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PSY3301 > Final > Flashcards

Final Flashcards

Sleep, Neuropsychological Assessment, Dementia and Multiple Sclerosis

1
Q

What is chronobiology?

A

The study of biological rhythms

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2
Q

What are biological rhythms?

A

Inherent timing mechanisms that control various biological processes –> Circadian rhythm

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3
Q

What drives behaviour in biological rhythms?

A

External cues i.e. Sunlight, and internal cues i.e. melatonin

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4
Q

What are the 4 biological rhythms?

A

Circannual –> yearly, i.e., bird migration
Circadian –> daily, i.e., sleep-wake cycle
Ultradian –> less than a day, i.e., eating cycles
Infradian –> more than a day, i.e., menstrual cycle

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5
Q

What are free running rhythms?

A

Rhythm that the body devises in absence of all external cues, for example sleeping patterns when deprived of sunlight and darkness.

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6
Q

What are zietgerbers?

A

A cue from the environment that signals a “reset” in the biological rhythm, i.e., light and dark

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7
Q

What is suggested to be the neural basis of the biological clock?

A

The suprachiasmatic nucleus, located at the base of the hypothalamus.

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8
Q

What happens if the superchiasmatic nucleus is damaged or disrupted?

A

Damaged: Issues with timing of daily activities
Disrupted: Issues with length and timing of sleep

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9
Q

Where does the suprachiasmatic nucleus receive its information?

A

The retinohypothalamic tract –> light signals the release of excitatory neurotransmitters to entrain the rhythmic activity of the SCN

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10
Q

How does the Suprachiasmatic nucleus control our biological rhythms?

A

By giving input about the appropriate timing of behaviours through the circadian timing system

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11
Q

What is the circadian timing system?

A

The control of behaviours by slave oscillators that affect another behaviour.

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12
Q

How can we objectively measure sleep?

A

Recording equipments such as polysomnography through electroencephalogram, electromyogram and electrooculogram.

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13
Q

How do the three measures of polysomnography work?

A

Electronic equipment records readouts from electrodes attached to the sleeper. (A) EEG made from a point on the skull relative to a neutral point on the ear. (B) EMG made between two muscles, such as those on the chin and throat. (C) EOG made between the eye and a neutral point on the ear.

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14
Q

What are the 5 stages of sleep?

A

W – Waking
N1 - NREM stage 1
N2 - NREM stage 2
N3 - NREM stage 3
R-sleep – REM

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15
Q

What rhythm is active during the Waking state?

A

Beta rhythms, but may also produce alpha rhythms when relaxed

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16
Q

What occurs during non-rem sleep 1 (NREM1)?

A

Sleep onset–> Moves from beta activity to theta-wave activity

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17
Q

What occurs during non-rem sleep 2 (NREM2)?

A

Asleep –> Theta-waves, sleep spindles and k-complexes

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18
Q

What occurs during non-rem sleep 3 (NREM3)?

A

Deep sleep–> Difficult to arouse and groggy when woken up, delta rhythms

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19
Q

What occurs during r-sleep (REM sleep)?

A

Atonia, EEG pattersns are similar to the beta, alpha and theta-wave activity (possibly because they are dreaming)

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20
Q

What is characteristic of a typical night’s sleep?

A

Progressing through the sleeping stages in order, replacing the W-stage with REM as the cycle reverses.

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21
Q

What is a somnogram?

A

A sleep graph of an individual’s sleep cycling throuhgh their stages in the night.

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22
Q

What is true about sleep patterns as humans age?

A

Time asleep tends to decrease, REM sleep makes up less of that sleep too

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23
Q

What are some feats of NREM sleep (all stages)?

A

Maintain muscle tone – can sleep in various postures/positions
Body temperature and heart rate drop; growth hormone release increases
Can talk in our sleep, grind our teeth, flail our limbs – restless leg syndrome
Sleepwalking occurs
Dreaming can occur, though it is usually less vivid than during REM
Can have lucid dreaming during NREM, where we are aware of the dreams as we dream them.

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24
Q

What are some feats of REM sleep?

A

Our eyes move.
Our toes, fingers, and mouth will twitch.
Erections in males – regardless of whether accompanying dreams had sexual content in them or not
Mechanisms that regulate body temperature stop.
Body temperature moves toward whatever the room temperature is, so you might wake up extremely cold or extremely hot…
Experience paralysis and atonia.

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25
Q

What are two psychoanalytic theories of dreams?

A

Freud: Dreams are the symbolic fulfillment of unconscious desires and wishes; often emphasising sexual desires and wishes
Jung: Dreams allow us to relive the memories/history of the human race - our “collective unconscious”

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26
Q

What does recent research suggest about dreams?

A

Dreams are related to recent events and tend to concern ongoing problems in our lives

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27
Q

What is the activation-synthesis hypothesis of dreaming (as a means of meaningless brain activity)?

A

Cortex produces characteristic patterns of waking EEG during REM, which generates random meaningless dreams.

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28
Q

What does sleep accomplish?

A

Sleep serves as an energy-conserving strategy. The brain is a major user of the body’s energy supply, so decreasing brain activity by sleeping can help conserve this energy.

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29
Q

What is some evidence for the energy-conservation theory of sleep?

A

Animals sleep during non-optimal times

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30
Q

What is true about average sleep time in animals?

A

Total sleep times differ between species, and largely reflects the amount of time required to obtain food and by their risk of predation.

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31
Q

Why is sleep a restorative process?

A

Chemical processes in our bodies that provide energy to cells are depleted during waking periods and are replenished during sleep.

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32
Q

What is REM sleep deprivation and its effects?

A

Subjects take less time than usual to get back to REM sleep

The “need/pressure/desire” for the brain to enter REM sleep increases – “REM rebound”

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33
Q

What is REM rebound?

A

When finally given the chance to enter REM sleep subjects spend almost double the amount of time in REM than normal.

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34
Q

Why is sleep a factor in memory storage?

A

Sleep helps solidify and organize our memories and allows for better memory retention.

Place cells (hippocampal neurons for spatial memory) fire during sleep as a “remembering and replaying” event.

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35
Q

What is the role of melatonin on the neural basis of sleep?

A

Hormone secreted from the pineal gland of the brain in response to darkness that causes sleepiness

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36
Q

What is the role of the Reticular Activating System on the neural basis of sleep?

A

Associated with both sleeping behavior and our ability to wake up from sleep
RAS stimulation by sensory information causes us to wake up
Damage to the RAS
Produces a slow-wave EEG (sleep-like)
Can result in a coma – a prolonged state of deep unconsciousness that resembles deep sleep.

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37
Q

What are two brainstem nuclei in the ascending pathway of the RAS that influence waking EEG?

A

Basal forebrain nucleus and the median raphe nucleus.

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38
Q

What is the role of the Peribrachial area on the neural basis of sleep?

A

Part of RAS; cholinergic nucleus in the dorsal brainstem that projects to the medial pontine reticular formation.

Initiates REM sleep and REM-related behaviors.

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39
Q

What is the role of the Medial pontine reticular formation on the neural basis of sleep?

A

Nucleus in the pons participating in REM sleep and REM-related behaviors
Connections with the spinal motor neurons and inhibits them = produces the atonia/paralysis characteristic of REM sleep

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40
Q

What are some disorders of sleep

A

Insomnia
Sleep-paralysis
Narcolepsy
Cataplexy

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41
Q

What is insomnia?

A

The most common sleep disorder, resulting in a prolonged inability to fall asleep due to dysfunction of slow waves (Delta-waves)

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42
Q

What is sleep-paralysis?

A

A REM-sleep disorder
Atonia and dreaming when a person is still “awake”, usually after just falling asleep or more commonly right before waking up

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43
Q

What is narcolepsy?

A

Slow-wave sleep disorder in which a person uncontrollably falls asleep at inappropriate times
Can be a secondary symptom of sleep apnea

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44
Q

What is cataplexy?

A

Form of narcolepsy; animal suddenly experiences atonia, as if they are in REM, while still awake
Often tied to an emotional event (ex. overexcitement)

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45
Q

What is the applied science that is concerned with the behavioural expression of brain dysfunction?

A

Clinical psychology

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46
Q

What are some of the origins of neuropsychological assessments?

A

Screening, diagnosis, monitoring and rehabilitation of people in the wars

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47
Q

What are dynamic imaging techniques?

A

Electroencephalography, Positron Emission Tomography and functional MRIs

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48
Q

What are static imaging techniques?

A

X-rays, CT scans and MRIs

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49
Q

What are 5 reasons neuropsychological assessments are used in clinical examinations?

A

Diagnosis
Patient Care and Planning
Treatment
Research
Forensic Questions

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50
Q

What are some ways a diagnosis can be useful?

A

Neurological symptoms vs psychiatric
Distinguishing between similar conditions
Early detection and prediction
Behavioural data

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51
Q

What are some ways a neuropsychological assessments can be useful in patient care and planning?

A

Can help provide information on cognitive functioning and capacity –> provides factual information

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52
Q

What are some ways a neuropsychological assessments can be useful in treatment?

A

A diagnosis can help determine the most appropriate type of treatment by determining an individual’s strengths and weaknesses

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53
Q

What are some ways a neuropsychological assessments can be useful in research?

A

They can evaluate specific questions in research

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54
Q

What are some ways a neuropsychological assessments can be useful in forensic neuropsychology?

A

Assessments can be undertaken for legal purposes to determine whether an individual is deemed at fault for a crime, or whether they have a disability from an accident.

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55
Q

What are some components of a neuropsychological assessment?

A

Collateral information, clinical interviews

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56
Q

What are some examples of collateral information?

A

Previous neuropsychological assessments, chart review, family questioning, imaging, psychiatric history and diagnoses, etc.

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57
Q

What is collected during a clinical interview for a neuropsychological assessment?

A

Basic orientation information to time and place, medications, languages of origin, subjective complaints, emotional issues, developmental history, etc.

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58
Q

What are 3 dimensions of behaviour?

A

Cognitive, emotion and executive functioning

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59
Q

Why is cognition most important in a neuropsy assessment?

A

For most patients these tend to be their most prominent symptoms/complaints.

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60
Q

What are two approaches to neuropsychological assessments and measurement?

A

Quantitative data and qualitative data

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61
Q

What would be an example of quantitative data from a neuropsychological assessment?

A

Drawing conclusions based on the scores obtained using standardized tests
Each test has cut-off scores for impaired or not impaired
A set battery of tests is used.
Drawback: Doesn’t consider how the individual performed the task

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62
Q

What would be an example of qualitative data from a neuropsychological assessment?

A

Focus is on behavioural observations/how the person went about the task
Uses a flexible battery of tests (can pick and choose based on theory/hypothesis)
Drawback: Lacks objective standardization

63
Q

How can we assess cognitive domains?

A

Orientation - The awareness of oneself in relation to one’s surroundings in time and space
Sometimes we use the WMS-III

64
Q

What is Pre-morbid Intellectual Functioning?

A

A ”rough guess” measure of general cognitive ability reflective of the individual’s level of functioning prior to the onset of the disease/illness/etc.

65
Q

How do we measure attention and information processing speed?

A

There aren’t tests that purely measure attention, BUT we can evaluate attention and processing speed through tasks such as:
- Reaction time
- Working memory tasks (letter-number sequencing)
- Symbol digit modalities test

66
Q

What is the name for impairments in language functioning; the inability to comprehend and/or formulate language due to damage in specific brain regions?

A

Aphasia

67
Q

What is characteristic of Wernicke’s aphasia?

A

Difficulties with language comprehension (paraphasias and circumlocution)

68
Q

What is characteristic of Broca’s aphasia?

A

Difficulties with language production
Difficulty with multisyllabic words –> harder to string together multiple syllables

69
Q

How can we test language when assessing cognitive domains, while considering all aspects of verbal functions and language skills?

A

Free conversation, repetition, comprehension (token test), Reading, writing, naming (boston naming task), verbal fluency (FAS)

70
Q

What is semantic dementia?

A

Difficulty with naming pictures or objects, categorizing, or knowing the uses and features of object

71
Q

Why is it important to distinguish between a language or a speech disorder?

A

In some disorders, speech may seem unintelligible (i.e., looks like aphasia), but when asked to express through written language, the context, syntax, grammar, etc. are often normal

72
Q

What is dysarthria?

A

Difficulty in articulation of speech sounds due to weakness, paralysis, or poor coordination of the muscles of the vocal cords, tongue, lips, etc.

73
Q

What are measures of visual perceptual abilities?

A

Measures of perception along with a motor and spatial component
For example:
- Visuoconstruction (house or cube drawing)
- Line orientation task
- Neglect (crossing out lines task)

74
Q

What is nonverbal confabulation?

A

filling in gaps in memory with distorted, or misinterpreted information– typically by using environmental cues

75
Q

What are some behaviours that may come up when testing visual perceptual abilities?

A

In detailed oriented people (such as OCD, but also other individuals), they can take forever to do the task as they try to measure everything.

75
Q

What are some behaviours that may come up when testing visual perceptual abilities?

A

In detailed oriented people (such as OCD, but also other individuals), they can take forever to do the task as they try to measure everything.

75
Q

What are some behaviours that may come up when testing visual perceptual abilities?

A

In detailed oriented people (such as OCD, but also other individuals), they can take forever to do the task as they try to measure everything.

76
Q

What is stimulagnosia

A

Inability of an individual to perceive more than a single object at a time –> balint syndrome

77
Q

What is the use of the clock-drawing test?

A

Monitoring dementia progression through visual perceptual abilities, but also through hemispheric neglect, motor issues.

78
Q

How can we test for learning and memory?

A

Working memory tasks, active recall, wisconsin card sorting task…

79
Q

How can we measure executive functions (generally)

A

Sorting tasks, color word tasks (stroop), conceptual tasks, proverbs task (abstract reasoning), tower test (planning)

80
Q

What is malingering?

A

Fabricating symptoms of a cognitive impairment for a personal gain

81
Q

How can we avoid scoring malingering people?

A

Tests are administered which, by design, are incredibly easy to complete however the instructions give the impression they are difficult

Tests of Memory Malingering (TOMM) can be used.

82
Q

How do we interpret scores on cognitive assessment tasks?

A

Comparing to normative data

83
Q

What is the cutoff score for impaired individuals in score interpretation?

A

-1.50SD

84
Q

What is the formula used to calculate how a patient compares to normative data?

A

z = Score minus Mean divided by Standard Deviation

85
Q

What is dementia?

A

An umbrella term for an acquired set of symptoms affecting brain function that are caused by neurodegenerative and/or vascular diseases/injuries.
- Generally a decline in cognitive abilities resulting in functional impairment

86
Q

What is different between mild cognitive impairment and dementia?

A

Mild cognitive impairment (MCI) is a pattern of forgetfulness, but the cognitive issues (particularly outside of memory) aren’t as severe
–> About 15-20% will go on to AD
–> Potential for early detection/treatment before AD

87
Q

What is amnesia?

A

A striking impairment in memory (even more so than MCI) and the striking inability to learn new information
Other cognitive areas are generally intact

88
Q

What is delirium?

A

An acute state that results in a change in mental, emotional and behavioural disturbances and results in disorientation

89
Q

How many new dementia cases occur each year in Canada?

A

80,000+

90
Q

What is true about dementia and genders?

A

Women are more likely to develop dementia

91
Q

What is Alzheimer’s Disease?

A

The most common form of dementia.

A cortical dementia characterized by a slow, progressive loss of cognitive function

Primarily a disorder of older adults above the age of 80

92
Q

What are some proposed causes of AD?

A

Beta amyloid plaque buildup
Neurofibrillary tangles
Brain atrophy
Cholinergic cell loss

93
Q

What is the main risk factor for AD?

A

Age

94
Q

What is the protein associated with the genetic predisposition of AD?

A

ApoE gene.

95
Q

How is AD diagnosed?

A

No single, definitive diagnostic test exists

Obtain medical and family history, including psychiatric history, to look for cognitive and behavioural changes

Ask a family member or close friend to provide input about any changes they observe

Conduct cognitive testing and/or neurological exams

Undergo blood tests and neuroimaging to rule out other potential causes

AD is often a diagnosis of exclusion

96
Q

What are some symptoms of temporal damage in AD?

A

Progressive memory loss that disrupts daily life
Misplacing things
Initial word finding difficulties progressing to anomia
Impaired comprehension
Losing the ability to retrace their steps

97
Q

What are some signs of parietal/frontal damage in AD?

A

Difficulties in planning or solving problems
Decreased/poor judgement
Withdrawal from work or social activities
Changes in mood and personality (apathy, depression)
Decreased awareness/concern of their deficits
Delusional thinking can occur later in the disease
Being stolen from, interacting with a dead person, etc.
Confusion with person, place, or time
- Visuoconstruction deficits

98
Q

What are Lewy body dementias?

A

The second most prevalent category of dementia

Two subtypes: dementia with Lewy bodies (DLB), and Parkinson’s disease dementia (PDD)

Characterized by the presence of Lewy bodies
Abnormal clumps of protein deposit buildup that interfere with cellular processes

99
Q

In what cohort do LBDs occur most often?

A

Men over the age of 60

100
Q

What are some core features of LBD?

A

Fluctuating cognitive symptoms
Parkinsonism
Vivid hallucinations and psychotic symptoms

101
Q

What is the difference between LBD and AD?

A

LBD is more mild in memory impairments and has much more effects on functioning early on.

102
Q

What is the difference between dementia with lewy bodies and parkinson’s disease dementia?

A

DLB: Lewy bodies present primarily in the cortex (“cortical dementia”)

PDD: Lewy bodies primarily in the basal ganglia (“subcortical dementia”)

A distinction is also made based on the timing of cognitive and motor symptoms
Cognitive before motor? – DLB
Motor before cognitive? - PDD

103
Q

What is frontotemporal dementia?

A

A group of neurodegenerative disorders resulting from progressive degeneration of the temporal and frontal lobes.

Characterized/distinguished by progressive disturbances in language, behaviour/personality, and “other” (motor disorders).

104
Q

What are the 3 categories of frontotemporal dementias?

A

Language variant, behavioural variant, other variant

105
Q

What is true about the onset of FTDs?

A

They tend to be early onset, occuring between the ages of 45-65… Risk does not increase with age

106
Q

What are some characteristics of the Behavioural Variant of FTD?

A

Onset is in the 50s, and is insidious – comes on slowly, no obvious symptoms right away, often unaware of it developing

Characterized by progressive changes in personality, issues with social conduct, emotional blunting and/or loss of empathy, disinhibition, difficulty seeing the point of view of others, hypersexuality, and impulsivity

Repetitive motor behaviours (ex. throat clearing) are often present

107
Q

What is the difference between Primary Progressive Aphasia (an FTD) and Broca’s aphasia?

A

evolves more slowly/progressively over time; rather then suddenly appearing after an acute stroke

108
Q

What is apraxia of speech?

A

Difficulty in planning the movements of the lips and tongue needed for speech

Speech production is effortful, slowed, and hesitant.

Results in incorrect speech sounds (paraphasias)

Simplified and agrammatic (leave out “connecting” words)

Multisyllabic words are the most difficult

109
Q

What are some variants of PPAs?

A

Nonfluent/aggramatic variants
Semantic variants
Logopenic variants

110
Q

What are two core features of logopenic variants of PPAs?

A

Impaired repetition
Impaired single-word retrieval

111
Q

What are FTD with motor variants?

A

Have FTD cognitive symptoms in the presence of various motor issues… Examples: FTD-ALS/Motor Neuron Disease, Corticobasal Syndrome, Progressive Supranuclear Palsy

112
Q

What is Vascular Dementia?

A

A large group of dementias due to impaired blood flow to the brain

Typically a result of recurrent cerebrovascular dysfunction, which builds up over time leading to permanent changes in brain structure/function

Clinical feature: Perseveration

113
Q

What are toxic-metabolic dementias?

A

Dementia due to metabolic/toxic changes in the body

114
Q

What is Alcohol-related dementia (ARD)?

A

Due to the neurotoxic effects of alcohol on the brain (inflammation, excitotoxicity)
Results in extensive brain atrophy/neuronal loss – particularly of the frontal lobes
If abstinent, can halt progression

115
Q

What is Wernicke’s Encephalopathy?

A

Severe thiamine deficiency (Vitamin B1) due to poor nutrition and chronic alcoholism
–> affects superchiasmatic nucleus

Triad of symptoms: weakness in moving the eyes, ataxia (lack of voluntary coordination), confusion

60-85% with WE will go on to develop Korsakoff’s syndrome

116
Q

What are some characteristics of Korsakoff’s syndrome?

A

KS is characterized by a profound memory dysfunction with marked anterograde amnesia and an inability to learn new information

117
Q

What is Marchiafava-Bignami disease?

A

Presence of acute demyelination/atrophy/destruction of the corpus callosum

Primarily observed in Italian males with excessive red wine intake; with only about 300 cases ever reported

118
Q

What are examples of other dementias?

A

Transmissible spongiform encephalopathies (i.e., prion diseases), Chronic traumatic encephalopathy (CTE), Multiple sclerosis, Huntington’s disease, Epilepsy, Infectious Agents

119
Q

What is multiple sclerosis?

A

A chronic, and progressive degenerative disease of the central nervous system

One of the most commonly acquired neurological diseases in young adults

120
Q

What are some imaging characteristics of MS?

A

Characterized by lesions/plaques in the brain and spinal cord (and optic nerve…)

121
Q

What is the mean age of symptom onset in MS?

A

25/26 years old

122
Q

What is the mean age of diagnosis of MS?

A

30-35 years old.

123
Q

What is true about the world distribution of MS?

A

Temperate areas (away from the equator) tend to have higher prevalence rates compared to tropic areas (near the equator) –> about 45* distance from the equator.

124
Q

What is true about risk adoption of MS during developmental periods?

A

Immigration modifies risk until about 15 years old… So if you move to another country before 15 years old, you adopt the risk of MS of the country you move to.

125
Q

What are some causes/risk factors for MS?

A

Multifactoral. There is no cause that appears to be sufficient on its own for developing MS.

Some suggestion for genetic predisposition, suggesting that the human leukocyte antigen (HLA) gene complex may play a role.

126
Q

How does geographic latitude play a role in risk factors for MS?

A

Likely vitamin D exposure lessens the risk of MS

127
Q

How do infections pose as a risk factor for MS?

A

Infectious agents may initiate or maintain the pathological immune response in MS

128
Q

How do hormones modulate risk for MS?

A

Inflammation, relapse rates, and MS lesion activity typically decline during pregnancy –> progesterone?

129
Q

How does gut microbiome act as a risk factor for MS?

A

Significant differences between the gut bacteria of people with MS vs. those without

130
Q

What is the typical pathology of MS?

A

Widely accepted to be an autoimmune-mediated inflammatory disorder

Inflammation causes the lesions (demyelinated nerve cells) in the brain and spinal cord

Myelin sheath of axons are the target of the inflammatory response
Immune system attacks its own myelin sheath surrounding the axons of nerves = demyelination

131
Q

What is the typical pathology of MS?

A

Widely accepted to be an autoimmune-mediated inflammatory disorder

Inflammation causes the lesions (demyelinated nerve cells) in the brain and spinal cord

Myelin sheath of axons are the target of the inflammatory response
Immune system attacks its own myelin sheath surrounding the axons of nerves = demyelination

132
Q

What is the role of myelin?

A

Allows neurons to communicate more rapidly. Instead of generating action potentials along each point, the action potential can “jump” over the myelin between each node of Ranvier

133
Q

What are lesions (plaques) found in MS?

A

Lesions (plaques) = patches of inflammation (scarring) as a result of these autoimmune processes/demyelination

134
Q

What are the two types of lesions we can see in imaging scans for MS?

A

Wet lesions and dry lesions

135
Q

What is a temporal sequence of pathological events?

A

Begins as a focal inflammatory disease with circumscribed plaques
Chronic = diffuse inflammation with slowly progressive axonal injury and cortical demyelination/atrophy

136
Q

What is true about the clinical features of MS?

A

Symptoms vary considerably between individuals (both physical and cognitive)

137
Q

What are some initial symptoms of MS?

A

Visual symptoms – optic neuritis, loss/impaired visual acuity
Numbness/tingling/weakness
Vertigo

138
Q

What are the 4 recognized disease courses of MS?

A

Relapsing-remitting MS (RRMS)

Primary-progressive MS (PPMS)

Secondary-progressive MS (SPMS)

Progressive-relapsing MS (PRMS)

139
Q

What is characteristic of relapsing-remitting MS?

A

Clearly defined disease relapses with i) full recovery, or ii) with residual deficits upon recovery

The periods between relapses are characterized by a lack of disease progression

140
Q

What are characteristics of primary progressive MS?

A

Steady disease progression from symptom onset with no discrete relapses.

141
Q

What are characteristics of secondary-progressive MS?

A

Initial diagnosis of relapsing-remitting MS, but eventually never come out of the relapse.

142
Q

What are characteristics of Progressive-relapsing MS?

A

Progressive disease from symptom onset with clear and acute relapses, without returning to baseline or recovery

143
Q

What is the McDonald criteria for MS?

A

Dissemination of lesions in both time and space… This meaning new lesions show up at follow-up scans (time) and lesions appear in new regions of the brain (space)

144
Q

What is clinically isolated syndrome?

A

Refers to a first episode of neurological symptoms that lasts at least 24 hours and is caused by CNS inflammation or demyelination

145
Q

What is radiologically isolated syndrome

A

Incidental findings of lesions that are in asymptomatic individuals.

146
Q

What is the Expanded Disability Status Scale?

A

Used to assess physical disability in neuological exams

147
Q

What are some cons of using the EDSS?

A

Weighted towards physical aspects of MS (ignores cognitive factors)

148
Q

What are some feats of cognitive impairment that are known to occur in MS?

A

Attention
IPS
Memory
Language
Fatigue

149
Q

What is a rapid way to test for information processing speed during a neuropsychological assessment for MS?

A

The relative consequence model

150
Q

What does the relative consequence model measure?

A

Deficits in information processing speed underlie deficits observed in all other cognitive domains

Impairments in a variety of cognitive processes are simply a by-product of slowed IPS

151
Q

How can we measure cognition in MS?

A

Using the Multiple Sclerosis Functional Composite

152
Q

What does the Multiple Sclerosis Functional Composite measure?

A

Lower extremity function/ambulation (timed 25-foot walk)
Upper extremity function (9-hole peg test)
Cognition (Paced Auditory Serial Addition Test: PASAT – a measure of IPS)

PSY3301 (6 decks)

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