exam 3 Flashcards

(36 cards)

1
Q

What is memory?

A

The ability to acquire, retain and recall information.
- a process, not a thing
- Inferred not observed
- different types of memory processes exist

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2
Q

short-term memory?

A

The amount of information that can be held in memory after a single exposure.
- insensitive to age
- digit span tests test this

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3
Q

long-term memory?

A

The ability to learn and retain information for longer periods after attention is lost.
- sensitive to age
- paragraphs, word lists, pictures, or drawings test this

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4
Q

Remote memory?

A

The ability to retain information from a long time ago.
- not sensitive to aging
- autobiographical, famous faces, public events test this

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5
Q

Learning vs. Retention?

A

Learning: the initial acquisition of material that is treated with immediate recall, also called encoding.

Retention: How much information is retained over time- requires delayed testing and is always relative to how much was learned.

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6
Q

Amount vs Rate?

A

Amount: how much a person has learned
Rate: how fast the person learned it

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7
Q

Retrieval vs Storage problem?

A

Retrieval Problem: information only appears to be forgotten, but it’s present it just needs help to access it.
- vascular dementia
- Parkinson’s
Storage problem: truly forgotten information
- Alzheimer’s
- korsakoffs

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8
Q

What is amnesic syndrome?

A

A permanent, stable, and global disorder of memory
- occurs in the absence of any other extensive perceptual or cognitive disturbance.
- never goes away, consistent, all stimuli effected(global)

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9
Q

What is a anterograde amnesia component?

A

A memory deficit that extends forward in time from the onset of amnesia and prevents the formation of new memories.
- Absolute ( episodic/sematic: our experience - medial temporal lobe and diencephalon)
- selective
- non-declarative memory not affected ( Procedural: skills - basal ganglia)

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10
Q

Memory types & the brain area?

A

Episodic/sematic: our experience - medial temporal lobe and diencephalon
Procedural: skills - basal ganglia
Priming- neocortex
Simple classical conditioning- the amygdala, cerebellum
habituation sensitization- reflex pathways

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11
Q

What is the retrograde amnesia component?

A

A memory deficit that extends backward in time from the onset of amnesia and prevents the recall of information acquired prior to the onset of amnesia.
- temporal gradient
- individual differences
- nondeclarative spared

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12
Q

Amnesia and anatomy: Medial temporal lobe amnesia?

A

Medial temporal lobes: hippocampus (H.M.)
- surgery for epilepsy, anoxic brain damage

Henry Molaison (H.M.):
- bilateral medial temporal lobectomy to treat epilepsy
- anterograde amnesia for decorative memories
- non-declarative memory relatively preserved

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13
Q

Amnesia and anatomy: Diencephalic amnesia?

A

Diencephalic: thalamus and mammillary bodies
- Wernicke Korsakoff syndrome, tumors of the 3rd ventricle, thalamic stroke, traumatic brain injury

Diencephalic Amnesia: (Wernickes)
- Damage to anterior and nuclei of the thalamus and mammillary bodies
- Thlakine deficiency (Vitamin B1)- alcoholism
- anterograde amnesia for declaritive
- retrograde amnesia to some degree

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14
Q

Normal aging: Neuroanatomical changes?

A
  • Brain mass/size decrease
  • ventricular dilation
  • cortical surface flattening
  • neuron loss
  • white matter thinning
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15
Q

Normal aging : cognitive changes?

A

Three domains
1) new learning
2) new problem solving
3) behavioral speed (walking, talking)

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16
Q

What is dementia?

A

An acquired, persistent impairment of intellectual function with compromise in multiple areas such as:
-memory
-language
-visuospatial
-emotion
-personality
-executive function
See in: AD, VD, FT, Picks, PPA, Parkinson’s, aids

17
Q

What is Alzheimers Disease (AD)?

A

Could be genetic or spontaneous. All three must be present:
1) clear evidence of declining memory and learning in other domains
2) progressive, gradual decline without extended plateaus
3) no mixed etiology (cognitive decline)
- most common dementia
-age increase
-diagnose definitive only postmortem
-terminal

18
Q

AD: Pathology

A
  • Amyloid plaques
  • Neurofibrillary tangles
  • Brain atrophy (nerve cell loss)
    winding of salci = more empty space = less volume in gyrui
    1ST Occur: anterior temporal lobe
    2ND: spread posterior and anterior
    3RD: majority of the brain
19
Q

AD: cognitive symptoms

A

-memory
-language
-visuospatial
- executive function
-personality/behavior

20
Q

AD CS: Memory

A

Slow progressive impairment of declarative memory, preclinical phase.
- mild cognitive impariment (MCI)
- subtle deficits of verbal and nonverbal anterograde memory
- deficits of retrograde memory with a temporal gradient
- implicit memory is partly preserved

21
Q

AD CS: language

A
  • starts with word finding and naming difficulties
  • continues to changes in speech and written language are noticeable
22
Q

AD CS: visuospatial

A

-orientation
-drawing
-construction

23
Q

AD CS: Executive functions

A

Impairments in:
-inhibition
-concept formation reasoning
-planning
-problem solving

24
Q

AD CS: behavioral/personality

A

-depression
-anxiety, irritability, apathy, agitation
-social isolation
-aggression
-delusions, hallucinations, dysphoria, euphoria
-sleep disturbances
-unawareness of deficits

25
Traumatic Brain Injury (TBI) Types?
1) Closed vs. penetrating - linear vs. nonlinear -coup vs. countercoup (blow- against the blow)
26
Primary effects of TBI
Skull fractures Focal damage - contusion -laceration -hemorrhage Diffuse damage
27
Secondary effects of TBI
-ischemia -hematoma -edema -intracranial pressure -herniation -infection -post-traumatic epilepsy
28
Severity of TBI
-mild -moderate -severe -Glasgow Coma Scale (GCS) -Post-traumatic amnesia (PTA)
29
Physical symptoms of TBI
-Headaches -Balance -Visual disturbances -sleep disturbances -fatigue
30
Cognitive symptoms of TBI
-attention -information processing speed -memory -executive functions
31
Behavioral symptoms of TBI
-aggression -irritability -impulse control -apathy depression anxiety, PTSD
32
Chronic Traumatic Encephalopathy (CTE)
A progressive neurodegenerative disease caused by repetitive head trauma (repetitive TBI).
33
CTE: Neuropathology
Grey matter atrophy: -frontal and temporal cortex -medial temporal lobe -thalamus, hypothalamus, and mammillary bodies White matter atrophy: -thinning of the corpus callosum -generalized atrophy of subcortical white matter Microscopic pathology: -neurofibrillary tangles -TDP-43 accumulations -Beta-amyloid plaques
34
CTE: Symptoms
Cognitive: -memory impairment -Executive dysfunction Mood: -depression -apathy -irritability -suicidality Behavior: -impulse control problems -disinhibition -substance abuse and addiction -aggression Motor: (like ALS) -parkinsonism -balance -gait -tremors -masked facies -dysarthric speech
35
CTE: Risk factors
-repetitive blows to the head -age -length of play -genetics
36
CTE: treatments
Prevention -protective equipment -limit contact during practice -remove injured players from the game -instruct safe tackling and hitting