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Parkinson's Disease

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Parkinson’s disease\: neurodegenerative disorder due to loss of dopaminergic cells from the substantia nigra.
Symptoms\: motor (bradykinesia, rigidity, tremor, postural instability), non-motor (cognitive impairment, autonomic
dysfunction).
Prevalence\: a
Pathophysiology\: loss of dopamine-producing neurons in the nigrostriatal pathway; formation of Lewy bodies.
Risk factors\: idiopathic, genetic associations (family history in up to 20%), male sex, increasing age.
History\: motor symptoms (slowness, sti
mood/cognitive symptoms (low mood, anxiety, apathy), sleep disturbances, anosmia.
Examination\: bradykinesia, rest tremor, rigidity, shu
confusion.
Di
supranuclear palsy, vascular parkinsonism, essential tremor.
Investigations\: bedside (lying and standing BP, cognitive assessment), lab (full blood count, urea & electrolytes, liver
function tests, in
Management\:
Medical\: levodopa (with carbidopa), MOA-B inhibitors (selegiline), dopamine agonists (ropinirole), COMT inhibitors
(entacapone).
Multidisciplinary\: physiotherapy, speech and language therapy, Parkinson’s nurse, occupational therapy.
Advanced\: deep brain stimulation for severe cases.
Complications\: falls, dementia (DLB, Parkinson’s dementia), hallucinations, paranoia, aspiration pneumonia.
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A comprehensive topic overview

Introduction

Parkinson’s disease (PD) is a neurodegenerative disorder occurring due to the loss of dopaminergic cells from the
substantia nigra area of the brain.
Cardinal symptoms of PD are those of movement disorder, although non-motor symptoms such as cognitive impairment
are also widely prevalent and account for a signi
neurodegenerative disorder.
1
Parkinson’s disease is the most common cause of parkinsonism, a syndrome of motor symptoms that involves
bradykinesia plus at least one of; rigidity, tremor or postural instability.
2

Aetiology

PD typically presents in those above 55 years old. It has a prevalence of 1-2% in people over 65 and this rises with age.
3
There is a higher prevalence of PD in men, with a male to female ratio of 1.5\:1.
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Pathophysiology

Dopamine is a key neurotransmitter used in the regulation of movement. It is produced in the substantia nigra within the
basal ganglia which is the key movement control centre of the brain (Figure 1).
In PD, there is a progressive loss of dopamine-producing (dopaminergic) neurons. There are several dopaminergic
pathways a
neurons in the nigrostriatal pathway, a motor control pathway that originates in the substantia nigra and terminates in the
striatum.
Figure 1. The structures of the basal
ganglia.
4
Physiologically, dopamine (an excitatory neurotransmitter) acts to upregulate the thalamus and ultimately the motor
cortex via the direct pathway of the basal ganglia. This results in increased movement.
Loss of these dopaminergic neurons results in a reduction in the action of the direct pathway of the basal ganglia and a
resultant increase in the antagonistic indirect pathway, which has a restrictive action on movement. Bradykinesia and
rigidity are therefore key features of parkinsonism.
In PD, there is also formation of protein clumps (Lewy bodies) within the remaining neurons. These typically begin to form
in the lower structures of the brainstem and progressively spread cranially towards the cortex. This progression can be
broken down into Braak stages, however, this is a post-mortem staging progress and is not used clinically.

Risk factors

PD is an idiopathic disease. It is not known what causes the loss of dopaminergic cells, although there appears to be some
genetic associations, with a
3
Male sex and increasing age are known risk factors for PD. Research is ongoing into environmental factors and triggers of
PD. Smoking is thought to be protective.

Clinical features

Parkinson's disease is usually a clinical diagnosis, based on history and examination
clinical for a prolonged period, with many features not clinically apparent until at least 50% of dopaminergic cells have
been lost.
3

History

Typical symptoms of Parkinson’s disease include\:
Motor symptoms\: slowness of movement, sti
Autonomic symptoms\: constipation, light-headedness on standing, excessive salivation or sweating, urinary dysfunction,
sexual dysfunction
Mood/cognitive symptoms\: low mood, anxiety, apathy
Sleep disturbance and daytime sleepiness
Anosmia or reduced sense of smell
Other symptoms which may be reported by family or carers include\:
Cognitive decline
REM sleep behaviour disorder\: manifests with behaviours such as punching, kicking or shouting during sleep
Altered handwriting\: micrographia
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Although motor symptoms are the diagnostic features of parkinsonism, non-motor features may precede motor symptoms
by years in PD.
Other important areas to cover in the history include\:
Past medical history\: history of known tremor or movement disorder, cognitive impairment, frequent falls
Drug history\: drug-induced parkinsonism must be excluded (see di
Family history\:
Social history\: smoking is thought to be protective for PD and alcohol withdrawal is a common cause of tremor. It is
important to ask about the patient's living situation, mobility, carers and activities of daily living.

Clinical examination

A thorough neurological exam should be carried out on all patients suspected of Parkinson’s disease. For more
information, see the Geeky Medics OSCE guide to Parkinson's disease examination.
Typical clinical
Bradykinesia\: Tested using
Tremor\: typically a ‘pill-rolling’ tremor of the hands at rest
Rigidity
Abnormal gait\: shu
arm swing, freezing (particularly when turning or when faced with doorways, obstacles or changes in terrain)
Postural instability\: tested using the pull test, although not usually present at diagnosis
Motor features usually begin unilaterally but will progress to become bilateral. The side a
worse causing persistent asymmetry.
Other clinical
Hypomimia\: decreased facial expression
Postural hypotension
Confusion
Reduced dexterity\: struggling with functional tasks such as fastening buttons

Di

Parkinsonism

Other causes of parkinsonism include\:
3,5
Lewy body dementia
Multiple system atrophy\: (MSA) unsteadiness, falls and autonomic dysfunction may be more predominant features of
early disease in MSA
Progressive supranuclear palsy (PSP)\: unsteadiness, dysphagia and gaze palsies may be more predominant features of
early disease in PSP
Vascular parkinsonism\: patients may report a history of cerebrovascular disease along with a sudden onset of symptoms
Drug-induced parkinsonism
Drug-induced parkinsonism
Any drug which acts by blocking dopamine or increasing its breakdown can cause parkinsonism.
Common causative drugs include\:
Antipsychotics\:
e
Anti-emetics\: prochlorperazine, metoclopramide
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Symptoms are more likely to be bilateral in drug-induced parkinsonism than in PD. Culprit drugs should be reduced,
replaced or stopped if clinically safe to do so to reduce parkinsonian symptoms.

Essential tremor

Essential tremors are common. They can occur at any age and patients will often have a family history of essential tremor.
Like drug-induced parkinsonism, essential tremor is usually bilateral.
The tremor in PD is typically noted in the hands, however, essential tremor is often present in the head, neck and trunk as
well as the hands.
Essential tremor increases on action and improves at rest, the opposite of PD. It also improves with alcohol or beta-
blockers but may be worse after ca
3

Investigations

Bedside investigations

Relevant bedside investigations include\:
Lying and standing blood pressure\: patients with PD may have postural hypotension
Cognitive assessment (e.g. Montreal cognitive assessment or abbreviated mental test)

Laboratory investigations

There is no routine testing for biochemical markers of Parkinson’s disease.
In the case of cognitive impairment, a ‘confusion screen’ set of tests should be considered, to exclude reversible causes of
confusion/delirium.
Relevant laboratory investigations as part of a confusion screen include\:
Full blood count\: low haemoglobin or raised white cell count may indicate anaemia or infection respectively
Urea & electrolytes\: electrolyte derangement
Liver function tests\: Hepatic encephalopathy
In
Glucose and HbA1c\: hypo/hyperglycaemia
Thyroid function tests\: hypothyroidism
Calcium\: hyper/hypocalcaemia
B12, folate and haematinics\: anaemia

Imaging

Dopamine active transporter (DaT) scans can be used. These scans measure dopamine uptake in the basal ganglia and
are therefore speci
Unfortunately, they are very costly and therefore reserved only for cases of diagnostic uncertainty.

Other investigations

Post-mortem

Diagnosis

A movement disorder/PD specialist should make the formal diagnosis of PD. Patients with suspected PD should be
referred promptly (and untreated) to a specialist clinic.
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Key diagnostic features are bradykinesia plus one of the following symptoms\:
2
Rigidity
Tremor
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Postural instability

Management

There is no cure for PD and current treatment does not halt or reverse the progression of the disease.

Medical management

Medical management should be initiated by a PD specialist.
Treatment aims to reduce symptoms by replacing dopamine or reducing dopamine breakdown. This can happen in a
variety of ways\:
6
Levodopa\: often
It is taken in conjunction with carbidopa (a dopamine decarboxylase inhibitor) to reduce metabolism into dopamine
before the drug crosses the blood-brain barrier. This reduces side e
Monoamine oxidase-B inhibitors (MOA-B inhibitors)\: these drugs block the breakdown of dopamine (e.g. selegiline).
Dopamine agonists\: these drugs bind to and stimulate dopamine receptors and therefore mimic the action of dopamine
(e.g. ropinirole and rotigotine patches). A major potential side e
control disorders. This is because alternative dopamine pathways in the limbic system are also agonised which can alter
attitude to risk.
Catechol-O-methyl transferase (COMT) inhibitors\: these drugs decrease dopamine breakdown and prolong the action
of levodopa (e.g. entacapone). COMT inhibitors are always taken alongside levodopa.
Anti-parkinsonian medications are ‘critical medications’ and are time-sensitive. Patients who miss doses or receive late
doses could experience freezing (akinesia). Suddenly stopping PD meds may also precipitate neuroleptic malignant
syndrome which can be life-threatening.
3
Response to medication deteriorates with time and side e
after taking medications due to overstimulation) or re-emergence of symptoms as each dose wears o
progression and increased loss of dopaminergic cells, increasing doses of medication are needed, leading to an increased
risk of side e

Multidisciplinary management

Multi-disciplinary input is a key part of the holistic bio-psycho-social management of PD. Professionals involved should
include\:
Physiotherapists
Speech and language therapists (SALT)
Parkinson’s nurse specialist
Occupational therapists

Deep brain stimulation

Deep brain stimulation is a specialised management option and not often used. It is reserved for those with severe
symptoms refractory to medical management yet still
6

Complications

Poor mobility can lead to increased falls and resultant injuries. Reduced independence is also seen as the disease
progresses and mobility deteriorates.
The risk of dementia is signi
and Parkinson’s dementia. These syndromes present clinically and pathologically very similarly, however, the clinical
timeline distinguishes them\:
DLB\: cognitive deterioration presents before or alongside parkinsonian motor symptoms
Parkinson’s dementia\: movement disorder symptoms preceded cognitive decline by a year or more
Hallucinations are a common complication of PD. Insight is generally good, however, if this is lost, patients can develop
paranoia.
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Aspiration pneumonia is frequently seen in end-stage PD as a complication of dysphagia. This increases morbidity and
mortality.

References

Patient.info. P a r k i n s o n i s m a n d P a r k i n s o n’ s D i s e a s e . Published in 2018. Available from\: [LINK]
Hughes, Daniel, Kilford, Lees. U K P a r k i n s o n’ s d i s e a s e s o c i e t y b r a i n b a n k c l i n i c a l d i a gn o s t i c c r i t e r i a . A c c u r a c y o f c l i n i c a l
d i a g n o s i s o f i d i o p a t h i c P a r k i n s o n' s d i s e a s e \: a c l i n i c o- p a t h o l o g i c a l s t u d y o f 1 0 0 c a s e s . Published in 1992. Available from\:
[LINK]
NICE Clinical Knowledge Summary. P a r k i n s o n’ s d i s e a s e . Published in 2022. Available from\: [LINK]
Beckie Port, adapted from original work by Jlienard, previously derived from work by Andrew Gillies’
, Mikael Häggström’s
and Patrick J. Lynch’s. T h e s t r u c t u r e s o f t h e b a s a l g a n g l i a . Licence\: [CC BY-SA]
Parkinson’s UK. T y p e s o f p a r k i n s o n i s m . Published in 2019. Available from\: [LINK]
Parkinson’s disease in adults. NICE Guideline. Published in 2017. Available from\: [LINK]

Reviewer

Professor Richard Walker
Consultant Geriatrician

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Di
Investigations
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