Lecture 15 - Language, Emotions, Mental Health Flashcards
1
Q
Where is language located?
A
Lateral surface of LEFT hemisphere
2
Q
What are the 3 most important structures involved in language?
A
- Wernicke’s area: responsible for recognition/comprehension of words
- Broca’s area: responsible for producing coherent speech
- Arcuate Fasiculus: pathway connecting Wernicke’s and Broca’s
3
Q
What is language?
A
Use of complex abstract symbols to represent one’s perception of world to another (both innate and learned)
4
Q
Pathway from auditory cortex…
A
- Primary Auditory area (hears something)
- Secondary auditory area (gets sent here)
- Wernicke’s area (sound is comprehended)
- Arcuate fasciculus (pathway from W to B)
- Broca’s area (instruction for language output)
- Lateral surface of motor cortex
- Cotricobulbar tract -> cranial nerves –> muscle
5
Q
Area responsible for understanding/recognizing words
A
Wernicke’s
6
Q
Area responsible for producing coherent speech
A
Broca’s
7
Q
Pathway connecting Wernicke’s and Broca’s
A
Arcute Fasciculus
8
Q
Give disorders of language
A
- Wernicke’s (receptive) Aphasia
- Broca’s (expressive) Aphasia
- Conduction aphasia
- Global Aphasia
9
Q
What is aphasia?
A
- Disturbance of language caused by insult to specific regions of brain
- Distinguished by dysphonia (difficulty in speaking) and dysarthria (unclear articulation of speech)
- Common cause is brain injury, stroke
- Symptoms may not always fall into one category
10
Q
Common cause of aphasia?
A
traumatic brain injury, stroke (cerebrovascular)
11
Q
Wernicke’s Aphasia
A
- Damage to Wernicke’s area (Left PTO)
- Deficit in comprehension of language
- Can produce words, but can’t understand
12
Q
Wernicke’s Aphasia language include…
A
- Meaningless speech - meaningless phrases that may be repeated
- Paraphrasia - word substitution
13
Q
These disorders can co-occur with Wernicke’s Aphasia
A
alexia, agraphia, hemiplegia, contralateral homonymous hemianopia
14
Q
Disorder characterized by deficit in comprehension of language
A
Wernicke’s Aphasia
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
16
Q
Broca’s Aphasia
A
Expressive. Damage to Broca’s area. Can understand everything but hard to produce verbal/written language
17
Q
Can’t produce verbal/written language, but can comprehend what you are saying. Answer by pointing.
A
Broca’s Aphasia
18
Q
Damage to frontal lobe, can’t send command to corticobulbar tract to talk
A
Broca’s Aphasia
19
Q
No language output, generate habitual phrases, slow deliberate speech with simple sentences, bad grammar, aware of errors
A
Broca’s Aphasia
20
Q
This disorder includes co-occurring disorders like difficult reading aloud, writing impaired, right hemiplegia always present
A
Broca’s Aphasia
21
Q
Where does secondary auditory cortex send info to?
A
Wernicke’s Area
22
Q
Where do corticobulbar tract connect to?
A
Cranial Nerves
23
Q
“Ah… Monday… ah, Dad and Paul… hospital. Two… ah… Example of what disorder?
A
Broca’s Aphasia
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
25
Damage to arcuate fasciculus is called...
Conduction Aphasia
26
Conduction Aphasia
Can speak fluently and expressive self, comprehend language but difficulty repeating phrases as they stumble over words they are attempting to pronounce (rare)
27
Global Aphasia
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.
28
Dyslexia
Inability to read at level commensurate with person's overall intelligence (less severe than alexia)
29
Acquired Alexia
Reading impairment that accompanies aphasia
30
Agraphia/Dysgraphia
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)
31
Disorders of reading and writing
Alexia/Dyslexia, Agraphia/Dysgraphia
32
Inability to perform mathematical calculations
Acalculia (think Calculus)
33
Damage to Left Hemisphere means...
Disorders of language
34
What is considered the non dominant hemisphere?
Right hemisphere
35
Hemisphere associated with nonverbal communication - gestures, facial expressions, tone of voice, posture
Right hemisphere
36
Aprosodia
Damage to right hemisphere, disturbance in affective nonverbal components of language
37
This area of brain interprets nonverbal signs from other people
Right Wernicke
38
This area has instructions producing nonverbal communication
Right Broca's
39
Damage to R. Wernicke means...
Person has difficulty understanding nonverbal communication (someone yells, they won't understand it means anger)
40
Damage to R. Broca's means...
Person has difficulty producing nonverbal motor responses (lack gesture, monotone, no facial expression)
41
Goal-oriented behaviors, self awareness
Dorsolateral Prefrontal Association (anterior part of frontal lobe)
42
Cognitive intelligence, perception/spatial, understanding language
PTO (Parietotemporal Occipital Association Area)
43
Personality, emotion, motivation
Ventral and Medial Prefrontal (limbic association area)
44
What are executive functions?
Correct mistakes, impulse control, follow plan, act in socially appropriate way, decide on a goal, judgment, mental flexibility, dividing attention
45
What main area controls executive function?
Dorsolateral Prefrontal Cortex
46
What happens if damage in Dorsolateral Prefrontal Cortex?
Difficulty planning, initiating, monitoring, maintaining behavior. (DLPC -> caudate nucleus -> globes pallicus -> ventral anterior nucleus thalamus
47
Damage to ventral and medial prefrontal
Emotion and personality (interfere with emotional response to emotional events, empathy, embarrassment, guilt, regret, personality, and can lead to risky behavior
48
What main areas control emotions?
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
Why should OT care about emotion?
Type of injury can influence occupation you choose to engage in
50
What does the HPA-axis/stress response do?
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
How does HPA-axis work?
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
What happens if stress response is prolonged?
Excessive amounts of cortisol floods system, causes phobias, panic disorder, PTSD, depressive disorder
53
What is PTSD?
Severe anxiety that can develop after exposure to event resulting in psychological trauma (post traumatic stress disorder), abnormality in HPA axis
54
Reduced relation of autonomic reactions to stimuli, decreased capacity to respond normally to emotional arousal, hyperarousal, hyper startle, disturbed appraisal process, learning, memory
Chronic physiologic arousal of PTSD
55
Characterized by combo of symptoms that interfere with person's ability to work, sleep, eat, study, enjoy pleasurable activities
MDD (Major Depressive Disorder) - more often person experience multiple episodes, study shows by 2020, MDD will be second leading cause of disability
56
Symptoms of MDD
sleep disturbance, fatigue, change in eating, decrease sex drive, poor memory, thoughts of dying, withdraws from social acts, etc
57
SSRI (increase available serotonin), SNRI (increase available serotonin and Cymbalta
Medications for major depressive disorder
58
Group of serious brain disorders in which reality is interpreted atypically, results in positive, negative, and cognitive symptoms
Schizophrenia (chronic, require lifelong treatment)
59
Etiology of Schizophrenia
Idiopathic (no idea what causes it), interaction with genes and environment (1% population, 10% relative) can show symptoms of stress during late adolescent
60
What are some neuroanatomical changes that occur in schizophrenia?
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
What are the 3 symptoms of Schizophrenia?
1. Positive
2. Negative
3. Cognitive
62
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)
Positive Symptoms (things that are there but shouldn't be)
63
Negative symptoms
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
People with these types of symptoms for Schiz. need help with everyday tasks
Negative symptoms
65
Alogia
Slow/lack of speech
66
Anhedonia
lack of pleasure in everyday life
67
Cognitive symptoms of Schiz
poor executive functioning, trouble focusing, problems with working memory (hard to lead normal life, cause emotional distress)
68
Which hypothesis points at positive symptoms?
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
Which hypothesis points at negative symptoms?
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
What is serotonin important in?
perception, attention, mood, aggression, sexual drive, appetite, motor behavior, sleep
71
Which hypothesis points at negative and positive symptoms?
NMDA receptor hypofunction: dysfunctional glutamatergic neurotransmission in prefrontal cortex because it inhibits mesolimbi DA pathway and excites mesocrotical DA neurons
72
Traditional antipsychotic drugs (first generation)
Manage positive symptoms, blocked all D2 receptors, decrease amount of DA, influence neurotransmission
73
Side effect of first generation drugs?
Tardive Dyskinesia (D2 becomes hypersensitive causing abnormal involuntary movements of face and tongue)
74
Atypical anti-psychotic medications (2nd generation)
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
Side effects of 2nd generation drugs?
Fewer motor effects but increase in metabolic side effects.
76
What is Tardive Dyskinesia?
- 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
What is schizophrenia?
A group of serious brain disorders in which reality is interpreted atypically, resulting in positive, negative, and cognitive symptoms.
78
What are the neural mechanisms involved in schizophrenia? What neurotransmitters?
- 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
Selective serotonin reuptake inhibitors such as Prozac are effective for some because...
they are blocking selective serotonin receptors (allow more serotonin in cleft)
80
Client has damage to most anterior portion of frontal lobe what kind of deficits expected?
Personality, executive function
81
Selective serotonin reuptake inhibitors such as Prozac are effective for some because...
they are blocking selective serotonin receptors (allow more serotonin in cleft)
82
Client has damage to most anterior portion of frontal lobe what kind of deficits expected?
Personality, executive function
83
Explain one theory that impacts positive and negative symptoms
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
2 neurotransmitters in pathways
NMDA receptors opened by glutamate (in hypothesis of positive and negative symptoms)
