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Bio Bases Of Bx > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

Visual Perception

A

Visuoperception is an active, creative, constructive process that transforms transient light patterns on retina into stable, coherent percepts that are affected by prior experience and other brain modules

(Hardwired by genes, but individual experience can modulate those systems and also modified by other systems)

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2
Q

Binding Mechanism

A

Perception of location, motion, depth, form, color are processed all along and between the two pathways–> involve different types of neurons and different brain structures (modules)

Selective attention affects what we perceive as most important

This attentional aspect of consciousness and the “binding problem” are considered to be among the most complex problems facing neuroscience

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3
Q

Ventral Stream

A

From occipital to inferior/ventral temporal lobe: processes object recognition (the “what” of vision, what it looks like)

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4
Q

Where is movement processed?

A

Medial temporal (MT/V5) and Medial Superior Temporal (MST)

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5
Q

Dorsal Stream

A

From occipital to parietal lobe to guide movements (the “how” of vision-where it is and if it’s moving)

Integrates visuospatial with data about movement from medial temporal, medial superior temporal

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6
Q

Parietal lobe is critical for…

A

SELECTIVE/FOCUSED ATTENTION

  • Selection of restricted sample of sensory data
  • Focusing on “target” stimulus & avoiding distractors
  • Bottom-up processes may bias attention by salient features of stimuli (limbic system could also active here and may affect ability to perceive accurately)
  • Top-down processes from cortex helps to avoid distractions.
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7
Q

Selective Attention

A

Separates signal from noise by quieting sensory system and amplifying signal

Like a “spotlight”

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8
Q

Posterior spotlights

A
  1. posterior parietal, especially right
    - Selects location
    - Critical for ability of neurons (especially visual) to highlight one sensory input while keeping others in background
  2. Right posterior parietal lobe (PPL) is critical for switching attention.
    - Posner’s “disengage, move, engage” model
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9
Q

Hemispatial (contralateral) neglect (“inattention”)

A

Neglect of contralateral side…people neglect information in one hemisphere.

  • Usually vision (but may include other sensory modalities)
  • Left side is much more commonly neglected because right PPL is involved in selective attention for both sides
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10
Q

Anosagnosia

A

Loss of awareness of deficits (physical & cognitive)

  • Left side of body is usually more “neglected.”
  • More common w/ right parietal lesions
  • May occur w/ right prefrontal lesions
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11
Q

Binding and consciousness

A

A unified, conscious experience is achieved through

  1. Connectivity
  2. Synchrony/timing
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12
Q

Agnosia

A

“Lack of knowledge” due to perceptual deficit w/ intact sensation

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13
Q

Visual Agnosia

A

Inability to recognize/perceive visual objects (or drawings) and to draw or copy them

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14
Q

Prosopagnosia

A

Inability to recognize familiar faces due to inability to disambiguate individual stimuli.

  • Memory and visual-perceptual issue
  • Usually due to bilateral lesions in occipito-temporal cortex & white matter
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15
Q

Aphasia

A

Acquired difficulty in comprehending or formulating verbal content of language.
-Thought-language disconnect
-May disrupt:
Syntax – Grammatical structure
Lexicon – “Dictionary” of word meanings
Word morphology – Combination of
phonemes to make words

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16
Q

Wernicke’s (receptive, sensory, fluent) aphasia

A

Difficulty comprehending verbal content of language

Three Impairments:

  1. Impaired phonemic recognition
  2. Impaired speech
  3. Impaired writing– also frequently experience apraxia (difficulty making movements), which extend beyond mere writing.
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17
Q

Anomia

A

Loss of naming ability, usually w/ left-hemisphere lesions

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18
Q

Receptive dysprosody

A

Difficulty comprehending emotion, intonation, inflection in language

Pt often experiences social, interpersonal difficulties due to failure to pick up subtle inflections and cues from others.

Usually from lesions in area homologous (same area in opposite hemisphere) to Wernicke’s area in right hemisphere.

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19
Q

Where is music primarily processed?

A

Right hemisphere, where prosody (loudness, pitch, timbre, & rhythm) is processed

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20
Q

Sensory Integration

A

integration of somatosensory, auditory, visual information

  • Generates knowledge - Understanding of meaning & relationships among recognized sensory inputs
  • Sends to frontal lobes for “final” integration with limbic input

Reading and math performed here

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21
Q

Acalculia

A

Loss of math ability

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22
Q

Alexia

A

Loss of reading ability. at one point had normal reading ability but loses it

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23
Q

Dyslexia

A

(Selected Reading Disorder). neurodevelopmental issue

24
Q

Apraxia

A

Loss of skilled or purposeful movement in absence of muscular weakness/paralysis, sensory loss, poor motivation, intellectual deterioration, poor comprehension, or other movement disorders such as tremor

-Especially an inability to make proper use of an object

25
Q

Agraphia

A

Loss of writing ability

26
Q

Movement order occurs with lesions in…

A

Sensory integration area:

Frontal lobe (responsible for formulating, elaborating, & executing motor acts) must have precise, highly integrated knowledge before acting

27
Q

Sample Question: Patients with Wernicke’s aphasia…

A

Have difficulty comprehending language but may also speak w/ “word salad,” which makes little sense.

28
Q

Sample Question: Loss of awareness of one’s own deficits is…

A

Anosagnosia

29
Q

Limbic System

A

Comprised of subcortical & cortical structures that encircle brainstem, thalamus, basal ganglia

Subcortical portion- involved with subconscious, fast responses to stimuli with positive or negative values (i.e. Fear reaction)

Cortical portion- mediates conscious feelings

30
Q

Amygdala

A
  1. Learning emotional significance of stimuli, particularly with biological significance (food, water, rivals)
  2. Prosody & facial expressions- particularly fear, anger, sadness. (Prosody is emotion in language)
31
Q

Amygdala and fear

A

***Responding to innate fears & learning new fears (conditioning)

The most important structure in brain for fear

Anxiety disorders associated w/ hyperactive amygdala

32
Q

Amygdala and emotional responses

A
  • Autonomic & endocrine responses via output to hypothalamus, brainstem
  • Defensive behavior via output to brainstem
  • Conscious awareness via output to prefrontal cortex, cingulate cortex
33
Q

Hippocampal Formation

A

Critical for declarative long-term memory

-Receives input from cortex
-Associates various inputs
-Sends processed information back to these
cortical areas where their synapses are modified
(stored in memory)
-Damage occurs in Alzheimer’s disease.

Long-term memory is stored throughout the cortex, but the storing or process of changing synapses occurs in the hippocampus

34
Q

Nucleus Accumbens (NA)

A

Major role in craving, pleasure, addiction

  • Mesolimbic pathway
  • Brain response to natural reinforcers & recreational drugs associated with elevated levels of extracellular dopamine in NA
35
Q

Sample Question: Considered the reinforcement pathway and involved in addictions..

A

Mesolimbic pathway from the substantia nigra to the hypothalamus

36
Q

Sample Question: The most important structure involved in fear conditioning…

A

Amygdala

37
Q

Sample Question: Has a critical role in associating stimuli and forming long-term, explicit memories…

A

Hippocampus

38
Q

Basal Ganglia

A

Complex set of subcortical nuclei that modulate movement, perception, cognition, emotion

Basal ganglia (BG) get information from cortex, modulate that information, and then modulate frontal cortex via thalamus.

Modulation results in either increased or decreased excitation of frontal cortex.
Slow= Parkinson’s
Fast= Huntington’s, tics, etc.

39
Q

Striatum

A

Three Nuclei:

  1. The caudate nucleus
  2. Putamen
  3. Nucleus accumbens

Receives input primarily from cerebral cortex, also from substantia nigra, which project primarily to thalamus and also frontal lobe, inhibiting cortical activity

40
Q

Four parallel circuits (“loops”)

A
  1. Skeletomotor Loop- Sensory-motor control (Parkinson’s, Huntington’s)
  2. Oculomotor Loop- Control of orientation and gaze
  3. Prefrontal Cortex (Executive) Loop- Cognitive processes (ADHD)
  4. Limbic Loop- Emotional and visceral responses
41
Q

Skeletomotor Loop

A

-Modulates force/rate/amount of movements, including initiation & control of movement

(Not involved in conscious desire to move, in planning details, or in activating muscles)

  • Helps to smooth movements
  • Automatic motor subroutines require basal ganglia & cerebellum–Subconscious habits, motor skills
42
Q

Hypokinetic Symptoms

A

Loss/decrease of motor/cognitive ability

43
Q

Hyperkinetic symptoms

A

Involuntary movements

44
Q

Parkinson’s Disease

A

AKA ideopathic Parkinsonism, primary Parkinson’s

  • Ideopathic- uncertain why pt has destruction of neurons in substantia nigra (50% cases)
  • Primary- not due to drug, but due to damage to substantia nigra

Motor sx’s due to loss of dopaminergic neurons of substantia nigra that project to striatum of BG.
Results in decreased excitation from BG to thalamus with resulting hypokinetic sx’s

45
Q

Akinesia (dyskinesia)

A
  1. Difficulty initiating activity
  2. Loss of postural reflexes (tends to fall backward)
  3. Shuffling gait, as if feet were stuck in place, w/ decreased arm swing and appearing stiff w/ little neck movement
  4. Sometimes followed by nearly normal gait but difficulty stopping or falling
46
Q

Bradykinesia

A

Slowed movements

47
Q

Hypokinetic dysarthria

A

(articulation problems with speech) – Decreased intonation, low volume, variable speed of speech

48
Q

Extrapyramidal Symptoms (EPS)

A

Due to improper balance of neurotransmitters in BG

1, Akathisia (restlessness, pace often), often seen
in Abilify
2. Muscular rigidity (bent over, “cogwheel rigidity”)
3. Resting (pill-rolling) tremor vs. intention tremor
(usually cerebellar problem)

49
Q

Other traits of PD

A
  • Depression is common
  • Mental deterioration, slowed cognition (bradyphrenia), memory deficit, in 20-50% (working memory and procedural)
  • About 31% of PD pts develop dementia
50
Q

Parkinsonism

A 
Syndrome of sxs of Parkinson’s due to:
- Side effect of antipsychotics (particularly typical 
  antipsychotics, Haldol)
- Metoclopramide (Reglan)
- Toxins
- TBI
- Stroke
- Encephalitis
- Meningitis
51
Q

Hyperkinetic Dysfunction

A

Results in increased excitation of thalamic neurons, which results in excessive stimulation of the cerebral cortex

52
Q

Choreiform movements

A

Generalized irregular dance-like movements of limbs

  • Sydenham’s chorea
  • Chorea gravidarum
  • Huntington’s disease
  • Part of tardive dyskinesia
53
Q

Athetoid movements

A

Conextremity- tinuous writhing of distal portions of Huntington’s disease

  • Sometimes in treated Parkinson’s disease
  • Part of tardive dyskinesia
54
Q

Huntington’s Chorea

A

Inherited disease causing abnormality in BG, which leads to over-stimulation of frontal cortex, resulting in choreiform & athetoid movements as well as cognitive dysfunction

Depression is the most common sx; high suicide rate

May experience mania or hypomania, anxiety, emotional lability, irritability, aggressiveness, apathy late in disease

55
Q

Tardive dyskinesia

A

Repetitive choreic or athetoid movements that affect face, trunk, hands, feet

  • Sxs may be temporary or permanent
  • Caused by chronic Rx w/ antipsychotics, especially neuroleptics (typical antipsychotics)
56
Q

Dystonia

A

Persistent contraction of muscles (neck, back, eyes, hand, foot)

Most common cause is SE of antipsychotic

57
Q

Tourette’s syndrome (Gilles de la Tourette’s)

A
  • Involuntary tics & involuntary movements
  • Multiple motor tics accompanied by at least one
    vocal tic for a period of at least 1 year
  • Excessive D2 activity in basal ganglia, especially
    right caudate
  • May involve circuit including prefrontal cortex

Bio Bases Of Bx (3 decks)

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