Neurology - Parkinson's disease Flashcards
What is Parkinson’s disease?
Progressive denegeration of the substantia nigra and therefore reduced production of dopamine leading to disorders of movement
Symptoms are characteristically asymmetrical (one side affected more than the other)
Classic triad of:
- Resting tremor
- Rigidity
- Bradykinesia
What is the usual function of the basal ganglia?
Coordinating habitual movements such as walking or looking around, controlling voluntary movements and learning specific movement patterns
What is the pathophysiology of PD?
Substantia nigra cell loss causing lack of dopamine production
Dopamine is required as a neurotransmitter in the coordination of movement
Presentation of parkinson’s
Typically in older people, more commonly males
Unilateral tremor
Cogwheel rigidity
Bradykinesia
Other features:
- Depression
- Sleep disturbance/insomnia (REM sleep disorder)
- Anosmia
- Postural instability
- Cognitive impairment and memory problems
How does the tremor in PD present?
Unilateral typically
4-6Hz (4-6 times/s)
Pill-rolling tremor
More pronounced at rest
Improves with movement
Tremor may worsen if the patient is distracted e.g. ask them to do a task with their other hand
How does the bradykinesia present?
Their handwriting gets smaller and smaller
They can only take small steps when walking (“shuffling gait”)
They have difficulty initiating movement (e.g. from standing still to walking)
They have difficulty in turning around when standing, having to take lots of little steps
They have reduced facial movements and facial expressions (hypomimia)
Differentiating between benign essential tremor and tremor seen in PD
PD tremor:
- Asymmetrical
- 4-6 hertz
- Worse at rest
- Improves with intentional movement
- Other Parkinson’s features
- No change with alcohol
Benign essential tremor:
- Symmetrical
- 5-8 hertz
- Improves at rest
- Worse with intentional movement
- No other Parkinson’s features
- Improves with alcohol
Subclassifications of hypertonia and what can cause them
Can be subcategorised into spasticity and rigidity
Spasticity is associated with pyramidal tract lesions e.g. stroke
- Is velocity dependent - worse the faster you move the limb
- There is typically increased tone in the initial part of the movement which then suddenly reduces past a certain point (known as “clasp knife spasticity”).
- It is also typically accompanied by weakness
Rigidity is associated with extrapyramidal tract lesions e.g. PD
- Velocity independent - hypertonia is the same whether you move the limb fast or slowly
What are the two main types of rigidity?
Cogwheel rigidity - tremor is superimposed on the hypertonia resulting in intermittent increases in tone during movement of the limb. e.g. Parkinson’s disease
Lead pipe rigidity - uniformly increased tone throughout the movement of the muscle e.g. Neuroleptic malignant syndrome
What other syndromes present with Parkinsonism features?
The parkinson’s plus syndromes:
- Multiple system atrophy
- Dementia with Lewy bodies
- Progressive supranuclear palsy
- Corticobasal degeneration
What is Multiple system atrophy and how does it present?
Degeneration of neurones in multiple areas in the brain including the basal ganglia
Parkinsonism
Autonomic dysfunction e.g. postural hypotension, constipation, abnormal sweating
Cerebellar dysfunction e.g. ataxia
What is Dementia with Lewy bodies and how does it present?
Features of Parkinsonism plus visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness
How is the diagnosis in PD made?
Clinical diagnosis based on symptoms and examination
Management of PD
Refer to neurologist or PD specialist
Aim of treatment to control symptoms and minimise side effects
Levodopa - first line
- Synthetic dopamine that boosts host dopamine levels
- Usually combined with a drug that stops it being broken down (peripheral decarboxylase inhibitors)
- Co-benyldopa (levodopa and benserazide)
- Co-careldopa (levodopa and carbidopa)
-COMT inhibitors e.g. entacapone can be given alongside levodopa - The COMT enzyme metabolises levodopa in both the body and brain so entacapone slows the breakdown of levodopa in the brain and extends half-life
Dopamine agonists:
- mimic dopamine in the basal ganglia and stimulate the dopamine receptors
- Less effective than levodopa
- usually used to delay the use of levodopa and are then used in combination with levodopa to reduce the dose of levodopa that is required to control symptoms
- Side effect is pulmonary fibrosis
- E.g. Bromocriptine, Pergolide, Cabergoline
Monoamine oxidase-B inhibitors
- MAO-B enzymes breakdown dopamine NT
- Therefore inhibitors increase circulating dopamine
- usually used to delay the use of levodopa and are then used in combination with levodopa to reduce the dose of levodopa that is required to control symptoms
- E.g. selegiline, rasagiline
What are the potential side effects of levodopa?
Dopamine becomes too high causing dyskinesias e.g.
- 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.
