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Neuropsychology Flashcards

1
Q

What are the two main divisions of the Nervous System?

A
  1. Central: brain + spinal cord
  2. Peripheral: afferent nerves (sensory or receptor nerves) that carry info from sense organs to CNS and efferent nerves (motor/effector nerves) that carry info from CNS to muscles/glands
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2
Q

3 Divisions of the Brain

A
  1. Hind brain
  2. Mid brain
  3. Fore brain
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3
Q

What are the 5 groups of the spinal cord?

A
  1. Cervical
  2. Thoracic
  3. Lumbar
  4. Sacral
  5. Coccygeal
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4
Q

What are afferent nerves?

A

AKA Sensory or Receptor nerves

Carry info from sense organs to the CNS

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5
Q

What are efferent nerves?

A

AKA Motor or Effector nerves

Carry info from CNS to the muscles and glands

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6
Q

What are the two brances of the Peripheral Nervous System?

A
  1. Somatic Nervous System
  2. Autonomic Nervous System
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7
Q

What is the role of the Somatic Nervous System?

A

Controls action of skeletal muscles

Voluntary movement

Relays signals from the senses

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8
Q

What is the role of the Autonomic Nervous System?

A

Contains nerves that are around smooth muscles, glands (e.g. all our organs)

Regulates things that are involuntary (e.g. digestion, respiration, heartrate)

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9
Q

What are the 2 Branches of the Autonomic Nervous System?

A
  1. Sympathetic NS: mobilizes resources to prepare for threat
  2. Parasympathetic NS: deactivates the F-F-F response. Active during states of relaxation
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10
Q

What are the 3 parts of a neuron?

A
  1. Cell Body: responsible for protein synthesis, contains the nucleus, mitochondria
  2. Dendrites: short fibers that come out of cell body. Respond to stimulation from other neuros and carry it to cell body
  3. Axon: carries info away from cell body
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11
Q

What is Conduction?

Other terms: resting potential, depolarization, action potential

A

The electrochemical process through which info is received and processed within a nerve cell

Resting Potential: inside of cell negatively charged, outside positively charged

Stimulation from other cells can lead to depolarization which triggers an action potential

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12
Q

What is Synaptic Transmission?

A

The transmission of info from one neuron to another

NT’s released following an action potential, float across to other neurons receptor site

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13
Q

2 processes of synaptic transmission termination

Reuptake & Enzynmatic Degradation

A
  1. Reuptake: terminal buttons suck in the excess NT’s and store for future
  2. Enzymatic Degradation: enzyms around the synapse break down the NT which is then removed as waste
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14
Q

What are the 2 chemical messengers of the nervous system?

A
  1. Neurotransmitters
  2. Hormones
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15
Q

What is a Neuromodulator?

A

A NT that increases or decreases the sensitive of neurons to the effects of other NT’s

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16
Q

What are Cholingeric Neurons?

A

Neurons that produce Acetylcholine

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17
Q

Acetylcholine (ACh): what does it do?

A

Involved in:
* Voluntary movement
* Learning & memory
* Sexual behaviour
* Sleep

Can be inhibitory or excitatory

Degeneration in the hippocampus associated with aging and Alzheimers

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18
Q

Where is Dopamine released in the brain?

A

Basal ganglia
Limbic system
Frontal lobes

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19
Q

What does Dopamine do?

A

Make me happy
Movement
Learning
Mood

Reinforcing effects of stimulants, opiates, nicotine

Abnormal levels linked to: depression, schizophrenia, Tourette’s, ADHD, Huntington’s, Parkinson’s

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20
Q

What does Norepinephrine do?

A

Mood
Dreaming
Learning
Automatic responses

Abrnomal levels: depression, mania, panic disorder

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21
Q

What does Serotonin do?

A

Regulates anxiety, mood, aggression
Memory
Pain
Sleep
Appetite
Sexuality

Low Levels: depression, aggression, PTSD, PCD, Bulimia

High Levels: Schizophrenia, Autism, Anorexia

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22
Q

What does Gamma-Amino Butyric Acid (GABA) do?

A

Main inhibitory NT of the CNS

Motor Control
Anxiety regulation

Abnormal levels: sleep, eating, anxiety, seizure disorders, Parkinson’s, Huntington’s

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23
Q

What does Glutamate do?

A

Excitatory NT in the CNS
Long Term Potentiation (LTP) which is needed for memory formation

High Levels: seizures, stroke, TBI, Alzheimers, Parkinsons, Huntingtons

Also contribute to anxiety disorders, schizophrenia, mood disorders

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24
Q

What are Endorphins?

A

The natural morphine, but it doesn’t make me puke

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25
Q

Hormones: Thyroxin

A

Controls metabolism
Low = hypothyroidism
High = hyperthyroidism
* At extreme: Grave’s Disease

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26
Q

Hormones: Insulin

A

Stimulates uptake of glucose and amino acids

Low = diabetes
Hyperglycemia: high appetite, weight loss, pee lots, thirsty, prone to infection, apathy, kidney problems

High = hypoglycemia (hunger, weakness, headaches, visual disturbance, palpitations, anxiety, depression, confusion)

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27
Q

Hormones: Cortisol

A

Regulates blood glucose levels

Low = Addison’s disease (weakness, fatigue, low BP, irritability, darkening of skin pigmentation)

High = Cushing’s disease (obesity, hypertension, impaired concentration & memory, depression/anx, low libido)

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28
Q

Hindbrain: 3 parts

A

Brain stem
1. Medulla Oblongata
2. Pons
3. Cerebellum

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29
Q

Role of Medulla Oblongata

Hindbrain

A

Controls:
* Breath
* Heart
* BP
* Digestion

Stimulates:
* Coughing
* Swallowing
* Salivating

Damage often fatal

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30
Q

Role of the Pons

Hindbrain

A

Connects 2 halves of cerebellum

Relays sensory & motor information

Role in: arousal, sleep, respiration

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31
Q

Role of the Cerebellum

Hindbrain

A

Role in:
* balance
* coordination
* posture

Damage: may cause ataxia (slurred speech, tremors, loss of balance)

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32
Q

What 2 parts make up the midbrain?

A
  1. Reticular Activating System
  2. Substantia Nigra
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33
Q

Role of the Reticular Activating System

Midbrain

A

Part of reticular formation (bunch of neurons from spinal cord to midbrain)

Regulates:
* Sleep-wake transition
* Screens incoming sensory info, esp. when sleeping
* Wakes us up if sensory info needs to be attended to (e.g. cat chaos)

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34
Q

Role of the Substantia Nigra

Midbrain

A

Role in:
* controlling movement
* reward-seeking
* addictive behaviour

Degeneration of dopamine neurons here can lead to Parkinson’s

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35
Q

Forebrain (Subcortical): 4 areas

A
  1. Hypothalamus
  2. Thalamus
  3. Basal ganglia
  4. Limbic system
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36
Q

Role of Hypothalamus

Forebrain

A

Controls ANS and Endocrine via teh pituitary
Role:
* Maintain homeostasis: temperature, metabolism
* Motivated behaviours: drinking, feeding, sex, aggression, maternal behaviour
* Expression of strong emotions, esp. rage, fear, excitement

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37
Q

What are the 2 parts of the Hypothalamus?

Forebrain

A

Suprachiasmatic Nucleus:
* Regulates circadian rhythm through light/dark cues
Mammillary Bodies:
* Important for memory
* Damage can result in Korsakoff’s Syndrome (antero/retrograde amnesia, confabulation). related to thiamine deficiency as a result of alcoholism

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38
Q

Role of the Thalamus

Forebrain

A

Central Relay Station
* Relay incoming sensory info to cortex (except for olfaction-it is relayed by LIMBIC)
* Process info between different cortical regions and between cortex & subcortical
* Language, memory, activity

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39
Q

3 parts of the Basal Ganglia

Forebrain

A
  1. Caudate nucleus
  2. Globus pallidus
  3. Putamen
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40
Q

What brain areas make up the Extrapyramidal Motor System?

A

Substantia nigra
Cerebellum
Basal Ganglia (caudate nucelus, globus pallidus, putamen)

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41
Q

Role of the Basal Ganglia

Forebrain

A

Process and relay info needed for control of:
* Voltuntary movement
* Motor expression of emotion
* Sensorimotor learning

Abnormalities:
* Tourette’s
* Huntington’s
* Parkinson’s
* Schizophrenia
* Mood disorders
* OCD
* ADHD

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42
Q

4 parts of the Limbic System

Forebrain

A
  1. Amygdala
  2. Septum
  3. Cingulate cortex
  4. Hippocampus
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43
Q

Role of the Amygdala

Forebrain

A
  • Integrates and directs emotional reactions
  • Attaches emotion to info it gets from the senses
  • Mediates aggressive/defensive behaviour

Damage: lack of fear, struggle reading tones/expressions

Kluver-Bucy Syndrome: low fear & aggression, increased docility, altered diet, psychic blindness, hypersexuality
occurred in monkeys w/ bilateral lesions in amygdala and anterior temporal lobe

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44
Q

Role of the Septum

Forebrain

A

Inhibits emotionality

Lesions may cause Septal Rage Syndrome (shown in rats)
* Hyperemotionality
* Viciousness

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45
Q

Role of the Cingulate Cortex

Forebrain

A

Regulates emotional responses and pain perception

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46
Q

Role of the Hippocampus

Forebrain

A

Role:
* Memory and Learning
* Memory consolidation

Damage:
* Anterograde amnesia
* Degeneration linked to memory loss

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47
Q

What is Contralateral Representation?

Forebrain

A

Each hemisphere controls the opposite side of the body

Olfactory is the exception.

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48
Q

Lateralization of Function

A

Each hemisphere dominates for certain behaviours

Left Hemisphere is often responsible for language, logic, positive emotion

Right Hemisphere for spatial relationships, creativity, negative emotion

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49
Q

What happened in studies with split brain patients?

A

Info in left visual field, people couldn’t verbally ID object or pick it out with right hand, but could with left hand

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50
Q

4 Lobes of the Cerebral Cortex

Forebrain

A
  1. Frontal Lobe
  2. Parietal Lobe
  3. Occipital Lobe
  4. Temporal Lobe
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51
Q

Role of the Frontal Lobe

A
  • Motor behaviour
  • Expressive language
  • Higher-level cognitive functions
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52
Q

4 Areas of the Frontal Lobe

Forebrain

A
  1. Primary motor cortex
  2. Premotor cortex
  3. Broca’s area
  4. Prefrontal cortex
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53
Q

Role of the Primary Motor Cortex

A

Part of the Pyramidal Motor System (pathway of neurons from motor cortex to brain stem and spinal cord. Mediates intricate movement, and speed/strength of movement)

Role in the control of voluntary movement

Lesions may produce weakness, paralysis, apraxia

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54
Q

Role of Premotor Cortex

Forebrain

A

Location: anterior to primary motor cortex

Active during motor actions, or when observing people do motor actions

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55
Q

Role of Broca’s Area

Forebrain

A

A primary language area, within the left frontal lobe

Broca’s Aphasia: deficits in production of written and spoken language
* slow, simple speech
* difficulty repeating phrases
* anomia

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56
Q

Role of the Prefrontal Cortex

Forebrain

A

High order cog functions:
* planning
* judgement
* problem solving
* memory (WM & prospective memory)
* regulate emotion & motor responses

Damage:
* Dorsolateral Prefrontal Area: ‘Dysexecutive syndrome’ (impaired problem solving, planning, abstract thinking, highly distracticle, apathetic)
* Medial Frontal:” pseudodepression
* Pseudopsychopathy

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57
Q

Temporal Lobe: 2 main roles

A
  1. Auditory input
  2. Long-term memory
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58
Q

2 areas of the Temporal Lobe

A
  1. Auditory Cortex
  2. Wernicke’s area
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59
Q

Role of Auditory Cortex

Temporal Lobe

A

Mediation of auditory input

Damage:
* auditory agnosia (can’t distinguish sound)
* auditory hallucinations

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60
Q

Role of Wernicke’s Area

Temporal Lobe

A

Location: left temporal lobe
Role: language comprehension
Damage:
* Wernicke’s Aphasia: trouble understanding language. they produce fluent speech but it is nonsensical. Anomia, difficulty w/ repetition

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61
Q

What is Conduction Aphasia? What causes it?

Temporal Lobe

A

What? comprehends language and speaks fluently, but has anomia and difficulties repeating what has been heard

Cause: lesions in the arcuate fasciculus (connects Broca and Wernickes)

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62
Q

What may cause deja vu?

Temporal lobe

A

Electrical stimulation of certain parts of the right temporal lobe

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63
Q

Medial Temporal Lobe and Memory

H.M. example

A

Tumors here may affect verbal or nonverbal memory

H.M had a bilateral medial temporal lobectomy to treat epilepsy
ST memory and pre-surgery memory were intact
Couldn’t acquire new information, or recall info retained shortly before the surgery

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64
Q

Parietal Lobe & the Somatosensory Cortex Role

A
  1. Role:
    * process somatosensory input and integrates it w/ other info
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65
Q

Parietal Lobe Damage: 3 types of Somatosensory Agnosia

A

Somatosensory Agnosia:
* tactile agnosia: can’t ID objects by touch
* asomatognosia: can’t recognize own body parts
* anosognosia: can’t recognize own symptoms

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66
Q

Parietal Lobe Damage: Contralateral Neglect

A

Loss of knowledge of or interest in one side of the body or things in the environment

Location: right parietal lobe

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66
Q

Parietal Lobe Damage: 3 types of Apraxia

A

Apraxia
* can’t do purposeful movement.
* Ideomotor Apraxia: can’t carry out request to do an action, but can do it spontaneously
* Constructional Apraxia: can’t draw or copy simple figures or arrange blocks in pattern

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67
Q

Parietal Lobe Damage: Gerstmann’s Syndrome

A

Cause: lesions in left hemisphere

Impact:
* Agraphia: difficulties w/ writing
* Acalculia: difficulties w/ math
* Finger agnosia: can’t recognize our fingers
* Left-right disorientation

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68
Q

Occiptal Lobe & the Visual Cortex

A

Role: process visual info
Damage:
* Total damage = complete blindness
* Less extensive = blind spots, after-images, loss of depth perception, alexia (can’t recognize printed words), visual agnosia (can’t recognize familiar objects)

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69
Q

What is Prosopagnosia and what causes it?

Occipital Lobe

A

What? inability to recognize familiar faces
Cause: damage that affects junction of occipital/temporal/parietal lobes

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70
Q

What are the 3 Components of Emotions?

Physiological Foundations of Behaviour

A
  1. Autonomic arousal
  2. Feelings
  3. Behaviour
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71
Q

Ekman’s 6 Primary Emotions

Physiological Foundations

A
  1. Happiness
  2. Sadness
  3. Fear
  4. Anger
  5. Disgust
  6. Surprise
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72
Q

Papez’s role in the study of emotions

Physiological foundations

A

One of the first to research brain mechanisms underlying emotions

Neural circuit that mediates experience and expression of emotions

Circuit = hippocampus, mammillary bodies, anterior thalamic nuclei of thalamus, cingulate gyrus

Ended up being more involved w/ memory than emotion

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73
Q

3 Brain areas involved in emotion

Physiological foundations

A
  1. Hypothalamus: physical expression of emotion through ANS and pituitary
  2. Amygdala: attach emotional content to memory, esp. fear & anxiety, mediate aggression, recognize fear in others
  3. Cerebral Cortex: left linked to positive emotions; damage = depression, anxiety. Right linked to negative emotions; damage = indifference
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74
Q

James-Lange Theory of Emotion

Physiological Foundations

A

Emotions happen when an autonomic response occurs to stimuli, which is then interpreted as an emotion

e.g. I’m trembling, so I must be scared.

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75
Q

Cannon-Bard Theory of Emotion

Physiological Foundations

A

Stimulus triggers thalamus to engage SNS and cerebral cortex

Arousal and emotional experience occur together

Thinks all emotions have same physiological response

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76
Q

Schacter & Singer’s Cognitive Arousal Theory

Physiological Foundations

A

Emotion is a combo of physical arousal and cognitive attributions for the arousal

Physical sensations similar for most emotions

77
Q

What part of the brain starts puberty?

A

The hypothalamus-pituitary-gonadal axis (HPG)

Genetic, but affected by diet, health, climate, etc.

78
Q

What 4 parts of the brain shows sexual dimorphism?

A
  1. The corpus callosum
  2. Amygdala
  3. Hippocampus
  4. Cerebellum
79
Q

HRT for Cisgender People?! WHY?

A

To reduce the effects of menopause (e.g. osteoporosis, heart disease, all the other great stuff)

Increase sex drive (T given to both men and women for this purpose)

80
Q

Describe Stage 1 Sleep

A
  • Transitional stage
  • fast alpha waves replaced by slower theta waves
  • Drowsy, muscles relax, heart slows
81
Q

Describe Stage 2 Sleep

A
  • Starts in a few minutes
  • Theta waves w/ sporadic sleep spindles and K-Complexes (bursts of higher activity)
  • Moderately light sleep
82
Q

Describe Stage 3 Sleep

A
  • Transition stage
  • large & slow delta waves appear
83
Q

Describe Stage 4 Sleep

A
  • Large, slow delta waves
  • Deep breath, slowed heart, low BP
  • Deep sleep
84
Q

Describe REM Sleep

A

Deep sleep, but brain waves are similar to stage 1/2
Breath and heart similar to awake
AKA Paradoxical Sleep
Dreams here are more vivid and easily remembered

85
Q

What happens to sleep as we age?

A

We sleep less
Less time spent in REM and in Stages 3/4
We start to wake more throughout the night
May shift to earlier bed time, earlier wake time

86
Q

What happens in REM Deprivation?

A

Alters sleep patterns
Anxiety, irritability
Impair cog functioning
Effects go away once allowed to sleep
A REM rebound occurs once asleep

87
Q

Hippocampus Role in Memory

A

Memory consolidation (ST to LT)

Consolidation happens during sleep

88
Q

Amygdala Role in Memory

A

Forms emotional memories by linking emotions to stimuli and events

89
Q

Prefrontal Cortex Role in Memory

A

Working Memory
Prospective Memory: remember something in the future

90
Q

Temporal Lobes Role in Memory

A

Storage of LT declarative memory

91
Q

Long Term Potentiation Role in Memory

A

High-frequency stim of neurons increases sensitivity and structure of dendrites

These changes may underlie memory formation

92
Q

Proteins Role in Memory

A

ST memory = modification of preexisting proteins

LT memory = synthesis of new proteins

Meds that block the synthesis of protein or RNA prevent formation of LT memory

93
Q

What is Sensation?

A

receipt of info by sensory receptors and the translation of that info into nerve impulses that get sent to the brain

94
Q

What is Perception?

A

The process of becoming aware of and interpreting what has been sensed

95
Q

Vision: What are rods?

A

A photoreceptor that are adapted for low levels of light

See in black, white, grey

Location: periphery of retina

96
Q

Vision: What are cones?

A

Photoreceptors specialized for detecting colour, visual acuity, function best in bright light

Location: clustered around centre of retina (fovea)

97
Q

What is the stimulus pathway from the photoreceptors to the optic nerve?

A

Photoreceptors –> Bipolar Cells –> Ganglion Cells

Axoms of the Ganglion Cells form the optic nerve

98
Q

Young-Hemholtz Trichromatic Theory of Colour Vision

A

There’s 3 types of color receptions that respond to a primary colour

What are the colours?! red, blue, green

applies only to 1st level of processing @ retina

99
Q

Hering’s Opponent-Process Theory of Colour Vision

A

3 types of opponent-process cells (stimulated by 1-inhibited by another)
1. red-green
2. yellow-blue
3. white-black
Patterns of stimulation produce colours

Explains why we see after images

Applies to 2nd level of processing (retina to visual cortex)

100
Q

What causes colour blindness?

A

Genetic: anomaly on X chromosome
Injury/Disease

Most common is red-green colour blindness

101
Q

What is the Auditory Pathway?

A

Sound wave enters –> auditory canal –> ear drum –> ossicles –> oval window –> cochlea –> hair cells (auditory receptors) –> transformed to neural activity –> auditory nerve –> thalamus –> auditory cortex

102
Q

Components of Sound: What is Loudness?

A

Intensity
Amplitude of sound waves
Measures in decibels
Pain threshold is 120db

103
Q

Components of Sound: What is Pitch?

A

Frequency of sound waves
Measured in cycles per second (Hertz)
Human range: 20-20,000 Hz

104
Q

Components of Sound: What is Timbre?

A

Tonal quality of sound, related to the sound waves complexity

Makes it possible to distinguish between two sounds that have same loudness and pitch

105
Q

Pain: What is one of its distinguishing features?

A

It is not caused by a single type of stimulus, but a variety

106
Q

What affects pain sensitivity?

A
  • Past experience with pain (more past exp = more sensitive)
  • Expectations of pain relief
  • Anxiety/depression
  • BPD/ASD/etc
107
Q

Gate Control Theory of Pain

A

**2 types of nerve fibres: **
-large myelinated fibres
-Small, unmyelinated fibres

Activation of large inhibits transmission of pain by small fibres

How to activate? massage, temperature therapy, etc.

108
Q

What is Neuropathic Pain?

A

Caused by nervous system trauma, surgery, disease, drugs

E.G. Phantom Limb Pain: thought to be caused by damage to central/peripheral NS

Treatment: anti-depressants, opioids, anticonvulsants, topical analgesics, transcutaneous nerve stimulation (TENS)

109
Q

What is Synesthesia?

A

An involuntary perceptual condition in which stim of one sensory mode elicits a sensation in another mode

Types:
-Grapheme Synesthesia: numbers/letters are associated with a colour

110
Q

What causes Synesthesia?

A

Cytowic (1993) said the limbic system

Others say increased connectivity of neural connections between associated regions

Genetic, sensory deprivation, drug use, brain damage

111
Q

What is Psychophysics?

A

Study of the relationship between magnitude of physical stimuli and psychological sensations

112
Q

Psychophysics: Fechner’s 2 Thresholds

Absolute Threshold & Difference Threshold

A
  1. Absolute Threshold: weakest stimuli that a person can detect . Its the intensity at which a stimulus is detected 50% of the time by people
  2. Difference Threshold: AKA Just Noticeable Difference. Smallest physical difference between two stimuli that is recognized as a difference (e.g. with a 10lbs weight, you don’t notice a difference between 8 lbs or 12lbs. JND is 2lbs)
113
Q

Psychophysics: Weber’s Law

A

The just noticeable difference for any stimulus increases in size in direct proportion to the magnitude of the stimulus

114
Q

Psychophysics: Fecher’s Law

A

There’s a logarithmic relationship between psychological sensation and magnitude of physical stimulus

Intensity of internal sensation increases arithmetically as the stimulus increases

115
Q

Psychophysics: Steven’s Power Law

A

There’s an exponential relationship between psychological sensation and magnitude of a physical stimulus, and it varies between stimuli

Method of Magnitude Estimation: participants rated intensity value to different stimuli. It showed that the perception varied based on type of stimuli.

E.g. doubling intensity of a light may double perception of its brightness, but doubling the temp of a room more than doubles the perception of heat

116
Q

What are Neurological Disorders? Give 5 examples.

A

Disorders of the nervous system
1. stoke
2. TBI
3. motor disorders
4. seizures
5. headaches

117
Q

What are the 2 types of brain imaging techniques?

A
  1. Structural techniques
  2. Functional techniques
118
Q

Structural Brain Imagining Techniques

A

ID structural changes
Types:
CT/CAT (computerized axial tomography) scan: xray
MRI: magnetic & radio waves

Show cross sections of brain

119
Q

Functional Brain Imaging Techniques

A

Brain structure and activity
Types:
1. PET (positron emission tomography): radioactive injection. Map NT’s and find dysfunction
2.* SPECT* (single photon emission computed tomography): like PET, but lower resolution
3. fMRI: shows brain activity based on blood oxygenation

120
Q

What are the 2 types of stroke?

A
  1. Ischemic: artery is blocked
  2. Hemorrhagic: blood vessel in brain ruptures or leaks
121
Q

What are the risk factors of stroke?

A
  1. Hypertension
  2. Athersclerosis
  3. Atrial fibrillation
  4. Diabetes
  5. Cigarettes
  6. Age/Gender/Race
122
Q

Symptoms of a Middle Cerebral Artery Stroke

A

Most common one
Contralateral hemiplegia & hemiparesis (face + arm)
Contralateral visual field loss
Aphasia
May not notice some symptoms

123
Q

Symptoms of Anterior Cerebral Artery Stroke

A

Contralateral hemiplegia (leg)
Impaired judgment and insight
Personality change
Incontinence

124
Q

Symptoms of Posterior Cerebral Artery Stroke

A

Cortical blindness
Visual agnosia
Language impairment
Memory loss

125
Q

2 types of TBI

A
  1. Open Head Injury: symptoms focal to area affected, resolves quickly, rare to lose consciousness
  2. Closed Head Injury: more wide spread damage, often lose consciousness. Often has emotional, behavioural, physical, cognitive symptoms
126
Q

What 3 measures are often used for TBI?

A
  1. Glasgow Coma Scale
  2. Duration of Post Traumatic Amnesia
  3. Duration of Loss of Consciousness

All rated as mild/moderate/severe

127
Q

What is Postconcussional Syndrome?

A

When a TBI results in prolonged symptoms such as:
* dizziness
* headaches
* memory impairment
* fatigue
* emotional instability

Could meet DSM-5 for Major/Mild Neurocognitive Disorder

128
Q

Huntington’s Disease: Symptom Progression

A

Initial Symptoms:
* Depression
* Anxiety
* Mania
* Emotional lability

Middle Symptoms:
* Forgetfulness
* Personality changes
* Motor symptoms (clumsiness, fidgetting, incoordination)

Later Symptoms:
* Athetosis: slow, writhing movement
* Chorea: involuntary movement of face, limbs, trunk
* Disarthria: struggle articulating words
* Dysphagia: difficulty swallowing
* Immobility
* Mild/Major neurocog

Age of Onset: 30-50

129
Q

Huntington’s Disease: Causes

A

Genetics:
* autosomal dominant gene

Brain:
* smaller basal ganglia
* abnormal cortex
* reduced metabolic brain activity

Neurotransmitter:
* Glutamate
* ACh
* GABA
* Dopamine

130
Q

Parkinson’s: Symptoms

A

Tremor:
* first symptom
* “Pill rolling” hand movement
Rigidity:
* neck, arms, legs
* ‘Cogwheel Rigidity’ = tremor + rigid = jerky movement
Postural Instability:
* unsteadiness
* Stooped posture
Bradykinesia:
* difficulty initiating/completing movements
* Face: blank mask

131
Q

Parkinson’s: Cause

A

Loss of dopamine producing cells in the substantia nigra

Basal ganglia, thalamus and cortex then affected

132
Q

Symptoms of a Simple Partial Seizure

A

No loss of consciousness
Uncontrollable movements
Sensory (hallucinations, paresthesias)
Autonomic (nausea, sweating)

133
Q

Symptoms of a Complex Partial Seizure

A

Start with aura
Alteration in consciousness
Automatisms: involuntary complex movements

Most often originating in lobes of cerebral cortex, esp. temporal

134
Q

Generalized Seizures: Tonic Clonic

A

AKA grand mal
Symptoms:
* altered consciousness
* Tonic (stiffening of body) followed by clonic (jerky movement of arms and legs)
* Once conscious, may be depressed, irritable, confused, have amnesia

135
Q

Generalized Seizures: Absence Seizures

A

AKA petit mal
Symptoms:
* brief loss of consciousness
* Vacant stare

136
Q

Migraine: causes

A

Low serotonin that leads to constriction of blood vessels

But really, they don’t know

137
Q

Migraine: Treatment

A

Medication:
* NSAIDs
* Ergotamine
* Sumatriptan
* SSRI
* Beta-blockers

Other:
* thermal biofeedback
* autogenic training

138
Q

Tension Headaches: Causes

A

Usually muscle tension
Serotonin may be involved

139
Q

Cluster Headaches: Treatment

A

Medication:
* sumatriptan
* lidocaine

Other:
* oxygen therapy

140
Q

Sinus Headaches: Causes and Treatment

A

Causes:
* Sinusitis

Treatment:
* Antihistamines
* Decongestants
* Antibiotics
* Corticosteroids

141
Q

Quantitative Genetic Methods: what does it look at?

A

calculates the net impact of genetic and environmental variables on specific traits

142
Q

Molecular Genetic Methods: what does it look at?

A

Used to ID what genes are responsible for specific traits

143
Q

What effect does an Agonist have?

Psychopharmacology

A

Produce similar effects as do neurotransmitters

144
Q

What effect does an Inverse Agonist have?

Psychopharmacology

A

Produce effects opposite to those of a neurotransmitter

145
Q

What effect does an Antagonist have?

Psychopharmacology

A

Produce no activity on their own; they reduce/block the effects of a NT or agonist

146
Q

What are the effects of race/ethnicity on psychoactive drugs?

Psychopharmacology

A

Asians and African Americans may metabolize some isoenzymes slower than White peoples

This leads to increased sensitivity to the therapeutic and side effects of meds

147
Q

What are the 5 types of antidepressants?

Psychopharmacology

A
  1. Tricyclic (TCA’s)
  2. SSRI’s
  3. Monoamine Oxidate Inhibitor (MAOIs)
  4. Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)
  5. Norepinephrine-dopamine Reuptake Inhibitors (NDRI’s)
148
Q

Tricyclic Antidepressant: how does it work? Name 3

Psychopharmacology

A

How? block reuptake of norepinephrine and serotonin

Common Ones:
1. Imipramine (Tofranil)
2. Clomipramine (Anafranil)
3. Amitriptyline (Elavil)

149
Q

Tricyclic Antidepressants: 8 Uses

Psychopharmacology

A
  1. MDD w/ hopelessness and anhedonia
  2. Relieve physicals symptoms: appetite, sleep, energy
  3. Dysthymic Disorder
  4. Panic attack
  5. Agoraphobia
  6. OCD (clomipramine)
  7. Enuresis (imipramine)
  8. Chronic pain
150
Q

Tricyclic’s: Side Effects

Psychopharmacology

A
  • Anticholinergic: dry mouth, constipation, urinary retention, blurred vission
  • Gastrointestinal
  • Impaired sexual functioning
  • Drowsiness
  • Weight gain
  • Confusion/memory impairment

Less common:
* tachycardia
* arrhythmia
* Orthostatic hypotension

Very toxic in overdose

151
Q

SSRI’s: How do they work? Name 3

Psychopharmacology

A

Work? increase the availability of serotonin at synapses

Common Ones:
1. Fluoxetine (prozac)
2. Sertraline (Zoloft)
3. Paroxetine (Paxil)

152
Q

SSRI: Uses

A
  1. MDD
  2. Dysthymic disorder
  3. OCD
  4. Panic disorder
  5. Social phobia
  6. Binge eating
  7. Premature ejaculation
153
Q

SSRI’s: Side Effects

Psychopharmacology

A

Common:
* Nausea
* Loss of appetite
* Impaired sex functioning
* Dizziness
* Agitation
* Headaches

Safer in overdose
Combined with other meds may cause Serotonin Syndrome

154
Q

Monoamine Oxidase Inhibitors (MAOI’s): How do they work? Name 2

Psychopharmacology

A

How? block an enzyme that breaks down norepinephrine & serotonin

Common Ones:
1. Phenelzine (Nardil)
2. Tranylcypromine (Parnate)

155
Q

MAOI’s: Uses

Psychopharmacology

A

Atypical depression (increased appetite, hypersomnia, RSD, reactivity, hypochondriasis)

Depression that hasn’t responded to other meds

156
Q

MAOI’s: Side Effects

Psychopharmacology

A

Common:
* dry mouth
* anti-cholinergic
* nausea
* weight gain
* dizziness
* insomnia
* tremoe
* Tachycardia
* Impaired sex functioning

Overdose:
* Seizures
* Coma
* Cardiac arrest

Combined with other drugs/food containing tyramine can cause Hypertensive Crisis

157
Q

Serotonin-Norepinephrine Reuptake Inhibitors (SNRI’s): Name 3

A
  1. Venlafaxine (Effexor)
  2. Duloxetine (Cymbalta)
  3. Desvenlafaxine (Pristiq)
158
Q

SNRI’s: Side Effects

Psychopharmacology

A
  1. Sleep disturbance
  2. nausea
  3. gastrointestinal
  4. sex dysfunction
  5. headache
  6. high BP
158
Q

SNRI’s: Uses

Psychopharmacology

A
  1. MDD
  2. GAD
  3. SAD
  4. Panic Disorder
159
Q

Norepinephrine-Dopamine Reuptake Inhibitors (NDRI’s): Name 1

Psychopharmacology

A
  1. Buproprion: Wellbutrin, Zyban
160
Q

Lithium: 2 main types, 4 sub

Psychopharmacology

A

Lithium carbonate:
1. Eskalith
2. Lithonat
3. Duralith

Lithium citrate:
1. Cibalith

161
Q

Lithium: Side Effects

Psychopharmacology

A

Common:
* nausea
* diarrhea
* metallic taste
* weight gain
* hand tremor
* fatigue
* mild cog impairment

162
Q

Anti-Seizure Drugs: what are they used for? Name 2

Psychopharmacology

A
  1. Cabamazepine (Tegretol)
  2. Valproic acid (Depakote)

Used to treat mania and mania w/ rapid cycling

163
Q

Anti-Seizure Drugs: Side Effects

Psychopharmacology

A
  1. Vomiting
  2. Lethargy
  3. Tremor
  4. Ataxia
  5. Visual disturbances

Monitor closely for liver failure, low white blood cell count, anemia

164
Q

Traditional Antipsychotics: how do they work? Name 3

Psychopharmacology

A

How? block dopamine receptors

Common ones:
1. Phenothiazines: clorpromazine (Thorazine), thioridazine (Mellaril)
2. Butyrophenones: haloperidol (Haldol)

165
Q

Traditional Antipsychotics: Uses?

Psychopharmacology

A
  1. Schizophrenia (only work on + symptoms)
  2. Psychosis
  3. Tourette’s
  4. Acute mania
166
Q

Traditional Antipsychotics: Side Effects

Anticholinergic
Extrapyramidal
Neuroleptic malignant syndrome

A

Anticholinergic:
* Dry mouth
* Urinary retention
* Blurred vision
* Tachycardia
* Gastric distress
* Sex dysfunction

Extrapyramidal:
* Parkinsonism
* Dystonia (muscle contraction, involuntary movement)
* Akathisia
* Tardive dyskinesia

Neuroleptic malignant syndrome: life threatening. ridity muscle, fever, unstable blood pressure, cog disturbances, autonomic dysfunction

166
Q

Sedatives/Hypnotics/Anxiolytics: 2 types

Psychopharmacology

A
  1. Benzodiazapines
  2. Barbituates
167
Q

Benzodiazapines: how do they work? Name 5

Psychopharmacology

A

How? enhance GABA

Common ones:
1. Diazepam (valium)
2. Alprazolam (xanax)
3. clonazepam (klonapin)
4. Lorazepam (ativan)
5. Triazolam (Halcion)

168
Q

Benzos: uses

Psychopharmacology

A

Anxiety
Insomnia
Muscle spasms
Seizures
Moderate/severe alcohol withdrawal

169
Q

Benzos: Side Effects

Psychopharmacology

A

Common:
* Drowsiness/sedation
* Ataxia
* Incoordination
* Anterograde amnesia
* Reduced concentration
* Anticholinergic
* Sex dysfunction

Very addictive
Severe withdrawal
Fatal mized with other CNS depressants

170
Q

Barbituates: how do they work? Name 3

Psychopharmacology

A

How? affect GABA in reticular activating system, medulla, parts of cortex

Common ones:
1. thiopental (pentothal)
2. amobarbital (amytal)
3. secobarbital (seconal)

171
Q

Barbituates: Uses

Psychopharmacology

A

General anesthetic
Manage agitated patients
ST insomnia treatment
Used to be for anxiety

172
Q

Barbituates: Side Effects

Psychopharmacology

A

Common:
* Drowsiness
* Dizziness
* Confusion
* Ataxia
* Cog impairment
* Paradoxical excitement

Very addictive
Withdrawal: seizures, delirium, death
Too much fatally suppresses breathing

173
Q

Azaspirones (sedative): how do they work? name 1

Psychopharmacology

A

How? affects dopamine, norepinephrine, serotonin

Med: Buspirone (BuSpar)

174
Q

Azaspirones: Side Effects

Psychopharmacology

A

Common:
* Dizziness
* Light headedness
* Nausea
* Headache

Doesn’t have strong sedative effect
Seems to be less addictive

175
Q

Narcotic-Analgesics: how do they work? Name 3 main types

Psychopharmacology

A

How? mimic the bodies natural analgesics (endorphins, enkephalins)

Types:
1. Natural opioids: opium, morphine, codeine
2. Synthetic opioids
3. Semi-synthetic opioids: heroin, methadone, oxycodone (Percodan, OxyContin), hydrocodone (Vicodin), meperidine (Demerol)

176
Q

Narcotic-Analgesics: Side Effects

Psychopharmacology

A

Common:
* Dry mouth
* Nausea
* Pupil constriction
* Hypotension
* Cough suppression
* Sex dysfunction
* Respiratory depression

Overdose: decreased pulse, convulsions, coma, death

Chronic Use: dependence, tolerance, withdrawal.

177
Q

Psychostimulants: how do they work? Name 3 main prescription types

Psychopharmacology

A

How? mimic norepinephrine & dopamine

Common Ones:
1. Methylphenidate: ritalin, concerta
2. Pemoline: cylert
3. Amphetamine-dextroamphetamine: adderall

178
Q

Psychostimulants: uses

Psychopharmacology

A

ADHD
Narcolepsy

They decrease motor activity & impulsiveness

179
Q

Psychostimulants: side effects

Psychopharmacology

A

Common:
1. Insomnia
2. Decreased appetite
3. Weight loss
4. Stomachaches
5. Dysphoric mood

May worsen tics

Kids may have a drug holiday

180
Q

Norepinephrine Reuptake Inhibitor (NRIs)

How do they work?
Uses
Side Effects

A

How? block reuptake of norepinephrine
Med: atomoxetine (strattera)
Use: non-stim drug for ADHD
Side Effects:
* Decreased appetite
* dizziness
* fatigue
* irritability
* sexual dysfunction
* menstrual cramps
* may increase SI in kids and teens

181
Q

Beta-Blockers: how do they work? Name 1

Psychopharmacology

A

How? inhibit SNS by blocking beta-adrenergic receptors. Slow HR and lower BP

Med: propranolol (Inderal)

182
Q

Beta-Blockers: Uses

Psychopharmacology

A
  1. Hypertension
  2. Cardiac arrythmias
  3. Migraine
  4. Essential tremor
  5. Physical symptoms of anxiety
183
Q

Beta-Blockers: Side Effects

Psychopharmacology

A

Common:
* brachycardia
* hypotension
* sex dysfunction
* fatigue
* nausea
* vision changes
* dizziness
* depression

Abrupt withdrawal:
* headache
* tremors
* confusion
* hypertension
* arrhythmia

184
Q

Anti-Alcohol Drugs

2 common ones
How do they work?
Side effects

A

Meds:
1. Disulfiram (Antabuse)
2. Naltrexone (ReVia, Vivitrol)

How?
No. 1 causes nausea, vomit, shortness of breath, tachycardia when taken with booze
No. 2 reduces pleasurable effects of booze and cravings for it

Side effects:
* No.1: drowsy, rash, headache, restless, impotence, blood dyscrasias, metallic/garlic taste. Overdose may be fatal
* No 2.: stomach pain, nausea, vomit, fatigue, headache, joint/muscle pain, liver damage

185
Q

Cognition Enhancer

Name 4

How do they work?

Psychopharmacology

A

How? inhibit breakdown of acetylcholine

Meds:
1. Tacrine Hydrochloride (Cognex)
2. Donepezil hydrochloride (Aricept)
3. Rivastigmine (Exelon)
4. Galantamine (Razadyne)

186
Q

Cognition Enhancer

Side effects

Uses

Psychopharmacology

A

Uses:
* slow down memory loss & other cog impairments in Alzheimers
* Donepezil: approved for mild/mod/severe Alzheimers
* Others approved only for mild/moderate

Side Effects:
* Diarrhea
* Nausea
* Loss of appetite
* Weight loss
* Stomach pain
* Tacrine Hydrochloride can cause liver failure; rarely prescribed

187
Q

Practical Clinical Trials

What are they?
How to formulate them? (5 steps)

Psychopharmacology

A

Focus: effectiveness of intervention in typical community settings
Formulation:
1. Hypothesis about clinical concern
2. Objective/measurable goals that capture clinical significance
3. Randomized design
4. Selection criterion
5. Large sample size

188
Q

3 types of genetic screening methods

C;B;M

Psychopharmacology

A
  1. Cytogenetic: examine chromosomal abnormalities
  2. Biochemical: examine proteins instead of gene
  3. Molecular: directly analyze DNA sequence

EPPP (9 decks)

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