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OT 441: Neuroscience - Summer 2017 > Cognition: Language... (15 A) EXAM 4 > Flashcards

Cognition: Language... (15 A) EXAM 4 Flashcards

1
Q

The use of complex abstract symbols to represent one’s perception of the world to another:

A

Language

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2
Q

T or F: Language is both innate and learned, verbal and nonverbal?

A

True

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3
Q

Language is located on which area of the brain?

A

Lateral surface of LEFT hemisphere

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4
Q

Language pathway from auditory cortex:

A

Primary auditory area –> secondary auditory area –> Wernicke’s Area –> Arcuate Fasciculous –> Broca’s Area –> Lateral surface of motor cortex (because face is most lateral)

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5
Q

Wernicke’s Area

A

Responsible for the recognition and comprehension of words

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6
Q

Broca’s Area

A

Responsible for producing coherent speech (NOT motor, sends instructions to UMN).

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7
Q

Arcuate fasciculus

A

The pathway connecting Wernicke’s Area and Broca’s area

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8
Q

Three key features of language:

A
  1. Wernicke’s Area
  2. Broca’s Area
  3. Arcuate Fasciculus
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9
Q

What is a disturbance of language caused by an insult to specific regions of the brain?

A

Aphasia

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10
Q

T or F: Aphasia is similar to dysarthria (slurred speech) and dysphonia (tightness of larynx)?

A

FALSE, Aphasia is caused by trauma to brain, dysarthria and dysphonia are mechanical disorders of speech

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11
Q

What is the most common cause of Aphasia?

A

Traumatic brain injury, stroke (cerebrovascular accident)

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12
Q

Wernicke’s Aphasia is caused by damage where?

A

PTO area

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13
Q

What disorder is characterized by deficit in comprehension of language? (listening to other people speak is meaningless)

A

Wernicke’s Aphasia

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14
Q

Which disorder is characterized by meaningless speech and meaningly phrases that may be repeated?

A

Wernicke’s Aphasia

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15
Q

Paraphrasia:

A

Word substitutions

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16
Q

What are co-occuring disorders with Wernicke’s Aphasisa?

A

Alexia, Agraphia, Sensory & Motor impairments (hemiplegia), contralateral homonymous hemianopia

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17
Q

What is Broca’s Aphasia caused from?

A

Damage to Broca’s area in the frontal lobe

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18
Q

What disorder is characterized by difficulty getting words out

A

Broca’s Aphasia

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19
Q

What are co-occuring disorders with Broca’s Aphasia?

A

Difficulty reading aloud, writing impaired, R hemiplegia almost always present

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20
Q

What type of aphasia is damage to arcuate fasciculus?

A

Conduction Aphasia

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21
Q

T or F: In conduction aphasia the person can understand written and spoken language?

A

TRUE

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22
Q

Which disorder is this:
Can speak fluently, but speech does not make sense; can write, but writing does not make sense and there is a severe deficit in repeating out loud?

A

Conduction Aphasia

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23
Q

What disorder is caused by an extreme of the L lateral cerebrum?

A

Global Aphasia

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24
Q

Which disorder is this?
Deficits in all aspects of spoken and written language
Can’t produce understandable speech, comprehend spoken language, speak fluently, read or write

A

Global Aphasia

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25
Q

Alexia

A

Loss in reading the printed word

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26
Q

Dyslexia

A

Impairment in reading the printed word

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27
Q

Loss in reading the printed word

A

Alexia

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28
Q

Impairment in reading the printed word

A

Dyslexia

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29
Q

Acquired Alexia

A

A reading impairment that accompanies or is part of aphasia

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30
Q

Dyslexia:

A

Inability to read at a level commensurate with the person’s overall intelligence

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31
Q

Inability to read at a level commensurate with the person’s overall intelligence

A

Dyslexia

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32
Q

A reading impairment that accompanies or is part of aphasia

A

Acquired Alexia

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33
Q

Agraphia / Dysgraphia:

A

Loss/impairment of writing ability in the absence of limb dysfunction

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34
Q

Loss/impairment of writing ability in the absence of limb dysfunction

A

Agraphia / Dysgraphia

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35
Q

Acalculia

A

Inability to perform mathematical calculations

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36
Q

Inability to perform mathematical calculations

A

Acalculia

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37
Q

T or F: The right hemisphere typically does not process language?

A

True

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38
Q

Aprosodia

A

damage to right hemisphere that is a disturbance in the affective, nonverbal components of language

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39
Q

What is the right hemisphere associated with controlling?

A

Nonverbal communication, gestures, facila expressions, tone of voice, posture

40
Q

Right Wernicke’s

A

Interpretation of nonverbal signs from other people

41
Q

Right Broca’s

A

Instruction for producing nonverbal communication (emotional gestures, speech intonation)

42
Q

Damage to “R Wernicke’s”

A

Difficulty understanding nonverbal communication

ex: Statement said in jest vs. anger

43
Q

Damage to “R Broca’s”

A

Difficulty in producing nonverbal motor responses

ex: speak in monotone, lack emotional facial expressions, lack gestures

44
Q

Parietotemporal Occipital Association Area (PTO)

A

Cognitive intelligence, perception/spatial relationships, understanding language

45
Q

Dorsolateral Prefrontal Association Area

Anterior part of frontal lobe)

A

Goal-oriented behaviors, self-awareness, executive function

46
Q

Limbic Association Area

Ventral and medial prefrontal association cortex

A

Personality, emotion, motivation

47
Q

If there is damage to the dorsolateral prefrontal association area, what is the outcome?

A

Profound influence on compliance and outcomes, can negatively impact daily life (deciding on a goal, planning a goal, impulse control, etc…)

48
Q

If there is damage in the ventral and medial prefrontal association cortex, what is the outcome?

A

Can lead to inappropriate and risky behavior, poor social judgement (empathy, embarrassment, guilt, regret)

49
Q

What 5 structures recognize emotional stimuli and generate and perceive emotions?

A
  1. Amygdala
  2. Area 25
  3. Mediodorsal Nucleus of thalamus
  4. Ventral striatum
  5. Anterior insula
50
Q

When an individual’s reaction to an experience disrupts homeostais, this is called:

A

The stress response

51
Q

What activates in the physiological aspect of the stress response?

A
  1. Somatic nervous system (muscles)
  2. Sympathetic division of the ANS (blood flow, stop digestion)
  3. Neuroendocrine system (release stress hormones - HPA axis)
52
Q

What is the HPA Axis?

A

Hypothalamus, Pituitary, Adrenal

53
Q

What does the HPA axis do (broadly)?

A

Starts and stops the stress response through a cascade of events

54
Q

Steps in HPA Axis response:

A
  1. Hypothalamus: Neurons in hypothalamus synthesize and secrete CRH / CRF
  2. Pituitary: CRH causes pituitary gland to release ACTH
  3. Adrenal: ACTH acts on adrenal gland to produce cortisol (stress response) and other glucocorticoids
55
Q

What does the production of cortisol in the HPA Axis stress response do?

A
  1. Mobilizes energy
  2. Suppresses immune response
  3. Acts as anti-inflammatory agent
56
Q

What does the production of glucocorticoids in the HPA Axis stress response do?

A

Acts on the hypothalamus and other structures to suppress CRH and ACTH production

57
Q

What disorders is the HPA Axis involved in the neurobiology of?

A
  1. Panic disorder
  2. Phobias
  3. Post-traumatic stress disorder
  4. Major depressive disorder
58
Q

Excessive amounts of cortisol are associated with what?

A

Stress-related diseases

59
Q

Post-Traumatic stress disorder

A

Severe anxiety disorder that can develop after exposure to any event that results in psychological trauma

60
Q

In PTSD, there is an abnormality where?

A

HPA Axis

61
Q

Symptoms of PTSD:

A
  1. Reduced regulation of autonomic reactions to internal and external stimuli
  2. Decreased capacity to respond normally to emotional arousal or external stressors
  3. Hyperarousal and hyperstartle
62
Q

What disorder is characterized by a combination of symptoms that interfere with a person’s ability to work, sleep, study, eat and enjoy once-pleasurable activities?

A

Major Depressive Disorder

63
Q

Medications for Major Depressive Disorder:

A
  1. Selective serotonin reuptake inhibitors
  2. Serotonin and norepinephrine reuptake
  3. Tricyclics
  4. Monoamine oxidase inhibitors (MAO)
64
Q

Selective Serotonin Reuptake inhibitors (SSRI’s)

Prozac, Zoloft

A

Increase available 5HT (Serotonin) by blocking it from being reuptaken by presynaptic neuron

65
Q

Serotonin and Norepinephrine reuptake inhibitors (SNRI’s)

Symbalta and Effector

A

Increase available 5HT and NE

66
Q

Tricyclics

A

Inhibit reuptake of 5HT and NE, less specific, not selective what they are blocking

67
Q

Monoamine oxidase inhibitors (MAOI’s)

A

Prevent MAO from metabolizing the NE, 5HT and DA in the brain
(usually cause severe side effects so not used unless other drugs have been tried)

68
Q

Schizophrenia

A

A group of serious brain disorders in which reality is interpreted atypically. Results in positive, negative and cognitive symptoms

69
Q

Is Schizophrenia a chronic or acute condition?

A

Chronic, requires lifelong treatment

70
Q

Etiology of Schizophrenia

A

Idiopathic

typically develops in late adolescence/early adulthood when person is under a lot of stress/changes

71
Q

Neuroanatomical changes in Schizophrenia

A
  1. Reduction in the volume of gray matter (esp in frontal and temporal lobes)
  2. Hippocampus and Amygdala shrinks
  3. Enlarged ventricles
  4. Differences in brain activities in certain areas
  5. Imbalance in Neurotransmitters
72
Q

In Schizophrenia, Where is the reduction of gray matter most seen?

A

Frontal and temporal lobes

73
Q

What happens to the ventricles in Schizophrenia?

A

They become enlarged

74
Q

What happens in the hippocampus and amygdala in Schizophrenia?

A

They become reduced

75
Q

What are the positive symptoms of schizophrenia (things that are there that shouldnt be)?

A
  1. Hallucinations
  2. Delusions
  3. Thought Disorders
  4. Movement Disorders
76
Q

What are the negative symptoms of schizophrenia?

A
  1. Alogia (Speaking less)
  2. Blunted / flat affect
  3. Avolition
  4. Anhedonia
77
Q

Blunted/Flat affect

A

Reduction in range/intensity of emotional expression

78
Q

Avolition

A

Difficulty/loss of ability to initiate and persist in goal-directed behavior

79
Q

Anhedonia

A

Lack of pleasure in everyday life

80
Q

Cognitive symptoms of Schizophrenia

A
  1. Poor executive functioning
  2. Trouble focusing or paying attention
  3. Problems with working memory
81
Q 
Neurochemical Hypothesis:
Dopamine Hypothesis (Schizophrenia):
Too much dopamine
A

Over activity in the mesolimbic DA pathway

causes positive symptoms because DA binds over and over again

82
Q 
Neurochemical Hypothesis:
Dopamine Hypothesis (Schizophrenia):
Too little dopamine
A

Under activity in the mesocortical DA pathway causes negative and cognitive symptoms because there is not enough DA binding

83
Q

Neurochemical Hypothesis:
Serotonin Hypothesis (Schizophrenia)
Hypoactivity
(Likely to be indirectly related to Schizophrenia)

A

Decreased density of serotonin 5-HT(2) receptors int he prefrontal cortex causing negative and cognitive symptoms

84
Q

Neurochemical Hypothesis:
Serotonin Hypothesis (Schizophrenia)
Hyperactivity
(Likely to be indirectly related to Schizophrenia)

A

Too much 5HT hanging out in synaptic cleft

85
Q

Neurochemical Hypothesis:

NMDA receptor hypofunction:

A

Dysfunctional glutamatergic neurotransmission in prefrontal cortex

86
Q

What happens in NMDA receptor hypofunction to the mesolimbic DA pathway?

A

Can’t inhibit mesolimbic DA neurons –> mesolimbic hyperactivity –POSITIVE symptoms

87
Q

What happens in NMDA receptor hypofunction to the mesocortical DA pathway?

A
  1. Can’t excite mesocortical DA pathways –> mesocortical hypoactivity –> negative and cognitive symptoms
88
Q

What happens TYPICALLY in the mesolimbic and mesocortical pathways with NMDA receptors?

A
  1. Mesolimbic DA pathway is inhibited

2. Mesocortical DA neurons are excited

89
Q

Traditional Antipsychotic Drugs (1st generation) for Schizophrenia manage what symptoms?

A
  1. Manage POSITIVE symptoms
90
Q

Traditional Antipsychotic Drugs (1st generation) for Schizophrenia: How do they work?

A

Block ALL dopamine (D2) receptors

91
Q

What is a side effect of blocking ALL D2 receptors (1st gen Schiz drugs)

A

Tardive Dyskinesia

92
Q

Why is Tardive Dyskinesia developed with the use of 1st gen antipsychotic drugs for Schiz?

A

Because of the long term use of the antipsychotic drugs (the D2 receptors become hypersensitive)

93
Q

What is Tardive Dyskinesia?

A

Abnormal, involuntary movements, especially of the face and tongue (grimacing, tongue protrusion, lip smacking, puckering/pursing of lips)

94
Q

What symptoms do Atypical anti-psychotic medications (2nd gen) manage for Schiz?

A

Positive and negative symptoms

95
Q

What receptors do atypical anti-psychotic meds have an effect on (Schiz)?

A

Dopamine and Serotonin receptors

Dont block all D2 receptors, but rather specific DA receptors

96
Q

With atypical anti-psychotic drugs there are fewer ______ side effects but increased chance of ______ side effects?

A

Fewer motor side effects

Increased chance of metabolic side effects

97
Q

Examples of atypical anti-psychotic medications (Schiz)

A
  1. Clozapine
  2. Risperidone
  3. Olanzapine

OT 441: Neuroscience - Summer 2017 (11 decks)

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