Week 7, Lec 2 Flashcards

1
Q

what is a delusion

A

Belief is held despite being presented with evidence against it (“fixed” – firmly maintained)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what disorders can delusions be seen in

A

▪ Can be due to: mental disorder, neurological or
medical disorder
▪ Examples: schizophrenia, substance abuse, bipolar disorder, major depressive disorder (MDD), delirium and dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

delusion

A

▪ A belief that is clearly false and indicates an
abnormality in content of thought

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is hallucination

A

sensory perception in the absence of a corresponding external or somatic stimulus and described according to the sensory domain in which it occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

types of hallucinations

A
  • Most common are visual, auditory, tactile, olfactory
    ▪ gustatory, nociceptive, thermoceptive, proprioceptive are possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

formed vs unformed hallucinations

A

Formed (i.e. voice making a command) or unformed (i.e.non- specific sound)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hallucinations with insight or without insight

A

With insight–px is aware that she is experiencing a hallucination - OR without insight – patient believes the perception is real

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

causes of hallucinations

A

▪ Can occur in illness or during an adjustment disorder or without mental illness (i.e. grief)

▪ Can be due to: psychiatric, neurological or medical disorder

*Delirium, substance withdrawal, intoxication, CNS infection, seizures can all cause hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DSM criteria for schizophrenia

A
  1. delusions
  2. hallucinations
  3. disorganized speech (e.g. frequent derailment or incoherence)
  4. grossly disorganized or catatonic behaviour
  5. negative symptoms (i.e. diminished emotional expression or avolition)

must have 2+ of these and one of them has to be #1,2,or3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how long must have signs and how long for active symptoms of schizophrenia for DSM5 criteria

A

6 months have signs

1 month of active symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

other DSM criteria of schizo

A
  • Level of functioning in work/school, social relationships, self-
    care is markedly decreased
  • Can’t be due to another condition

ALONG WITH
(2+ characteristics) and last 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is disorganized speech and thoughts (schizophrenia)

A

Speech and thought – derailment, poverty of speech, tangentiality, lack of logic, perserveration, neologism, thought blocking, clanging, echolalia… these are part of a phenomenon known as “thought disorders”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

catatonia in schizo

A

move their body erratically or not at all.

  • Psychomotor disturbances motor immobility
  • Stupor, rigidity, strange postures, “waxy
    flexibility”

▪ excessive activity
* Echolalia, echopraxia

▪ Sometimes both can be present at different times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

derailment in schizo

A

Also known as “loose associations,” this is when a person’s thoughts shift abruptly from one topic to another unrelated topic, making their speech difficult to follow. There may be a lack of logical connection between ideas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

poverty of speech in schizo

A

This refers to limited verbal output, where the person’s speech is reduced in quantity or content. They might give brief or monosyllabic answers, which lack detail or elaboration, even when more is expected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

tangentiality in schizo

A

this occurs when a person goes off-topic or provides an irrelevant answer during conversation. The response is loosely related or completely unrelated to the question or topic at hand.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

lack of logic (illogical thinking) in schizo

A

This involves making conclusions or statements that don’t follow a logical sequence or have faulty reasoning. The person may present ideas in a way that defies conventional logic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

perseveration in schizo

A

Repetitive thoughts or speech, where a person repeats the same word, phrase, or idea over and over, often despite a change in the topic or context.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

neologism in schizo

A

The creation of new, often nonsensical, words that only have meaning to the person using them. These made-up words are often unrecognizable and not based on any known language.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

thought blocking in schizo

A

This is when a person’s thoughts are interrupted or stopped abruptly, often in the middle of speaking. The person may pause for an extended period or appear to lose their train of thought.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

clanging in schizo

A

Speech characterized by the use of rhyming or alliteration, often with words linked together based on sound rather than meaning. The focus is on the phonetic aspects of words, which can make the content nonsensical.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

echolalia in schizo

A

The repetition or mirroring of words or phrases spoken by someone else, often without understanding the meaning. This behavior can be seen in individuals with autism or certain types of psychosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

disorganized behaviour in schizophrenia

A

-incoherent or erratic behaviour (i.e. inappropriate dressing, cant complete tasks, aimless wandering)

-inappropriate emotional responses (laugh cry at wrong time)

-difficulty planning an sequencing (i.e. make a meal, hygiene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

catatonia

A

omplex psychomotor syndrome characterized by abnormal movements, behaviors, and reactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

7 psychomotor disturbances seen in catatonia (decrease vs increase activity)

A
  1. motor immobility (reduced or lack of movement)
  2. stupor (unresponsive)
  3. ridigity (muscle stiff)
  4. strange postures (catalepsy)
  5. excessive motor activity
  6. echolalia (autonmatic repetition of words)
  7. echopraxia (imitate or mirror movements)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

echolalia and echopraxia

A

echolalia- repeat words

echopraxia- imitate or mirror movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

negatove symptoms in schizophrenia

A

-less speech
-less emotions
-less social activity
-less motivation
-less psychomotor activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

onset of schizo

A

3rd decade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

pathogenesis of schizophrenia

A

▪ Psychosis and other positive symptoms thought to be
associated with dysregulation in dopaminergic systems
▪ Neurological basis for cognitive symptoms are poorly understood

30
Q

cognitive symptoms of schizophrenia

A
  • Problems with working memory and attention
  • Executive functions, such as ability to organize information
  • Social cognition – difficulty understanding/noticing subtle interpersonal cues, difficulty with forming relationships with others
31
Q

what happens to the dopaminergic system in schizophrenia

A

hyper responsive

32
Q

2 things that prove dopaminergic system is hyperresponsive in schizophrenia

A

▪ (1) Antipsychotic drugs block DA via D2 receptors

▪ (2) Drugs that increase DA (L-dopa, amphetamines)
will cause increase in psychosis

33
Q

what are the last interneurons to be incorporated into the Brian and are vulnerable to developmental insults

A

GABA interneurons

34
Q

what is GABA interneurons susceptible to damage from

A

Highly susceptible to damage from oxidative stress and glutamatergic drive – particularly in the early postnatal developmental period before puberty

35
Q

monoamines in the dipaminergic system

A

dopamine, norepinephrine, serotonin

36
Q

where are most of the neuronal cell bodies that release dopamine located

A

midbrain

37
Q

2 midbrain area for releasing dopamine

A

ventral tegmental area (VTA) and substantia nigra

38
Q

which midbrain area for reward and motivation

A

VTA

39
Q

which midbrain area for motor function

A

substantia nigra

40
Q

which midbrain area for executive fucntion

A

VTA and dorsal substantia nigra

41
Q

where does VTA project to for reward

A

nucleus accumbens and ventral striatum (of the basal ganglia)

42
Q

where does substantia nigra project to for motor function

A

striatum (of basal ganglia)

43
Q

where do VTA and dorsal susbstantia nigra project to for executive function

A

many cortical areas

44
Q

what is tonic firing

A

Dopaminergic (DA) neurons fire in a slow, pacemaker fashion “at rest”

45
Q

what area of the brain slows down tonic firing and by release of what

A

the ventral pallidum (basal ganglia) slows down this activity via GABA release

46
Q

what is phasic firing

A

reticular activating system detects a stimulus ! glutamate release onto DA neurons ! rapid bursts of action potentials

47
Q

what happens in interesting or acutely stressful stimuli

A

Activation of part of the hippocampus (subiculum)! enhanced tonic firing ! “stronger” phasic firing in response to a stimulus

48
Q

2 types of firing in dopaminergic system

A

tonic firing (at rest) and phasic firing

49
Q

what happens to firing in chronic stress

A

Activation of the amygdala ! decreased tonic firing ! “weaker” phasic firing

50
Q

acute vs chronic stress effects on firing of DA system

A

acute: increase tonic and phasic firing

chronic: decrease tonic and phasic firing

51
Q

what do antipsychotic medications block? what symptoms does this make worse?

A

block D2 receptors, and L- dopa (dopamine precursor) as well as amphetamines (cause “leak” of dopamine into synaptic cleft) worsen positive symptoms
▪ However, antipsychotics do not seem to help cognitive or negative symptoms

52
Q

what areas in the DA system are hyper functioning in schizophrenia

A

he hippocampal areas that stimulate tonic activity are hyperfunctioning! inappropriately increased tonic activity

▪ VTA neurons that release dopamine do not seem to be abnormal
▪ Reduced inhibitory GABA-ergic neurons in the hippocampus

53
Q

changes to gaba and dopamine in schizo

A

▪ VTA neurons that release dopamine do not seem to be abnormal

▪ Reduced inhibitory GABA-ergic neurons in the hippocampus

54
Q

what is the theory for delusions/hallucinations in schizo in relation to DA system

A

hyperactive dopaminergic activity due to “hippocampal overdrive” –> all stimuli are seen as “important” or real –> delusions/hallucinations

55
Q

DA system and getting cognitive and negative symptoms in schizo?

A

The dopaminergic system projects to a wide variety of brain areas
▪ May explain some of the cognitive or negative symptoms of schizophrenia

56
Q

risk factors for developing schizo ?

A

stress in childhood

lead to loss of inhibitory GABA-ergic neurons in the hippocampus

▪ (Over)activation of the amygdala may be linked to loss of these neurons

57
Q

inflammation and schizo?

A

Elevations in pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1beta) during psychosis, normalize with antipsychotic treatment

  • Pro-inflammatory cytokines –> kynureneic acid production (a metabolite of the amino acid tryptophan)
  • Kynurenic acid blocks NMDA receptor, which can cause psychosis

▪ Activation of microglial cells–>Cognitive dysfunction and grey matter volume loss?
* Microglia are key in pruning synapses – possibility that “overactivated” microglia are involved in volume loss

58
Q

what input does the pain in migraine come from

A

trigeminovascular input

59
Q

pathway for migraine

A

pain in migraine –> trigeminovascular input
* from the meningeal vessels –> trigeminal ganglion–> synapses on second-order neurons in the trigeminocervical complex (TCC) in the brainstem
* TCC–> thalamus–> cortex

60
Q

what inputs modulate the trigeminovascular nociceptive (pain) input in migraines?

A

midbrain areas: dorsal raphe nucleus, locus coeruleus, and nucleus raphe magnus

61
Q

cause of migraines

A

Problems with modulation of pain sensation from these trigeminal afferents seems to be the cause

▪ Abnormal pain sensation related to vascular dilation and constriction? (vasomotion)

62
Q

which 2 homrones/ neurotransmitters are acted on by medications in migraines?

A

serotonin and CGRP

63
Q

medications effecting migraine

A

▪ 5-HT1 receptors – important in the trigeminal nucleus and the thalamus, bind to serotonin
* Blocked by drugs known as “-triptans” (i.e. sumatriptan)

▪ CGRP (calcitonin-gene- related peptide) seems to mediate neurotransmission at the trigeminal ganglion and at the vasoactive efferents (it’s a vasodilator and a pain modulator)

64
Q

neuromuscular theory of migraine

A

▪ primary neural dysfunction – wave of “spreading depression” (slowly travelling wave of neural excitability) travels through the cortex and leads to activation of the trigeminal complex

  • leads to vascular-generated pain
  • spreading depression wave thought to be linked to other neurological findings
  • may also be linked to modulation of nociceptor afferents by locus ceruleus and dorsal raphe nucleus
65
Q

central sensitization; what do pro inflammatory cytokines cause the release of

A

release of nerve growth factor from mast cells –> increase release of BDNF from C fibers

C fibers are pro pain in dorsal horn network

66
Q

orthodromic and antidromic movement of action potentials in pain C fibre

A

▪ From periphery –> spinal cord = orthodromic

▪ From spinal cord –> periphery = antidromic

67
Q

what do C fibers release

A

substance P and CGRP

rom dendrites into peripheral tissues when action potentials move antidromically
▪ Substance P can cause mast cell degranulation, vasodilation, and edema
▪ CGRP can cause vasodilation
▪ These substances can increase inflammation – this is known as neurogenic inflammation

68
Q

what does substance P and CGRP cause

A

neurogenic inflammation via

▪ Substance P can cause mast cell degranulation, vasodilation, and edema
▪ CGRP can cause vasodilation

69
Q

migraines and gut microbiome?

A

eradicated h pylori (which triggers CGRP release and sensitizes nerves) –> improve migraine

70
Q

IBS and migraines

A

IBS= visceral hypersensitivity

migraine= central hypersensitivity

IBS at risk for migraine

  • Food intolerances can trigger both IBS and migraine episodes
  • Higher amount of circulating serotonin in IBS
  • Pharmaceuticals modulating serotonin receptors are effectively used in both IBS and migraines
71
Q

how can pro inflammatory cytokines (IL-1Beta, IL-6, IL-8, TNF-alpha, IFN ) that are increased in migraines cause visceral pain

A

sensitize afferent ending and induce visceral pain

72
Q

dysbiosis

A

▪ Increase gut permeability –> LPS leakage –> pro-
inflammatory cytokine release

▪ Some bacterial strains can metabolize tryptophan thus may affect local gut serotonin metabolism

  • Serotonin receptors are found on various immune cells (unclear if it is involved in modulating inflammation)