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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4 types of learning
* 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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Hebb Rule-
repeatedly activating an unconditioned stimulus with the excitation of an automatic response, you strengthen the weak/CS by pairing.
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HM
- 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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Hippocampus
short term memory and memory consolidation into LTM
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Hippocampal formation
- 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.
30
long-term potentiation (LTP)
A long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high-frequency activity.
31
Huntington's
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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Parkinsons
* 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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2 Types of Apraxia
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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Apraxia
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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Monosynaptic stretch reflex
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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Agonist muscle
contraction produces or facilitates a movement.
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Antagonist muscle
contraction resists or reverses a movement.
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Cerebellum Disorder
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
Cerebeller Disorder may include:
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
Primary Motor Cortex
• (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.
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Frontal Association Cortex
* 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
Primary Motor Strip
• 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.
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Primary Motor Circuit,
corticospinal tract, pyramidal tract, descending pyramidal
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Basil ganglia
Extra pyramidal movements. 5 major nuclei include putamen, caudate nucleus, globus pallidus, subthalamic nucleus and substantia nigra.
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Long-term Potentiation
long-term increase in excitability of neuron to particular synaptic input caused by repeated high-frequency activity
46
Pyramidal Cell
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
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Perforant Path
system of axons that travel from cells in entorhinal cortex to dentate gyrus granule
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Entorhinal cortex
region of limbic cortex that provides major source of inputs to hippocampal formation
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Hippocampal Formation
highly plastic structure of temporal lobe, includes Ammons horn, dentate gyrus, subiculum
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Dentate Gyrus
Part of hippocampal formation; receives inputs from entorhinal cortex and projects to pyramidal cells of field CA3 of hippocampus proper via granule cells
51
Hippocampus
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
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4 types of Learning
1) Perceptual (recognition) 2) Stimulus-Response (CC, OC) 3) Motor (muscle memory) 4) Relatioal (akin to shaping)
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Anterograde Amnesia
think ANTICIPATE | Amnesia from damage forward/inability to make new memories
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Retrograde Amnesia
think RETROACTIVE | Amnesia from before (usually just before and surrounding) damage
55
Korsakoffs
permanent anterograde amnesia via alcoholism or malnutrition
56
confabulation
Reporting of events that never happened
57
2 Pathways for Conditioning
1) Direct transcortical connections, episodic memory | 2) Connections via basal ganglia and thalamus, over-learned behaviors/cerebellum
58
James-Lange Theory
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
Hemisphere Dominance
Right: comprehension of emotion, tone Left: language
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Volitional Facial Paraesis
You can't smile when you decide to but you usually can when you accidentally/naturally do
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Emotional Facial Paraesis
You can't smile when you are happy/laughing and naturally would
62
Kluver-Bucy Syndrome
Breakdown in fear response Increased aggression, sexuality, eating/drinking, memory impairment, increased impulsivity
63
Ventromedial Prefrontal Cortex
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
Ventral Prefrontal Cortex
Involved in automatic emotional response and control f complex behaviors (such as appropriate social demeanor)
65
Amygdala
(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
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Aphasias
``` Broca's Wernicke's Pure Word Deafness Conduction Anomia Transcortical Sensory ```
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Broca's Aphasia
Comprehends but cannot talk
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Wernicke's Aphasia
Talks but cannot comprehend or follow instructions to name or repeat
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Pure Word Deafness
Talks and Names/Identifies but neither comprehends not repeats Damage to Wernicke's area &/or connectors to PAC
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Conduction Aphasia
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
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Anomia Aphasia
Can speak, comprehend, repeat but cannot NAME/identify "tip of the tongue" Parietal/temporal damage regions A-NOMia: without name/label
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Transcortical Sensory
Can speak and repeat but can neither comprehend nor name Damage to Posterior Language Area
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Huntington's
HYPERkinetic neurological disease Degeneration of caudate nucleus and putamen enlarged lateral ventricles uncontrollable jerking, writing, psychiatric symptoms; Cohrea. Anticipation and Amplification
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Parkinson's
HYPOkinetic movement disorder Results from degradtion of cell bodies and dopaminergic neurons in Substantia Nigra (BG) TRAP
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Parkinson's TRAP
Tremor; Rigidity; Akinesia (psychomotor slowing); Postural Instability
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Limb Apraxia: Callosal
left hand due to damage to anterior corpus callosum
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Limb Apraxia: Sympathetic
left hand, right arm/hand impairment due to left frontal lob
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Limb Apraxia: Left Parietal
damage to left parietal lobe, results in difficulty producing sequenced movement on verbal request
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Constructional Apraxia
Difficulty drawing pictures of geometrical qualities
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Apraxia
A-Prax | not able to do purposeful movement w/o weakness orparalysis (especailly over-learned/practiced)
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Agonist Muscle
contraction produces or facilitates a movement think: facilitates movement of a plot, e.g. agonist character
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Antagonist Muscle
contraction resists or reverses a movement think: hero of the story/antagonist character
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Monosynaptic stretch reflex
Reflex when muscle contracts to quick stretch | involves sensory neuron and motor neuron, one syanpse betwen them
84
Cerebellum
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
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Nystagmus
involuntary rapid eye movement
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Dysmetria
disordered measure of distance in muscular acts
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Dysdiadochokinesia
disordered alternation of movement
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Intention Tremor
Tremor during purposeful movements
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Cerebral Coorniation Issues from Alcohol
wide gate, affects of vermis