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ABPP > Domains of Function > Flashcards

Domains of Function Flashcards

1
Q

How is intellectual disability defined/diagnosed?

A

Must have onset before age 18, requiring a substantially subnormal IQ (about 2 or more SD below mean) combined with significant deficits in 2 or more adaptive skills.

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2
Q

How is anterior cingulate and limbic system relevant to attention?

A

Determines saliency of stimuli and associated emotion/motivation

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3
Q

How is prefrontal area relevant to attention?

A

Response selection, control, sustained attention, switching

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4
Q

How is orbitofrontal area relevant to attention?

A

Inhibition of responses

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5
Q

How is dorsolateral frontal area relevant to attention?

A

Initiation of responses

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6
Q

How is superior colliculus relevant to attention?

A

Shifting of attention and eye movements (orienting)

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7
Q

How is parietal lobe relevant to attention?

A

Spatial attention. Damage may be associated to hemispatial inattention/neglect.

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8
Q

What is hemispatial inattention?

A

Impairment in awareness of visual (and other) stimuli on the side contralateral to a brain lesion that is not the result of a primary sensory deficit and is manifested in hemi-inattention. Associated features can include anosognosia or denial of illness, extinction of stimuli, and asomatognosia (denial of a body part). Underlying pathology is usually associated with lesions in the right temporal-parietal region, leading to left side of space being ignored.

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9
Q

What disorders and modifiable factors can negatively impact attention?

A 
Delirium
ADHD
Hemispatial inattention/neglect
TBI
Depression
Anxiety
Fatigue
Medications
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10
Q

What is aphasia?

A

Aphasia is the acquired loss or impairment of language following brain damage or disease. Primary etiology is stroke (as many as 40% of patients after stroke have some degree of aphasia). Other potential etiologies include neoplasm, intracranial tumor, infection, TBI, and neurodegenerative diseases.

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11
Q

What are different areas to assess language functions (think of aphasias)

A
  1. Spontaneous speech
  2. Comprehension of spoken and written language
  3. Repetition
  4. Naming
  5. Reading
  6. Writing
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12
Q

Which aphasia syndromes are fluent?

A
  1. Wernicke’s
  2. Conduction
  3. Anomic
  4. Subcortical
  5. Transcortical sensory

Fluent aphasias involve dysfunction of posterior language areas.

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13
Q

Which aphasia syndromes are nonfluent?

A
  1. Broca’s
  2. Global
  3. Subcortical
  4. Transcortical motor
  5. Transcortical mixed

Nonfluent aphasias involve dysfunction of anterior language areas.

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14
Q

Which aphasia syndromes have repetition problems?

A
  1. Broca’s
  2. Wernicke’s
  3. Conduction
  4. Global

Remember: Disorders with repetition difficulties are located in the perisylvian areas.
Syndromes that are “extrasylvian” are the transcortical aphasia syndromes.

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15
Q

Does anomic aphasia localize?

A

No

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16
Q

Describe what is impaired in Broca’s aphasia

A

Impaired: nonfluent speech, impaired repetition, impaired naming, impaired reading, impaired writing

Intact: comprehension

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17
Q

Describe what is impaired in Wernicke’s aphasia

A

Impaired: comprehension, repetition, naming, reading, and writing

Fluent spontaneous speech

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18
Q

Describe what is impaired in Conduction aphasia

A

Impaired: repetition, naming, and writing

Intact: fluent spontaneous speech, comprehension, and reading

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19
Q

Describe what is impaired in global aphasia

A

Everything is impaired - nonfluent speech, impaired comprehension, repetition, naming, reading, and writing

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20
Q

Describe what is impaired in anomic aphasia

A

Impaired naming and impoverished content in writing. Spontaneous speech is empty in content

Intact: comprehension, repetition, and reading

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21
Q

Describe what is impaired in transcortical motor aphasia

A

Impaired: nonfluent spontaneous speech, limited naming, and impaired writing.

Intact: comprehension, repetition, and reading

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22
Q

Describe what is impaired in transcortical sensory aphasia

A

Impaired: comprehension, naming, reading, and writing

Intact: fluent spontaneous speech, repetition

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23
Q

Describe what is impaired in transcortical mixed aphasia

A

Impaired: spontaneous speech is nonfluent, comprehension, repetition, naming, reading, and writing.

Intact: repetition

24
Q

Farah proposed which 2 streams of higher order visual processing are present?

A
  1. Analyzing the form or the “what” of visual stimuli

2. Analyzing the location or the “where” of visual stimuli

25
Q

What is agnosia?

A

An acquired disorder, caused by brain disease or injury, resulting in an inability to recognize formerly familiar objects.

26
Q

What is a visual agnosia?

A

Disturbance of visual perceptual function concerning the identification and recognition of faces, objects, or their representation, forms, colors, and spatial information. The disturbance is not the result of a deficit in vision, attention, or naming.

27
Q

Visual object agnosia

A

The inability to visually recognize and appreciate the meaning or character of an object. Although patients with visual agnosia may be able to describe features of the object, such as its color or shape, they are unable to recognize what the object is.

Usually a result of left occipital lesions with extension into subcortical white matter, but also bilateral lesions involving peristriate angular gyrus and the lingual and fusiform lobules.

Visual agnosias are an example of a problem with the “what” pathway.

28
Q

Which tests could test the “what” pathway?

A

Picture Completion, Hooper Visual Organization Test

29
Q

Which tests could test the “where” pathway?

A

JOLO, Block Design

30
Q

What are disorders in spatial analysis/processing?

A

Impairments in spatial processing can include difficulties locating objects in space, difficulties discriminating between complex visual stimuli, and difficulty constructing simple and complex shapes.

One disorder example is constructional apraxia, which involves loss of ability to carry out purposeful movements (like an apraxia), but is really a visuospatial disorder that signals an inability to construct shapes and geometric designs and to assemble block arrangements.

Usually these disorders stem from right hemisphere (parietal) lesions.

31
Q

Name the steps of the information processing model

A
  1. Encoding (active organization or manipulation of incoming stimuli through rehearsal and repetition).
  2. Storage (transfer of transient memory to where it can be made more permanent)
  3. Consolidation (process by which encoded information undergoes a series of processes that render the memory representations progressively more stable and permanent).
  4. Retrieval (the ability to access previously stored information by way of cues).
32
Q

Name the steps of the “3-stage model”

A
  1. Sensory memory (holds information for a few seconds)
  2. Short-term memory (limited capacity, 7 plus or minus 2 chunks; temporary store where information can be held for up to several minutes, often equated with working memory and attention.
  3. Long-term memory (a more permanent memory store where information is stored by way of consolidation or learning. Requires the hippocampus where structural change takes place due to long-term potentiation [LTP])
33
Q

What is an amnestic disorder?

A

Amnestic disorder is an isolated loss of memory without loss of any other cognitive functions. Declarative (explicit) memory is affected, whereas procedural (implicit) memory is not.

34
Q

What is retrograde amnesia?

A

Amnesia for events prior to an accident, illness, or event; it is typically temporally graded, whereby events immediately before are lost, whereas more remote memories remain intact. Ribot’s Law states that the oldest memories are the most resistant to amnesia. There is an association between severity of retrograde amnesia and extent of hippocampal pathology.

35
Q

What is anterograde amnesia?

A

Amnesia for new information. Inability to learn or encode new information or form new memories.

36
Q

What results from anoxia or hypoxia?

A

Damage to the medial temporal lobe, particularly area CA1 of the hippocampus. Mammillary bodies, cingulate cortex, fornix, and entorhinal cortex also affected. Essentially hippocampal pathway affected.

May result in dense amnesia (usually ANTEROGRADE amnesia).

In some cases, the amnesia is profound but in others memory performance improves with retrieval cues. Unlike other amnestic disorders, insight may be preserved and confabulation is NOT present.

37
Q

What may result from ACoA (anterior communicating artery) aneurysm?

A

Rupture of the ACoA (which connects/bridge between anterior cerebral arteries) often results in basal forebrain, striatal, and frontal system damage.

This in turn causes a frontal amnesia characterized by confabulation, attentional problems, disorientation, some apathy/lack of insight, and variable retrograde amnesia

38
Q

What does STRIATAL and STRIATUM and STRIATE refer to?

A

CAUDATE (NUCLEUS) AND PUTAMEN!

39
Q

What is Wernicke-Korsakoff’s syndrome?

A

Occurs as a result of chronic alcohol use and thiamine deficiency.
Affects anterior nucleus of thalamus, dorsomedial nucleus of thalamus, fornix, and mammillary bodies.

Korsakoff’s syndrome involves BOTH anterograde and retrograde amnesia (loss of remote memory), confabulation, and poor insight.
It is also associated with gait ataxia, oculomotor palsy, and encephalopathy.

40
Q

What results from herpes encephalopathy?

A

Virus preferentially affects the medial and inferior temporal lobes and the amygdala.
Often this initially results in severe RETROGRADE amnesia, aphasia, and agnosia.

41
Q

What might results from surgical ablation of medial temporal lobes bilaterally?

A

Think of H.M. - he underwent resection due to epilepsy. He suffered severe anterograde amnesia.

42
Q

What happens with posterior cerebral artery (PCA) stroke?

A

The brain areas affected, and the resulting AMNESIA, depends on the laterality of the lesion; however, the pathology involves medial temporal and posterior occipital lobes. Associated cognitive deficits include visual deficits, hemianopic alexia, color agnosia, and object agnosia.

43
Q

What are the memory pattern differences between Alzheimer’s disease and others?

A

AD affects memory encoding.
Patients with dementias impacting frontal-subcortical systems (e.g., vascular dementia, MS, PD) typically display retrieval difficulties and thus are helped with recognition cueing.

44
Q

List the syndromes in which particular deficits results from damage of discrete areas.

A
  1. dorsolateral prefrontal syndrome (dysexecutive syndrome). Dorsolateral prefrontal area damaged. Characterized by poor problem-solving, working memory, word list generation, planning/organization, abulia/amotivation, and sometimes perseveration
  2. orbitofrontal syndrome. Orbitofrontal area damaged. Characterized by emotional lability, impulsivity, disinhibition, stim bound behaviors, childishness, personality change, and distractibility.
  3. Medial frontal/cingulate syndrome. Anterior cingulate area damaged. Characterized by decreased initiation and apathy/indifference, but can also have amnesia, incontinence, and leg weakness.
45
Q

Which dementias present with executive dysfunction?

A 
Cortical dementias (FTD, Lewy body disease)
and frontal-subcortical dementias (PD and Huntington's)
46
Q

What other etiologies can results in executive dysfunction?

A

TBI, brain tumor, strategic vascular lesions among others

47
Q

What is autotopagnosia?

A

one loses the ability to identify parts of one’s body to command or imitation (finger agnosia is one example of this)

48
Q

Finger agnosia

A

Loss of the ability to name or identify the fingers of one’s own hands or the fingers of the hands of another person. Occurs as a result of lesion to left angular gyrus in parietal lobe.

49
Q

What is Gerstmann’s syndrome?

A

Collection of 4 symptoms:

  1. Finger agnosia
  2. Acalculia
  3. Agraphia
  4. Right-left disorientation
50
Q

What is right-left disorientation?

A

Another example of autotopagnosia. One loses the ability to identify parts of one’s body to command or imitation, or to identify such parts in another person. Occurs as a result of lesion to left angular gyrus in parietal lobe.

51
Q

What is apraxia?

A

Impairment of the ability to carry out purposeful skilled movements despite normal primary motor skills and comprehension of the act to be performed.

52
Q

What is ideational apraxia?

A

Loss of the ability to plan and execute complex gestures, as though one lost the “idea” behind the gesture or use of a tool. Assessment of serial acts is important in identifying this disorder. Has been associated with bilateral, nonfocal lesions and with left hemisphere lesions, especially the posterior temporal-parietal junction.

53
Q

What is ideomotor apraxia?

A

Loss of the ability to perform transitive or intratransitive gestures on command and to imitate, although spontaneous production of the gesture is intact. Involves difficulty making believe one is using a tool and is manifest in tool use and gestures. Patients may uses a body part as if it were an object (hand as comb). Usually involves lesions in the left inferior parietal lobe or supplementary motor area or a lesion in the corpus callosum.

54
Q

What are transitive movements?

A

Those done as a goal-directed movement with an object.

55
Q

What are intransitive movements?

A

Movements done without a specific goal and without use of an object, like hand gestures

56
Q

Describe differences in hemispheres with respect to emotion

A

Damage to the right parietal and frontal systems is associated with no emotional concern/distress about symptoms. Alexithymia, inability to understand, label emotions, is also associated with the right hemisphere.

57
Q

Damage to which area may result in confabulation?

A

Diencephalic area, making sense as Korsakoff’s and ACoA aneursym damage this and are associated with confabulation

ABPP (20 decks)

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