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3A Neurology > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

What is Parkinson’s disease (PD) definition?

A

Parkinson’s Disease (PD) is a neurodegenerative disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta (SNPC) of the basal ganglia (nigrostriatal pathway).

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2
Q

Epidemiology of PD

A
  • Parkinson’s Disease is the second most common neurodegenerative disease (after Alzheimer’s Disease)
  • It’s progressive, adult-onset disease, and it gets more common with age
  • Prevalence of 1% in those aged 60-70 and up to 1-3% in those ≥80 years old
  • M>F
  • 3% > 65 yr.
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3
Q

RFs for PD

A
  • Age:prevalence of 1% in those aged 60-70 and up to 1-3% in those ≥80 years old
  • Gender:males are 1.5 times more likely than females to develop PD
  • Family History
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4
Q

What is PD?

A
  • Parkinson’s disease is a condition where there is a progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement.
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5
Q

Key genes involved in Parkinson’s ?

A

Those which code for α-synuclein and the ubiquitin-protease system.

the result is a loss of transmission between the basal ganglia, thalamus, and motor cortex, resulting in unimpaired control of voluntary movements.

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6
Q

What is the histological hallmark of PD?

A

eosinophilic inclusion bodies consisting of misfolded α-synuclein in the dopaminergic neurones of the SNPC called Lewy bodies.

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7
Q

What are the significance of these inclusion bodies

A

misfolded α-synuclein may spread to neighbouring brain regions in a prion-like fashion.

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8
Q

What is the basic pathophysiology of PDs

A

There is diminished substantia nigra

Susceptibility factors + Inherited factors + Parkinsons Genes > Cell loss in substantia Nigra < Risk Factors + Environmental factors + Toxin induced

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9
Q

‘Parkinsonism’ symptoms

A
  • Bradykinesia
  • Tremor (at rest, maybe unilateral)
  • Rigidity (Pain, problems with turning in bed)
  • Postural instability
  • non motor brain functions
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10
Q

What other conditions is Parkinsons associated with?

A
  • lewy body dementia
  • multiple system atrophy
  • progressive supranuclear palsy
  • corticobasal degeneration
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11
Q

What do PD symptoms usually start and then later become?

A

Start unilaterally
Then become bilateral later in the disease course

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12
Q

Bradykinesia symptoms

A
  • Slow movements
  • Difficulty initiating movement
  • Shuffling gait with reduced arm swing
  • Problems with doing up buttons, keyboard etc
  • Writing smaller
  • Walking deteriorated: Small stepped, dragging one foot etc
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13
Q

Tremor symptoms

A
  • Resting ‘pill-rolling’ (4-6 Hz) tremor
  • At rest - better with voluntary movement
  • May be unilateral
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14
Q

Rigidity symptoms

A

Cogwheel rigidity occurs due to a tremor superimposed on a rigid movement

Lead- pipe rigidity describes stiffness throughout the entire movement

Pain

Problems with turning in bed

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15
Q

Other features of motor symptoms

A
  • Micrographia - (abnormally small, cramped handwriting)
  • Hypomimia (reduced degree of facial expression)
  • Postural instability
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16
Q

Non motor symptoms of PD

A
  • Anosmia (smell blindness)
  • Sleep disturbance: REM sleep is impaired
  • Psychiatric symptoms
    • Depression
    • Anxiety
    • Dementia: usually develops after motor symptoms, unlike in Lewy-body dementia
  • Constipation
  • Increased urinary frequency
  • Urinary incontinence not typical
17
Q

What does the increased pressure of the hydrocephalus in PD cause?

A

Magnetic gait
Incontinece
Dementia

18
Q

What symptoms are not found in PD?

A
  • Incontinence
  • Dementia
  • Symmetry
  • Early falls

These especially not found in early PD

19
Q

PD investigations

A
  • PD is a clinical diagnosis: it should be suspected in a patient who has bradykinesia and atleastoneofthe following:
    • Tremor
    • Rigidity
    • Postural instability
20
Q

What investigations can you consider for PD

A
  • MRI brain:may help exclude other causes of neurological disease but should not be used to diagnose PD
  • SPECT (DaT scan):single-photon emission computed tomography (SPECT) will show reduced dopamine uptake in the basal ganglia
21
Q

DDs FOR Parkinson

A

Benign Essential Tremor

22
Q

Benign Essential Tremor - Treatment

A
  • Take it seriously!
  • 1/3 of pat have to re-train!
  • Beta-blockers
    Up to 100 mg bd
    Contraindicated in pat with asthma or diabetes
  • Primidone
    Start off with low doses
  • Others
    Gabapentin, clonazepam
23
Q

1st line management for PDs
Motor symptoms affecting quality of life

A
  • Levodopa + decarboxylase inhibitor
    • Co-benyldopa (levodopa and benserazide)
    • Co-careldopa (levodopa and carbidopa)
    • Boosts dopamine levels and decarboxylase inhibitor prevents levodopa breakdown before it reaches the brain
24
Q

1st line medications for motor symptoms not affecting quality of life

A

A choice of one of the following:

  • Dopamine agonist(non-ergot derived)
    • Pramipexole, ropinirole
    • Ergot derived medications (e.g. bromocriptine) should be avoided as they are associated with cardiac and pulmonary fibrosis
  • Monoamine oxidase B inhibitor
    • Selegiline, rasagiline
    • Stop breakdown of circulating dopamine
  • Levodopa + decarboxylase inhibitor
25
Q

L-Dopa features

A

Most powerful drug
The higher the dose, the greater the risk of SE

26
Q

2nd line management of PDs

A
  • Catechol-O-methyltransferase inhibitors (Rasagiline - Selegiline)
  • Amantadine
  • Subcutaneous apomorphine
  • Deep Brain stimulation
27
Q

MAO- B inhibitor (Catechol-O-methyltransferase inhibitors) features

A

Not very powerful, but does help some patients
If any of the currently licensed PD drugs have neuroprotective effect, it’ s this one!

28
Q

What is the monitoring for Parkinson’s disease

A

Those with confirmed disease should be reviewed 6-12 monthly

29
Q

What are motor complications usually related to in Parkinson’s disease

A

These are usually related to the use of anti-parkinsonian medication

30
Q

Motor complications of Parkinson’s

A
  • Motor fluctuations:symptoms are initially well-controlled (on period) but then re-emerge prior to the next dose (off period). The off period gets longer and more unpredictable as PD advances
  • Freezing:sudden stoppage of movement
  • Dyskinesia:excessive involuntary movements related to levodopa use (excess dopamine)
    • Dystonia: This is where excessive muscle contraction leads to abnormal postures or exaggerated movements.
    • Chorea: These are abnormal involuntary movements that can be jerking and random.
    • Athetosis: These are involuntary twisting or writhing movements usually in the fingers, hands or feet.
31
Q

Motor complications of late stage PD

A
  • Motor fluctuations:symptoms are initially well-controlled (on period) but then re-emerge prior to the next dose (off period). The off period gets longer and more unpredictable as PD advances
  • Freezing:sudden stoppage of movement
  • Dyskinesia:excessive involuntary movements related to levodopa use (excess dopamine)
    • Dystonia: This is where excessive muscle contraction leads to abnormal postures or exaggerated movements.
    • Chorea: These are abnormal involuntary movements that can be jerking and random.
    • Athetosis: These are involuntary twisting or writhing movements usually in the fingers, hands or feet.
32
Q

Non motor complications of PD

A
  • Psychiatric:impulse control disorders, depression, anxiety, dementia
  • ## Autonomic:postural hypotension, constipation
33
Q

When should treatment for motor symptoms be started?

A

No one knows
Take into consideration:
Severity
Side effects
L-Dopa - phobia
Neuroprotection

Decide with patient

34
Q

Prognosis of PD

A

PD is a chronic and slowly progressive condition with no cure.

Overall, life expectancy is reduced with the mortality being 2-5 times higher for those aged 70-89 years old. Also, the risk of dementia is up to 6 times higher in PD patients.

No disease modifying treatment

35
Q

How do you help with Parkinson’s

A

Compensate for loss of dopamine

Increase availaibility of dopamine + Slow the loss of dopamine + Reduce aCH activity

36
Q

Drugs that could help with PDs

A

L- Dopa > Dopamine > Dopamine receptor
Dopamine agonist works on dopmaine receptor (Permax, Parlodel)
COMT/MAO-B inhibitors: Stop chemicals that “eat” dopamine - allows dopamine to bind to dopamine receptors

37
Q

Surgical correction of PD?

A

Ventriculoperitoneal Shunt placement

A bit of shunt can result in imporovement of Dementia, incontinence and walking problems

3A Neurology (24 decks)

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