Neuro 5 and 6) Neurobiology and neurochemistry in mental health Flashcards

1
Q

What are the symptoms of schizophrenia?

A

Positive - voices, delusions, thought insertion / withdrawal / broadcast
Negative - neglect, isolation, lack of emotional expression, avolition
Cognitive - reduced concentration and attention. Reduced executive functioning

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2
Q

What is dopamine?

A

Monoamine neurotransmitter

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3
Q

What is the precursor of dopamine?

A

Tyrosine

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4
Q

What are the functions of dopamine?

A
Executive functions
Motor control
Motivation
Reward
Lactation
Nausea
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5
Q

Why do typical antipsychotics cause side effects?

A

Reduce dopamine causing hyperprolactinaemia

Too little dopamine in nigrostriatum causes extrapyramidal side effects

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6
Q

Describe the link between glutamate and psychosis

A

Too little cortex in prefrontal cortex causes psychosis
Reduction in glutamate release leads to direct loss of dopamine in the prefrontal cortex via the mesocortiyal pathway.
Reduction in glutamate release increases positive symptoms by mesolimbic pathway

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7
Q

Describe the link between GABA and psychosis

A

Reduction in glutamate release decreases GABA so there is less inhibition. This increases positive symptoms due to hyperactivity in the mesolimbic pathway

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8
Q

What neuroanatomical changes occur in schizophrenia?

A

Enlarged ventricles
Reduced grey matter volumes
Decreased gyrification
Loss of asymmetry of planet temporale

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9
Q

Why is it important to understand the neuroanatomical changes in schizophrenia?

A

Understand therapeutic drug development
Identify appropriate treatment goals in schizophrenia
Understand side effect profiles

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10
Q

What are some organic causes of psychosis?

A
NMDA receptor autoimmune encephalitis
Huntington's chorea
Temporal lobe epilepsy
Wilson's disease
Parkinson's disease
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11
Q

Describe NMDA receptor autoimmune encephalitis

A

Associated with teratomas
Presents with flu like illness, encephalitis or psychotic symptoms
Requires immunosuppression with steroids.
May need ITU due to autonomic instability

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12
Q

How does NMDA receptor autoimmune encephalitis cause psychosis?

A

Antibodies form against NR1 and NR2 subunits of NMDA receptor which reduces glutamate binding

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13
Q

Describe the genetics of Huntington’s chorea

A

Autosomal dominant
CAG triplet repeats in Huntington gene
Every generation increases instability of CAG triplets and risks increasing the number of repeats (genetic anticipation)

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14
Q

Describe the link between temporal lobe epilepsy and psychosis

A

May have no impairment of consciousness during seizure
Depending on part of temporal lobe, can have hallucinations in all modalities, extreme fear, amnesia, dissociation
Post-ictal or inter-octal psychosis

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15
Q

What is Wilson’s disease and how does it cause psychosis?

A

Autosomal recessive
Faulty ATP7B gene affecting Wilson’s disease protein which leads to copper deposition in liver and brain
Affects basal ganglia
Neuropyschiatric complications including cognitive impairment, depression and psychosis
Will have Kayser-Flesicher rings

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16
Q

Describe the link between Parkinson’s disease and psychosis

A
Multiple contributing factors:
PD medications (L-DOPA)
Visual dysfunction
brainstem, sleep dysfunction
Cortical pathology
Deep brain stimulation surgery
Genetic, neurochemical abnormalities
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17
Q

What is autism?

A

Spectrum from severe classical autism to high functioning asperger’s
Deficits in social interaction, restricted repertoire, communication

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18
Q

What is classical autism?

A
Tapping feet
Screeches
Spins in circles
Struggles when routine is changed
Can be aggressive
Obsessed with numbers
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19
Q

What is high functioning ASC?

A

Wears same clothes
Eats same coloured foods
Interest in playing violin and practices every evening and weekend
Excels at maths

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20
Q

What are the current autism theories?

A

Empathising - systemising theory

  • decreased empathy
  • increased systemising

Theory of mind
- empathy deficit

Navon test
- over systemising

21
Q

Describe autism and the social brain

A

Hypoactivation of fusiform gyrus in response to faces leading to reduced ability to recognise emotions in others
Hypoactivation of social brain on fMRI
- IFG during facial expression imitation
- pSTS during perception of facial expression and gaze tasks
- SFG during theory of mind tasks

22
Q

What is ADHD?

A

Neurodevelopmental disorder

Triad of attention difficulties, impulsivity, hyperactivity

23
Q

What is the DSM criteria for ADHD?

A

At least 6 inattentive symptoms present for 6 months

At least 6 hyperactive-impulsive symptoms present for 6 months

24
Q

Describe the neurophysiology with ADHD

A

Can be viewed as deficit in executive functioning and delayed rewards
- executive functioning comes from frontal lobe
- delayed rewards come from amygdala and front lobe
Abnormalities in dopamine and noradrenaline

25
Q

What medication can be given for ADHD?

A

Methylphenidate (ritalin) and atomoxetine (non-stimulant options) - noradrenaline and dopamine reuptake inhibitors

26
Q

What are the 2 types of bipolar affective disorder?

A

Bipolar type 1 = depression and mania

Bipolar type 2 = depression and hypomania

27
Q

What are the roles of the limbic system?

A

Emotional regulation
Memory formation
Learning

28
Q

What are the components of the limbic system

A
Cingulate gyrus
Fornix
Thalamus
Hippocampus
Amygdala
Mammillary bodies
Hypothalamus
Orbitofrontal cortex
Insula
29
Q

What is the cingulate gyrus involved with?

A

Smells and sights with pleasant memories, emotional reaction to pain, aggressive behaviour

30
Q

What is the role of the prefrontal cortex in bipolar disorder?

A

Underactivation seen using fMRI
Volume loss as disease progresses
Reduced connectivity between PFC and amygdala

31
Q

What is the role of the amygdala in bipolar disorder?

A

Overactivity in response to faces

Complex models of toxic signalling, oxidative stress, inflammatory responses and calcium dysregulation

32
Q

Describe what happens to the PFC and amygdala as bipolar progresses

A

Loss of prefrontal cortex and progressive hypoactivation

Sustained hyperactivity of amygdala and increasing volume size

33
Q

Describe the prevalence of depression

A
Depressive symptoms in 13-20% 
Depressive disorder 5.8%
Major depressive disorder lifetime prevalence 20%
Peak 25-35 years
Female : male 2:1
34
Q

What are the symptoms of depression?

A

Low mood, anhedonia, tiredness
Cognitive - hopelessness, helplessness, guilt, worthlessness, poor concentration, poor attention
Somatic - early morning waking, loss of appetite, weight loss, libido decreased
Slow motor movements

35
Q

What is the pathophysiology of depression?

A

Monoamine hypothesis
Receptors act downstream on adenyl cyclase or phospholipase C
Designated monoamine transports
All broken down by monoamine oxidase
Serotonin, dopamine, histamine, adrenaline, noradrenaline

36
Q

How does reserpine cause depression?

A

Antihypertensive that causes rapid depletion of serotonin in synaptic cleft

37
Q

What are the types of anxiety disorders?

A
Generalised anxiety disorder
PTSD
Social anxiety
Phobia
Agoraphobia
Panic disorder
38
Q

What is the role of the amygdala in anxiety?

A

Differentiates sensory information sent by the thalamus to identify threat from no threat
If a threat is perceived, initiates a physiological response

39
Q

What parts of the brain does the amygdala act on?

A
Lateral hypothalamus
Dorsal vagal nuclei
Parabrachial nuclei
Basal forebrain
Reticular pontis caudalis
Central grey area
Paraventricular nuclei
40
Q

What is the effect of the amygdala on the lateral hypothalamus?

A

Heart rate

BP

41
Q

What is the effect of the amygdala on the dorsal vagal nuclei?

A

Bradycardia

Ulcers

42
Q

What is the effect of the amygdala on the parabrachial nuclei?

A

Panting

Respiratory depression

43
Q

What is the effect of the amygdala on the basal forebrain?

A

Arousal
Vigilance
Attention

44
Q

What is the effect of the amygdala on the reticular points caudalis?

A

Increased startle response

45
Q

What is the effect of the amygdala on the central grey area?

A

Freezing

Social interaction

46
Q

What is the effect of the amygdala on the paraventricular nuclei?

A

Corticosteroid release

47
Q

Describe the pathway of HPA overstimulation in anxiety

A

Sensory input to thalamus to amygdala or prefrontal cortex.
From amygdala to hypothalamus which releases corticotrophin releasing hormone which causes anterior pituitary to release adrenocorticotrophic hormone which causes adrenals to produce cortisol.
Chronic stress with elevated cortisol causes anxiety disorders

48
Q

What is PTSD characterised by?

A

Hypervigilance
Flashbacks
Nightmares
Avoidance

49
Q

Describe the pathology path of PTSD

A

1) Trigger e.g. smell
2) Hippocampus recalls fragment of memory e.g. image
3) Amygdala reacts to memory causing flashback
4) Prefrontal cortex is unable to rationalise situation and unable to recognise person is safe
5) Person attempts to avoid or escape