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Clinical and Neuropsychology 2 > NP Ch21: Parkinson's disease > Flashcards

NP Ch21: Parkinson's disease Flashcards

1
Q

What is the Parkinson’s spectrum?

A

A group of progressive neurodegenerative diseases which involve various motor symptoms.
It was first described in 1817 by James Parkinson
It’s also known as Hypokinetic-rigid syndrome and parkinsonism

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2
Q

What is the prevalence of Parkinson’s disease (PD)

A

7-10 million worldwide

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3
Q

Whose more likely to get PD? Males or females?

A

According to her slides, its men, acccording to the book its women.
Id say go with slides, cus the book is based on NL

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4
Q

What is the typical age of onset?
Is age related to risk?

A

Onset is typically 50-70. (There’s also early onset, but thats rarer).
Beyond 65, likelihood increases

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5
Q

Why is the number of ppl with PD expected to increase?

A

Aging population
Increased life expectancy
Industrialization/pollution

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6
Q

What types of Parkinson’s are apart of hypokinetic-rigid syndrome?

A

Its split between Parkinson’s disease and Atypical Parkinsonism.
Parkinson’s is further split into Familial and Idiopathic

See Figure 21.1

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7
Q

What are the different forms of Atypical parkinsonism?

A
  1. Drug-induced (secondary)
  2. Vascular Parkinson (secondary)
  3. Mutiple system atrophy (MSA)
  4. Cortico-basal degeneration (CBD)
  5. Lewy body dementia (DLB)
  6. Progressive supranuclear paralysis (PSP)
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8
Q

What are some differences between typical PD and atypical?

A
  • On average more rapid progression in atypical
    • Shorter survival time
    • More prominent cog. deterioration
  • More limited reaction to specific drugs in atypical
    • People with Vascular Parkinsonism don’t respond to anti-Parkinson’s drugs
  • Non-motor symptoms occur relatively often in atypical primary parkinsonian syndromes
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9
Q

What causes Parkinson’s?

A

Degeneration of dopamine(DA)-producing neurons in part of substantia nigra (SN)

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10
Q

What is the substantia nigra involved in?

A

Part of the basal ganglia, interacts w. thalamus and cortex (Which are involved in motor control and cognitive/motivational processes)

Long description, don’t need but cool.
A decrease in dopamine (1) disrupts the balance between the cortico-basal ganglia-thalamocortical circuit in which the subthalamic nucleus (STN) becomes hyperactive and causes decreased activation of the motor cortex via the thalamus.

(1) first in dorsal striatum, later in ventral striatum and mesocorticolimbic dopamine system

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11
Q

What are Lewy bodies?

A

Abnormal encapsulations of proteinaceous material, which develop in the SN and cortically.
α-synuclein is most important protein in Lewy bodies

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12
Q

Why is it important to identify if Lewy bodies are present

A

Because it’s important to differentiate parkinsonism with and without α-synuclein pathology.
This is because Parkinson’s disease, DLB, and MSA are all synucleinopathies.
PSP and CBD are tauopathies.

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13
Q

What are the motor symptoms of PD?

A
  • Lack/slowness of movement (Bradykinesia)
  • Rigidity
  • Rest tremor
  • Postural instability

More info about them on next slide

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14
Q

How can lack/slowness of movement present itself?

A
  • Akinesia
    • People cannot start movement. (This can be lessened by constantly rocking on their feet so the motor system is active)
  • Hypokinesia (decreased bodily movement)
    • Limited facial expression, loss of automatic movement.
  • Bradykinesia (making slow movement)
    • Most basic symptom of hypokinetic-rigid syndrome
  • Sudden stiffening of a movement, ‘freezing’, is a late syndrome.

You don’t need to know all of this word by word, but generally what each is and that bradykinesia is the most important part.

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15
Q

What causes rigidity?
What are the characteristics of postural instability?

A

Rigidity results from simultaneous tightening of agnostic/antagonistic muscles.

Postural Instability is characterised by
Ppl. w. PD often have a forward-bent posture, which can result in falls.
Usually occurs later in the course, if it starts with this, an atypical PD should be considered.

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16
Q

What are the non-motor symptoms of PD?

A
  • Fatigue/sleep disorders
  • Sensory/pain (Esp. smell/ around two-thirds suffer from pain)
  • Autonomic
  • Neuropsychiatric and cognitive impairment.
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17
Q

What are the characteristics of fatigue and sleep disorders?

A
  • Around half struggle with fatigue
  • 60-98% have sleep impairments.
    • Often difficulty getting to sleep and long periods of wakefulness during the night
  • REM sleep behaviour disorder (RSBD) is when patients move, cry out, and flail their arms when dreaming because normal motor suppression is lacking
    • This often doesn’t disturb the patient, but their partner
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18
Q

What are the subtypes for Parkinson’s?

A

Tremor-dominant
Balance-dominant
Hypokinetic-rigid subtypes (the atypical ones)

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19
Q

Why is important to differentiate between subtypes?
Why is it important to know the initial symptoms?

A

Distinction is important because the course and treatment differ for the various subtypes.

There are indications that patients whose symptoms first occur on the left side (thus right hemisphere affected) experience more cognitive problems than those on the right.

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20
Q

What is needed for diagnosis?

A

You need Bradykinesia and at least one other motor symptom.
The course of the symptoms is an important supporting part of the diagnosis.

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21
Q

What are supporting factors for PD?

A

Unilateral lateralised start (HY Scale stage 1)
Increase in the symptoms over time
Improvement in the motor symptoms once anti-Parkinson’s drugs are taken.

22
Q

Does neuroimaging provide support for diagnosis?

A

Not really, MRI scans are only useful in very advanced stages, or to initially exclude other causes (vascular, tumours).
A SPECT scan can’t differentiate between Parkinson’s disease and CBD, MSA, or PSP.
It can be used to discover Parkinson’s, but it can’t differentiate.

Look at figure 21.2 for example of how PD can be visible.

23
Q

What factors provide evidence against Parkinson’s, and FOR atypical syndromes

A
  • Visual hallucinations and a dementia syndrome occur prior or during the first year of motor symptoms.
    • DLB is more likely
  • Severe balance disorders or eye movement disorders are observed in the early stages
    • Other atypical parkinsonian syndromes are more likely
  • Severe autonomic disorders occur
    • Other atypical parkinsonian syndromes are more likely
  • If motor symptoms do not improve after treatment with medication.
23
Q

What symptoms are typical of Multiple system atrophy (MSA)

A

Decreased balance of the torso and a strongly forward-bent posture
Relatively rapid progression
Severe speech disorders and dysphagia
Cold blue hands and feet

As a result patients become wheelchair dependent relatively quickly

23
Q

What symptoms are typical of Cortico-basal degeneration (CBD)

A

Cognitive (Cortical) problems, including apraxia and aphasia
Strong asymmetrical parkinsonism.

24
Q

What symptoms are typical of Progressive supranuclear paralysis (PSP)

A
  • Straight or slightly backward-bent posture
  • In early stage
    • Impairments in eye movements
    • Disinhibition
    • Emotional instability
25
Q

What is the most common scale to rate Parkinson’s?

A

The Unified Parkinson Disease Rating Scale (UPDRS): Used to determine severity
Hoehn & Yahr Scale (HY Scale): To determine stage. (It’s a component of UPDRS)

26
Q

What stages of the disease are there?

A

Preclinical, prodromal, and clinical

Look at figure 21.3 for examples of progression

27
Q

How many patients have cognitive impairments? How do they develop over time?

A

24% already have impairments when diagnosed
25-40% has cognitive impairments
Over time these impairments may gradually develop into dementia.
Indications that all patients with PD eventually develop substantial cognitive impairments.

28
Q

What are typical cognitive impairments

A
  • Executive dysfunctions
  • Attention problems
  • Reduction of processing speed
  • Problems with processing emotional information
  • Learning new skills is hard (because shift from control to automation doesn’t happen)
  • Problems with explicit episodic learning, because of deficiencies in delayed active retrieval.
29
Q

What occurs because of executive dysfunctions?

A
  • Visuo-spatial dysfunctions
    • Primary perception impairments, and sometimes neglect.
  • Problem in internal generation of automatisms
    • Patients have to do automatic actions in a goal-oriented manner.
30
Q

What factors increase the risk of cognitive impairments?

A
  • Attention problems and reduction of processing speed are especially at risk because of mood disorders.
  • Use of levodopa may be good for cognitive flexibility, but it’s detrimental for implicit learning, feedback learning, and suppression of undesirable behaviours.
  • It may have an inhibitory effect on learning to avoid negative outcomes, which may result in the development of impulsive behaviour.
31
Q

What types of neuropsychiatric symptoms are seen in Parkinson’s disease?
How common are they in general?

A
  • Depression
  • Anxiety
  • Apathy
  • Psychosis
  • Impulsivity
  • Sleep disorders

90% of PD patients have at least one neuropsychiatric symptom
First 3 are most common, 4th and 5th are kinda common, the last had no info.

32
Q

What are the characteristics of depression in PD?

A
  • 35-70% have depression symptoms (1:3) (3 criteria of depression are apart of PD, so its easy to see it)
  • 17% have formal depressive mood disorder
  • Sometimes decreased mood during ‘off’ moments
  • Differential diagnosis: similarities with apathy, MCI, dementia
  • Severity is often mild to moderate. Suicide is relatively rare, but is slightly higher risk after DBS surgery, due to impairment of impulse inhibition.
33
Q

What are the characteristics of anxiety in PD?

A
  • 40-50% have anxiety symptoms
  • Approximately 30% have a formal anxiety disorder
  • Sometimes increase during ‘off’ moments or transition from ‘on’ to ‘off’
33
Q

What are the characteristics of apathy in PD?

A
  • This affects families a lot as patient becomes passive, which can be perceived as lazy.
  • Plays a role in 20-40% in patients without dementia
  • up to 60% of PD patients develop dementia within 5-10 years
  • Differential diagnosis: similarities with fatigue, depression, hypoactive delirium, MCI, dementia
    • Especially difficult to differentiate from depression in PD.
34
Q

What are the characteristics of psychosis in PD?

A

Usually develops later in the disease.
Manifested as delusions and predominantly visual hallucinations and illusion.

34
Q

What are the characteristics of impulsivity in PD?

A

Caused by anti-Parkinson’s drugs and DBS
I.e. perseverative stereotypical behaviour, impulse control disorders, intense fascination with and involvement in irrelevant activities (punding).

35
Q

What is PD dementia?

A

A specific type of dementia caused by parkinsons.
For the next couple flashcards if i refer to a disorder, i’m referring to someone with the disorder who have developed dementia.

36
Q

What are the diagnostic criteria for PD dementia?

A
  • PD diagnosis diagnosed before dementia
  • Cognitive impairments are progressive
  • Cognitive impairments that interfere with daily function
  • Cognitive impairment in 2+ domains
37
Q

What cognitive domains are affected?

A
  • In memory, Active retrieval impaired, recognition maintained (different to Alzheimer’s)
  • Cognitive deterioration is most prominent in attention and psychomotor speed.
  • Aphasia, apraxia, agnosia less prevalent in PD dementia vs other dementia’s
    • However some speech difficulties occur, but thats more motor symptoms
38
Q

What are some general points about PD dementia?

A

MMSE < 26
Prevalence PD dementia 25-30%
After 10-20 years, majority of ppl w. PD develop dementia
Patients who develop dementia are younger on average.
Parkinsonism is more distinct than in patients with DLB

39
Q

How does dementia present itself in DLB?

A
  • More fluctuation in cog. performance and hallucinations
  • DLB is diagnosed if these symptoms develop prior or within 1 year of motor symptoms
  • Patients display more cognitive deficiencies and psychiatric symptoms.
40
Q

Do PD dementia and DLB have similar pathologies?

A

There is a mixed evidence for the underlying pathology of the two disorders, it’s likely they share a common pathology, but what it is? who knows. (book rambles about different evidence points, but i dont think thats necessary)

41
Q

How does dementia present itself in PSP and CBD?

A

Cognitive profiles of patients with PSP and CBD show significant cortical deficiencies, so it’s easier to identify due to similarity to Alzheimer’s.

42
Q

Do we know the risk factors for cognitive deterioration in PD?

A

Risk factors for cognitive deterioration in later stages are unknown or have little research.
There is some evidence for increased risk if onset occurs at an advanced age.
Theres also evidence that sleep disorders, like RBSD, are associated with dementia in PD, as well as DLB and MSA.

43
Q

What treatments exist for PD?

A

Parkinson’s can’t be cured, nor slowed down, so treatment is focused on suppressing symptoms.
It consists of medication, neurosurgery, and paramedical care.

44
Q

What is the most common anti-Parkinson drug?
What does it do?

A

Levodopa
Dopamine agents/agonists are also common, but remember Levodopa.
These drugs work by either increasing dopamine, or increasing the effect of dopamine to make up for the degeneration in the SN

45
Q

What are the side effects of Levodopa

A

Side effects: From narcolepsy to psychosis, hyperkinetic movements and dyskinesia,
Impairments in impulse control are particular associated w. levodopa and dopamine agonists.
Many patients experience side effects in motor control (such as hyperkinetic movements or dyskinesias, twisting movements) after taking the drugs for a while.

46
Q

What happens in the long term use of levodopa?

A

First, tolerance develops so meds wear off quickly or have delayed response
As the disease progresses, the effects of levodopa may become unpredictable and arbitrary response fluctuations may occur, meaning that the medication suddenly no longer works.
At times like this, ‘off’ symptoms may occur, such as stiffening and severe bradykinesia.

47
Q

When is brain surgery considered? What is the typical brain surgery?

A

If medication no longer works or there are negative side effects, brain surgery is considered
Deep brain stimulation (DBS)

48
Q

What does DBS do?

A

It stimulates cerebral nuclei, commonly in the subthalamic nucleus (STN).
It works really well on motor symptoms, but it does cause cognitive and affective side effects, so patients get a remote to turn it on and off when needed.

Clinical and Neuropsychology 2 (12 decks)

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