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Year 2 Semester 4 Neuroscience and anatomy > Session 12 > Flashcards

Session 12 Flashcards

1
Q

What are the features of depressive disorders?

A

Patient usually have the symptoms continually for 2 weeks and consist of • CORE SYMPTOMS – Low mood – Lack of energy – Lack of enjoyment & interest • Depressive thoughts • Somatic symptoms/Biological symptoms • In severe cases may have psychotic symptoms

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2
Q

What are the differences between a ‘normal’ adjustment reaction and clinical depression

A

Adjustment reaction • Symptoms develop sudden after and ‘event’ • Symptoms fluctuate • Time limited • Preoccupation with ‘event’ • Energy not low • No particular pattern to sleep disturbance • Reduced or increased appetite • Feelings of anger and frustration more typical

Depression • Symptoms develop gradually • Symptoms continuous • Usually at last two weeks • Lack of interest • Low energy • Sleep disturbance with typically EMW • Loss of appetite and weight loss are typical • Low self esteem and feelings of guilt and blame are typical

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3
Q

What are the features of mania?

A

• Elated Mood • Increased energy • Pressure of speech • Decreased need for sleep • Flight of ideas • Normal social inhibitions are lost • Attention cannot be sustained • Self esteem is inflated, often grandiose • May have psychotic symptoms

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4
Q

What is Bipolar Affective Disorder?

A
  • Diagnosis is made following 2 episodes of a mood disorder at least one of which is mania or hypomania.
  • Therefore you don’t ever have to have a diagnosis of depression to be given the diagnosis bipolar disorder.
  • Bipolar 1 – discrete episodes of mania only or mania and depression
  • Bipolar 2 – discrete episodes of hypomania or hypomania and depression.
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5
Q

What are the physical health differentials for depression?

A

• Hormone disturbance such thyroid dysfunction • Vitamin deficiencies such as vitamin B12 • Chronic disease e.g. renal, CVS & liver failure • Anaemias • Substance misuse e.g. alcohol, cannabis & stimulants • Hypoactive delirium

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6
Q

What are the physical health differentials for Mania?

A

• Iatrogenic e.g. steroid induced • Hyperthyroidism • Delirium • Infection e.g. encephalitis, HIV, syphyllis • Head injury • (intoxication with stimulants)

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7
Q

What brain structures are involved in mood disorders?

A

• Limbic system • Frontal lobe • Basal ganglia

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8
Q

What determines mood?

A

The main hypothesis is that mood is determined by functional circuits between these brain areas. E.g. the frontal lobe projects to parts of the limbic system which in turn connects to the basal ganglia and the brainstem. This affects:

• Cognitive processed (thoughts) • Sympathetic output • Parasympathetic output • Motor systems

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9
Q

What is the limbic system

A

panopto

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10
Q

What are the main functions of the limbic system?

A

• Emotion • Motivation • Memory

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11
Q

Possible limbic system changes in mood disorders

A

insert slide

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12
Q

What are the functions of the frontal lobe?

A

The frontal lobe form 2/3 of the total cortex

• Motor function • Language (Broca’s area) • Executive functions (purposeful goal directed behaviours) • Attention • Memory • Mood • Social and moral reasoning

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13
Q

The prefrontal cortex

A

• The ventromedial prefrontal cortex – is thought to be involved in the generation of emotions. • While the orbital prefrontal cortex is thought to be involved in emotional responses – possibly via connection with the amygdala.

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14
Q

Possible frontal lobe changes in mood disorders

A

insert slide

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15
Q

Human basal ganglia

A

insert slide

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16
Q

Basal ganglia functions

A

• Motor function; malfunction of the basal ganglia are implicated in neurological illnesses such as - Parkinson’s disease - Wilson’s disease - Huntington’s disease • Psychological function: - Emotion - Cognition - Behaviour

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17
Q

Possible basal ganglia changes in mood disorders

A

insert slide

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18
Q

Overall – involvement several circuits could account for symptoms • For depression:

A
  • Prefrontal cortex: Slowing of thought, executive dysfunction. Altered emotional processing.
  • Amgydala: Abnormal emotional processing
  • Basal ganglia: Impaired incentive behaviour. Psychomotor changes.
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19
Q

What neurotransmitters are involved in mood disorders?

A

The two main neurotransmitters for depressive disorders are:

– Serotonin

– Noradrenaline (aka norepinephrine)

• Both are monoamines. • Monoamine hypothesis suggests that depressive disorder is due to abnormality in the availability of these neurotransmitters. • Less evidence re. role of neurotransmitters in mania.

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20
Q

Serotonin

A
  • Produced in the brain stem (Raphe nuclei) and transported to cortical areas and limbic system
  • Thought to have roles in:

– Sleep – Impulse control (link with suicide) – Appetite – Mood

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21
Q

Role of serotonin in mood disorders

A

• Serotonin is thought to be low in depression. • Evidence to support this:

– SSRI’s, SNRI, TCA’s & MAOi’s all successfully treat depression by increasing levels of serotonin in synaptic cleft

– 5HIAA (metabolite of serotonin) is low in the CSF of patients with depression (particularly those who have attempted suicide).

– Tryptophan (precursor for serotonin) depletion causes depression

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22
Q

Noradrenaline

A

• Produced in the locus coeruleus (pons) and projects to limbic system and the cortex

Functions in the brain: • Mood • Suggests a role in behaviour (arousal and attention) – fight or flight response • Implicated in memory functions

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23
Q

Role of noradrenaline in mood disorders

A

• NA thought to be decreased in depression:

– Antidepressants (e.g. SNRI’s, NARI’s and some TCA’s) that increase NA successfully treat depression.

– Patients who have recovered from depression who show decreased NA levels, have significantly higher rates of relapse.

– Postmortem studies of depressed patients vs controls

24
Q

Treatment of Depression

A

• Biological - First line = Selective Serotonin Reuptake inhibitors.
Other options: SNRI’s, TCA’s etc Life threatening/treatment resistant: ECT

  • Psychological – First line treatment for depression: CBT
  • Social – Help with e.g. isolation, social stressors (including housing, finances)
25
Q

Treatment of Bipolar

A

panopto

26
Q

Treatment of mania

A

• Biological – First line: antipsychotics
Alternatively: mood stabiliser

  • Psychological – Acutely unlikely to be helpful, longer term – psychoeducation re. BPAD, triggers and signs of relapse.
  • Social – Treat in a place of safety – where risk to self and others is minimal. Consideration of implications of mania e.g. debts (excessive spending).
27
Q

Treatment of bipolar depression

A

• Biological – Can use antidepressant – but ONLY with mood stabiliser cover.
ECT Lithium
• Psychological – CBT

• Social – as for unipolar depression

28
Q

Maintaining stability in bipolar disorder

A

• Biological – Mood stabilisers e.g. lithium, sodium valproate Antipsychotic (used as a mood stabiliser e.g. Quetiapine)

• Psychological – Psychoeducation re. bipolar affective disorder.
CBT – to help prevent relapses

• Social – Consideration of BPAD on employment e.g. shift work. Involvement of family, education of family etc

29
Q

Extra

A

extra

30
Q

extra

A

extra

31
Q

Define psychosis

A

The presence of hallucinations or delusions Describes symptoms, not a diagnosis in itself

32
Q

What are hallucinations?

A

Perception without a stimulus Can be in any sensory modality Visual hallucinations are usually organic (caused by problem with brain or eyes)

33
Q

Hallucinations in the ‘normal’ population

A

Hypnogogic – going to sleep

Hypnopompic – waking up

34
Q

What are delusions?

A

Delusion – a fixed false belief, which is unshakeable. Outside of cultural norms.

35
Q

Presentation of schizophrenia

A

Patients with schizophrenia don’t have a split mind or personality

Patients with schizophrenia are generally no more ‘dangerous’ than any other patient.

5% of violent crimes are committed by patients with severe mental illness, which means that 95% are committed by ‘normal people’!

36
Q

First Rank Symptoms of schizophrenia

A

• Auditory hallucinations - Thought echo – hearing thoughts aloud
Running commentary –’He’s brushing his teeth, he’s sitting down’
Third Person - Voices referring to patient in third person and conversing with each other about the patient
• Passivity experiences - Patient believes an action or feeling is caused by an external force,
‘MI5 have been moving my leg’
• Thought withdrawal, broadcast or insertion -Thought withdrawal – thoughts are being taken out of the mind

Thought broadcast – everyone knows what the person is thinking.

Thought insertion – thoughts implanted by others
• Delusional perceptions - ‘attribution of new meaning, usually in the sense of self-reference, to a normally perceived object’

New meaning cannot be understood as arising from patient’s affective state or previous attitudes
‘The traffic lights went red and I knew this was a sign that aliens were going to land soon’
• Somatic hallucinations - Mimics feeling from inside the body

37
Q

Positive vs negative symptoms of schizophrenia

A

Positive symptoms: Delusions, hallucinations, thought disorder, lack of insight Added symptoms

Negative symptoms: Underactivity, low motivation, social withdrawal, emotional flattening, Self neglect Symptoms that take away from the patient

38
Q

Do schizophrenia patients present the same?

A

All patients with Schizophrenia are different
• While patients with Schizophrenia might have the same cluster of symptoms e.g. delusions, hallucinations, absence of insight.

• How each patient experiences these symptoms will be completely different e.g. • Delusions MI5 are following them • Delusions witchcraft is being performed on them • Delusions family are poisoning them

39
Q

Pathophysiology of Schizophrenia

A

Dopamine pathways
Brain changes
Limbic system

40
Q

Dopamine (DA) theory of Schizophrenia

A
  • Drugs e.g. amphetamines which cause the release of DA induces psychotic symptoms.
  • All medications that antagonise DA receptors, help treat psychosis & those with the strongest affinity to D2 receptions are most clinically effective.
  • 4 DA pathways in the brain.
41
Q

Mesolimbic pathway

A

From Ventral tegmental area

To Limbic structures (amygdala, septal area, hippocampal formation) and Nucleus accumbens
Thought to be overactive in schizophrenia

42
Q

Mesocortical pathway

A

From Ventral tegmental area

To Frontal cortex and Cingulate cortex
Thought to be underactive in schizophrenia

43
Q

Brain changes in schizophrenia

A

Enlarged ventricles

Reduced grey matter (with reduced brain weight)

Decreased temporal lobe volume

Reduced hippocampal formation, amygdala, parahippocampal gyrus and prefrontal cortex

44
Q

Neuropathology of Schizophrenia

A
  • Decreased pre-synaptic markers • Decreased oligodendroglia • Fewer thalamic neurons
  • Together these changes have led to a theory of “aberrant connectivity” causing schizophrenia.
45
Q

Other theories not relted to brain changes, mesocortical pathway, mesolimbic pathway and dopamine for causation of schizophrenia?

A

Involvement of the limbic structures – as they have a role in regulating emotional behaviour

Basal ganglia – even untreated patients can present with motor symptoms

46
Q

Treatment of Schizophrenia

A

Typical antipsychotics • Block D2 receptors in all CNS dopaminergic pathways • Main action as antipsychotics is on mesolimbic and mesocortical pathways. But side effects come from antagonising D2 receptors in other pathways

Atypical antipsychotics • Lower affinity for D2 receptors • Milder side effects as dissociate rapidly from D2 receptor • Also block 5HT2 receptors

47
Q

Dopamine receptors

A

panopto

48
Q

Problems in the treatment of Schizophrenia

A

Antipsychotic medications cause side effects!

49
Q

Basal ganglia input, processing and ouput

A

insert slide

50
Q

Nigrostriatal pathway & EPSE’s

A

From Substantia nigra pars compacta

To Striatum (caudate nucleus and putamen)

51
Q

So if dopamine promotes movement, why do untreated patients develop catatonia?

A

More than two weeks, one or more of • Stupor / mutism • Excitement • Posturing • Negativism • Rigidity • Waxy flexibility • Command automatism
Probably due to less GABA binding so loss of inhibitory effect

52
Q

Tuberoinfundibular pathway

A

From Arcuate and periventricular nuclei of Hypothalmus

To Infundibular region of hypothalamus

53
Q

Hyperprolactinaemia & antipsychotics

A
  • Dopamine normally inhibits prolactin release from the pituitary.
  • DA antagonists, which lower DA lead to loss of DA’s inhibitory function, and therefore increased prolactin levels.
  • This can lead to: amenorrhoea, galactorrhoea, decreased fertility, reduced libido and long term can lead to osteopenia/osteoporosis
54
Q

Difficulties treating people with SCZ

A
  • Lack insight
  • Medications therefore often not taken.
  • Medications can be given in different ways: PO (inc orodispersible), short acting IM, depot.
55
Q

Prognosis for schizophrenia patients

A
  • Earlier someone is treated the better the prognosis.
  • Moderately good long term global outcome in about 50%
  • Good prognostic factors Absence of family history Good premorbid function Acute onset Mood disturbance Prompt treatment Maintenance of initiative and motivation
  • Mortality is twice as high as in general population • Shorter life expectancy • Higher incidence of CVS disease, respiratory disease and cancer • Suicide risk is 9x higher than in general population • Death from violent incidents in 2x as high • About 50% have a substance misuse problem • Higher rate of cigarette smoking

Year 2 Semester 4 Neuroscience and anatomy (12 decks)

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