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345A > Hallucinations: November 5th > Flashcards

Hallucinations: November 5th Flashcards

1
Q

what does a psychedelic

A

positive connotation to hal: releasing the mind with drugs

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2
Q

what is the other posotive way hallucinogens were viewed?

A

generating the devine within

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3
Q

T: generating the devine within- liberating spiritual self

A

enthenogenic

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4
Q

what hal used in spiritual settings

A

ayawaska others because of pleasure

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5
Q

negative connotations to hal?

A

psychomimetic

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6
Q

what is psychomimetic

A

appearance of psychosis

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7
Q

T: negative connotation: mind distrupting and mind dissolving- loose sense of self

A

psychosleptic/ psycholytic

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8
Q

how do we operationalize hallucinogens

A

any chemical that induces perceptions of something that does not exist in the enviro

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9
Q

problem with the operationalization? 2

A
  1. according to this definition many hallucinogens arent hallucinogenic: arent changing what you see but how you interpret it = distorted reality
  2. anything can be hallucinogenic at high doses
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10
Q

what should hallucinogenics really be called

A

illusiongenic

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11
Q

… is a state in which individuals disconnected from enviro (perceptual state of being poisoned)

A

dellerium (relates to toxicity)

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12
Q

so how do we tell if its a hal or delirium

A

differentiate from primary or toxic effect

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13
Q

why is it hard to study hal effects

A

Hard to quantify subjective experience of hallucination/delusion and delirium

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14
Q

what drug fits closest with current definition of hal?

A

DMT

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15
Q

what are the 3 categories of hal we talk about?

A

psychedelics, dissociatives, deliriants

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16
Q

T: “reducing valve”; subjective feeling that the brain’s filter is being disabled by the drug (seeing beyond scope of brain and body)

A

psychedelics

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17
Q

“how did I not see it before” what drug

A

psychedelics

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18
Q

T: Physical “numbing” ; analgesia, amnesia, anesthesia

−Psychological detachment

A

dissociatives

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19
Q

which used as rape drugs

A

dissociatives

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20
Q

T: perception of dream-like state or unreal

A

Derealization

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21
Q

T: detached or removed from the body (out-of- body) not in control of body but not sedative= still awake

A

Depersonalization

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22
Q

which drug used as an anethetic

A

dissociatives bcs numbing

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23
Q

T: Confusion, inability to control behaviour, rage

A

deliriants

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24
Q

what system messed with that makes you feel detached from brain and body in dissociatives

A

thalamus= switchboard from signals from brain and body

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25
Q

problem with deliriants

A

toxic, dehydration, mydriasis

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26
Q

debate with deleriants?

A

is it a different category (deliriant state) or potency response = Quantitative or qualitative difference?

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27
Q

all deliriants are toxic

A

t

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28
Q

what happens on deliriants

A

Confusion, inability to control behaviour, rage (used before war)

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29
Q

what is mydriasis

A

pupil dialation

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30
Q

how do we make categorical distinctions

A

based on the receptors cells they target

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31
Q

which hal target 5 HT (2)

A

DMT and LSD (predominantly)

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32
Q

what hal target non ep (2)

A

ecstacy (MDMA) and mescaline

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33
Q

what targets Achetycholine

A

scopolamine

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34
Q

what does scopolamine do

A

makes you sleepy in gravol

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35
Q

what NT do PCP ketamine and salvia target

A

target second messenger systems and transcription factors so effect many NT

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36
Q

does targeting the same NT make the effects the same

A

no dif combo of effects= structural sim doesnt tell you about effects

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37
Q

what schedule are most hal?

A

3 =Legal to possess with prescription/license, illegal to produce or traffic= no big drug busts

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38
Q

what flower is illegal

A

peyote = mescaline

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39
Q

what kinds of sensory distortions?

A

visual, auditory and smell, taste touch

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40
Q

what 3 things change in visual feild?

A

size, color and contrast= low level sensory perceptions

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41
Q

what 2 things happen to sounds?

A

louder but not always clearer

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42
Q

T: crossing of sensory modality

A

synesthesia

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43
Q

is there euphoria in synesthesia

A

no

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44
Q

what are the 2 common stages all hal move through

A

1: visual images

2. meaningful images of people/animals/places

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45
Q

do the hallucinations exist even when external stimuli removed?

A

yes stimulation from inside

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46
Q

clearer percpetion of signals picked up on in stage 1= what is this expereinced as

A

categories crossed

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47
Q

how often do images change in stage 2

A

rapidly (in first stage changes will have a conceptual pattern)

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48
Q

why is rapidly changing images important to understanding moa

A

we know its top down

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49
Q

do people know the hallucinations arent real

A

yes unless high doeses= swept up in hal= freak out (toxicity?)

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50
Q

what does LSD stand for

A

Lysergic Acid Diethylamide

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51
Q

is LSD alkaloid

A

yes ergoline fungus similar analogue

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52
Q

what was LSD used for medically

A

Reduce bleeding/increase contractions

53
Q

why is ergoline not used globally for medical use

A

extremely toxic

54
Q

was LSD synthesized from ergoline?

A

isolated

55
Q

when was LSD found

A

1943

56
Q

street name for the indole nucleus that looks just like seretonin structurally

A

acid

57
Q

what does it mean that acid is a volatile substance

A

interacts with water easily (stamps dont work as well)

58
Q

what does it mean to say acid oxidates?

A

?

59
Q

does acid react to sun

A

yes photosensitive

60
Q

Powder “..”, gelatin “…”, “blotters”

A

pellets, chips

61
Q

how potent is LSD

A

very

62
Q

1 dose (“hit”) of LSD= ug

A

50 -150

63
Q

what happens if you take more than the effective dose

A

doesnt do much more for you system is saturated

64
Q

T: LSD Mimic/simulate activity of the sympathetic nervous

system

A

sympathomimetic

65
Q

does nonep cause the increased altertness is LSD

A

no

66
Q

2 ways LSD works on the system

A
  1. arouse sympa= fight or flight

2, supress para

67
Q

what does arouse sympa effects of LSD do

A

Alertness, arousal: Increase blood pressure, temperature

68
Q

what does supressing para effects of LSD

A

Anorectic effects (appetite suppressant)

69
Q

does permissive hyp apply to hal?

A

more about chemicals have similar effects depending on which receptor site

70
Q

an alteration in the rate, sequential ordering, and goal-directness of thinking processes

A

temporal disintegration (cannabis)

71
Q

how would the sympathomimetic effects of hal be explained by permissive hyp

A

nonep system getting things started then influece seretonin= chemical reaction (focus on other reactions not these NT)

72
Q

other explanation for sympatho response

A

emotional reaction to whats happening visually happening

73
Q

what happens after forst 30 min after dropping LSD

A

nothing: no physiological effects, but sensation of relaxing or “release of tension”

74
Q

what causes the relaxation before LSD trip

A

could be anticipation (opposite of sympathomimetic)

75
Q

four stages that person goes through on LSD trip from 30 min to 2 h (as drugs manifest each area of brain)

A

1) “Images” with eyes closed (low level)
2) Synaesthesia
3) Perception of “multilevel reality” (can see beyond meaning)
4) Distorted (exaggerated/strange) visual input

76
Q

which area of brain associated with each stage

A
  1. brainstem
  2. thalamus and insula
  3. insula (hearing angels?)
  4. Visual cortex/Locus Coeruleus
77
Q

what additional function on top of seretonin influence is the drug having at peak

A

preffrontal= glutamate involved= reality monitoring effected

78
Q

what stage do emotions get involved

A

stage 4 due to what they are experiencing or chemically induced mood changes

79
Q

what time does peak occur

A

3-5 hour

80
Q

3 things you experience at peak

A

1) Emotion/panic swings
2) Feelings of timelessness
3) Disembodiment or “ego-disintegration”

81
Q

Disembodiment or “ego-disintegration” what does this mean

A

stop feeling seperate from their enviro= one with the universe= prefrontal

82
Q

how does stage 1-4 differ from peak

A

sensory perceptual vs perceptual iterpretive

83
Q

what are the chemical mechanisms in LSD

A

2 types of seretonin agonism

84
Q

which 2 ser receptors

A

5-HT1A, 5-HT2A

85
Q

which reeptor is infleunced in all the hal

A

5-HT2A

86
Q

are the hal discriminatible from one another

A

yes due to their unique targets aside from 5HT2A

87
Q

where are 5-HT1A, 5-HT2A infleuced in LSD

A

ocipital lobe

88
Q

what is happening to ser receptors in ocip lobe

A

not inhibited but decrease activity

89
Q

what does lateral inhibtition mean

A

when ones activated the other shuts up

90
Q

how does brain code for neurons that are signalling input vs ones just firing to stay alive?

A

rhythms (when they syncronize they are just signaling to stay alive)

91
Q

what is object model completion

A

filling in image

92
Q

how is object model completion influenced in LSD

A

disruption (signal not getting past the noise)

93
Q

would someone on LSD see the triangle from the 3 pac men

A

no

94
Q

4 brain areas LSD goes through

A

brainstem visual cortex, locus coeruleus, cerebral cortex

95
Q

in the LC what receptor gets the talking stick

A

5-HT2A active on both glutamate and GABA

96
Q

excite 2A receptor on Glutamate1 and GABA2 what does this do to sensory signaling

A

some activated some inhibited: sensory signals getting through the threshold are decreasing

97
Q

what happens to sensory threshold on LSD

A

lowering = noise getting through increase sensory signals

98
Q

what happens to noise on LSD

A

decrease “spontaneous” signals

99
Q

what does glutamate activation cause

A

spontaneous signals erratic= lower threshold and throwing signals around

100
Q

2 roles of 5 ht 2A

A

1: increase sensory signals (threshold)
2: decrease “spontaneous” signals (noise)

101
Q

what does LSDs effect on ht52A receptors do

A

Refinement and Salience of signals no longer occurs because of agonism = perceptions emerge as if they are there

102
Q

how does synesthesia occur in regards to neuron signaling

A

coordinating between populations of neurons that are completely disconnected

103
Q

what happens in the PFC

A

induce glutamate released not GABA

104
Q

what part of LSD MOA explains why perception is altered

A

hyeractive cerebral cortex glutamate singals tell the brain to make snese of all that= illusions= apply logic to whats happening to you

105
Q

how does james lange theory apply to LSD

A

react to our bodily responses based on whats happening in our enviro

106
Q

Interaction between … and … explains psychotic actions (i.e. when things get scary)

A

Dopamine and Serotonin

107
Q

is there tolerance in LSD

A

debate due to emotionality

108
Q

the first LSD trip is scary second and third not so much why?

A

tachyphylaxis or expectation= knowing whats coming

109
Q

how long does it take for LSD to work again

A

3 days to one week

110
Q

what is the danger of LSD tolerance

A

people keep taking more to try and get high but cant in next week= toxicity

111
Q

is there cross tolerance? to what

A

yes for other things in the Tryptamine family (shrooms, DMT)

112
Q

is there dependance

A

no, no withdrawal psysiological

113
Q

is there psycholoigcal dependance

A

no its not an easy high= 8 hour “trips” ; physically/psychologically exhausting

114
Q

Alternating between pleasant and terrifying: how does this change psychological tolerance

A

(not as rewarding, unpredictable)

115
Q

is there psysioligcal effects

A

yes Chronic pupil dilation (sympathomimetic: live life behind shades)

116
Q

T: Chronic pupil dilation

A

Myadrasis

117
Q

psychological effects if you keep taking LSD?

A

wont keep getting effect but saturating system in chemical that looks like seretonin

118
Q

The accumulation of excess serotonin in the CNS that is psycholigcal effect of LSD :T

A

seretonin syndrome

119
Q

3 categorites of symptoms of seretonin syndrome

A

cognitive, autonomic, somatic

120
Q

coginitve effects of seretonin syndrome? 3

A

hypomania, confusion, hallucinations (see sports and shapes not on it)

121
Q

autonomic effects of seretonin syndrome? 4

A

sweating, hyperthermia, vasoconstriction (BP up), tachycardia

122
Q

somatic effects of seretonin syndrome?

A

tremor, twitchiness

123
Q

what is lasting twitchiness of LSD called

A

myoclonus

124
Q

seretonin syndrome feels like Lasting “… reactions”

A

Panic

125
Q

Re-experiencing symptoms from the trip when sober “flashbacks” (somehow hal persisting in the system) :T

A

Hallucinogen Persisting Perception Disorder (HPPD)

126
Q

HPPD: Chronic (mostly …) or episodic (..)

A

visual, all sensory modality)

127
Q

when does HPPD hal happen most often

A

Before going to sleep, in darkness, driving, (stress)= low sensory stimulation

128
Q

LSD Long-Term Effects? Used one of either LSD, Mescaline, or Psilocybin at any point of their lives= results

A

no difference in rates OR onset of the 11 indicators of mental-health problems when compared to controls

129
Q

so is there no such thing as HPPD

A

found in non users as well… but was correlational study

345A (20 decks)

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