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Y4 - CCC & PC > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is Parkinson’s disease?

A
  • a progressive neurodegenerativve condition
  • caused by degeneration of dopaminergic neurones in the substantia nigra
  • this is part of the basal ganglia, which has a role in regulation of motor signalling

there is a gradual but progressive fail in the production of dopamine

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2
Q

What is the classic triad of symptoms?

What is significant about these symptoms?

A
  • bradykinesia
  • resting tremor
  • rigidity
  • these symptoms are ASYMMETRICAL with one side being affected more than the other
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3
Q

Who is typically affected by Parkinson’s disease?

A
  • it is twice as common in men
  • the mean age of diagnosis is around 65 years
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4
Q

How is the tremor in Parkinson’s disease described?

A

“pill rolling tremor”

  • it looks as though they are rolling a pill between their fingertips and thumb
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5
Q

What is the frequency of the tremor?

A

4-6 Hz

it occurs 4 to 6 times each second

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6
Q

When is the tremor worse / better?

A
  • the tremor is more pronounced when resting
  • it improves during voluntary movement
  • it becomes worse when the patient is distracted or stressed / tired

ask the patient to perform a task with the other hand (e.g. mime the motion of painting a fence) will exaggerate the tremor

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7
Q

What is significant about the tremor?

A

it is unilateral

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8
Q

How is the rigidity in Parkinson’s disease described?

A

“cogwheel rigidity”

  • when passively flexing / extending the arm at the elbow, there is tension in the arm that gives way to movement in small increments (small jerks)
  • this is due to the superimposed tremor

this is different to “lead pipe rigidity” in which there is uniform resistance to movement

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9
Q

What is meant by bradykinesia?

A
  • this describes how movements beome smaller and slower
  • there are often hesitations / pauses during continued movement

sometimes described as hypokinesia = this is a decrease in amplitude of movement

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10
Q

What symptoms result from the development of bradykinesia?

A
  • handwriting becomes smaller and smaller (micrographia)
  • they have a “shuffling gait” as can only take small steps when walking
  • difficulty initiating movement (e.g. from standing still to walking)
  • difficulty in turning around, having to take many small steps
  • hypomimia - reduced facial movements + facial expressions
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11
Q

How is gait changed in Parkinson’s disease?

A
  • they have a “shuffling gait” as they take many small steps
  • there is reduced arm swinging
  • they also have a stooped posture
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12
Q

What other features can sometimes affect patients with Parkinson’s disease?

A
  • depression
  • sleep disturbance / insomnia
  • REM sleep behaviour disorder
  • anosmia (loss of sense of smell)
  • postural instability
  • cognitive impairment + memory problems
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13
Q

What are the differences between a Parkinson’s tremor and benign essential tremor?

A
  • BET tends to improve at rest
  • it is symmetrical
  • it is worse with intentional movement
  • it improves with alcohol
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14
Q

What are the 4 main Parkinson’s-plus syndromes?

A
  1. multiple system atrophy
  2. dementia with Lewy Bodies
  3. progressive supranuclear palsy
  4. corticobasal degeneration
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15
Q

What is multiple system atrophy?

A
  • the neurones of multiple systems in the brain degenerate
  • the degeneration of the basal ganglia results in a Parkinson’s presentation
  • the degeneration in other areas leads to autonomic + cerebellar dysfunction
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16
Q

What are the additional symptoms seen in multiple system atrophy?

A

cerebellar dysfunction:

  • ataxia

autonomic dysfunction:

  • constipation
  • postural hypotension
  • abnormal sweating
  • sexual dysfunction
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17
Q

What is dementia with Lewy bodies?

A
  • a type of dementia associated with features of Parkinsonism
  • it causes progressive cognitive decline
  • there is a decline in thinking, reasoning + independent function
17
Q

What is dementia with Lewy bodies?

A
  • a type of dementia associated with features of Parkinsonism
  • it causes progressive cognitive decline
  • there is a decline in thinking, reasoning + independent function
18
Q

What are some of the symptoms associated with Lewy body dementia?

A
  • REM sleep behaviour disorder
  • fluctating consciousness
  • recurrent visual hallucinations / delusions
  • spontaneous changes in attention / alertness
19
Q

What is REM sleep behaviour disorder?

A
  • a sleep disorder in which the patient physically acts out vivid, unpleasant dreams during REM sleep
  • this involves vocal sounds and sudden, often violent arm and leg movements
20
Q

How can Lewy body dementia be differentiated from isolated Parkinson’s disease?

A
  • cognitive impairment typically occurs before parkinsonism
  • both features tend to occur within 1 year of each other
  • in PD, the motor symptoms tend to present at least one year before the cognitive symptoms
21
Q

What is the characteristic pathological feature of Lewy body dementia?

A
  • positive immunohistochemistry staining for alpha-synuclein
  • the Lewy bodies within the substantia nigra stain brown
22
Q

What 2 main features are unique to Lewy body dementia and do not occur in other forms?

A
  • cognition is fluctating - this does not occur in other forms of dementia
  • there are early impairments in attention + executive function (in Alzheimer’s there is just memory loss)
23
Q

What medication must be avoided in Lewy body dementia?

A

neuroleptics

  • patients are very sensitive and may develop irreversible parkinsonism
  • the patient will deteriorate rapidly following introduction of an antipsychotic agent

neuroleptics = medications that block dopamine receptors

e.g. haloperidol, olanzapine, clozapine, paliperidone, thioridazine etc.

24
Q

What is the treatment for Lewy body dementia?

A
  • the same treatment for Alzheimers
  • acetylcholinesterase inhibitors and memantine are used
  • ACh esterase inhibitors = donepezil + rivastigmine
25
Q

How are the symptoms of drug-induced parkinsonism different?

A
  • the motor symptoms are rapid onset and bilateral
  • rigidity and resting tremor are uncommon
26
Q

How is Parkinson’s disease diagnosed?

A
  • diagnosis is clinical by a specialist with experience in diagnosing Parkinson’s
  • NICE recommend using the UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria
  • SPECT can be considered if there is difficulty differentiating from BET

SPECT = single photon emission computed tomography

27
Q

Who can initiate treatment for Parkinson’s disease?

A
  • management is guided by a specialist
  • management is tailored to each individual patient and their response to different medications
28
Q

What is the most effective drug for controlling motor symptoms in PD?

Who is this offered to?

A

levodopa

  • this is synthetic dopamine
  • it is offered to newly diagnosed patients whose motor symptoms are significantly affecting their QoL
  • it tends to be reserved for when other treatments are not managing to control symptoms
  • this is because it becomes less effective over time
29
Q

What must levodopa be co-prescribed with?

A

peripheral decarboxylase inhibitors

  • these stop the levodopa from being broken down before it enters the brain
  • e.g. carbidopa and benserazide
30
Q

What combination drugs can be given that include levodopa + peripheral decarboxylase inhibitor?

A

co-benyldopa:

  • levodopa + benserazide

co-careldopa:

  • levodopa + carbidopa
31
Q

What is the main side effect associated with levodopa?

A
  • when the level of dopamine is too high, patients can develop dyskinesias
  • these are abnormal movements associated with excessive motor activity
32
Q

What are the 3 main dyskinesias associated with excessive dopamine?

A

chorea:

  • abnormal involuntary jerking movements

athetosis:

  • involuntary writhing movements, usually in the fingers or feet

dystonia:

  • excessive muscle contraction results in abnormal postures / exaggerated movements
33
Q

What medication may be given to extend the effective duration of levodopa?

A

entacapone

  • this is a COMT inhibitor
  • the COMT enzyme metabolises levodopa in the body / brain
  • inhibiting COMT enzyme slows the breakdown of levodopa to extend its effective duration

COMT = catechol-o-methyltransferase

34
Q

How do dopamine agonists work?

What are examples?

A
  • they mimic dopamine in the basal ganglia to stimulate dopamine receptors
  • examples include:
  1. bromocryptine
  2. pergolide
  3. carbergoline
35
Q

When are dopamine agonists used in the treatment of PD?

A
  • they are used to delay the use of levodopa
  • and then in conjunction with levodopa to reduce the dose of levodopa needed to control symptoms
  • they are LESS EFFECTIVE than levodopa in controlling symptoms
36
Q

What is the most significant side effect of dopamine agonists?

A

pulmonary fibrosis

37
Q

How do monoamine oxidase-B inhibitors work?

A
  • monoamine oxidase enzymes break down neurotransmitters such as adrenaline, serotonin & dopamine
  • MAO-B is more specific to dopamine
  • MAO-B inhibitors block this enzyme to increase circulating dopamine
38
Q

When are MAO-B inhibitors used to treat PD?

A
  • they are used to delay the use of levodopa
  • they are then used in conjunction with levodopa to reduce the dose needed to control symptoms
39
Q

What are examples of MAO-B inhibitors?

A
  • selegiline
  • rasagiline

Y4 - CCC & PC (34 decks)

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