dysfunction

A

BILATERAL injury in LATERAL OCCIPETAL-TEMPORAL AREAS

fMRI data showed that Visual Object Agnosia patient had no activity that could be observed for the real objects over and above what was seen for the scrambled objects.

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32
Q

Prosopagnosia

Memory Access Dysfunction

A

They are unable to:
-recognize a person by looking at their face (but know that a face is a face).

They can:

  • discriminate whether 2 faces are the same or different
  • recognize individual based on their voice
  • recognize objects
  • describe features of a face
  • can interpret facial expressions
  • “implicit face recognition may be spared (“guilty knowledge test” uses electro-dermal electrodes to measure responses to faces. Get increase response to faces they know.)
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33
Q

Prosopagnosia Lesion

Memory Access Dysfunction

A

BILATERAL but can be UNILATERAL RIGHT hemisphere lesion

  • Ventral & medial temporal-occipetal
  • R hemisphere FUSIFORM & PARAHIPPOCAMPAL GYRI

will also have difficulty recognizing their car from another car of the same model.

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34
Q

Auditory Agnosias

A

Affecting the recognition of sounds…

Lesions in LEFT & RIGHT auditory cortex.

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35
Q

Word Deafness

A
  • Normal pure tone hearing
  • Normal recognition of nonverbal sounds
  • Can’t recognize or discriminate speech
  • Speaking, reading, writing intact
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36
Q

Word Deafness Lesion

A
  • BILATERAL ANTERIOR PART OF SUPERIOR TEMPORAL GYRUS

- UNILATERAL L SUBCORTICAL TEMPORAL (destroying axonsentering Wernicke’s Area

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37
Q

Ventral Simultagnosia Lesion

Perceptual Dysfunction

A

DON’T ACT BLIND ALL THE TIME

  • can’t recognize more than 1 object but can see other objects. (Abnormal limits on object recognition).
  • lEFT VENTRAL TEMPORAL- OCCIPETAL DAMAGE
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38
Q

Auditory Agnosias- Specific:

A
  • Agnosia for nonverbal (environmental) sounds

- Amusia (agnosia fro musical sounds only)

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39
Q

Amusia

A

Lesion in INSULA, inferior frontal gyrus, temporal lobe

  • can be congenital
  • specific aspects of music impaired after different injuries.
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40
Q

Amusia Case Studies

-Classical composer

A

LEFT hemisphere injury

  • Wernicke’s Aphasia
  • could recognize melodies
  • good pitch and musical judgement
  • COULD NO LONGER COMPOSE OR READ MUSIC.
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41
Q

Amusia Case Studies

-Music Professor

A

RIGHT hemisphere injury

  • retained musical knowledge
  • “lost interest” in composing
  • did not enjoy listening to music
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42
Q

Topographic Disorders

Spatial Disorders and Attention

A
  • route-finding problems
  • loss of familiarity for typical routes and places
  • map reading problems
  • problems learning new environments/ routes
  • can describe some familiar routes from memory
  • can recognize building types but can’t be used as spatial cues.

-Often associated with prosopagnosia

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43
Q

Topographic Disorders Lesions

Spatial Disorders and Attention

A
  • Right paraphippocampal gyrus, hippocampus

- LEFT OR RIGHT LINGUAL GYRUS

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44
Q

Constructional Disorders

Saptial Processing and Attention

A
  • Deficits reproducing detailed spatial figures, relations among component parts.
  • Deficits in drawing. assembling, building
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45
Q

Constructional Disorders Lesions

Spatial Processing and Attention

A 
Left Hemisphere (Parietal) 
-poor performance at LOCAL LEVEL
Right Hemisphere (Posterior)
-poor performance at GLOBAL LEVEL, greater deficit overall.
46
Q

Hemi-Neglect

A
  • appears to ignore stimuli/events on side of space CONTRALATERAL to lesion. If severe fail to acknowledge own contralateral limbs.
  • impaired at line bisection, drawing, copying, reading/writing (on neglected side).
47
Q

Hemi-Neglect Lesions

A

Left Hemi-Neglect
-RIGHT posterior PARIETAL cortex (ESP. SUPRAMARGINAL GYRUS)

-Right dorsofrontal cortex, and right cingulate gyrus

48
Q

Hemi-Neglect Treatments

A
  • Stimulate Left side of vistibular system by putting cold H20 into Left ear.
  • Stimulate Left side of neck muscles
  • TMS on Left side to shift locus of attention.
  • Reward patients for seeing things on their left.
49
Q

Hemi-Neglect

Posner Components of Spatial Attention

A

-DISENGAGE attention from current locus
(posterior parietal cortex)

-MOVE attention to new location
(Superior Colliculus)
-ENGAGE attention at new location
(Thalamus)

50
Q

Default Network

A
  • MEDIAL PREFONTAL CORTEX
  • POSTERIOR CINGULATE/ RETROSPINAL CORTEX
  • INFERIOR PARTETAL CORTEX

abnormal Default network activity reported for Autism, Schizophrenia, and Alzheimer’s disease.

51
Q

Aphasia

A

Any language disorder due to brain injury which is not attributable to motor or sensory loss or diminished intelligence.

52
Q

Aphasia

in general

A
  • Some disturbance of speech ANOMIA
  • Comprehension impairment varies from minor to profound
  • Usually both auditory & visual language impaired
  • Speech ‘formulas’ preserved (Swearing, ouch etc.)
  • Gestures impaired to similar extent as speech
  • Social interaction skills intact (will make eye contact, will know when it’s their turn to talk)
53
Q

Broca’s Aphasia

A
  • Dysfluent, hesitant speech
  • Speech and writing are agrammatic (inability to use/comprehend grammatical forms)
  • Repetition mildly impaired
  • Comprehension spared
  • Will try to self correct
54
Q

Broca’s Aphasia Lesions

A

-Broca’s area (45,44)

55
Q

Wernicke’s Aphasia

A
  • Comprehension very impaired
  • Speech is fluent, well-articulated
  • Speech is empty of meaning
  • Semantic (word that is produced is related in meaning to what they want to say) and Phonemic (word they produce is related to word they want to make in that it sounds similar) paraphasias
  • Syntax and grammar are intact
  • Repetition impaired similar to speech
  • Speech/ writting can be meaningless sequence of actual words or neologistic jargon (Things that look and sound like words but really aren’t words).
  • Does not try to self correct
56
Q

Conduction Aphasia

A
  • Very good comprehension (better than Broca’s or Wernicke’s)
  • Speech is normal, except for phonemic paraphsias (word they make sounds similar to word they intended to say)
  • VERY IMPAIRED REPETITION
  • Writing usually impaired
57
Q

Conduction Aphasia Lesion

A

Usually in LEFT PARIETAL CORTEX and subcortical may include supramarginal gyrus

58
Q

Hypothesized “circuit” for repeating a spoken word

A

Auditory cortex&raquo_space;>Wernicke’s area»> via Arcuate Fasciculus&raquo_space;> Broca’s area & Motor Cortex

59
Q

Anomic Aphasia

A

Word finding problems (content words)

  • complete block
  • circumlocution
  • semantic paraphasia (say a related word)
  • indefinite forms

Good comprehension and repetition
Speech is empty, but well articulated and grammatical
Often seen in recovery of other Aphasias (patients with other aphasias are often left with Anomia)

60
Q

Anomic Aphasia Lesion

A

Could be a result to lesions almost anywhere in the Left Hemisphere.

61
Q

Global Aphasia

A

Large LEFT HEMISPHERE lesions usually involving the PERISYLVIAN AREA.

  • dysfluent speech
  • very poor comprehension, naming, repetition, writing
62
Q

Transcortical Motor Aphasia

A

Lesion in LEFT FRONTAL LOBE just above (but not including) Broca’s area

  • diminished spontaneous speech and writing
  • auditory and reading comprehension intact
  • reading aloud and repetition spared

INABILITY TO TURN THOUGHTS INTO LANGUAGE

63
Q

Transcortical Sensory Aphasia

A

Lesion in LEFT TEMPORAL OCCIPETAL LESIONS (sparing V1 and Wernicke’s area)

  • fluent, irrelevant speech
  • preserved repetition
  • comprehension impaired
  • little or no ability to read and write
  • often shows good recovery
64
Q

Pure Alexia

A

Different from dyslexia in that reading and writing were normal until injury to brain.

  • usually have right visual field hemianopsia (Lesion at V1 in LH).
  • all language functions intact, expect reading
  • can’t read what they have just written
  • some have LETTER-BY-LETTER reading
65
Q

Left Middle Temporal Cortex

A

activated in word COMPREHENSION tasks

66
Q

Left Inferior Temporal-Occipital Cortex

A

activated by VISUAL word forms

“VISUAL WORD FORM AREA”

67
Q

Alexia Lesions

A

Left VENTRAL OCCIPITAL TEMPORAL REGION (visual word form area)

Lesion involves left primary visual cortex and splenium of corpus callosum ( cutting off input to visual word form area)

68
Q

Language Deficits in RH-injured patients

A
  • Prosody (can’t process the tone of speech)
  • Inferencing and Discourse Comprehension (fail to get the main point)
  • Impaired ability to apperciate nonliteral language (metaphors, idioms, sarcasm, verbal humor)
69
Q

Hickok Poeppel Speech Processing Model

A

2 Parallel processing pathwways
-Dorsal (LH only): Acoustic»> Phonological Interface»> Articulatory system

Language Learning, Verbal Working Memory

-Ventral (LH & RH): Acoustic»> Phonological»> Word LevelSemantics»> Sentence Meaning

Comprehension of Speech

70
Q

Amnesia Symptoms

A
  • Anterograde Amnesia (AA): difficulty learning new information
  • Retrograde Amnesia (RA): difficulty remebering information learned before onset of amnesia (can be graded… remote memories easier to remember, and more recent memories more difficult to remember.)
71
Q

Amnesia Lesions

A
  • Mammilary Bodies
  • Dorsal Medial Nucleus of the Thalamus
  • Medial Temporal Lobe (HIPPOCAMPUS,AMYGDALA)
72
Q

Causes of Amnesia (7)

A
  • Korsakoff’s Syndrome
  • Alcoholic Blackout
  • Closed Head Injury
  • Transient Global Amneisa
  • Encephalitis
  • Dementia
  • Temporal Lobe Removals
73
Q

Korsakoff’s Syndrome

Causes and Lesions

A
  • Chronic alcoholism
  • THIAMINE DEFICIENCY

Lesion
-Bilateral degeneration of MAMMILARY BODIES, DM NUCLEUS OF THALAMUS

74
Q

Korsakoff’s Syndrome

Symptoms

A
  • Anterograde Amnesia
  • Retrograde Amnesia (extending back to decades)
  • Confabulation, lack of insight, apathetic
75
Q

Alcoholic Blackout

Temporary Amnesia

A
  • During blackout: complete AA, no RA

- After blackout: no AA, but RA for blackout period

76
Q

Neumonic to learn brain development….

I.S.C.G.

A

I (Interhemispheric) (8 weeks)
S (Sylvian) (14 weeks)
C (Central Sulcus) (20 Week)
G (Gyrus) (24-28)

Late 20s Corpus Collosum

77
Q

Closed Head Injury

A
  • AA for some period
  • Shrinking RA

Damage in the Medial Temporal Lobe area

78
Q

Transient Global Amnesia

Temporary and usually seen in people 50 yrs+

A
  • sudden onset of AA and RA
  • can last for hours or several days
  • complete recovery

Reduction of POSTERIOR CEREBRAL CIRCULATION a possible cause… posterior cerebral artery supplies medial temporal lobe structures

79
Q

Encephalitis

A

Primarily attacks medial temporal lobe structures and some frontal lobe structures

-viral brain infection and produces the most dense and severe amnesia.

80
Q

Temporal Lobe Removals

A

Bilateral removal of Anterior temporal lobes
(Unilateral… no amnesia)

H.M. had anterior temporal lobes removed which included the amygdala, hippocampus…

  • short term memory intact
  • major difficulty forming new memories (AA)

can still learn skills, procedural learning

  • mirror drawing, reading, and writing
  • tower of hanoi (cognitive skill)
81
Q

Procedural Learning & Repetition Priming

A
  • DON’T REQUIRE INTENTIONAL RETRIEVAL
  • show influence of prior experience on later behavior, w.o memory for the experience itself

ANTEROGRADE AMNESIA IS THEN NOT THAT YOU CAN’T STORE NEW MEMORIES BUT INSTEAD THAT YOU CAN’T CONSCIOUSLY RETRIEVE MEMORIES. Hence why H.M. showed improvement in mirror tasks.

82
Q

Memory Network

A

-Medial Temporal-Diencephalic
-Cortical-subcortical Interactions
Prefrontal Cortex

83
Q

Frontal Cortex

A
  • Precentral gyrus (motor strip)
  • Premotor
  • Prefrontal (dorsolateral, medial, and orbitofrontal surfaces)
84
Q

Prefrontal Cortex Inputs

A
  • Inferior Parietal Cortex
  • Amygdala, Hypothalamus (emotions)
  • Olfactory Cortex (sensory)
  • Dorsal Medial Nucleus of Thalamus (executive control of memory process)
85
Q

Prefrontal Cortex Outputs

A
  • Cingulate gyrus (emotions)
  • Caudate & Putamen (motor output system)
  • Hippocampus (executive control of memory process)
86
Q

Frontal Lobe Deficits

A
  • Out-put type disorders
  • Disorders of planning, organization, goal-directed behavior
  • Judgement disorders
  • Personality disorders
  • Memory disorders (working memory)
87
Q

Frontal Lobe Deficits

output type disorders

A

Lesion to PREMOTOR CORTEX

Problems initiating, controlling, and stopping action.
-unable to inhibit motor responses
-impaired activity level
(Dorsolateral Injury get hypokinetic movement (slow non-spontaneous), Orbitofrontal Injury get hyperkinetic movement (restless, impulsive))
-Fluency disorder
-Disorders of gaze, visual search

88
Q

Frontal Lobe Deficits

Disorders of planning, organization, goal-directed behavior

A
  • Impulsivity
  • Failure to execute steps

(Wisconsin Card Sort Task, Stylus Maze)

89
Q

Frontal Lobe Deficits

Disorders of Judgement

A
  • Confabulation
  • Cognitive Estimation (make estimates that don’t really make sense).

(Rey-Os. Drawing… exhibit no planning)

90
Q

Frontal Lobe Deficits

Personality Disorders

A
  • Unconcerned, don’t complain of pain (don’t seem to process general feedback not even pain)
  • Tactless, Callous towards others
  • Loss of creativity
  • Decreased spontaneity
  • Inattentive and careless
  • Lack of insight and self-criticism
91
Q

Frontal Lobe Deficits

Personality Disorders

A

Dorsolateral

  • Pseudodepressed, apathy, inability to plan, unconcern for self
  • Movement disorder, cognitive deficits

Orbitofrontal

  • Pseudopsychopathic, euphoric, irritable, disinhibited, poor social judgment, unconcerned for others
  • Poor impulse control, judgment problems, inconsistent pattern of responses
92
Q

Prefrontal Injury

Memory Problems

A

-delayed comparisons
-memory of recency, temporal order
-self-ordered pointing
LACK OF ABILITY TO INHIBIT

93
Q

Traumatic Brain Injury (TBI)

A

Brain injury caused external force that may produce diminished/altered consciousness, resulting in impaired cognitive abilities.

94
Q

Concussion

A

Mild TBI

Rapid onset, usually resolving within weeks

95
Q

Subconcussion

A

Milder injury without neurological symptoms.

96
Q

Concussion rate in HS vs College Sports

A
  • Higher rate in College vs HS

- Higher rate of Female vs. Males usually.

97
Q

Causes of TBI

A
  • Falls
  • Automobile Accidents
  • Assaults
  • Sports Injuries
  • War Injuries
  • Blast Injuries
98
Q

What are some Immediate Symptoms of TBI?

A
  • Confusion
  • Drowsiness
  • Unsteady
  • Headache
  • Memory loss
  • Nausea
  • Sleep Disturbance (too much or too little)
  • “In a fog”
99
Q

Mechanical Forces Producing Head Injury

A
  • Linear Acceleration
  • Rotational Acceleration
  • Focal Injuries: Coup and Countercoup
  • Diffused Injuries: Axonal sheering

-Rapid acceleration/deceleration

100
Q

TBI Coup and Countercoup Injuries

A

Coup Injury: focal damage at the site of impact

Countercoup Injury: focal damage on the opposite side of impact

101
Q

Mechanism of Blast Injuries

A

Primary: Effects of blast wave itself aka pressure

Secondary: Effects of missiles being propelled by blast force

Tertiary: Effects of impacts with other objects (coup-countercoup)

102
Q

What are Diffuse Axonal Injuries of TBI?

A

Microscopic white matter injury due to axonal shearing (esp. coritcal sulci)

  • Axons can swell and degenerates causing impairment to pathway.
  • APP (Amyloid Precursor protein) accumulates in damaged axons
  • Not seen in CT, MRI scans
  • DTI can detect abnormality to pathway organization.
103
Q

Acute Effects of TBI

A
  • Possible loss of consciousness
  • “Shearing” of axons
  • Increased levels of activation on fMRI
  • Depolarization of neurons, glutamate release
  • Inflammation, disruption of blood brain barrie
  • Increased amyloid beta
  • If severe, intracranial bleeding.
104
Q

What happens if second injury while symptomatic?

A

Metabolic dysfunction (increased demand, but reduced energy)

Rare: diffuse cerebral swelling. (DCS)

105
Q

What are Chronic Effects of TBI?

A

1 .Post- Concussion Syndrome

2. Chronic Traumatic Enecephalopathy (CTE)

106
Q

What is Post-Concussion Syndrome?

A

A concussion that persists 3 most or more after single, mTBI
-Headaches, dizziness, poor memory and attention, executive dysfunction, mood and personality symptoms

-DTI Findings

107
Q

Chronic Traumatic Enecephalopathy (CTE)

A

DELAY ONSET neurodegeneration; latent period

Linked to repeated TBIs (There is no specific threshold)

First identified as “Punch drunk”

Memory loss, attention, new learning and executive deficits

Neuropsychiatric symptoms

Motor symptoms

108
Q

What is Dementia Pugilistica?

A

“Punch Drunk”

109
Q

What is the Gross Pathology for CTE?

A
  • Diffuse brain atrophy
  • Enlarged Ventricles, cavum septum pellucidum
  • White matter loss (especially in corpus callosum)
110
Q

What is CTE Histology?

A
  • Neurofibrillary tangles -tau Pathology
  • Amyloid beta plaques
  • Neuronal loss
  • Neuroinflammation
  • White and Grey Matter Pathology
111
Q

How is TBI considered a risk factor for Alzheimer’s Disease?

A

Increased risk, accelerated onset

  • Dose dependent relationship
  • Increased risk for APOE4?
  • CTE vs Alzheimer’s (similar pathological features)

No way to predict who will develop CTE

112
Q

What is the relationship between Aging and TBI

A

Increased severity of TBI will lead to earlier onset of Aging

Neuropsychology (4 decks)

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