Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Management of Disorders > Neuropsychiatry of Parkinson's Disease > Flashcards

Neuropsychiatry of Parkinson's Disease Flashcards

1
Q

What percentage of patients with PD exhibit psychiatric symptoms?

A

70%

(risk increase the longer you have had PD)

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

What transmission is affected by neuronal degeneration in PD?

A

▪️ Catecholaminergic (dopamine and noradrenaline)
▪️ Cholinergic (acetylcholine)

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

What are Lewy bodies?

A

Intracellular inclusion bodies of abnormal alpha-synuclein

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

What pathological changes may precede movement disorder and dopamine dysfunction in prodromal PD?

A

▪️ Neurodegeneration in noradrenergic, serotonergic, and cholinergic nuclei
▪️ Causing extensive frontal and posterior cortical compromise

(up to 10 years before?)

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

What is most commonly associated with psychosis in PD?

A

Medications such as dopamine agonists and levodopa)
▪️ Associated with starting DRT and improved with dose reduction

Rarely seen in absence of medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common manifestation of PD psychosis?

A

Visual hallucinations (8-40%)
▪️ Typically complex, and when alert/eyes open
▪️ More common at night
▪️ Predominance of human or animal forms, sometimes emotionally significant

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

What delusions are most commonly seen in PD psychosis?

A

▪️ Spouse infidelity (Othello syndrome)
▪️ Persecution
▪️ Theft
▪️ Abandonment - linked to Othello?

(Can occur without hallucinations but rare)

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

How much insight is usually seen in people with PD psychosis?

A

Usually do have insight and ‘know’ they are hallucinating (benign hallucinations)

~5% lack insight

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

How should psychosis be viewed in PD?

A

As a spectrum instead of focusing on individual symptoms

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

What might PD psychosis be a biomarker for?

A

▪️ PD stage
▪️ Disease distribution
▪️ Progression of disease

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

What are some of the earlier symptoms of PD psychosis?

A

▪️ Passage and presence of hallucinations
▪️ Illusions
▪️ Formed hallucinations with preserved insight
▪️ Unidentified figures (executive dysfunction?)

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

What are some of the later symptoms of PD psychosis?

A

▪️ Loss of insight
▪️ Delusions
▪️ Misidentification (associated with lower MMSE)
▪️ Auditory, tactile, and olfactory hallucinations

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

How does prevalence of PD psychosis change during the duration of PD?

A

Often increases with longer duration of illness

(~60% by end of 10-12 year follow-ups)

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

What are the main risk factors for psychosis in PD?

A

▪️ Thinning of retinal ganglion layer (in hallucinating PD)
▪️ Visual perception deficits
▪️ Executive dysfunction (inhibitions, verbal fluency)
▪️ Progressive deterioration in cognition
▪️ Presence of depression, RBD, and vivid dreams

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

What is the association between cognition and risk of PD psychosis?

A

Bidirectional relationship:
▪️ Those with visual hallucinations at increased risk of dementia
▪️ Those with worse cognition at increased risk of psychosis

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

How might changes in neuropathology explain the progression from minor visual hallucinations to fully formed multi-modality hallucinations in PD?

A

▪️ Braak progression of Lewy bodies from brainstem to the forebrain
▪️ Becomes multi-modal as spread through cortex (+ loss of insight and delusions)

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

What role does antiparkinsons medications play in the development of PD psychosis?

A

Likely a modifier rather than a necessary feature as still see cases in unmedicated patients

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

What are the main steps for managing PD psychosis?

A
  1. Exclude causes of delirium
  2. Withdraw antiparkinsonian medications
  3. Keep L-dopa therapy at lowest dose possible to maintain motor function
  4. Antipsychotics or cholinesterase inhibitors?
  5. Other options (e.g., supportive treatment, ECT)
  6. Pimavanserin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why should risperidone and olanzapine be avoided in PD psychosis?

A

Can cause significant motor deterioration

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

What antipsychotic shows the most promise for the treatment of PD psychosis?

A

Clozapine - BUT use is limited to routine settings as must be monitored closely

21
Q

What is use of antipsychotics for PD psychosis associated with?

A

Increased mortality

22
Q

Why do clozapine and quetiapine show the best effectiveness for PD psychosis?

A

▪️ They are serotonin 2A and 2C receptor antagonists
▪️ Able to use them effectively at low doses with low occupancy of D2 receptors
▪️ Increased serotonin 2A receptor binding in ventral visual pathway associated with VH in PD

23
Q

Why might pimavanserin be a promising medication for PD psychosis?

A

It is based on evidence for serotonergic activity so avoids dopaminergic activity that may worsen motor function

24
Q

What have trials of pimavanserin in PD psychosis found?

A

▪️ ~74% improvement
▪️ Nearly 14% complete resolution
▪️ Reductions in positive symptoms for PD
▪️ Importantly, no worsening of motor symptoms

25
Q

What is the evidence for the use of cholinesterase inhibitors for PD psychosis?

A

▪️ Limited - not yet specifically studied in PD
▪️ Rivastigmine may possibly be more useful for hallucinations than delusions but not much evidence

26
Q

How might supportive treatment be used for PD psychosis?

A

▪️ In addition to pharmacological treatment
▪️ Develop coping mechanisms such as focusing on false object, looking away etc
▪️ Interacting with hallucinations can often help it to disappear

27
Q

What percentage of PD patients experience anxiety and when is it most common?

A

▪️ Up to 40%
▪️ Especially in younger patients

28
Q

What are the most common forms of anxiety in PD?

A

▪️ Panic disorder
▪️ GAD
▪️ Social phobia
▪️ Panic attacks with onset of “freezing”/”off” episodes

29
Q

How does anxiety in PD interact with motor symptoms?

A

Often report worsening of tremor when anxious

30
Q

How is anxiety thought to be related to dopamine dysfunction in PD?

A

▪️ Inverse relationship between anxiety in untreated PD and striatal DAT availability
▪️ Involvement of hypofunction of nigrostriatal dopaminergic system?

31
Q

What percentage of people with PD present with depression and when?

A

▪️ Up to 50%
▪️ Can often precede movement disorder - predictor of future diagnosis?

32
Q

How can medication for PD affect depression and mood?

A

▪️ Levodopa and dopamine agonists can cause mood changes ranging from euphoria to mania
▪️ Sometimes see hypomanic symptoms during times of peak dose
▪️ Can fluctuate alongside motor fluctuations

33
Q

What approaches to psychotherapy may be considered for PD patients with anxiety and/or depression?

A

▪️ CBT - helpful in reducing both
▪️ Metacognitive therapy - helpful in reducing distress

34
Q

What is the main problem with CBT for anxiety and depression in PD?

A

There is a limit on the ability to reality-test negative beliefs

E.g., ‘there is no cure for this disease’

35
Q

What is the theoretical basis of metacognitive therapy?

A

Psychological distress results from perseverative cognitive processes (e.g., rumination) and attentional strategies (e.g., hypervigilance)

36
Q

What is the theoretical model of off-period distress in PD?

A

▪️ Trigger = off period
▪️ Positive metabelief = “worrying & monitoring symptoms helps me better control them”
▪️ Cognitive attentional syndrome
▪️ Negative metabelief = “worry is uncontrollable and cannot focus on anything but symptoms”

37
Q

What is the first line of pharmacological treatment for anxiety and depression in PD?

A

SSRIs
▪️ Fluoxetine/sertraline (‘activating’)
▪️ Paroxetine (sedating)
▪️ Citalopram (helpful for anxiety, less potential for drug interactions)

38
Q

What medications could be considered if SSRIs are ineffective for anxiety/depression in PD?

A

Atypical antidepressants
▪️ Mirtazapine (depression + anxiety, insomnia)
▪️ Venlafaxine
▪️ Bupropion (apathy, fatigue and poor concentration)
▪️ Trazodone (helpful for neurodegeneration in mice?)

39
Q

What medications may be considered as third line treatments for anxiety/depression in PD?

A

Tricyclic antidepressants
▪️ Amitriptyline/Imipramine (most sedation)
▪️ Nortriptyline (less sedation and hypotension)

40
Q

Why are tricyclic antidepressants typically avoided in PD?

A

▪️ Anticholinergic effects can cause confusion/worsen cognition
▪️ Hypotension can increase risk of falls
▪️ Other common side effects such as sedation, weight gain, and sexual dysfunction

41
Q

What symptoms might occur with the interaction of antidepressants with PD medications rasagiline and selegiline?

A

Serotonin syndrome:
▪️ Fever
▪️ Confusion/stupor
▪️ Agitation
▪️ Sweating
▪️ Diarrhoea
▪️ Delusions
▪️ Mania
▪️ Tremor
▪️ Rigidity

42
Q

How might you treat apathy in PD?

A

DA agonists or cholinesterace inhibitors

43
Q

What is the aetiology of ICDs in PD?

A

▪️ Dopamine depletion in motor dorsal striatum
▪️ Ventral striatum relatively preserved
▪️ Thus antiparkinsonian medications to compensate for dorsal dopamine depletion may ‘overdose’ the limbic ventral system

44
Q

What could you consider for ICD treatment?

A

▪️ Reduce dopamine replacement therapies
▪️ CBT

Possibly:
▪️ Antipsychotics
▪️ Amantadine
▪️ Naltrexone

45
Q

What are the two schools of though for DBS use in ICDs?

A
  1. ICDs can occur de novo post DBS - spread to limbic areas?
  2. DBS allows reduction of DRT and offers more consistent stimulation, reducing likelihood of ICDs?
46
Q

What can DBS help with in cases of ICD?

A

▪️ Allows for 74% DRT reduction when stimulate STN
▪️ Restores impaired learning
▪️ Reversible ventral striatum hypersensitivity and abnormal decision making?

47
Q

What is the psychosocial theory for increased risk of suicide post-DBS?

A

▪️ Due to expectations not being realised despite clinical improvement
▪️ Changes in social situation, roles or coping strategies
▪️ ‘burden of health’

48
Q

What is dopamine agonist withdrawal syndrome?

A

▪️ Resembles other psychostimulant withdrawal
▪️ Anxiety, panic, depression, agitation, dysphoria, insomnia, cravings etc
▪️ Improvement with agonist replacement
▪️ Associated with tendency to develop ICDs

49
Q

How might DBS be used for DLB?

A

▪️ Target nucleus basalis
▪️ Improves attention, concentration and alertness?
▪️ Possibly also for AD if increases cholinergic output?

Management of Disorders (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions