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My Physiology of Behavior > Exam II > Flashcards

Exam II Flashcards

1
Q

Broca’s Aphasia Chart

A
  • Frontal cortex rostral to base of primary motor cortex (Broca’s area)
  • Nonfluent speech
  • Good comprehension
  • Poor Repetition or Naming
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2
Q

Wernicke’s Aphasia Chart

A
  • Posterior portion of superior temporal gyrus (Wernicke’s area) and posterior language area
  • Fluent speech
  • Poor comprehension, repetition, naming
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3
Q

Pure Word Deafness Chart

A
  • Wernicke’s area or its connection with primary auditory cortex
  • Fluent speech
  • Good Naming
  • Poor comprehension, repetition
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4
Q

Conduction Aphasia Chart

A
  • White matter beneath parietal lobe superior to lateral fissure (arcuate fasciculus)
  • Fluent speech
  • Good comprehension and naming
  • Poor repetition
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5
Q

Anomic Aphasia Chart

A
  • Various parts of parietal and temporal lobes
  • Fluent speech
  • Good comprehension, repetition
  • Poor naming
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6
Q

Transcortical Sensory Aphasia Chart

A
  • Posterior language area
  • Fluent speech
  • Good repetition
  • Poor comprehension or naming
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7
Q

Broca’s Aphasia, add’l

A
  • Prototypic nonfluent aphasia.
  • Damage to inferior left frontal lobe or insular cortex
  • Articulation difficulty-no expressive language, painful
  • Anomia-word finding/naming difficulties
  • Agrammatism-telegraphic speech. Grammatical trouble.
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8
Q

Wernicke’s Aphasia, add’l

A
  • Poor insight.
  • Prototypic fluent aphasia
  • Damage to posterior portion of left superior temporal gyrus
  • Hallmarks include poor receptive language/comprehension, cannot identify spoken words. And fluent meaningless speech, word salad.
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9
Q

Pure Word Deafness, add’l

A
  • Disorder of word recognition, without other deficits. Presents normally.
  • Reading and writing intact. Damage to Wernickes Area.
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10
Q

Conduction, add’l

A
  • Arcuate fasciculus- bundle of axons connecting wernickes and brocas area, damaged.
  • Anomia- everything is good except naming (Tip of the tongue phenomena) Parietal and temporal lobes damaged
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11
Q

Transcortical Sensory, add’l

A
  • Same as wernicks but w/out ability for repetition.

* Posterior language area damaged.

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12
Q

Emotion Structures: Amygdala

A

o fight, flight, feed fornicate.
• Medial – olfaction and sensory input relays to medial basal forebrain and hypothalamus.
• Lateral – sensory information from neocortex, and sends to basal, and central nucleus of amygdala. Hippocampus learning of lesson, connection of response to emotion
• Central – expression of emotional response to aversive stimuli. learning of a threatening situation. PTSD

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13
Q

Ventral prefrontal cortex

A

• involved in automatic emotional response and control of complex behaviors (such as appropriate social demeanor).

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14
Q

Ventromedial prefrontal cortex

A
  • base of anterior frontal lobes
  • receives input from dorsomedial thalamus, etc. outputs to cingulate, hippocampus, etc. inputs provide information of planning environmental stimuli and responses organized by amygdala.
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15
Q

Kluver-Bucy Syndrome

A

• from bilateral anterior temporal removal or injury. breakdown of fear and response/conditioning, increased aggression, sexuality, eating/drinking and memory impairment. Hypothalamic increase (increase in species behaviors) increased inpulsivity, etc.

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16
Q

Emotional facial paresis

A

lack of facial movement during genuine response to emotions on the ipsilateral side of damage, usually to insular prefrontal cortex, subcortical white matter or thalamus.

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17
Q

Volitional facial paresis

A

cannot move facial muscles voluntarily even though they feel the emotion. Damage to subcortical connections in primary motor cortex

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18
Q

Hemisphere Dominance

A
  • R hemisphere → comprehension of emotion, tone.

* L → language

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19
Q

James-Lange Theory

A

feelings of emotion are an after effect of the internal autonomic response to what we feel/biologically respond with after an experience. Ie: experience causes you to sweat , your feelings/insight about sweating cause emotion of it.

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20
Q

2 primary pathways for conditioning

A
  • Direct transcortical connections, episodic memory.

* Connections via basal ganglia and thalamus, overlearned behaviors/cerebellum.

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21
Q

Anterograde

A

amnesia after trauma

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22
Q

Retrograde

A

amnesia before trauma

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23
Q

Korsakoffs

A

permanent anterograde amnesia via alcoholism or malnutrition

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24
Q

Confabulation

A

reporting of events that never happened

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25
Q

4 types of learning

A
  • Perceptual- stimulus recognition and familiarity/understanding of what you see
  • Stimulus-response, learned response to stimulus (CC, OC)
  • Motor- Strong neural circuits are formed in motor systems of brain to become “well learned”.
  • Relational- increased complexity of learned behavior, relationship between stimuli. Episodic learning is remembering sequences of events.
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26
Q

Hebb Rule-

A

repeatedly activating an unconditioned stimulus with the excitation of an automatic response, you strengthen the weak/CS by pairing.

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27
Q

HM

A
  • bilateral mesial temporal resection (including hippocampus)
  • antegerade amnesia.

Thus, hippocampus:
• (1) is not the location of long-term memories or their retrieval
• (2) is not the location of immediate (‘short-term’) memories
• (3) is involved in converting immediate (‘short-term’) into long-term memories

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28
Q

Hippocampus

A

short term memory and memory consolidation into LTM

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29
Q

Hippocampal formation

A
  • highly plastic forebrain structure of temporal lobe in limbic system which includes the Ammon’s horn dentate gyrus (input from entorhinal cortex and projects pyramidal cells to hippocampus) and subiculum
  • A forebrain structure of the temporal lobe, constituting an important part of the limbic system; includes Ammon’s horn (cornu ammonis or CA), dentate gyrus, and subiculum.
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30
Q

long-term potentiation (LTP)

A

A long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high-frequency activity.

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31
Q

Huntington’s

A

Hyperkinetic neurologic disorder, degeneration of caudate nucleus and putamen, englarged lateral ventricles, characterized by uncontrollable jerking movements, writhing, psychiatric symptoms and dementia. F>M early onset. Psychosis. Cohrea-dancing, throwing of limbs. Anticipation-each subsequent generation is worse. Amplification, and more debilitating with each onset.

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32
Q

Parkinsons

A
  • hypokinetic movment disorder that results from degradation of cell bodies and dopaminergic neurons within the substantia nigra (basal ganglia) in midbrain.
  • TRAP: resting tremor, rigitidy =, Akinesia (psychomotor slowing) and postural instability. breakdown of planning and drawing of the clock would be too small. Cannot “right” themselves (find balance).
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33
Q

2 Types of Apraxia

A
  1. Limb apraxia:
    • a. Callosal apraxia (apraxia of left hand caused by damage to anterior corpus callosum.
    • b. Sympathetic apraxia (d/o of left hand by damage to left frontal lobe, impairment of right and left arm.
    • c. Left parietal apraxia – caused by damage to left parietal lobe, difficulty producing sequenced movement on verbal request. damage to right parietal lobe.
  2. Constructional apraxia – difficulty drawing pictures of geometrical qualities,
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34
Q

Apraxia

A

difficulty carrying out purposeful movement in absence of paralyses and muscle weakenss. Esp for overlearned tasks. Breakdown of sequenced movment, and becomes concrete, breakdown of initiation, innap. Or excessive behavior.

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35
Q

Monosynaptic stretch reflex

A

a reflex when a muscle contracts in response to its being stretched quickly, involving sensory neuron and motor neuron w/ one synapse between them. Righting, given response at spinal level. Single muscle spindle gets activated (stretching of muscle) which sends action potential down dorsal root ganglion to spinal cord (grey matter) meeting at alpha motor neuron. Then the ventral root takes the message/potential back to the extrafusal muscles (w/many dendritic spines).

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36
Q

Agonist muscle

A

contraction produces or facilitates a movement.

37
Q

Antagonist muscle

A

contraction resists or reverses a movement.

38
Q

Cerebellum Disorder

A

Signs of cerebellar disorder:
Ataxia (ipsilateral to side of lesion): disordered movement, wide gate, not apraxia
Abnormal movement including errors in rate, range, direction, timing, and force of motor activity.

39
Q

Cerebeller Disorder may include:

A

May include:
Dysmetria (disordered measure of distance in muscular acts)
Dysdiadochokinesia (disordered alternation of movement); alternating movements, (tested via palm down then up slapping knee)
Intention tremor (tremor with movement)
Ataxic or wide-based gait (e.g., as result of alcoholism)
Nystagmus
Involuntary rapid eye movements that may be horizontal, vertial, rotary, or mixed.

40
Q

Primary Motor Cortex

A

• (rostral to central sulcus). pyramidal movements, receives information from primary somatosensory (topographically organized mapping of body parts in particular regions of the brain.) cortex, premotor cortex, supplementary motor area.

41
Q

Frontal Association Cortex

A
  • rostral to PMC. Receives sensory info from parietal/temporal lobes, efferent. Includes supplemental motor area (SMA) which region of association motor cortex, dorsal. Planning and preforming sequenced behaviors. Includes premotor cortex, in lateral frontal lobe, involved in learning/executing complex movements.
  • (mirror neurons, within ventral premotor cortex and inferior parietal lobule).
42
Q

Primary Motor Strip

A

• Listed from medial to lateral: Genitals, Buddocks, Toes, leg, abdomen, Shoulder, Arm, forearm, palm, fingers, Thumb, eyelids, face, lips neck, tongue, jaw and swallowing. Supplementary motor area, medial, closes to top of list.

43
Q

Primary Motor Circuit,

A

corticospinal tract, pyramidal tract, descending pyramidal

44
Q

Basil ganglia

A

Extra pyramidal movements. 5 major nuclei include putamen, caudate nucleus, globus pallidus, subthalamic nucleus and substantia nigra.

45
Q

Long-term Potentiation

A

long-term increase in excitability of neuron to particular synaptic input caused by repeated high-frequency activity

46
Q

Pyramidal Cell

A

Category of large neurons with pyramidal shape; found in cerebral cortex and Ammon’s horn of hippocampal formation.
Pyramidal dendrite and branches are studded with 30000 dendritic spines

47
Q

Perforant Path

A

system of axons that travel from cells in entorhinal cortex to dentate gyrus granule

48
Q

Entorhinal cortex

A

region of limbic cortex that provides major source of inputs to hippocampal formation

49
Q

Hippocampal Formation

A

highly plastic structure of temporal lobe, includes Ammons horn, dentate gyrus, subiculum

50
Q

Dentate Gyrus

A

Part of hippocampal formation; receives inputs from entorhinal cortex and projects to pyramidal cells of field CA3 of hippocampus proper via granule cells

51
Q

Hippocampus

A

involved in consolidation of STM to LTM
HM’s LTM and Working memory/immediate STM were not affected by Bilateral medial temporal resection aka removal of hippocampus

52
Q

4 types of Learning

A

1) Perceptual (recognition)
2) Stimulus-Response (CC, OC)
3) Motor (muscle memory)
4) Relatioal (akin to shaping)

53
Q

Anterograde Amnesia

A

think ANTICIPATE

Amnesia from damage forward/inability to make new memories

54
Q

Retrograde Amnesia

A

think RETROACTIVE

Amnesia from before (usually just before and surrounding) damage

55
Q

Korsakoffs

A

permanent anterograde amnesia via alcoholism or malnutrition

56
Q

confabulation

A

Reporting of events that never happened

57
Q

2 Pathways for Conditioning

A

1) Direct transcortical connections, episodic memory

2) Connections via basal ganglia and thalamus, over-learned behaviors/cerebellum

58
Q

James-Lange Theory

A

Feelings of emotion are an affect effect of internal autonomic response to what we feel/biologically respond with after an experience.

IE experience causes you to sweat, you then feel/insight that “I am nervous”

59
Q

Hemisphere Dominance

A

Right: comprehension of emotion, tone
Left: language

60
Q

Volitional Facial Paraesis

A

You can’t smile when you decide to but you usually can when you accidentally/naturally do

61
Q

Emotional Facial Paraesis

A

You can’t smile when you are happy/laughing and naturally would

62
Q

Kluver-Bucy Syndrome

A

Breakdown in fear response

Increased aggression, sexuality, eating/drinking, memory impairment, increased impulsivity

63
Q

Ventromedial Prefrontal Cortex

A

Base of anterior frontal lobes
receives input from dorsomedial thalamus, etc. outputs to cingulate, hippocampus, etc. inputs provide information of planning environmental stimuli and response organized by amygdala

64
Q

Ventral Prefrontal Cortex

A

Involved in automatic emotional response and control f complex behaviors (such as appropriate social demeanor)

65
Q

Amygdala

A

(four “f’s”)
Medial: olfaction and sensory input relays to medial basal forebrain and hypothalamus

Lateral: sensory information form neocortex, sends to basal, central nucleus of amygdala. Hippocampus learning of lesson, connection of response to emotion

Central: expression of emotional response to aversive stimuli; learning of threatening situation; PTSD

66
Q

Aphasias

A 
Broca's
Wernicke's
Pure Word Deafness
Conduction
Anomia
Transcortical Sensory
67
Q

Broca’s Aphasia

A

Comprehends but cannot talk

68
Q

Wernicke’s Aphasia

A

Talks but cannot comprehend or follow instructions to name or repeat

69
Q

Pure Word Deafness

A

Talks and Names/Identifies but neither comprehends not repeats

Damage to Wernicke’s area &/or connectors to PAC

70
Q

Conduction Aphasia

A

Can speak, comprehend, name/identify but cannot repeat (cannot be conducted, as it were)

Damage to white matter beneath parietal lobe superior to lateral fissure

71
Q

Anomia Aphasia

A

Can speak, comprehend, repeat but cannot NAME/identify
“tip of the tongue”

Parietal/temporal damage regions

A-NOMia: without name/label

72
Q

Transcortical Sensory

A

Can speak and repeat but can neither comprehend nor name

Damage to Posterior Language Area

73
Q

Huntington’s

A

HYPERkinetic neurological disease
Degeneration of caudate nucleus and putamen
enlarged lateral ventricles
uncontrollable jerking, writing, psychiatric symptoms; Cohrea.
Anticipation and Amplification

74
Q

Parkinson’s

A

HYPOkinetic movement disorder
Results from degradtion of cell bodies and dopaminergic neurons in Substantia Nigra (BG)
TRAP

75
Q

Parkinson’s TRAP

A

Tremor; Rigidity; Akinesia (psychomotor slowing); Postural Instability

76
Q

Limb Apraxia: Callosal

A

left hand due to damage to anterior corpus callosum

77
Q

Limb Apraxia: Sympathetic

A

left hand, right arm/hand impairment due to left frontal lob

78
Q

Limb Apraxia: Left Parietal

A

damage to left parietal lobe, results in difficulty producing sequenced movement on verbal request

79
Q

Constructional Apraxia

A

Difficulty drawing pictures of geometrical qualities

80
Q

Apraxia

A

A-Prax

not able to do purposeful movement w/o weakness orparalysis (especailly over-learned/practiced)

81
Q

Agonist Muscle

A

contraction produces or facilitates a movement

think: facilitates movement of a plot, e.g. agonist character

82
Q

Antagonist Muscle

A

contraction resists or reverses a movement

think: hero of the story/antagonist character

83
Q

Monosynaptic stretch reflex

A

Reflex when muscle contracts to quick stretch

involves sensory neuron and motor neuron, one syanpse betwen them

84
Q

Cerebellum

A

Responsible for coordinated movement
Signs of disorder [IPSILATERAL]

disordered movement, wide gate, not apraxis, abnormal movement (rate, range, direction, timing, force of motor activity).

Nystagmus, Dysmetria, Disdiadochokinesia, Ataxia, Intention Tremor

*can be caused by alcohol

85
Q

Nystagmus

A

involuntary rapid eye movement

86
Q

Dysmetria

A

disordered measure of distance in muscular acts

87
Q

Dysdiadochokinesia

A

disordered alternation of movement

88
Q

Intention Tremor

A

Tremor during purposeful movements

89
Q

Cerebral Coorniation Issues from Alcohol

A

wide gate, affects of vermis

My Physiology of Behavior (3 decks)

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