Parkinson's Disease Flashcards

(40 cards)

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
What is the treatment for Lewy body dementia?
* the same treatment for Alzheimers * acetylcholinesterase inhibitors and **memantine** are used * ACh esterase inhibitors = **donepezil + rivastigmine**
25
How are the symptoms of drug-induced parkinsonism different?
* the motor symptoms are **rapid onset** and **bilateral** * rigidity and resting tremor are uncommon
26
How is Parkinson's disease diagnosed?
* 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 ## Footnote SPECT = single photon emission computed tomography
27
Who can initiate treatment for Parkinson's disease?
* management is **guided by a specialist** * management is tailored to each individual patient and their response to different medications
28
What is the most effective drug for controlling motor symptoms in PD? | Who is this offered to?
**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
What must levodopa be co-prescribed with?
**peripheral decarboxylase inhibitors** * these stop the levodopa from being broken down before it enters the brain * e.g. **carbidopa** and **benserazide**
30
What combination drugs can be given that include levodopa + peripheral decarboxylase inhibitor?
**co-benyldopa:** * levodopa + benserazide **co-careldopa:** * levodopa + carbidopa
31
What is the main side effect associated with levodopa?
* when the level of dopamine is too high, patients can develop **dyskinesias** * these are **abnormal movements** associated with excessive motor activity
32
What are the 3 main dyskinesias associated with excessive dopamine?
**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
What medication may be given to extend the effective duration of levodopa?
**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 ## Footnote COMT = catechol-o-methyltransferase
34
How do dopamine agonists work? What are examples?
* they mimic dopamine in the basal ganglia to **stimulate dopamine receptors** * examples include: 1. ***bromocryptine*** 2. ***pergolide*** 3. ***carbergoline***
35
When are dopamine agonists used in the treatment of PD?
* 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
What is the most significant side effect of dopamine agonists?
pulmonary fibrosis
37
How do monoamine oxidase-B inhibitors work?
* 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
When are MAO-B inhibitors used to treat PD?
* 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
What are examples of MAO-B inhibitors?
* selegiline * rasagiline