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4th Year Neuro > Parkinson’s disease > Flashcards

Parkinson’s disease Flashcards

1
Q

Pathology of Parkinson’s disease

A

Dopaminergic neurones in the substantia nigra degenerate.

Progressive, adult onset movement disorder.

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2
Q

What are the two parts of the substantia nigra and which is affected in Parkinson’s disease?

A

Pars reticulata

Pars compacta - affected area

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3
Q

Which neuro pathway is affected in Parkinson’s disease and what is its function?

A

Nigrostriatal pathway - helps to stimulate the cerebral cortex and initiate movement

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4
Q

What are the cardinal motor signs of Parkinson’s disease?

A
  • Bradykinesia
  • Resting tremor
  • Rigidity
  • Postural instability
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5
Q

What does bradykinesia look like in a patient?

A
  • Slow to initiate movement
  • Actions slow and decrease in amplitude with repetition
  • Festinant gait, pitched forward, turning en bloc
  • Decreased arm swing and freezing at obstacles or doors (due to poor simultaneous motor and cognitive function)
  • Hypomimia (expressionless face)
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6
Q

Is Parkinson’s disease unilateral or bilateral?

A

Symptoms often begin on one side of the body or even in one limb on one side of the body. As the disease progresses, it eventually affects both sides. However, the symptoms may still be more severe on one side than on the other.

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7
Q

Non motor symptoms of Parkinson’s disease

A
  • Reduced sense of smell (can lose sense of smell years before motor symptoms)
  • Sleep disturbances
  • Autonomic dysfunction
    • postural hypotension
    • constipation
    • urinary symptoms
    • dribbling of saliva
  • Neuropsychiatric complications
    • depression
    • dementia
    • psychosis
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8
Q

Does Parkinson’s disease have a treatment that will stop the progressive neurodegeneration?

A

No - treatments only aim to control symptoms and will not affect the underlying disease

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9
Q

What are the pharmacological treatments for Parkinson’s disease?

A
  • Levodopa
  • Dopamine agonists
  • MAO-B inhibitors
  • COMT inhibitors
  • Anticholinergics
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10
Q

Why is levodopa (precursor to dopamine) given instead of dopamine?

A

Levodopa can cross the blood brain barrier while dopamine cannot.

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11
Q

What is levodopa combined with and why?

A

Levodopa is administered with carbidopa - a dopa decarboxylase inhibitor that isn’t able to cross the blood brain barrier

  • Levodopa is converted to dopamine by dopa decarboxylase (within nigrostriatal neurones and by peripheral dopa decarboxylase)
  • Periperal dopa decarboxylase can metabolise levodopa into dopamine before it gets to the blood brain barrier. Dopamine can be further metabolised into other catecholamines such as epinephrine which can have side effects such as arrhythmias
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12
Q

Risk factors for Parkinson’s disease

A
  • Age: prevalence of 1% in those aged 60-70 and 1-3% in those aged over 80
  • Gender: males 1.5x more likely to develop than females
  • Family history
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13
Q

Side effects of levodopa

A
  • Compulsive gambling, hypersexuality, binge eating, or obsessive shopping (can develop in patient on any dopaminergic therapy)
  • Dyskinesia - involuntary movements
  • Wearing off - the effects of the drug wear off before the next dose
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14
Q

Why should levodopa not be withdrawn suddenly?

A

It risks acute akinesia and neuroleptic malignant syndrome

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15
Q

How do anticholinergics work? Who should they be used for?

A

They balance acetylcholine with dopamine

They cause confusion in the elderly and have multiple side effects - limit use to younger patients

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16
Q

How do COMT inhibitors and MAO-B inhibitors work?

A

They inhibit enzymes which metabolise dopamine which increases the dopamine concentration in the brain

17
Q

MAO-B inhibitor examples, use and side effects

A

Rasagiline, selegiline

An alternative to dopamine agonists in early Parkinson’s disease

Side effects include postural hypotension and atrial fibrillation

18
Q

Other causes of Parkinsonism

A
  • Lewy body dementia
  • Wilson disease
  • Pick disease
  • Encephalitis
  • Neurosyphilis
  • Side effects of:
    • antipsychotics (haloperidol) - blocks dopamine receptors
    • metclopramide - dopamine antagonist used to treat vomiting
19
Q

Parkinson’s disease is a clinical diagnosis.

Which investigations might be considered in Parkinson’s disease?

A
  • DaT scan: single-photon emission computed tomography (SPECT) will show reduced dopamine uptake in the basal ganglia
  • MRI brain: to exclude other causes of neurological disease but should not be used to diagnose PD
  • Ceruloplasmin and urinary copper: if suspecting Wilson’s disease, ceruloplasmin is reduced and urinary copper is raised
20
Q

What is the first line treatment given to patients with motor symptoms affecting quality of life?

A
  • Levodopa and decarboxylase inhibitor (Co-beneldopa)
21
Q

What is the first line treatment given to patients with motor symptoms not affecting quality of life?

A
  • Dopamine agonist (pramipexole or ropinirole)
  • MAO-B inhibitor (selegilline, rasagilline)
  • Levadopa and decaboxylase inhibitor (Co-benyldopa)
22
Q

Adjuvant treatments suitable for patients with dyskinesia

A
  • COMT inhibitors (entaxapone)
    • indicated in those with motor fluctuations or dyskinesia
    • reduces breakdown of levodopa peripherally
  • Amantadine
    • increases dopamine release and reduces reuptake
23
Q

Which adjuvant treatment may be suitable in advanced disease with significant motor symptoms?

A

Deep brain stimulation

24
Q

Which part of the brain is the target for deep brain stimulation?

A

Subthalamic nucleus and globus pallidus internus are the main targets.

25
Q

OSCE examination of patient with Parkinson’s disease

A
  • Upper limb examination
    • ​Rigidity, bradykinesia and tremor (ask patient to close and open fist repeatedly to demonstrate bradykinesia)
  • Lower limb
    • ​Gait assessment
  • Screen for other causes
    • ​Ask for a lying and standing BP
    • Check vertical eye movements
    • Check for cerebellar signs
    • Offer to do a screen of cognition eg MMSE
26
Q

If a patient with symptoms of Parkinson’s disease had difficulty looking down, what would this suggest?

A

This is characteristic of progressive supranuclear palsy which is a Parkinson-plus syndrome. Patients have a vertical gaze palsy.

27
Q

What are the structures of the basal ganglia?

A
  • Striatum
    • Caudate
    • Putamen
  • Globus pallidus
  • Subthalamic nucleus
  • Substantia nigra
    • Pars compacta
    • Pars reticulata
28
Q

How can you differentiate Wilson’s disease from Parkinson’s disease?

A

Wilson’s disease is seen in younger patients with liver disease and Parkinsonian symptoms

29
Q

How can you differentiate Lewy body dementia from Parkinson’s disease?

A

In Lewy body dementia cognitive impairment usually precedes motor symptoms. Patient usually have visual hallucinations.

4th Year Neuro (12 decks)

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