Lecture 15 - Language, Emotions, Mental Health Flashcards

1
Q

Where is language located?

A

Lateral surface of LEFT hemisphere

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2
Q

What are the 3 most important structures involved in language?

A
  1. Wernicke’s area: responsible for recognition/comprehension of words
  2. Broca’s area: responsible for producing coherent speech
  3. Arcuate Fasiculus: pathway connecting Wernicke’s and Broca’s
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3
Q

What is language?

A

Use of complex abstract symbols to represent one’s perception of world to another (both innate and learned)

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4
Q

Pathway from auditory cortex…

A
  1. Primary Auditory area (hears something)
  2. Secondary auditory area (gets sent here)
  3. Wernicke’s area (sound is comprehended)
  4. Arcuate fasciculus (pathway from W to B)
  5. Broca’s area (instruction for language output)
  6. Lateral surface of motor cortex
  7. Cotricobulbar tract -> cranial nerves –> muscle
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5
Q

Area responsible for understanding/recognizing words

A

Wernicke’s

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6
Q

Area responsible for producing coherent speech

A

Broca’s

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7
Q

Pathway connecting Wernicke’s and Broca’s

A

Arcute Fasciculus

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8
Q

Give disorders of language

A
  1. Wernicke’s (receptive) Aphasia
  2. Broca’s (expressive) Aphasia
  3. Conduction aphasia
  4. Global Aphasia
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9
Q

What is aphasia?

A
  1. Disturbance of language caused by insult to specific regions of brain
  2. Distinguished by dysphonia (difficulty in speaking) and dysarthria (unclear articulation of speech)
  3. Common cause is brain injury, stroke
  4. Symptoms may not always fall into one category
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10
Q

Common cause of aphasia?

A

traumatic brain injury, stroke (cerebrovascular)

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11
Q

Wernicke’s Aphasia

A
  1. Damage to Wernicke’s area (Left PTO)
  2. Deficit in comprehension of language
  3. Can produce words, but can’t understand
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12
Q

Wernicke’s Aphasia language include…

A
  1. Meaningless speech - meaningless phrases that may be repeated
  2. Paraphrasia - word substitution
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13
Q

These disorders can co-occur with Wernicke’s Aphasia

A

alexia, agraphia, hemiplegia, contralateral homonymous hemianopia

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14
Q

Disorder characterized by deficit in comprehension of language

A

Wernicke’s Aphasia

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15
Q

Can speak, but words mean nothing. People with this disorder are unaware that what they say makes no sense.

A

Wernicke’s Aphasia

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16
Q

Broca’s Aphasia

A

Expressive. Damage to Broca’s area. Can understand everything but hard to produce verbal/written language

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17
Q

Can’t produce verbal/written language, but can comprehend what you are saying. Answer by pointing.

A

Broca’s Aphasia

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18
Q

Damage to frontal lobe, can’t send command to corticobulbar tract to talk

A

Broca’s Aphasia

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19
Q

No language output, generate habitual phrases, slow deliberate speech with simple sentences, bad grammar, aware of errors

A

Broca’s Aphasia

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20
Q

This disorder includes co-occurring disorders like difficult reading aloud, writing impaired, right hemiplegia always present

A

Broca’s Aphasia

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21
Q

Where does secondary auditory cortex send info to?

A

Wernicke’s Area

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22
Q

Where do corticobulbar tract connect to?

A

Cranial Nerves

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23
Q

“Ah… Monday… ah, Dad and Paul… hospital. Two… ah… Example of what disorder?

A

Broca’s Aphasia

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24
Q

“Ah, where do I start the tesseineme from? They tell me that my brain, physically, my brain is perfect, the attitudes is fine, but the silence now.” Example of what disorder?

A

Wernicke’s Aphasia

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25
Q

Damage to arcuate fasciculus is called…

A

Conduction Aphasia

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26
Q

Conduction Aphasia

A

Can speak fluently and expressive self, comprehend language but difficulty repeating phrases as they stumble over words they are attempting to pronounce (rare)

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27
Q

Global Aphasia

A

Extreme lesion of Left lateral cerebrum (both Wernicke’s and Broca’s). Deficit in all aspects of spoken and written language. Can’t read, write, speak fluently, understand.

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28
Q

Dyslexia

A

Inability to read at level commensurate with person’s overall intelligence (less severe than alexia)

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29
Q

Acquired Alexia

A

Reading impairment that accompanies aphasia

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30
Q

Agraphia/Dysgraphia

A

Loss/impairment of ability in dysfunction, writing (spelling errors, impaired word order and other manifestations of faulty written language (not damage to limb but damage to brain)

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31
Q

Disorders of reading and writing

A

Alexia/Dyslexia, Agraphia/Dysgraphia

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32
Q

Inability to perform mathematical calculations

A

Acalculia (think Calculus)

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33
Q

Damage to Left Hemisphere means…

A

Disorders of language

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34
Q

What is considered the non dominant hemisphere?

A

Right hemisphere

35
Q

Hemisphere associated with nonverbal communication - gestures, facial expressions, tone of voice, posture

A

Right hemisphere

36
Q

Aprosodia

A

Damage to right hemisphere, disturbance in affective nonverbal components of language

37
Q

This area of brain interprets nonverbal signs from other people

A

Right Wernicke

38
Q

This area has instructions producing nonverbal communication

A

Right Broca’s

39
Q

Damage to R. Wernicke means…

A

Person has difficulty understanding nonverbal communication (someone yells, they won’t understand it means anger)

40
Q

Damage to R. Broca’s means…

A

Person has difficulty producing nonverbal motor responses (lack gesture, monotone, no facial expression)

41
Q

Goal-oriented behaviors, self awareness

A

Dorsolateral Prefrontal Association (anterior part of frontal lobe)

42
Q

Cognitive intelligence, perception/spatial, understanding language

A

PTO (Parietotemporal Occipital Association Area)

43
Q

Personality, emotion, motivation

A

Ventral and Medial Prefrontal (limbic association area)

44
Q

What are executive functions?

A

Correct mistakes, impulse control, follow plan, act in socially appropriate way, decide on a goal, judgment, mental flexibility, dividing attention

45
Q

What main area controls executive function?

A

Dorsolateral Prefrontal Cortex

46
Q

What happens if damage in Dorsolateral Prefrontal Cortex?

A

Difficulty planning, initiating, monitoring, maintaining behavior. (DLPC -> caudate nucleus -> globes pallicus -> ventral anterior nucleus thalamus

47
Q

Damage to ventral and medial prefrontal

A

Emotion and personality (interfere with emotional response to emotional events, empathy, embarrassment, guilt, regret, personality, and can lead to risky behavior

48
Q

What main areas control emotions?

A
  1. Amygdala
  2. Area 25
  3. Mediodorsal nucleus of thalamus
  4. Ventral striatum
  5. Anterier insula
  6. Voluntary emotional regulation in dorsolateral prefrontal cortex
49
Q

Why should OT care about emotion?

A

Type of injury can influence occupation you choose to engage in

50
Q

What does the HPA-axis/stress response do?

A

Complex system controlling stress response, fight or flight behavior. Occurs when person’s reaction to experience disrupts homeostasis -> activation of somatic NS, sympathetic division, nueroendocrine system (release stress hormone HPA axis)

51
Q

How does HPA-axis work?

A

Produce cortisol - stress response which mobilizes energy, suppresses immune response, acts as anti-inflammatory agent (secrete CRH causes pituitary gland release ACTH to produce Cortisol)

52
Q

What happens if stress response is prolonged?

A

Excessive amounts of cortisol floods system, causes phobias, panic disorder, PTSD, depressive disorder

53
Q

What is PTSD?

A

Severe anxiety that can develop after exposure to event resulting in psychological trauma (post traumatic stress disorder), abnormality in HPA axis

54
Q

Reduced relation of autonomic reactions to stimuli, decreased capacity to respond normally to emotional arousal, hyperarousal, hyper startle, disturbed appraisal process, learning, memory

A

Chronic physiologic arousal of PTSD

55
Q

Characterized by combo of symptoms that interfere with person’s ability to work, sleep, eat, study, enjoy pleasurable activities

A

MDD (Major Depressive Disorder) - more often person experience multiple episodes, study shows by 2020, MDD will be second leading cause of disability

56
Q

Symptoms of MDD

A

sleep disturbance, fatigue, change in eating, decrease sex drive, poor memory, thoughts of dying, withdraws from social acts, etc

57
Q

SSRI (increase available serotonin), SNRI (increase available serotonin and Cymbalta

A

Medications for major depressive disorder

58
Q

Group of serious brain disorders in which reality is interpreted atypically, results in positive, negative, and cognitive symptoms

A

Schizophrenia (chronic, require lifelong treatment)

59
Q

Etiology of Schizophrenia

A

Idiopathic (no idea what causes it), interaction with genes and environment (1% population, 10% relative) can show symptoms of stress during late adolescent

60
Q

What are some neuroanatomical changes that occur in schizophrenia?

A
  1. Reduction in volume of gray matter (frontal and temporal)
  2. Reduced size of hippocampus and amygdala
  3. Enlarged ventricles
  4. Diff in brain activity in certain areas
  5. *** imbalance in NTs **
61
Q

What are the 3 symptoms of Schizophrenia?

A
  1. Positive
  2. Negative
  3. Cognitive
62
Q

Hallucinations (hearing things not there is most common), delusions (radio waves talking to me), thought disorders (thought blocking, neologism make up words, movement disorders (repeating same movements)

A

Positive Symptoms (things that are there but shouldn’t be)

63
Q

Negative symptoms

A

Things that should be there but are not

  1. Alogia- slow/lack of speech
  2. blunted affect - underlying NT issues, reduction in range of emotional expression
  3. Avolition - difficulty initiating in goal directed behavior
  4. Anhedonia - lack pleasure in everyday life
64
Q

People with these types of symptoms for Schiz. need help with everyday tasks

A

Negative symptoms

65
Q

Alogia

A

Slow/lack of speech

66
Q

Anhedonia

A

lack of pleasure in everyday life

67
Q

Cognitive symptoms of Schiz

A

poor executive functioning, trouble focusing, problems with working memory (hard to lead normal life, cause emotional distress)

68
Q

Which hypothesis points at positive symptoms?

A
  1. Dopamine hypothesis (too much dopamine activity) midbrain to limbic
  2. Serotonin hyperactivity (too much serotonin)
  3. NMDA receptor hypofunction (can’t inhibit mesolimbic pathway, becomes hyperactive
    (mainly traditional dugs)
69
Q

Which hypothesis points at negative symptoms?

A
  1. Dopamine hypothesis (not enough dopamine in pathway) decreased activity midbrain to cortex
  2. Serotonin hypoactivity (too little serotonin)
  3. NMDA receptor hypofunction (can’t excite mesocortical pathways, mesocortical hypoactive
70
Q

What is serotonin important in?

A

perception, attention, mood, aggression, sexual drive, appetite, motor behavior, sleep

71
Q

Which hypothesis points at negative and positive symptoms?

A

NMDA receptor hypofunction: dysfunctional glutamatergic neurotransmission in prefrontal cortex because it inhibits mesolimbi DA pathway and excites mesocrotical DA neurons

72
Q

Traditional antipsychotic drugs (first generation)

A

Manage positive symptoms, blocked all D2 receptors, decrease amount of DA, influence neurotransmission

73
Q

Side effect of first generation drugs?

A

Tardive Dyskinesia (D2 becomes hypersensitive causing abnormal involuntary movements of face and tongue)

74
Q

Atypical anti-psychotic medications (2nd generation)

A

Manage both positive and negative symptoms, work on DA and 5HT receptors (don’t block all D2 receptors but specific ones) drugs include Clozapine, Ripseridone, Olanzapine

75
Q

Side effects of 2nd generation drugs?

A

Fewer motor effects but increase in metabolic side effects.

76
Q

What is Tardive Dyskinesia?

A
  • Disorder due to long-term treatment with antipsychotic drugs
  • Abnormal, involuntary movements, especially of the face & tongue.
  • With long-term use of traditional antipsychotic drugs that block all the D2 receptors, the nigrostriatal pathway becomes hypersensitive to DA, resulting in unusual movements; especially in the mouth & tongue
77
Q

What is schizophrenia?

A

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

78
Q

What are the neural mechanisms involved in schizophrenia? What neurotransmitters?

A
  • Excess DA in the mesolimbic DA pathway, causing positive symptoms; DA
  • Underactivity in mesocortical DA pathway, causing negative symptoms; DA
  • Decreased 5HT receptors in the prefrontal cortex, possibly (negatively) affecting: mood, aggression, sexual drive, appetite, motor behavior, sleep; 5HT
  • 5HT hyperactivity: possibly (positively) affecting: mood, aggression, sexual drive, appetite, motor behavior, sleep → causing positive symptoms; 5HT
  • NMDA receptor hypofunction: excess DA in mesolimbic pathway; underactivity (not enough DA) in mesocortical pathway → leading to both positive and negative symptoms; glutamate
79
Q

Selective serotonin reuptake inhibitors such as Prozac are effective for some because…

A

they are blocking selective serotonin receptors (allow more serotonin in cleft)

80
Q

Client has damage to most anterior portion of frontal lobe what kind of deficits expected?

A

Personality, executive function

81
Q

Selective serotonin reuptake inhibitors such as Prozac are effective for some because…

A

they are blocking selective serotonin receptors (allow more serotonin in cleft)

82
Q

Client has damage to most anterior portion of frontal lobe what kind of deficits expected?

A

Personality, executive function

83
Q

Explain one theory that impacts positive and negative symptoms

A

In the mesolimbic pathway if there is functioning pathway should be inhibit. If not inhibiting, there will be hyperactivity of mesolimbic pathway leading to positive symptoms. Other pathway is mesocortical, NMDA usually excite, but if not exciting pathway it will be underactivated leading to negative cognitive symptoms.

84
Q

2 neurotransmitters in pathways

A

NMDA receptors opened by glutamate (in hypothesis of positive and negative symptoms)