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Anatomy > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

Overview with specific relevance to SLT

1
Q

What is Parkinson’s?

A

A progressive neurodegenerative disorder affecting the brain

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2
Q

What are the main characteristics of Parkinson’s

A

Tremor, Rigidity, Slowness of Movement

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3
Q

What causes Parkinson’s?

A

Most cases are sporadic but there may be a genetic component. A small % is genetic - this cases have earlier onset and progress more rapidly

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4
Q

What the pathology of Parkinson’s? (i.e. what is damaged)

A

Damage to extrapyramidal system.

Involved pathological changes affecting dopaminingic neurons in the substantia nigra in the midbrain

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5
Q

What happens in the earlier stages of Parkinson’s? (i.e. what is damaged in the earlier stages)

A

Dopaminingic neurons are damaged - therefore they have less ability to manufacture and store dopamine.
The neurons accumulate Lewy bodies

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6
Q

What happens in the later stages of Parkinson’s? (i.e. what is damaged in the later stages)

A

Brain shows depigmentation, loss of neurons and gliosis (scarring) in the substantia nigra

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7
Q

Besides motor control, what else is the nigrastatal system involved in?

A

Cognitive and executive function, and reward (addictive behaviours can emerge)

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8
Q

What might be happening at a cellular level in Parkinson’s?

A

abnormal protein processing, oxidative stress, mitrochondrial dysfunction, excitotoxicity, inflammation, immune responses (don’t know what is primary event)

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9
Q

List two secondary causes of Parkinson’s

A

Drug-Induced Parkinson’s

Traumatic Parkinson’s

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10
Q

Describe the tremor in PD

A

slow pill rolling tremor, present only at rest
usually begins unilaterally in one hand
often noticed first by family/spouse
can involve the leg, lips, jaw or tongue
worse with anxiety, stress or emotional excitement

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11
Q

Describe Bradykinesia

A

generalised slowness of movement and major factor of disability associated with PD
Patients find it hard to describe
in arms it starts with reduced manual dexterity of fingers
Reduced arm swinging when walking
Legs dragging (shorter shuffling steps)

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12
Q

Describe Rigidity

A

increased tone -> resistance to passive movement

‘Cog wheel’ rigidity = increased tone with superimposed tremor

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13
Q

Features of More Advanced PD?

A

Postural Instability

Freezing

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14
Q

What are the communication difficulties in PD?

A 
Hypokinetic Dysarthria (difficulty fractioning complex movements, articulation is unclear) 
Hypophonia 
Hypomimia 
Pallilalia
Micrographia
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15
Q

Are there swallowing difficulties in PD?

A

Yes in the advanced stages of PD. Difficulty initiation voluntary movements is a contributed factor

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16
Q

What are the non-motor features of advanced PD

A

Anosmia - reduced smell
Autonomic dysfunction (e.g. constipation, bladder and sexual dysfunction)
Cognitive Impairments (decision making, abulia)
Fatigue
Disordered sleep
Neuropsychiatric (depression, anxiety, psychosis and hallucinations)

17
Q

How do you diagnose PD

A

Neurological exam and history taking
Essential criteria: bradykinesia and either rigidity or tremor
PLUS: 2 supportive criteria - rest tremor, response to dopaminergic meds, presence of leva-dopa induced dyskinesia, no red flags for other diagnoses

18
Q

What does L-dopa do?

A

Chemical building block that is converted to dopamine in the brain. Effective for many motor symptoms, but less effective as the disease progresses and there are significant side effects

19
Q

What does a dopamine agonist do?

A

Mimics the action of dopamine by binding to dopamine receptions and acting like dopamine.
Less effective but less side effects

20
Q

What does MAO-BI do?

A

It blocks dopamine breakdown - preserving existing dopamine.
Less effective than L-dopa but less side effects
used as an adjunct to boost/prolong L-dopa

21
Q

What does COMT inhibitors?

A

Blocks L-dopa breakdown.

Less effective

22
Q

How would you treat someone with Minimal PD?

A

might not treat, or might use MAO-BI (to boost dopamine)

23
Q

How would you treat someone with Mild PD?

A

First - dopamine agonist

24
Q

Hoe would you treat someone with Mod/severe PD?

A

Generally, will treat with L-dopa

25
Q

What are the motor side effects of drug treatment?

A 
Motor fluctuations (between on and off periods) 
Wearing off phenomenon 
Unpredictable off period 
Gait freezing 
Failure of 'on' response
26
Q

What type of L-dopa dyskinesia is during the on phase?

A

Chorea - irregular jerking movements

27
Q

What type of L-dopa dyskinesia is during the off phase?

A

Dystonia

28
Q

Dopamine agonist side effects?

A

Impulse Control Disorders

Mood disorders

29
Q

Main type of dopamine agonist?

A

Apomorphine
Administered subcutaneously via a pump
Side effect: nausea

30
Q

Why should you not stop PD meds suddenly?

A

Risk of akinesia (no movement)
Risk of life-threatening neuroleptic malignant syndrome
NB - think of how people with dysphasia will be administered drugs

31
Q

If a patient can’t swallow a tablet what other alternatives are there?

A

crushed tablets in NG tube
dispersible tablets
transdermal patches
apomorphone infusions

32
Q

How does lesion surgery work for people with PD?

A

involves creating a permanent small lesion in the basal ganglia circuitry

33
Q

How does deep brain stimulation work?

A

alleviates the symptoms so meds can be reduced so that medication related disability can be reduced
the surgically implanted brain electrodes stimulate the key basal ganglia
thought to work by altering the balance of excitatory and inhibitory activity in the basal ganglia motor circuits

34
Q

Who is deep brain stimulation suitable for?

A

People who respond well to L-dopa

Those without cognitive or mental health difficulties

35
Q

What the benefits of deep brain stimulation?

A

Better symptom control
Increased ‘on’ time
reduced need for meds
lasts 3-5 years
speech MAY improve if dysarthia is responsive to pre-op L-dopa
Verbal fluency can be adversely affects and overstimulation can worsen speech

36
Q

What is the prognosis for PD?

A

from impairment to disability 3-7 years
live between 6-22 years post onset
Prevalence of dementia in PD is around 40%

37
Q

What are the atypical parkinsonian disorders?

A

Multiple System Atrophy (prominent autonomic symptoms)
Progressive Supranuclear Palsy (+ difficulties looking up and down, prone to falls)
Corticobasal degeneration - spasiticity, cortical sensory loss

38
Q

What is dementia with Lewy Bodies

A

Parkinsonism with early dementia and visual hallucinations

Anatomy (12 decks)

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