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Week 10 Flashcards

1
Q

What is schizophrenia

A

Schizophrenia ‘divided mind’
Severe psychiatric disorder
Distortion of thoughts and perception also mood
[cognitive impairment]
Affects ~1% population

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2
Q

Clinical features

A

Onset in adolescence or early adulthood
Males=females
Repeated episodes
Or chronic-> progressive decline
Chronic schizophrenics account for most of the patients in long stay psychiatric hospitals

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3
Q

Positive symptoms Type I

A

Presence of abnormal thoughts and behaviours
-delusions (often paranoid)
-hallucinations (auditory ie hearing voices)
-disorganised speech
-grossly disorganised or catatonic behaviour
-[thought disorder (“inserted” thoughts)]

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4
Q

Negative symptoms Type II

A

Absence of normal responses/behaviours
Reduced expression of emotion
Social withdrawal (avolition)
[cognitive impairment- not currently diagnostic]
Not just one illness, more a spectrum with subtypes
Eg paranoid schizophrenia; catatonic

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5
Q

Aetiology of schizophrenia

A

Strong but not invariable hereditary component
-suggest environment has an impact
Possible factors include:
-slow viral infection
-associated autoimmune process
-poor maternal nutrition
-developmental abnormality (arising from above?)
Genetic predisposition with environmental trigger

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6
Q

Dopamine hypothesis of schizophrenia

A

States that dopaminergic hyperactivity underlies schizophrenia
Evidence in support comes from the effects of a number of dopaminergic agents

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7
Q

Dopamine hypothesis of schizophrenia: evidence

A

Amphetamine abuse (dopamine releasing drug)
Can lead to toxic psychosis, manifesting:
-paranoid delusions
-either visual or auditory hallucinations
-compulsive behaviours
Ie type I like symptoms in non-schizophrenic
Exacerbates symptoms of schizophrenic (type I not type II)
Dopamine D2 receptor agonists-> type I like symptoms (eg apomorphine, bromocriptine)
-also exacerbates patient symptoms (type I not type II)
Too much L-dopa-> type I symptoms
-disappear when dose reduced

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8
Q

Chlorpromazine: the first antipsychotic

A

Originally developed as an antihistamine (Thorazine)
Attenuates positive symptoms without excessive sedation
Part of a group of related drugs termed typical or first generation neuroleptics

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9
Q

Typical neuroleptics: chemical classes

A

Neuroleptic= antischizophrenic= antipsychotic= major tranquilliser
Typical neuroleptics 3 main classes
Phenothiazines eg chlorpromazine, fluphenazine
Butyrophenones eg haloperidol, droperidol
Thioxanthines eg flupenthixol, clopenthixol

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10
Q

Typical neuroleptics: receptor antagonists

A

‘Dirty drugs’ especially phenothiazines
Block a variety of receptor sites
-dopamine (D1 and D2 receptor families)
-ACh (muscarinic)
-histamine H1
-noradrenaline
-5-HT
Antipsychotic activity through dopamine receptor block

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11
Q

Atypical (second generation) neuroleptics

A

Distinction from typical on the basis of:
-different pharmacological profile. Eg higher dopamine receptor selectivity
-fewer motor (extrapyramidal) side effects (EPS)
-more effective against negative symptoms
-more effective against treatment-resistant schizophrenia (TRS) (~30%)

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12
Q

Atypical neuroleptics

A

Sulpiride, amisulpride
-selective dopamine receptor antagonists D2/D3
Clozapine, olanzapine
-multi acting receptor targeted agents MARTAs. Les’s side effects
Risperidone, zotepine, sertindole
-serotonin-dopamine antagonists
Quetiapine:
-Novel type

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13
Q

Therapy with antipsychotic drugs

A

Effective treatment for ~70%
‘Treatment resistant’ group (particularly chronic sufferers)
Typical neuroleptics:
-control positive symptoms
-negative symptoms not so well treated
-side effects problematic
Atypical drugs better for negative symptoms (eg clozapine)
-side effect less marked (eg clozapine)
-some efficacy in TRS (eg clozapine)

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14
Q

Dopamine pathways and schizophrenia

A

Mesocortical pathway:
-hypofunction
—negative symptoms. Antagonists dont work as well
Mesolimbic pathway:
-hyperfunction
—positive symptoms. Antagonists help
Positive symptoms respond best to neuroleptics

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15
Q

Side effects of neuroleptic drugs: anti-emetic

A

Due to dopamine receptor block in the chemoreceptor trigger zone (CTZ)
H1 receptor block also important
Beneficial

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16
Q

Side effects of neuroleptic drugs: endocrine- increased prolactin release

A

Prolactin (hormone) released by pituitary gland
Release normally inhibited by dopamine
D2 receptor mediated
Neuroleptics block inhibition
-> breast swelling, pain, lactation

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17
Q

Dopamine pathways-motor side effects

A

Due to blockade of striatal dopamine receptors
Nigrostriatal pathway

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18
Q

Motor side effects of neuroleptic drugs

A

Due to blockade of dopamine receptor in the striatum
Dystonias
-involuntary movements (face, tongue, neck)
-Parkinsonism: tremor at rest, muscle rigidity, decease mobility
Developed relatively rapidly
Reversible

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19
Q

Tardive dyskinesia

A

Severely disabling motor disturbance
Involuntary movements of face/tongue, limbs and trunk
Slow developing (tardive), chronic treatment
Generally irreversible
Serious side effect
Not produced by all neuroleptics

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20
Q

Side effects of neuroleptic drugs: non-dopaminergic

A

Related to blockade of other receptor sites
Anti-muscarinic effects: dry mouth, constipation, visual disturbances etc
Postural hypotension due to alpha adrenoceptor block
Sedation due to histamine H1 receptors block

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21
Q

Side effects of atypical neuroleptics

A

Better side effect profiles
Mainly due to greater selectivity
Lower incidence of motor disturbances
Increased likelihood of compliance
Ie will continue to take the drugs

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22
Q

Not just D2 receptor block

A

Many neuroleptics block 5-HT2A with similar affinities as D2
MARTAs (clozapine, olanzapine): block D2, D4, 5-HT2A, ACh muscarinic
More effective for treatment of negative symptoms
(Risk of serious side effects with clozapine: agranulocytosis, myocarditis)

23
Q

Problems with the dopamine hypothesis

A

Neuroleptics take weeks to work therefore secondary effects important
Less effective on negative symptoms therefore too simplistic
Dysfunction of dopaminergic system may not be primary cause

24
Q

What is emotion

A

Aka “affect”
Combination of psychological and physiological responses to a stimulus
Normal= range
Individual and population
Disorder
Emotions can be positive or negative

25
Q

Why have emotion

A

Communication
Aids memory
Evidence for importance?
-motor cortex
—expression
-other species
We don’t have high degree of localisation of emotion in the cortex
-network of neurones across various structures that form circuits that underpin our emotional state

26
Q

Linking the limbic system and emotion

A

Papez circuit 1930s
‘Emotion system’
-expression of emotion. ANS.
-awareness
Neocortex (awareness)
<-> cingulate gyrus
-> hippocampus
-> hypothalamus (physiological expression)
-> anterior thalamic nuclei—> cingulate gyrus

27
Q

Papez circuit

A

Evidence:
-lesions/tumours
—anterior thalamus
—spontaneous laughing/crying
-neocortex
—prefrontal cortex. Phineas gage case
—orbitofrontal cortex and pleasure

28
Q

Current view

A

Some elements of the Papez circuit not just involved in emotion
-hippocampus
—decrease volume in chronic depression
Other parts of the brain involved:
-amygdala- one in either temporal lobe
-important in fear and negative emotions like aggression

29
Q

Amygdala

A

Temporal lobe
Medial surface
Closely associated with hippocampus
Corticomedial nuclei
Central nuclei
Basolateral nuclei

30
Q

Role for the amygdala in emotion

A

Why do we think it is involved?
-experimental lesions . Temporal lobectomy in monkeys
-Kluver-Bucy syndrome
-decreased fear. Range of behavioural abnormalities
Human evidence:
-urbach-weithe disease
-“fearless” inability to recognise emotional facial expressions
-TLE- temporal lobe epilepsy. Feeling dread or fear before, involves amygdala
Stimulation (humans and animals):
-produces a fear response
Amygdala important for emotional memory

31
Q

Why do you need emotional memory

A

Interpretation of sensory input
Stimulus
-sensory cortex
- central nuclei: hypothalamus
—ANS
-central nuclei: PAG (periaqueductal grey)- freezing behaviour
—behavioural response
-cortex
—emotional experience

32
Q

Aggression

A

Many controlling factors
-amygdala
-hypothalamus
Overlap between fear and aggression pathways

33
Q

Role for amygdala in emotion

A

Clinical relevance of a dysfunctional amygdala
-anxiety disorders
-PTSD
-depression
-autism
-aggression

34
Q

Treating emotional disorders

A

Can we explain psychiatric disorders-> circuitry dysfunction?
Manipulation of the circuitry
-psychosurgery -surgery on brain impacts emotional state
-eg frontal lobectomy: no effect on intelligence, reduced anxiety/agitation, other behaviours affected. Eg decision making
-DBS and depression
-drugs to manipulate circuits

35
Q

Lateralisation

A

Right hemisphere so right amygdala specialised for recognising emotions in others
Both hemispheres don’t work the same

36
Q

Mental illness

A

Human behaviour
Highly variable
Within and between individuals
Biological and cultural factors
DSM-5 anxiety disorders
-depression and bipolar -disorders of mood or affect
Neurological bases
-incompletely understood
-inferred from mechanisms of useful drug therapies

37
Q

Anxiety disorders

A

An inappropriate or excessive anticipatory manifestation of the fear response often to a stressor
-defensive behaviours
-autonomic reflexes
-corticosteroid secretions
-negative emotions

38
Q

Types of anxiety disorder

A

Multiple types
-general anxiety disorder
-somatic and autonomic effects
-restlessness/agitation, tachycardia, sweating, sleep disturbance
Phobic anxiety
Panic disorder
DSM IV vs V classification
Normal anxiety-> pathological anxiety
-what is the relationship with psychological stress
-neuroendocrine response
Implications of multiple types:
-psychopathology the same?
-single treatment method

39
Q

Hypothalamic-pituitary-adrenocortical HPA axis

A

Anxiety disorders: presence of stressor not necessary, HPA overactive in anxiety?. Negative feedback control not as accurate
Stressor -> Hypothalamus(paraventricular nucleus)—Corticotropin releasing factor CRF->+anterior pituitary—adrenocorticotropic hormone ACTH—> +adrenal gland —>cortisol negative feedback - hypothalamus
Cortex—>amygdala->+ hypothalamus.
Cortex—> hippocampus—>-hypothalamus
Neuroplasticity?

40
Q

Treatment of anxiety disorders

A

Self help
Psychological Neuroplasticity reversed?Pharmacological
-prescribed
-self medication: ethanol known anxiolytic reduce anxiety but has problems
Diverse: common neurobiology about changing synaptic activity

41
Q

Anxiolytic drugs B-adrenoceptor antagonists

A

Choice influenced by: nature of predominant symptoms, duration of treatment needed
B-adrenoceptor antagonists:
-reduced somatic symptoms
-used for situational phobias

42
Q

Anxiolytic drugs benzodiazepines

A

Short term use:
-eg diazepam, nitrazepam, midazolam
Useful effects:
-reduction in anxiety
-sleep inducing- hypnotic
Mechanism:
-GABAa receptor, binds to allosteric site, increase GABA affinity, increase Cl-
-in prefrontal cortex, amygdala and other places
Problems:
-sedation
-acute overdose-> profound sedation -> with alcohol, serious respiratory depression
Long term use:
-tolerance, ‘tissue tolerance’
-dependence. Withdrawal increased anxiety, tremor, seizure, insomnia, depression
Therefore short term <4 weeks use

43
Q

Anxiolytic drugs monoaminergic drugs

A

Buspirone
Antidepressant drugs
-eg serotonin selective re uptake inhibitors SSRI
-link between anxiety and depression

44
Q

Major depressive disorder

A

~20% experience during lifetime
Symptoms
-misery, despair, loss of motivation, appetite, suicidal thoughts
Might not be one neurobiological process

45
Q

The monoamine theory of depression

A

“Depression is due to hypo activity at monoaminergic (NA and 5-HT) synapses in brain”
Evidence for:
-ADs increase MA in brain rapidly
Evidence against:
-ADs take >1-3 weeks to work

46
Q

Treatment of MDD

A

Psychotherapy
-Neuroplasticity
Antidepressant drug classes:
Electroconvulsive therapy ECT

47
Q

Antidepressant drug classes

A

Selective serotonin re uptake inhibitors SSRIs
Tricyclic antidepressant TCAs
Monoamine oxidase inhibitors MAOIs
Newer antidepressants
Drug choice?
~efficacy
Side effect profiles vary
-SSRI<TCA<MAOI

48
Q

Selective serotonin reuptake inhibitors SSRIs

A

Eg Fluoxetine (Prozac), paroxetine, sertraline, citalopram
5-HT increases all over body.
Unwanted effects:
-GI and nausea/vomiting
-weight changes
-suicidal thoughts . Prefrontal cortex thoughts
(Serotonin syndrome)

49
Q

Mechanism SSRIs

A

Inhibits reuptake of serotonin so increases intrasynaptic [MA]

50
Q

Tricyclic antidepressants

A

Eg amitriptyline pain medication for neuropathic pain, but dose MDD is much higher
Mechanism:
-5-HT/NA reuptake inhibition
Unwanted effects:
-anti-muscarinic
-sedative (H1 antagonism)

51
Q

Newer drugs

A

Various uptake/receptor mediated effects for 5-HT, NA, dopamine
Melatonin receptor agonism
-agomelatine
Better adverse effect profile
-targeting in brain
-but still delay to action

52
Q

Do AD drugs work

A

~30% patients may not respond
Trial and error required
MDD not a single neurobiological entity
Pharmacogenomics? Different neurobiological changes?

53
Q

New theory- network hypothesis

A

MDD-> increase [CRF] and [cortisol]
Negative feedback blunted
Reversed by AD
?hyperactivity/sensitisation of the neuroendocrine stress response-> depression
Stress—> anxiety—> depression
Network hypothesis chronic stress-> changes
Mechanism:
-cortisol receptors on hippocampus
—decrease glucocorticoid receptors and BDNF (neurotrophic factors)
—decrease neurogenesis and Neuroplasticity (change synaptic structure and function)
AD -> Increase MA-> increase neurogenesis-> restore neuronal network
?latency to clinical effect

54
Q

Future developments

A

Link MA and neuroendocrine dysfunction
Requires:
-increased understanding of role of
—Neuroplasticity and/or neurogenesis
—BDNF
Non pharmacological and pharmacological interventions

BAB (10 decks)

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