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Ageing and Complex Health > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

What are the main symptoms of parkinsonism?

A
  1. Bradykinesia
    - Slowness of initiating voluntary movement
    - Difficulty in sustaining repetitive movements
  2. Rigidity (cogwheel)
    - Involuntary increase in muscle tone (hypertonia)
  3. Tremor
    - Rhythmic involuntary movements - pill rolling
  4. The last one is less common but postural and gait instability
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2
Q

What are the types of parkinsonism?

A
  • Idiopathic - PD (asymmetrical)
  • Drug induced e.g. metoclopramide, cyclizine, haloperidol (symmetrical)
  • Vascular (loss of blood to the synapse)
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3
Q

What are the signs of vascular parkinsonism?

A
  • Gradual or step wise
  • Small vessel disease
  • Symmetrical
  • Legs&raquo_space; arms - profound gait abnormality
  • Acute onset
  • Usually associated with HTN, hypercholesterolaemia, diabetes etc
  • Tremor less common
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4
Q

What are the features of essential tremor?

A
  • Action tremor e.g. worse when eating/drinking
  • No bradykinesia
  • Usually bilateral, usually in legs and jaw
  • Coarse tremor
  • Familial
  • Non-specific beta blockers can reduce this e.g. propanolol
  • Alcohol can help with tremor
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5
Q

When do you use imaging when suspecting PD?

A

DaTSCAN which examines the dopamine transporter system - PD would be abnormal so asymmetrical and small.
CT/MRI can be used to rule out other likely differentials e.g. subdural haemorrhage

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6
Q

What tremors are worse on movement?

A
  • Drug induced
  • Essential tremor
  • Hyperthyroidism
  • Dystonic tremor
  • Exaggerated physiological tremor
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7
Q

What are additional clinical motor features of PD?

A
  • Quiet voice (hypophonia)
  • Small handwriting (micrographia)
  • Stooped posture (camptocormia)
  • Reduced or absent arm swings when walking
  • Freezing of gait
  • Festinant (fenestrated) gait - difficulty initiating gait and once mobile, rapid, short steps with accelerating speed, often with a stooped posture
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8
Q

What are facial features of PD?

A
  • Reduced facial expression

- Reduced rate of blinking

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9
Q

What is step 1 of the diagnosis for Parkinsonism?

A

Bradykinesia and at least one of:

  • Muscular rigidity
  • Rest tremor (4-6Hz)
  • Postural instability unrelated to primary visual, cerebellar, vestibular or proprioceptive dysfunction
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10
Q

What is in step 2 (exclusion criteria for PD) in the diagnosis of parkinsonism?

A
  • Repeated strokes with stepwise progression
  • Repeated head injury
  • Antipsychotic or dopamine depleting drugs
  • More than one affected relative
  • Sustained remission
  • Negative responses to large doses of levodopa
  • Strictly unilateral features after 3 years
  • Other neurological features
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11
Q

What is in step 3 (supportive criteria for PD) in the diagnosis of parkinsonism?

A

3 or more required for definitive diagnosis:

  • Unilateral onset
  • Rest tumour present
  • Progressive disorder
  • Persistent asymmetry affecting the side of onset most
  • Excellent response to levodopa
  • Severe levodopa induced chorea
  • Levodopa response for over 5 years
  • Clinical course of over 10 years
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12
Q

What is the 1st line treatment for PD?

A
  • Levodopa e.g. co-Beneldopa (Madopar) or co-careldopa (sinemet) for patients whose motor symptoms impact on their QoL
  • Dopamine agonist e.g. ropinirole, pramipexole and rotigotine (transdermal patch)
  • MAO-B inhibitor e.g. rasagaline, selegiline
  • Dopamine agonists, levodopa or MAO-B inhibitors for those in early stages whose motor symptoms do not impact on QoL.
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13
Q

What are the non-motor features of PD?

A
  • Drooling of saliva
  • Psychiatric features: depression, dementia, psychosis and sleep disturbances
  • Impaired olfaction (anosmia)
  • REM sleep behaviour disorder
  • Fatigue
  • Autonomic dysfunction - postural hypotension
  • Dysphagia
  • Bowel/bladder issues - constipation, urgency/freuquency
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14
Q

Describe the action of levodopa

A
  • Usually combined with a decarboxylase inhibitor e.g. carbidopa or benserazide, to prevent peripheral metabolism of levodopa to dopamine.
  • Reduced effectiveness with time (around 2yrs).
  • It is important not to acutely stop levodopa e.g. if a patient is admitted to hosp. If they can’t take it orally, can be given as a dopamine agonist patch.
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15
Q

What are the side effects of levodopa?

A
  • Dyskinesia (involuntary writhing movements)
  • On-off effect
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis
  • Drowsiness
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16
Q

Describe dopamine receptor agonists

A
  • e.g. bromocriptine, ropinirole, cabergoline, apomorphine, rotigotine, pramipexole
  • These have been associated with pulmonary, retroperitoneal and cardiac fibrosis. Advise echo, ESR, creatinine and CXR before and monitor patients closely.
  • SEs: impulse control disorders, excessive daytime somnolence, nasal congestion, postural hypotension
  • Pramipexole and ropinirole are oral
  • Rotigotine is a patch
  • Apomorphine SC injection - bolus or continuous infusion
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17
Q

Describe the action of MAO-B inhibitors

A
  • e.g. selegiline

- Inhibits the breakdown of dopamine secreted by the dopaminergic neurones

18
Q

Describe the action of amantadine

A
  • Mechanism not fully understood, probably increases dopamine release and inhibits uptake at dopaminergic synapses
  • SEs: ataxia, slurred speech, confusion, dizziness, livedo retivularis
19
Q

Describe the action of COMT inhibitors

A
  • e.g. entcapone, tolcapone
  • COMT is an enzyme involved in the breakdown of dopamine and hence may be used as an adjunct to levodopa therapy
  • Used in conjunction with levodopa in patients with established PD
20
Q

Describe the action of antimuscarinics

A
  • Block cholinergic receptors
  • More for drug-induced parkinsonism
  • Help tremor and rigidity
  • e.g. procyclidine, benzotropine, trihexyphenidyl (benzhexol)
21
Q

How is physiotherapy involved in the management of PD?

A
  • Gait re-education, improvement of balance and flexibility
  • Enhancement of aerobic capacity
  • Improvement of movement initiation
  • Improvement of functional independence, including mobility and activities of daily living
  • Provision of advice on safety in home
22
Q

How is occupational therapy involved in the management of PD?

A
  • Maintenance of work and family roles, home care and leisure activities
  • Improvement and maintenance of transfers and mobility
  • Improvement of personal self care activities such as eating, drinking, washing and dressing
  • Education on environmental issues to improve safety and motor function
  • Cognitive assessment and appropriate intervention
23
Q

How is speech and language therapy involved in the management of PD?

A

Improvement of vocal loudness and pitch range, including speech therapy programmes, such as Lee Silverman voice.

24
Q

What are further treatment options for PD?

A
  • Deep brain stimulation (may help those who are partly dopamine repsonsive)
  • Surgical ablation of overactive basal ganglia circuits (e.g. subthalamic nuclei)
25
Q

What are the first 2 stages of PD progression?

A
  1. Pre-diagnosis: during this phase nigrostriatal degeneration occurs without overt motor symptoms
  2. Diagnosis/maintenance: drug treatment is commenced with a good response and no motor complications
26
Q

What is the 3rd stage of PD progression?

A
  1. Complex: there may be the development of dyskinesias, unpredictable on/off motor problems and neuropsychiatric issues such as cognitive impairment and psychosis
27
Q

What is the 4th stage of PD progression?

A
  1. Palliative: poor drug response and the development of PD dementia predominate. The motor symptoms are eclipsed by multiple complications, swallowing can be impaired. Patients may need to have nutrition by PEG tube if deemed appropriate. Discussions should be undertaken about end of life care. Cognitive impairment and dementia are common in advanced PD.
28
Q

What is the background science of PD?

A

PD is a neurodegenerative condition of uncertain aetiology. Degeneration occurs in the pars compacta of the substantia nigra of the midbrain. Dopamine containing neurones project from the substantia nigra to the basal ganglia - as these degenerate over time there is a loss of dopamine delivery to the basal ganglia leading to motor signs and symptoms of PD.

29
Q

How can you tell the changes of PD has occurred in the brain?

A

Melanin-containing cells in this region are normally dark brown. Macroscopic sections of the midbrains of PD patient’s reveal depigmentation of the substantia nigra. This reflects the cell loss in this region during the disease process.

30
Q

What are Parkinson’s Plus syndromes?

A
  • Progressive supranuclear palsy
  • Multiple system atrophy
  • Cortico-basal degeneration
  • Lewy body dementia
31
Q

What are secondary causes of PD?

A
  • Vascular parkinsonism
  • Drugs (neuroleptics, metoclopramide, prochlorperazine)
  • Toxins e.g. manganese
  • Wilson’s disease
  • Trauma (dementia puglistica)
  • Encephalitis
  • Neurosyphilis
32
Q

What are the differentials for a tremor?

A
  • Parkinsonism - idiopathic PD, drug-induced
  • Hyperthyroidism
  • Cerebellar disorders
  • Essential tremor
  • Wilson’s (young and psychiatric)
  • Huntington’s (psychiatric and FH)
  • Alcohol/caffeine
  • Anxiety
33
Q

What are the features of cerebellar disorders?

A
  • Most common cause is stroke and alcohol
  • Nystagmus
  • Cerebellar tremor
34
Q

What are the early non-motor symptoms of PD?

A
  • Depression
  • Constipation
  • Anosmia
  • REM sleep behaviour disorder
35
Q

What are the early motor symptoms of PD?

A
  • Unilateral tremor
  • Reduced arm swing
  • Sometimes difficulty turning when walking
  • Reduced tone (not quite cogwheel)
  • 30% do not have a tremor - other symptoms can be worse as PD caught later
36
Q

What are the features of end stage PD?

A
  • Dementia (Lewy body) - visual hallucinations and talking to them
  • Loss of mobility (postural hypotension - disease and meds, gait instability - falls until cannot mobilise)
  • Incontinence (OAB symptoms progress to incontinence)
  • Dysphagia (high mortality, aspirate on own saliva even with PEG)
37
Q

What drugs can cause drug induced parkinsonism?

A
  • Metoclopramide
  • Haloperidol
  • Chlorpromazine
38
Q

What are the symptoms of Lewy Body dementia?

A

Triad of dementia, parkinsonism and visual hallucinations

39
Q

What are the neurological symptoms of idiopathic PD?

A
  • Cognitive impairment
  • Psychosis
  • REM sleep disorder
  • Depression
  • Anxiety
  • Apathy
  • Daytime somnolence
40
Q

What are the gastrointestinal symptoms of idiopathic PD?

A
  • Sialorrhoea (drooling)
  • Dysphagia
  • Reduced olfaction
  • Delayed gastric emptying
  • Constipation
41
Q

What are the genitourinary symptoms of idiopathic PD?

A
  • Nocturia
  • Urinary frequency and urgency
  • Urinary incontinence
  • Erectile dysfunction
  • Reduced libido
42
Q

What are the generalised symptoms of idiopathic PD?

A
  • Pain
  • Hypophonia
  • Restless leg syndrome
  • Postural hypotension

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