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Psych Prep Key Terms > Biological Bases of Behaviour > Flashcards

Biological Bases of Behaviour Flashcards

1
Q

central nervous system

A

spinal cord
+
brain (which includes the cerebrum, cerebellum, and brain stem)

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2
Q

peripheral nervous system

A

somatic nervous system
+
autonomic nervous system (which includes the sympathetic nervous system and the parasympathetic nervous system)

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3
Q

somatic nervous system

A

sends and receives messages that control voluntary motor movements of the skeletal muscles

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4
Q

autonomic nervous system

A

controls automatic or involuntary bodily functions of the smooth muscles and glands (digestion, heart rate, breathing)

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5
Q

sympathetic nervous system

A

the “mobilizing” system, dominant during times of stress, controls the fight or flight response

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6
Q

parasympathetic nervous system

A

the “energy conserving” system, dominant when a person is relaxed, rest and digest

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7
Q

Biofeedback helps people decrease what?

A

decrease sympathetic arousal by increasing the parasympathetic

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8
Q

Neuronal direction

A

Afferent = ascend to the brain
Efferent = exit the brain

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9
Q

Spinal cord regions

A

Cervical: C1-C7
Thoracic: T1-T12
Lumbar: L1-L5
Sacral: S1

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10
Q

quadriplegia

A
  • severing of the spinal cord anywhere between C1 and C5
  • all 4 limbs are paralyzed
  • reflexes remain intact
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11
Q

paraplegia

A
  • severing of the spinal cord at C6 or C7 = paralyzed legs and partial paralysis in arms
  • severing of the spinal cord at T1 or below = paralyzed legs only
  • reflexes remain intact
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12
Q

major brain divisions

A
  • cerebrum (cerebral cortex and subcortical areas)
  • cerebellum
  • brain stem
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13
Q

paresis

A
  • incomplete severing of the spinal cord
  • results in muscle weakness
  • can be the result of stroke
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14
Q

left hemisphere

A
  • dominant in about 97% of people
  • responsible for rational, analytical, logical, and abstract thinking
  • damage can result in aphasia, language problems, apraxia, and difficulties with the right side of the body
  • damage here impacts the RIGHT side
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15
Q

right hemisphere

A
  • responsible for perceptual, visuospatial, artistic, musical, and intuitive activities, maintenance of body image, understand/express emotions
  • damage can result in left-side hemi-neglect, prosopagnosia, visual perceptual disturbances, impulsivity, abnormal sexual behaviour
  • damage here impacts the LEFT side
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16
Q

Gyri

A
  • folds of the brain
  • they increase the surface areas of the brain without taking more space in the skull
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17
Q

corpus callosum

A

bundle of nerve fibres that serve as a bridge between the left and right hemispheres making it possible for the two to communicate

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18
Q

frontal lobes

A
  • largest portion of the brain
  • Broca’s area is here.
  • 3 main divisions = prefrontal cortex, premotor area, motor area
  • critical to personality, emotionality, inhibition, planning and initiative, abstract thinking, judgment, and higher mental functions
  • damage (stroke, TBI, tumour) can result in loss of movement of various body parts, changes in personality, emotional lability, perseveration, inattention, difficulty with problem-solving, Broca’s aphasia. DOESNT impact IQ (bc damage only impacts divergent thinking NOT convergent thinking which IQ tests measure)
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19
Q

occipital lobes

A
  • involved in sight, reading, and visual images
  • damage can result in difficulty recognizing drawn objects, and achromatopsia (difficulty seeing colours/identifying colours, visual agnosia (hallucinations and illusions), and inability to recognize words / problems with reading or writing, prosopagnosia (inability to recognize familiar faces), cortical blindness (loss of vision)
  • research: some people with cortical blindness experience blindsight= not consciously see things but reach for it or can feel/identify sad feeling when presented by a sad picture without seeing it (affective blindsight)
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20
Q

parietal lobes (and gertmans syndrome)

A
  • processes somatosensory information (shape, size, weight, texture, pain, heat, movement of the body) bc somatosensory cortex is here
  • right: directing attention, spatial skills
  • left: motor and linguistics

Damage causes:
- asomatognosia (not aware of body parts)
- Anosognosia (denial of illness)
- hemispacial neglect (contra lateral neglect; neglect one’s side of body ie. dress only one side of body)
- ideomotor apraxia (can’t carry our movements if told to do something)
- ideational apraxia (can’t conceptualize sequences or steps involved in movements)
- Gretsmann syndrome (left parietal lobe damage with four primary symptoms: agraphia, acalculia, right left finger agnosia and disorientation)

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21
Q

The a—ia’s

A

aPRAXia - motor
aNOMia - name objects
aGRAPHia - write
aLEXia - reading
aCALCULia - math
aPHASia - language
- Broca’s - broken speech
- Wernicke’s - no comprehension
- conduction - split between expressive-receptive, cannot repeat
- global - everything
- anomic - names
- transcortical - motor is like Broca’s, sensory is like Wernicke’s, mixed is like global, but can repeat
aGNOSia - things
- PROSOPAGNosia - recognize faces
- ANOSOGNosia - lack awareness of illness
aMNESia - memory loss
- retrograde amnesia - past memories
- anterograde amnesia - new memories

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22
Q

temporal lobes

A
  • contains the primary auditory cortex
  • connected to limbic system
  • also involved in emotional memory and behaviour
  • damage can result in increased aggression, increase or decrease in sexual behaviour, problems with declarative memory, Wernicke’s aphasia also auditory agnosia (inability to recognize familiar sound).
  • LEFT - verbal, language
  • RIGHT - visual
  • “temper temper” = emotions/aggression hearing
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23
Q

global aphasia

A
  • most language functions are impaired (fluency, comprehension, repetition, naming)
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24
Q

proprioception

A

ability to sense position, location, and movement of the body

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25
Q

Wernicke’s aphasia

A
  • located in the left temporal lobe
  • involved in verbal memory and language comprehension
  • damage results in an inability to comprehend speech
  • fluent spoken language but sentences are nonsensical
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26
Q

conduction aphasia

A
  • intact language comprehension, fluent speech but nonsensical
  • cannot repeat verbal phrases
  • can follow through with verbal commands because comprehension in not impaired (unlike Wernicke’s), no slowed speech like in Broca’s
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27
Q

Broca’s aphasia

A
  • located in left frontal lobe
  • controls muscles that produce speech
  • damage results in an inability to express language
  • speech is slow and effortful (short phrases and lengthy pauses)
    Broca’s = broken speech
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28
Q

split-brain patients

A
  • severed corpus callosum
  • information cannot be shared with or transferred to the opposite hemisphere of the brain
  • dichtonic listening task (language lateralization)
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29
Q

thalamus

A
  • sensory relay center
  • receives input from all senses (except smell), then processes and integrates it before projecting it to the appropriate other areas of the brain

Damage: schizophrenia, confabulation syndrome (Korsakoff), thiamine deficiency, anterograde amnesia, retrograde amnesia

Tha-Llamas feel hot (but don’t smell) so they tell the others.

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30
Q

hypothalamus

A
  • major role in homeostasis
  • regulates the five f’s: fever (temperature), feeding (hunger), thirst, eff’ing (sex), cyclic sex hormone secretion, fighting (aggression), falling asleep (the sleep-wake cycle) and involved in pituitary gland stimulation (important for oxytocin release)
  • electrical stimulation: trouble regulating emotions
  • suprachiasmatic nucleus (SCN) (body’s biological clock) is in the hypothalamus

To cool down Tha-Llamas that said they’re hot, you throw water on them to cool them down (hypo-thalamus = releases hormones that regulate homeostasis)

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31
Q

Kluver-Bucy syndrome

A
  • first described in monkeys that had their amygdala’s removed
  • results in placidity, apathy, hypersexuality, hyperphagia (overeating), and agnosias (problems with recognition), psychic blindness

A in amygdala for agression

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32
Q

septal rage syndrome

A

can be a result of damage to the septum (which moderates and or decreases aggression)

septum Simmers you down

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33
Q

cerebellum

A
  • excitatory, smooth movements and balance
  • responsible for maintaining smooth movement and coordinating motor activity
  • damage: ataxia
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34
Q

pons & medulla

A
  • involved in sleep, respiration, movement, and cardiovascular activity
  • damage can lead to failure of bodily functions and death
  • pons: connector and relays messages between cerebellum and cortex. Connects 2 halves of cerebellum and helps to coordinate movements on 2 sides.
  • medulla: BP, swallowing, heart rate and breathing
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35
Q

reticular activating system (RAS)

A

involved in the sleep-wake cycle, serves as a filler for incoming sensory information, and mediates alertness
- inside the reticular formation, projects into the thalamus

A tickle would wake you up

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36
Q

all or none law

A

A neuron, if sufficiently stimulated, will fire an action potential to its fullest extent. If it is not sufficiently stimulated, it will not fire at all.

(a local potentials build it up, but if it doesn’t build it up enough it won’t cause an action potential)

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37
Q

inhibitory neurotransmitters

A
  • decrease the likelihood of an action potential
  • GABA, endorphins, serotonin
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38
Q

excitatory neurotransmitters

A
  • increase the likelihood of an action potential
  • acetylcholine, norepinephrine, glutamate
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39
Q

action potential

A
  • involved in cell-to-cell communication
  • how it works: when dendrites receive sufficient stimulation.. depolarization occurs as positive charged ions (NA+) enter neuron. When stimulation reaches minimum threshold, complete depolarization occurs and it triggers action potential. After this, neuron returns to resting state.
  • sodium (Na+) outside of the cell membrane rushes into a cell, creating an action potential (electrochemical impulse)
  • potassium (K+) moves outside the cell

Outside the cell - more sodium (Na+)
Inside the cell - more potassium (K+)
The banana is floating on the ocean

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40
Q

agonists

A

enhances the effect of a neurotransmitter

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41
Q

antagonist

A

inhibits the effect of a neurotransmitter

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42
Q

acetylcholine (Ach)

A
  • two significant functions = voluntary movement and memory/cognition
  • role in parasympathetic system
  • in the hippocampus for memory consolidation

*Alzheimers (depletion of Ach)

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43
Q

catecholamines

A
  • dopamine + norepinephrine
  • Synthesized from dietary tyrosine and phenylalanine
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44
Q

role of dopamine in schizophrenia

A
  • psychotic (positive) symptoms are a result of an excessive amount of dopamine or hyperactivity of the dopaminergic receptors
  • revised dopamine hypothesis: hypersecretion of dopamine -> positive symptoms, hyposecretion-> negative symptoms
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45
Q

role of dopamine in Parkinsons

A
  • decrease of available dopamine in basal ganglia from neuron degeneration in substantia nigra (basal ganglia includes substantia nigra)
  • treatment for movement component (doesn’t heal it): L-Dopa or Levadopa
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46
Q

dopamine (DA)

A
  • involved in personality, mood, sleep, thought/memory, movement, and emotion
  • reward system of the brain

*linked to Tourette & Parkinson’s

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47
Q

norepinephrine (NE)

A
  • significantly involved in mood, attention, dreaming, learning and certain autonomic functions
  • also involved in pain perception and sleep
  • in the brain it’s a neurotransmitter, in the blood it’s a hormone involved in fight/flight
  • depression: - NE
  • mania: + NE
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48
Q

serotonin (5HT)

A
  • significantly involved in mood, sleep, appetite, aggression, sexual activity, temperature regulation, arousal, aggression, and pain perception
  • from dietary tryptophan
  • dysregulation: suicidality, impulsivity
    Low 5HT + low NE = depression
    Low 5HT + high NE = mania

*migraines, schizophrenia (high serotonin), anorexia

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49
Q

role of serotonin and norepinephrine in depression

A
  • deficiency in both
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50
Q

role of serotonin and norepinephrine in mania

A
  • low serotonin, excess norepinephrine
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51
Q

role of GABA in anxiety

A

insufficient levels of GABA

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52
Q

hypothyroidism

A
  • UNDERsecretion of thyroxin
  • unexplained weight gain
  • sluggishness
  • fatigue
  • impaired memory / intellectual functioning
  • sensitivity to cold

*sometimes mimics depression

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53
Q

hyperthyroidism

A
  • EXCESSIVE secretion of thyroxin
  • most common form: Grave’s Disease
  • weight loss despite increased appetite
  • heat sensitivity
  • sweating
  • diarrhea
  • tremor / palpitations
  • fatigue
  • agitated depression
  • insomnia
  • impaired memory / judgment
  • hallucinations / delusions

*sometimes mimics anxiety or manic episodes

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54
Q

corticosteroids

A

involved in the use of energy resources, inhibition of antibody formation, and inflammation

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55
Q

Addison’s disease

A
  • undersecretion of corticosteroids or adrenal insufficiency
  • symptoms = apathy, weakness, irritability, depression, gastrointestinal disturbance

ADD hormones to treat ADrenal insufficiency in ADDison’s.

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56
Q

Cushing’s disease

A
  • oversecretion of corticosteroids
  • symptoms = agitated depression, irritability and emotional lability, difficulties with memory and concentration, suicide, swelling of the face/neck/trunk

Theres too much cushioning from cushing’s = swelling, fattening

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57
Q

neurocognitive disorder

A

a decline in ONE OR MORE of 6 cognitive domains:
- complex attention
- executive function
- learning and memory
- receptive language
- perceptual-motor
- social cognition

mild to major NCD = level of interference with daily activities

Must specify the NCD cause disease: Alzheimer’s, vascular, Lewy body, Parkinson’s, Huntington’s, multiple etiologies, HIV, frontotemporal lobar degeneration, prion, other medical condition, TBI, substance/medication use, unspecified.

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58
Q

mild vs. major neurocognitive disorders

A
  • the distinction is based on the extent to which the cognitives symptoms interfere with daily functioning (how many domains or which domains are effected do not play a role)
  • if they interfere with independence in everyday activities = major
  • if they don’t interfere with independence in everyday activities = minor
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59
Q

delerium

A
  • a disturbance in attention and awareness
  • onset is rapid and course tends to fluctuate
  • cognitive disturbance
  • only diagnosed when symptoms have a physiological cause
  • reversible (unlike neurocognitive disorders), benefits from stable and quiet environment with memory cues
  • also called: acute confusional state
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60
Q

Alzheimer’s

A
  • most common neurocognitive disorder (60-80% of cases), prevalence increases with age.
  • symptom progression: memory, language, motor skills
  • first symptoms = short term memory loss, anomia, loss of spontaneity, depression/anxiety, apathy (2-4yrs)
  • progressive disease = anterograde/retrograde amnesia, hallucinations, sundowning, flat/liable mood, restless/agitation, sleep/language troubles (2-10yrs)
  • final stage of disease = severe cog functioning, urinary/fecal incontinence, loss of basic motor skills and self care skills, abnormal reflexes, seizures and frequent infections
  • high glutamate, low Ach in enthorial cortex/hippocampus
  • amyloid plaques(beta amyloid), intracellular neurofibrillary tangles (tau). First signs in locus caeruleous, high risk for Down syndrome.
    -Big 5= low concienciousness and high neuroticism
  • diagnosis: only can be confirmed by autopsy, brain biopsy. Can use molecular imaging, CF fluid protein test, CT/MRI, mental status exam, neuropsych testing.
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61
Q

vascular neurocognitive disorder

A
  • second most common neurocognitive disorder
  • first symptoms = impaired judgment / inability to make plans
  • onset is usually younger than Alzheimer’s
  • typically die within 2-3 years
  • stepwise progression
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62
Q

Huntington’s disease (chorea, globe)

A
  • fatal disease
  • involuntary movements
  • also known as chorea
  • early symptoms = irritability, apathy, disinhibition (emotional symptoms)
  • progressively deteriorating major NCD
  • choreiform movements (frequent, discrete, brisk jerking movements) and athetosis (slow writhing movements), facial grimaces
  • caused by autosomal dominant gene
  • linked to GABA (low), glutamate (high), dopamine in the basal ganglia and Ach (low)
    -degeneration in globus pallidus
  • it’s a form of subcortical dementia so it wouldn’t include apraxia, aphasia or agnosia* (which do occur in Alzheimer’s)
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63
Q

concussion vs. contusion

A

concussion = not hard enough to cause a cerebral contusion
contusion = bruising and bleeding of the brain

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64
Q

post-concussion syndrome

A
  • headache, dizziness, irritability, anxiety, insomnia, hypochondriacal concern, hypersensitivity to noise, hypersensitivity to light, fatigue
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65
Q

open head injuries

A

penetration of the skull

don’t generally loose consciousness

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66
Q

closed head injuries

A

the skull is not pierced or cracked

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67
Q

pseudodementia vs. NCD

A

pseudodementia = people complain about symptoms more and symptoms are relieved once depression is treated

NCD = people lack insight to symptoms and symptoms cannot be relieved

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68
Q

Korsakoff’s syndrome

A
  • common cause of alcohol-induced NCD
  • results from a chronic thiamine deficiency
  • retrograde amnesia and confabulation are common symptoms
  • lack of insight, limited spontaneous conversation, problems with executive functioning, disorientation, apathy, and labile irritability
  • short-term memory remains intact
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69
Q

retrograde amnesia

A
  • you can’t recall memories that were formed before the event that caused the amnesia.
  • recent memories typically more affected than remote memories from yrs ago
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70
Q

anterograde amnesia

A
  • the loss of the ability to form new memories after accident
  • information does not transfer from short-term memory to long-term memory
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71
Q

effects of bilateral vs. unilateral ECT

A
  • bilateral causes greater memory impairment than unilateral
  • some believe unilateral is less effective but if the dose of electricity is adequate it can be equally effective
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72
Q

gate control theory of pain

A
  • neural gates in the spinal cord allow pain signals to continue to the brain… pressure stimulation closes the gates (this is why rubbing a hurt area can relieve pain)
  • attitude/mood can affect the gates as well
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73
Q

stages of sleep (BATSDR)

A

Stage 1 - theta waves
Stage 2 - sleep spindles, K complex
Stage 3 & 4 - delta waves /deep sleep
Stage 5 - REM

*beta waves = be alert
*alpha waves = ahhh relax

OA= sleep advance, sleep latency or REM decreases as you get older BUT you still get about the same amount of REM sleep throughout life. Just spend less time in stage 3/4 sleep and REM and spend more time in stage 1/2 (lighter stages of sleep), have lucid dreaming in stage 1

74
Q

generalized seizures vs. partial seizures

A
  • generalized = affect the entire brain
  • partial = limited to one specific of one cerebral hemisphere
75
Q

tonic clonic vs. absence seizures
(generalized)

A
  • tonic clonic (grand mal, loss of consciousness, stiff muscles, jerking movements)
  • absence (petit mal, change in level of consciousness, between 0-30 seconds, blank stare or rolling eyes, continue on after as if nothing happened with whatever they were doing before! Looks like daydreaming. Common in kids)
76
Q

PET/SPECT scans

A

radioactive material injected into vein, inhaled, or swallowed - measures blood flow to detect abnormalities

77
Q

MRI/fMRI/MR spectroscopy

A

measure blood flow in brain during specific task, can determine diseases

78
Q

CT scan

A

shows brain structure

79
Q

positive symptoms of schizophrenia

A
  • hallucinations
  • delusions
  • disorganized thinking
  • positive symptoms tied to excess dopamine
80
Q

negative symptoms of schizophrenia

A
  • flat affect
  • lack of motivation
  • poverty of speech
  • Negative symptoms (like lack of motivation) and cognitive issues involve glutamate and low levels of dopamine. Serotonin’s role is less clear, but its believed to affect mood.
81
Q

side effects of antipsychotics

A
  • sedation, drowsiness, dizziness, weight gain, sexual dysfunction
  • anticholinergic and extrapyramidal symptoms
82
Q

mechanism of action for 1st gen antipsychotics & 2nd Gen antipsychotics

A
  • 1st Gen: dopamine D2 antagonists (positive symptoms)
  • 2nd Gen: dopamine & serotonin antagonists or inverse agonists that decrease effects of dopamine and serotonin (positive & negative symptoms, less side effects, equally as effective)
83
Q

anticholinergic effects

A

dry mouth, constipation, urinary retention, blurred vision, dry eyes, photophobia, nasal congestion, confusion, decreased memory

84
Q

extrapyramidal symptoms (DAPT + brady)

A

These symptoms are caused by decreased dopamine (DA) and increased acetylcholine (Ach) in the nigrostriatal pathway

  • dystonia or acute dystonia (occurs quickly, within hrs/days, looks like painful muscle spasms in face/neck/throat, often can’t open eyes and mouth is wide open/can’t close it)
  • akathisia (takes days/weeks to develop, looks like extreme restlessness, inability to sit still, jitteriness, associated with premature termination of treatment)
  • Parkinsonism (if taken for a few months this can occur, looks like Parkinson’s so tremors, muscle rigidity, mask like face, drooling, shuffling gait)
  • tardive dyskinesia (taken for 6+months this can occur, looks like repetitive muscle contraction particularly in the mouth &jaw, more common in W and OA). Ok to gradually withdraw, 50% experience full remission.
  • Bradykinesia: slowing down of spontaneous movement which may appear as decrease in facial expressions (symptom of Parkinsonism)
85
Q

tardive dyskinesia (what is it, who is it more common for, how to treat)

A
  • a side effect of antipsychotics
  • abnormal movements of the lips, tongue, and jaw
  • may involve the trunk and arms as well
  • not dangerous but adds to the stigma.
  • Irreversible sometimes.
  • more common in older adult and women ***
  • treatment: gradual withdrawal admin a BENZO or switch to 2nd Gen antipsychotic
86
Q

agranulocytosis

A
  • potentially lethal
  • sudden drop in white blood cell count
87
Q

TCAs vs. MAOIs vs. SSRIs vs. NDRI vs. SNRI

A
  • SSRIs = generally well tolerated, few side effects, minimal lethality, safer for OAs, less cardio toxic than TCA
  • SNRI = more efficacious than SSRI at severe depression, neuropathic pain here too (same as TCA)
  • TCAs = cardiotoxic, can be lethal if taken in overdose. Secondary (nortriptyline, desipramine) have fewer side effects. Good for neuropathic pain too.
  • MAOIs = oldest class of antidepressants, highly effective for atypical depression/treatment resistant, interact dangerously with certain foods/medications
  • NDRI: doesn’t cause sexual dysfunction, few anticholinergic effects and not cardiotoxic. NOT good for insomnia/anxious patients bc of energizing effect (norepinephrine). But GOOD: low motivation/energy bc of it.
88
Q

mechanism of action for antidepressants

A
  • block reuptake of serotonin or norepinephrine (increasing them in the brain)
89
Q

mechanism of action for benzos

A

enhance the effects of GABA

90
Q

withdrawal from alcohol and benzos

A
  • can be serious / fatal
  • stage 1 = tremors, sweating, agitation, increased autonomic reactions
  • stage 2 = hallucinations and panic
  • stage 3 = single / multiple grand mal seizures
91
Q

lithium toxicity

A
  • symptoms may mimic the flu
  • vomiting, abdominal pain, severe diarrhea
  • severe tremor, ataxia, coma, seizures, confusion, irregular heartbeat
92
Q

Parkinson’s disease

A
  • primarily considered a movement disorder, mask like expression in face.
  • caused by loss of dopamine producing cells in the substantia nigra which affects functioning of basal ganglia
  • characterized by tremors, rigidity, bradykinesia (slowed initiation of movement), and shuffling gait
  • symptoms result from decreased levels of dopamine
  • also see a degeneration of norepinephrine neurons in locus ceruleus (responsible for non motor symptoms- depression, cog deficits and sleep issues)
  • apoe gene (higher risk for Parkinson’s, Lewy bodies, vascular and Alzheimer’s)
  • more glutamate in basal ganglia at fault for progression of motor symptoms
93
Q

hemispacial neglect

A
  • one-sided neglect
  • most often results from damage to the right hemisphere
  • results in a lack of awareness of objects on the left side
94
Q

contralateral vs. ipsilateral

A

contralateral = opposite side

ipsilateral = same side

95
Q

Bottom-up vs top down

A

Bottom: starts with sensory —> brain (data driven)

Top: brain —> interprets sensory info (concept driven)

96
Q

Neuroleptic malignant syndrome

A

-rare life threatening/lethal.
- Physio symptoms (muscle rigidity, mutism, joint pain, altered consciousness) + altered mental state and autonomic dysfunction (high BP, tachycardia, sweating, fever)
-treatment: stop taking drug at first sign and put on supportive therapy (hydrate+ cool off)
- MEN under 40** MORE at risk
- occur in 1st Gen (typical/traditional) or 2nd Gen (atypical) antipsychotics

97
Q

Myasthenia Gravis

A

Ach receptors destroyed at neuromuscular junctions

98
Q

Low GABA disorders

A

Insomnia seizures and anxiety

99
Q

High glutamate disorders

A

Seizures, strokes, huntingtons and Alzheimer’s

100
Q

Tourette

A

High dopamine in caudate nucleus

101
Q

Low serotonin disorders

A

Depression, high risk for suicide, bulimia, ocd migraines

102
Q

High serotonin

A

Anorexia (high in brain causing obsessive thoughts & anxiety… food restriction lowers serotonin/symptoms).

ASD & chronic schizo (higher levels in blood)

103
Q

Homologous, compensatory, map expansion & cross modal

A

Homologous (same area opp side)
Cross modal (area now does something else since it was empty)
Map expansion (expands by recruiting from border)
Compensatory (compensates ability via other function like memorization when spatial abilities are impaired

104
Q

Dopaminergic pathways (Mesolimbic, mesocortical, tuberofundibular, nigrostriatal)

A

Mesolimbic- reward pathway (VTA- ventral striatum)
Mesocortical- exec function, motivation and emotional reg (VTA-PFC)
tubero- hormone regulation (prolactin) (hypothalamus- pit gland)
Nigrostriatal- purposeful movement (substantia nigra-dorsal striatum (caudate nucleus and putamen)

105
Q

Hemiparesis vs hemiplegia vs hemianopsia

A

Hemiplegia: paralysis
Hemiparesis: weakness
Hemianopsia: visual field loss

106
Q

Middle artery vs posterior artery vs anterior artery symptoms post stroke (key distinctions)

A

All have contra lateral sensory loss, Hemiparesis (weakness)

Middle: aphasia (when dominant is affected), apraxia, contralateral neglect and weakness**. Most common.

Posterior: náusea/vomiting, memory loss, Anosognosia (denial about illness)

Anterior: impaired insight, amnesia, depression, judgement, mutism, apathy, confusion and urinary incontinence

107
Q

PTE (post traumatic epilepsy) vs PTS (post traumatic seizures)

A

Pts (post traumatic seizures): seizures occur within 1 week of TBI. Treated well with anti seizure meds.

PTE (post traumatic epilepsy): seizures occur for + one week after TBI. Harder to treat, vagus nerve stimulation, responsive neurostimulation, surgery when meds don’t work.

108
Q

Seizures (brain areas)

A

Temp lobe, hippocampal atrophy and in simple partial we also see frontal lobe involved in Jacksonian seizures.

109
Q

Prognosis of TBI

A

anterograde amnesia duration

Most recover within 3 months & additional recovery within rest of 1st yr. Tho some may have injuries forever

110
Q

Diabetes mellitus (type 1 & 2) vs central diabetes insipidus vs hypoglycaemia

A

Mellitus: not enough insulin, increases blood sugar levels. can be trigg by 2nd Gen antipsychotic (atypical) use. Type 1: autoimmune d cause destruction of insulin producing cells in pancreas (trigg by viral infection) type 2: pancreas doesn’t produce enough insulin

Central diabetes insipidus: ADH (pit gland)

Hypoglycaemia: too much insulin, low blood sugar

111
Q

Neuroimages

A

NEBA: higher theta & beta wave ratio. Assist with ADHD diagnosis.

CT vs. MRI: mri preferred bc images are sharper/3D. Pros of CT: cheap, widely available. Cons: x-ray, MRI pro: better images con: have to stay still for long time

DTI: helpful to conj with ID of neurocog disorders, ASD, schizo, epilepsy & MS

FDG-PET: used to ID difference between Alzheimer’s and frontotemporal neurocognitive disorder

112
Q

Side effects of 2nd Gen antipsychotics (atypical)

A

Neuroleptic malignant syndrome, metabolic syndrome (weight gain, high BP, insulin resistance, hyperglycaemia, increased risk for diabetes mellitus and heart disease), anticholinergic effects and agranulocytosis

113
Q

SSRI side effects

A

Have a delayed onset (2-4 weeks sometimes 6-8 weeks for full effects). Also have suicidal ideation risk (especially for those under 24)

Mild anticholinergic effects, gastric problems, insomnia, anxiety, sexual dysfunction, weight gain.

Abrupt cessation: discontinuation syndrome (headaches, dizziness, mood lability, impaired concentration, sleep issues and flu like symptoms)

Can’t be combined with an serotinergic drug (MAOI, SNRI,TCA) : serotonin syndrome - potentially fatal (extreme agitation, confusion, autonomic instability, hyperthermia, tremor, seizures, and delirium.) Treatment: STOP

tachyphylaxis** (AD poop out, tolerance). Signs of this included: apathy, fatigue, imp. Cog functioning, sleep disturbance, sexual dysfunction. Treatment: increase dose, switch to different SSRi, SNRI (venlafaxine), TCA (clomipramine) which have lower rates of tachyphylaxis. Or combine with another med (TCA, bupropion, lithium, atypical antipsychotic) or depression focused therapy.

Tip: think of 7 SSSSSSS’s: sleep difficulty, size increase, stomach problems, serotonin syndrome, suicidal ideation (for under 24), stress/anxiety and sexual dysfunction

114
Q

SSRI vs SNRI

A

Similar in efficacy. SNRI may be more effective for severe depression

115
Q

SNRI side effects

A

norepinephrine: heart problems
Serotonin: same as SSRI discontinuation syndrome and serotonin syndrome

116
Q

PTSD brain & neurotransmitters

A

High glutamate, norepinephrine and dopamine. Low serotonin and GABA

brain: hyperactive amygdala/anterior cingulate, hypoactive vmPFC, reduced volume of hippocampus. Research finds that in PTSD reduced activity in vmPFCreduces inhibitory top/down control of amygdala> exaggerated fear responses.

117
Q

Cognitive appraisal theory (stress; primary, secondary and reappraisal)

A

Primary: what’s happening? Evaluate significance of situation. (Stressful/non stressful)

Secondary: what can I do about it? Stage involves assessing our ability to cope with/control situation. (Det what resources personal/environmental will be used)

Reappraisals: is my response appropriate? Ongoing. Make adjustments if necessary

118
Q

Research on treatment effects of chemo and cranial irradiation in children’s neurocognitive functioning?

A

Both associated with deficits in neurocognitive functioning

119
Q

Depression (heredity, neurotransmitters, brain)

A

Heredity: genetic link (higher rates in ID twins), larger rates for female pairs.

Neurotransmitters: low serotonin dopamine and norepinephrine

Brain: HPA axis (persistent hyperactivity/hypersecretion of cortisol associated with increased risk of depression). Abnormal activity levels in vmPFC & dlPFC.

120
Q

Models for understanding depression (social reinforcement theory, learned helplessness model, Beck’s CT)

A

lewinsohn’s Social reinforcement: d. Results from low rate of response contingent reinforcement for social behaviours. Lack of reinforcement» social isolation, low self esteem and pessimism

Seligman Learned Helplessness: d linked to repeated exposure to uncontrollable negative life events. Reformulared version emphasizes: negative cognitive style= stable, internal and global. Hopelessness theory: describes hopelessness as cause.

Beck: depresion due to cognitive triad.

121
Q

Sleep abnormalities in depression:

A

Reduced REM latency, prolonged sleep latency, INCREASED REM density, reduced slow wave sleep (stages 3/4),

122
Q

Anxiety (brain, neuroimaging)

A

Brain: abnormalities in vmPFC, dlPFC, anterior cingulate cortex, posterior parietal cortex, amygdala and hippocampus.

Neuroimaging: Reduced connectivity bw PFC, anterior cingulate cortex and amygdala

123
Q

OCD (brain)

A

Lower than normal levels of serotonin, elevated activity in caudate nucleus, orbito frontal cortex, cingulate gyrus and thalamus

124
Q

Highest concordance rate is to what disorder

A

Bipolar

125
Q

PFC damage (dorsolateral, orbitofrontal and Ventromedial PFC)

A

dorsolateral: role in executive functions, damage can cause concrete thinking, impaired judgment and insight, poor planning ability, deficits in working memory, perseverative responses*, and disinterest and apathy.
- causes dysexecutive syndrome. Decreased activity= depression. Think as exec part of brain.

Orbitofrontal: role in emotion regulation, response inhibition, and social behaviors. Damage can cause poor impulse control, social inappropriateness (e.g., immature behavior, offensive jokes), lack of concern for others, aggressive* and antisocial behaviors, distractibility, and affective lability*.

Ventromedial: role in decision-making, social cognition. Damage - impaired decision-making and moral judgment, lack of insight, deficits in social cognition (e.g., impaired emotion recognition, reduced empathy), confabulation, and blunted emotional responses.
- decreased activity= PTSD

126
Q

Atypical parkinsonism

A

*contraindicated for DBS

involves symptoms that are similar to Parkinson’s but is caused by other disorders (Lewy bodies, progressive supra nuclear palsy, multiple system atrophy). But unlike Parkinson’s it DOESNT respond to treatment with dopamine (levadopa) or DBS***

127
Q

What is an early sign of Alzheimer’s and what is a risk factor (hint: think of senses)

A

Sign: loss of smell
Risk factor: untreated hearing loss

128
Q

Ataxia vs apraxia

A

Ataxia: think x for shouldn’t drink bc then you walk with ataxia.
- Lack of coordination in voluntary muscle movements.
- Affects balance, coordination, and can result in unsteady movements.
- Caused by damage to the cerebellum in the brain.

Apraxia: think p for purposeful movement
- Inability to perform purposeful movements despite physical ability.
- Disconnect between intention and execution.
- Can affect speech (apraxia of speech) or limb movements.

129
Q

In response to a stressful situation the hypothalamus and the sympathetic NS stimulate which area of the brain to release epinephrine and norepinephrine?

A

Adrenal medulla

130
Q

Recovery of cognitive functions following TBI (think PT)

A

Retrograde (oldest memories return 1st)

Orientation to personal information 1st, place 2nd then time as 3rd. Patients who continue to be disoriented to personal information rarely exhibit orientation to time/place.

131
Q

Echolalia vs coprolalia vs echokinesis

A

Echolalia: repeat others vocalizations
Coprolalia: repeat socially undesirable words
Echokinesis: mimic others movements

132
Q

Anosognosia vs prosopagnosia vs asomatognosia

A

Anosognosia: fail to recognize own illness/neurological symptoms (ie. paralysis)

Prosopagnosia: inability to recognize familiar faces

Asomatopsia: damage to somatosensory cortex. Unable to recognize parts of their own body.

133
Q

Cingulate cortex (“cingle file”)

A

Think of the cingulate cortex as the emotional traffic controller in your brain. It helps regulate emotions, manage decision-making, pain, motivation and navigate the complexities of social interactions.

disruptions in the cingulate cortex can be linked to conditions like anxiety, depression, bipolar disorder and obsessive-compulsive disorder.

Damage: experience pain but not distressed by it

134
Q

Supplementary motor cortex vs premotor cortex vs primary motor cortex in movements

A

Supplementary: planning & organizing movements (determine trajectory and bilateral coordination)
Premotor: prep and generate motor commands (receives sensory info and transforms to motor commands- bottom up)
Primary: executing movements (what it receives from premotor)

135
Q

Research on stress and hippocampus size

A

Increased stress = increased cortisol impairs retrieval of declarative memories

Also it’s been found that in individuals with more trauma and ptsd= hippocampus size is smaller in volume. Therefore predisposing you to PTSD. Others say increased stress decreases volume and that leads to distressing memories from PTSD

136
Q

Basal ganglia includes what 3 structures

A

Nucleus accumbens, putamen and caudate nucleus (all part of striatum and all receive input from cortex)

Globus pallidus: transmits info to thalamus (messenger of sense signals throughout brain)

137
Q

Split brain pick up/say things study cheat sheet

A

You see something in your left you won’t be able to SAY it but will be able to pick it up (bc Broca’s is laterized in 95% to the left for right handlers and 50% for left handers)

You see something to your right you will be able to SAY IT!

138
Q

What 2 neurotransmitters are both inhibitory and excitatory

A

Dopamine and acetylcholine

139
Q

Partial Seizures (simple partial/focal onset AWARENESS* seizures vs complex partial seizures/focal onset IMPAIRED AWARENESS* seizures)

A

Simple: DONT lose consciousness (only seizure type that doesn’t) and can describe seizures after. Jacksonian seizures are an example of this type of seizure and can happen in frontal lobe.

Complex: always lose consciousness, auras right before are common and automatisms (involuntary movements like pacing, fidgeting or walking in circles). Example: temporal lobe epilepsy

140
Q

Alogia (negative symptom of schizophrenia)

A

Can speak but choose not to

141
Q

Positive and negative symptoms of schizophrenia & BRAIN

A

positive symptoms via MESOLIMBIC pathway

Negative symptom via MESOcortical pathway

142
Q

Serotonin syndrome (CAN)

A

Side effect of ADs. Think of CAN
- Cognitive changes: agitation, confusion, euphoria, insomnia, hypomania and hallucinations
- autonomic changes: sweating fever and tachycardia
- neuromuscular changes: seizures, tremors, difficulty coordinating movements

143
Q

Serotonin discontinuation syndrome (FINISH)

A

Think FINISH.* Get this when you stop serotonergic drug abruptly.

F= flu like symptoms
I= insomnia
N= nausea/upset stomach
I = imbalance (dizziness)
S= sensory disturbances (tingling, numbness
H= hyperarousal (increased energy and anxiety)

In SNRIs you also have: hypertension, anticholinergic and tachycardia

144
Q

MAOIs & side effects

A

MAOI: increase norepinephrine, dopamine and serotonin

Side effects: anticholinergic, hypertensive crisis, avoid tyramine foods, not good for OAs at falling risk, more likely to being on mania, weight gain, headaches, edema(swelling), paresthesia (pins/needles tingling), myoclonus (muscle spasm), insomnia, sedation, hypotension, serotonin syndrome. Not good for suicidal ideation.

145
Q

TCAs & side effects

A

TCA: increases/blocks reuptake of norepinephrine, dopamine and serotonin

Side effects: anticholinergic side effects, hypotension, weight gain, memory issues, drowsiness, cardiotoxic, not good for those with heart conditions/high BP/suicidal ideation, sexual dysfunction, can lead to death if overdose.

146
Q

Benzo side effects

A

Blocks reuptake of GABA.

Side effects: anticholinergic, drowsiness, weakness, confusion, agitation, memory problems, concentration difficulty, sexual dysfunction, rebound anxiety (if discontinued too abruptly, known as paradoxical reaction), easy to overdose, use with caution with OA bf they have higher risk of fractures, Cary accidents and cognitive impairments. Avoid with addicts due to addictive qualities.

  • caution: mixing with alcohol = synergic effect (BAD, sum 2 parts greater). Can’t withdraw too quickly. Withdrawal can be FATAL.
147
Q

Beta blocker side effects

A

Hypotension, bradycardia (slow heart rate), don’t give to people with asthma, insomnia, sexual dysfunction, nausea, dizziness, depression and memory impairment.

Work as antagonist for norepinephrine and epinephrine

148
Q

Psychostimulant and non stimulant side effects

A

Both good for ADHD and narcolepsy

Side effects: risk of abuse/dependence, hypertension*, lowers seizure threshold, can make tics worse, if dose too high=tremors, paranoia irritability, if overdose= heart failure stroke and seizure, don’t prescribe for those with history of heart problems schizophrenia BP 1, may increase anxiety, decrease appetite

149
Q

Mood stabilizer/anticonvulsants & side effects

A

Good for: BP, seizures, migraines, Major depressive disorder (lithium can help when ADs don’t respond), intermittent explosive disorder (lithium/carbamazepine)

Side effects: hypothyroidism, lithium toxicity (can be fatal, why you need to frequently monitor), polydipsia (super thirsty), polyuria (excessive urinating), weight gain, tremors, difficulty concentrating and memory impairment

  • with lithium: need to avoid salt intake caffeine alcohol NSAIDs like ibuprofen/Tylenol. Also have metallic taste.
150
Q

Migraine headaches with aura vs migraine headaches without aura

A

With aura: classic
Without aura: common

151
Q

Ideopathic vs nocebo vs latragenic

A

Ideopathic= unknown origin

Nocebo= opposite of placebo, when you take a sugar pill and believe it will make you worse (vs good in placebo)

Latragenic= infections/complications caused by receiving medical treatment

152
Q

Kandel research with sea slugs (aplysia)

A

Found that short term memory increased serotonin and long term memory created new synapses and changed structure of existing neurons

153
Q

Temporal lobe personality

A

Paranoid, aggressive and argumentative

154
Q

Most common type of synesthesia

A

Grapheme-colour synesthesia (see numbers as colours)

155
Q

Suprachiasmatic nucleus (SCN)

A

Group of cells inside hypothalamus.
Considered the body’s circadian clock.
Regulates the sleep-wake cycle.

156
Q

Limbic system

A
  • survival, emotions, basic drives, learning, olfactory, memory, autonomic nervous system, endocrine system.
  • inner border of cortex
  • primitive brain

HATCH:
Hippocampus
Amygdala
Thalamus
Cerebellum
Hypothalamus

157
Q

Hippocampus

A
  • memory from short term to long term

If there was a hippo on campus, you’d remember

158
Q

Amygdala

A
  • assigns emotion to input
  • controls the fear response
  • linked to PTSD

A mig fighter jet from war is scary

159
Q

Basal ganglia

A
  • coordination of movement, posture
  • is inhibitory, the breaks that allow us to stand still
  • Huntington’s: unwanted movement, degeneration of caudate nucleus and putamen, thrusting of face and limbs
  • Parkinson’s: difficulty with wanted movement, loss of dopamine this neurons in substantia nigra, tremors, rigidity, bradykinesia
  • Tourette’s
  • OCD
160
Q

Brain stem

A
  • extension of spinal cord
  • pons, medulla, reticular formation
161
Q

Wernicke’s vs Broca’s vs Gertsmann

A
162
Q

Amino acids

A

GABA, glycine, glutamate

163
Q

GABA and glycine

A
  • inhibitory
  • not enough = anxiety, epileptic seizures
164
Q

Glutamate

A
  • Excitatory
  • mediates fast synaptic transmission
  • involved in schizophrenia, OCD, autistic disorder, depression
165
Q

Peptide neurotransmitters

A
  • endogenous opioids (naturally occurring opioids)
  • enkephalins, endorphins
  • regulate stress and pain
166
Q

Grave’s disease

A

Most common form of hyperthyroidism

167
Q

Pituitary gland

A

Master endocrine gland
- releases hormones that work on other glands
- regulated by the hypothalamus
- hypo/hyper-pituitarism: under/over secretion of pituitary growth hormones

168
Q

Thyroid

A

Gland that controls metabolism through thyroxin hormone
- hyper/hypo thyroidism
- disorders in the thyroid should be suspected with psychiatric symptoms

169
Q

Pancreas

A
  • secretes insulin
  • regulates blood sugar levels
  • diabetes (type 1 doesn’t produce enough insulin, type 2 resistance to insulin is developed, gestational during pregnancy)
  • hyperglycemia (3Ps: polyuria, polydipsia, polyphagia) require just the right amount of insulin influx to bring down blood sugars level
  • hypoglycemia requires bringing up blood sugar levels
170
Q

Type I diabetes

A

Also known as Insulin Dependent Diabetes Mellitus (IDDM) (previously Juvenile Onset)
- usually develops before 30 years old
- requires insulin injections life long
- adolescents tend to be less compliant

171
Q

Type II diabetes

A

Also Non-Insulin Dependent Diabetes Mellitus (NIDDM) (previously adult onset)
- control by diet/excercise, sometimes need insulin injection or pills
- higher risk in Hispanic and African American groups

172
Q

Gestational diabetes

A

Develops in pregnancy
- can precede type II diabetes
- in 1 to 3% of pregnancies

173
Q

hypopituitarism

A
  • under secretion of pituitary growth hormones
  • causes dwarfism, puberty delays, gonadal failure, ++disorders.
174
Q

hyperpituitarism

A
  • over secretion of pituitary growth hormones
  • involves skeletal overgrowth (gigantism, acromegaly)
175
Q

Aphasias

A
  • Broca’s aphasia
  • Wernicke’s aphasia
  • conduction aphasia
  • global aphasia
  • anomic aphasia
  • transcortical aphasia (motor, sensory, mixed)
176
Q

Agnosia

A
  • loss of ability to recognize sensory stimuli (smells, objects, sounds, shapes, etc)
  • cause by damage to the parietal, temporal, or occipital regions
    Types:
  • PROSOPagnosia: inability to recognize faces (visual association cortex)
  • ANOSOgnosia: lack of awareness of illness/disability (frontal or parietal lobes)
177
Q

Agraphia

A
  • loss of ability to write
  • left hemisphere damage - frontal, temporal, or parietal lobes.
178
Q

Alexia

A
  • loss of ability to read/comprehend printed/written words
  • stroke in dominant (left) hemisphere
179
Q

Amnesia

A
  • partial or total memory loss
  • retrograde (past) or anterograde (new)
180
Q

Amnesia

A
  • partial or total memory loss
  • retrograde (past) or anterograde (new)

Psych Prep Key Terms (15 decks)

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