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Gwen - Neurology > Parkinsonism > Flashcards

Parkinsonism Flashcards

1
Q

What is parkinsonism?

A

Umbrella term that describes many conditions which share some of the symptoms of Parkinson’s. The main symptoms of Parkinson’s – tremor, rigidity and bradykinesia – are also the main symptoms of a number of conditions that are grouped together under the term parkinsonism

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2
Q

What are causes of parkinsonism?

A
  • Idiopathic Parkinson’s disease
  • Parkinson’s plus syndromes
    • ​Progressive supranuclear palsy (PSP)
    • Mutiple system atrophy (parkinsonism + autonomic + cerebellar signs)
    • Corticobasilar degeneration
  • Secondary parkinsonism
    • Encephalopathy (post-ecephaleptic)
    • Drug/toxin induced - antipsychotics, illicit drugs, copper (wilsons)
    • Strokes - in midbrain ganglia (multiple cerebral infarcts)
    • Hydrocephalus
    • Trauma - boxing
  • Degenerative Parkinsonism - alzheimers, lewy body
  • Genetic disorders - wilson’s, huntington’s
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3
Q

How does parkinson’s disease develop?

A
  • Arises from the death of dopaminergic in the pars compacta of the substantia nigra.
  • This leads to striatal actvitiy increasing due to lack of inhibitory influence of the substantia nigra.
  • Striatal activity exerts inhibitory affect on pallidum. As substantia nigra is no longer exerting excitatory effect on striatum, it reduces it’s inhibitory effect on the pallidum, which in turn grossly inhibits the thalamus.
  • This prevents excitatory signals being sent to the motor cortex, resulting in difficulty initiating movement

https://www.youtube.com/watch?v=I4XXoiWwoNc

SO:

  • Substantia Nigra degeneration (reduced dopamine)
  • Very high striatal activity (increased GABA)
  • Inhibition of pallidum
  • Hypokinesia
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4
Q

What are the characteristic features of the resting tremor in parkinson’s disease?

A
  • 4-6 cycles per second
  • Pill rolling - thumb over finger
  • Disappears with voluntary movement - so worse at rest and anxiety, imbroves by voluntary movement
  • Unilateral at presentation, progresses to bilateral

https://www.youtube.com/watch?v=ZMx07OagyJw

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5
Q

What are the characteristic features of rigidity in parkinsonism?

A
  • Lead-pipe rigidity - A hypokinetic disorder characterized by the inflexibility or stiffness of the limb that is maintained equally throughout the passive flexion
  • Cogwheel rigidity - series of catches/stalls when rapid movement performed by examiner
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6
Q

What are the features of bradykinesia/hypokinesia seen in parkinsonism?

A

Slow to initiate movement

  • Problems with fine motor tasks: writing, sewing or getting dressed.
  • Decreased blink rate (abnormal glabellar reflex)
  • Monotonous hypophonic speech
  • Micrographia - (small cramped handwriting)
  • Dead pan face

Gait changes

  • Decreased arm swing
  • Shuffling steps
    *
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7
Q

What are the core features of parkinson’s disease?

A
  • Bradykinesia/hypokinesia, plus one of:
    • Resting tremor
    • Rigidity
    • Postural instability
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8
Q

What is characteristic about the shuffling gait seen in parkinson’s disease?

A

Shuffling steps with reduced arm swing and flexed trunk, as if chasing one’s centre of gravity. Have difficulty turning on the spot, taking many steps

Classicalyl stooped posture with tendancy to fall

https://www.youtube.com/watch?v=MFA0aN8VpS4

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9
Q

What are non-motor symptoms of parkinson’s disease?

A
  • Ansomnia - Reduced sense of smell
  • Frequency/urgency
  • Dribbling of saliva
  • Neuropsychiatric - Depression, hallucinatnions, dementia, impulsive behaviour, bradyphrenia - slowed process of thought
  • Sleep disorders - insomnia, sleep fragmentation
  • GI and autonomic - drooling of saliva, excessive sweating, dysphagia, constipation
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10
Q

What is the typical age of onset of parkinson’s disease?

A

65 yrs old

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11
Q

What would be a diffirential diagnosis for tremor and bradykinesia?

A
  • Idiopathic parkinsons disease
  • Drug induced parkinsonism
  • Vascular parkinsonism
  • Essential tremor
  • Normal pressure hydrocephalus
  • Dementia with lewy bodies
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12
Q

What are parkinson’s plus syndromes?

A
  • Progressive supranuclear palsy
  • Multiple system atrophy
  • Corticobasal degeneration
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13
Q

What are causes of secondary parkinsonism?

A
  • Vascular
  • Drug induced
  • Hydrocephalus
  • Post-encephalitic
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14
Q

How would you investigate someone with parkinsonism?

A
  • Clinical examination - cardinal signs, positive pull test
  • Toxicology screen

May also do Imaging: CT/MRI, SPECT, Brain biopsy (Lewy body)

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15
Q

What would a resting tremor potentially indicate?

A

Parkinson’s disease

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16
Q

What could cause a tremor that occurs on maintaining a posture or with movement?

A
  • Essential tremor
  • Exaggerated physiological tremor
  • Hyperthyroidism
  • Drug-induced
  • Dystonic tremor
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17
Q

How would you manage someone with parkinson’s disease?

A
  • MDT involvement
  • Medical
    • Levodopa + Carbidopa - early disease
    • Dopamine agonists - early disease
    • MAO-B inhibitors - early disease
    • Anticholinergic drugs
    • COMT inhibitors
  • Neuropsychiatric conditions
  • Respite care
  • Deep brain stimulation
18
Q

What would you be thinking of if someone had the following tremor (improves during the action of reaching a target but is worse on reaching the target)?

https://www.youtube.com/watch?v=Imu1kk_gOKA

A

Cerebellar dysfunction - intention tremor - The amplitude of an intention tremor increases as an extremity approaches the endpoint of deliberate and visually guided movement

19
Q

How does levodopa work?

A

Levadopa is a natural precursor of dopamine. To prevent levodopa from being broken down peripherally, it is given in combination with a dopa-decarboxylase (carbidopa), which increases the amount available to the basal gnaglia.

Decreased efectiveness over time

20
Q

Long term SE of levodopa

A

Dyskinesia (invulntary movements)

On and off phenomenon

Psychosis

ABP reduced

Mouth dryness

Insomnia

N+V

Excess daytime sleepiness

Motor fluctuations (drug awareness)

Non motor SE = psychosis and visual hallucination

21
Q

How do dopamine agonists work?

A

Bind to dopaminergic post-synaptic receptors in the CNS and thereby increase dopaminergic neurotransmission

Echo/ESR/creatinine/CXR needed beofre

22
Q

Side effects of dopamine agonists

A

Drowsiness, compulsive behaviour, hallucinations

23
Q

Give examples of dopamine agonists

A

Cabergolin, bromoriptine, ropiniride,

24
Q

What is essential tremor?

A

Postural or kinetic tremor in the frequency range of 4 to 12 Hz (usually at the lower end of the range in older patients) is generally the only manifestation in patients with essential tremor. Occasionally, when severe, rest tremor and mild abnormalities of tone and gait may also occur.

25
Q

How do MOA-B inhibitors work?

A

Protects dopamine from being degraded within neurones

eg Selegiline

Alternative to dopamine agonists in early PD

26
Q

Side effects MOA-B inhibitor

A

Postural hypotension, arrhythmias

27
Q

What would indicate that someone had an essential tremor?

A

Reduces/disappears after consuming alcohol

28
Q

What are side effects of levodopa?

A
  • Dyskinesia
  • Psychiatric symptoms - hallucinations, delusions, nightmares, confusion
  • Unpredictable on/off switching
  • Hypotension and syncope
  • Dementia
  • Hypertension
  • Nausea/vomiting
29
Q

What are the side effects of Dopamine agonists?

A
  • Nausea, vomiting
  • Hypotension
  • Psychiatric symptoms - hallucinations, delusions, nightmares
  • Sleep disturbance and sudden onset of sleep
  • Impulse control disorders - compulsive sexual activity, overeating, gambling
30
Q

How do COMT inhibitors work?

A

Block the enzyme breakdown of dopamine and the drug levodopa and thereby reduces ‘off’ times. Because these medications affect levodopa levels directly the dose commonly needs to be reduced.

Eg entecapone

Used as an adjunvt to levodopa

SE = dry mouth, constipation

31
Q

In early parkinson’s disease, what is important to think about in terms of pharmacological intervention?

A

The decision of when to begin treatment can be a difficult one, particularly as levodopa is associated with more adverse effects the longer it is used

32
Q

What drugs would you use in early parkinson’s disease?

A
  • Levodopa + dopa decarboxylase inhibitor
  • Dopamine Receptor Agonists
  • Monoamine oxidase B inhibitors
33
Q

Outline the principles of parkisnons management

A

Delay in treatment until the onset of disabling symptoms and then to introduce a dopamine agonist

34
Q

What medication can be used in drug indiced parkinsonism?

A

Anticholinergics

SE - dry mouth, diziness,r educeed vision, urinary retention, confusion

35
Q

1st lin if parkinsons affecting quality of lfie

A

LEVODOPA

then add dopamine agonist, MAO-B or COMT as adjunct

36
Q

1st line if motor symptoms are not affecting pateints QOL

A

Dopamine agonist

Levodopa

MAO-B inhibitor

37
Q

Differences between essential tremor and parkinsons tremor

A

Essential bilateral, parkinsons unilateral.

Essential assocaited with purposeful movement, parkinsons tremor at rest.

Essential tremor affects arm mostly, parkinsons affects hands.

38
Q

What is a resting tremor? Cause?

A

Abolished on voluntary movement.

Parkinsonism

39
Q

What is an intention tremor? Causes?

A

Irregular large-amplitude, worse at end of purposeful acts eg finger pointing or using a remote control.

Finger nose touch (tremor worse when readching).

Causes: cerebellar damage eg MS, stroke

40
Q

What is postural tremor?

Cause

A

When body is voluntarily maintained against gravity

Absent at rest, present on maintined posture (arms otstretched)

When arms adopt a posture

May persist but is not worse on movement.

Causes: Benign Essential Tremor, anxiety B agonists.

Gwen - Neurology (38 decks)

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