Parkinson's disease Flashcards
What is Parkinson’s ?
Degeneration of dopaminergic neurons in the basal ganglia, particularly the substantia nigra.
What is the Parkinsonism triad/4 cardinal motor symptoms?
- Bradykinesia- slowness of movement (or hypokinesia/akinesia)
- Rigidity
- Resting tremor (“pill- rolling tremor”)
- Postural instability (later onset)
Asymmetrical tremors suggest idiopathic Parkinson’s
What are the risk factors for Parksinson’s?
Risk Factors → genetic, environmental factors, MPTP exposure (drug that damages the substantia nigra), drug-induced (anti-psychotics)
What are different conditions can also cause parkinsonism?
- Drug Induced ⇒ anti-psychotics (eg. haloperidol), typically bilateral
- Lewy Body Dementia ⇒ memory loss, visual hallucinations and parkinsonism
- Progressive Supranuclear Palsy ⇒ postural instability (falls), impaired vertical gaze, cognitive impairment, parkinsonism. STEELE RICHARDSON SYNDROME
- Multisystem Atrophy ⇒ autonomic features such as postural hypotension, incontinence and impotence
What presenting symptoms of Parkinson’s can be found in the history?
INSIDIOUS onset
Resting tremor (mainly in hands) – one side worse
Stiffness and slowness of movements
Difficulty initiating movements
Frequent falls
Smaller hand writing (micrographia)
Insomnia
Mental slowness (bradyphenia)
Subtle: sense of smell reduced, constipation, visual hallucinations, frequency/urgency, dribbling of saliva, depression
What signs of Parkinson’s can be found on physical examination?
- Tremor
- Pill rolling rest tremor
- 4-6 Hz
- Decreased on action
- Usually asymmetrical - Rigidity
- Lead pipe rigidity of muscle tone
- Superimposed tremor can cause cogwheel rigidity
- Rigidity can be enhanced by distraction - Gait
- Stooped
- Shuffling
- Small-stepped gait
- Reduced arm swing
- Difficulty initiating walking - Postural Instability
- Falls easily with little pressure
from the back or the front - Other features
- Frontalis overactivation (leads to furrowing of the brow)
- Hypomimic face
- Soft monotonous voice
- Impaired olfaction
- Tendency to drool
- Mild impairment of up-gaze - Psychiatric
- Depression
- Cognitive problems and dementia (in later stages)
What is Parkinson’s disease dementia?
PDD: Parkinson’s disease dementia is a decline in thinking and reasoning skills that develops in some people living with Parkinson’s
(very similar to LBD but onset of dementia happens many years after motor symptoms) FHAAV
Fluctuations (changes in the ability to move)
Hallucination
Aggression/anxiety
Amnesia (memory loss)
Visuospatial dysfunction (can’t draw a clock)
What investigations are used to diagnose/ manage Parkinson’s?
- Dopaminergic Agent Trial (DAT Scan) → results in improvement in symptoms
- Single Photon Emission Computed Tomography (SPECT)
- Bloods
- Serum caeruloplasmin - rule out Wilson’s disease as a cause of Parkinson’s disease - CT or MRI Brain
- To exclude other causes of gait decline (e.g. hydrocephalus) - Dopamine Transporter Scintigraphy (A DAT brain scan is a nuclear medicine test that looks at the function of dopamine transporters in your brain.)
Shows reduction in striatum and putamen
How is Parkinson’s Disease managed?
Urgent referral to neurology, medications can only be initiated by specialists
1. Drugs aim to increase amount of dopamine in substantia nigra:
a. If motor symptoms are affecting patients quality of life ⇒ Levodopa (dopamine)
- Can eventually cause on-off effect (inevitable consequence of sustained levodopa treatment)
b. If motor symptoms not affecting patients quality of life ⇒ Levodopa, Dopamine Agonists (ropinerole, pramipexole, apomorphine- SE: impulsive behaviour), MAO-B/COMT Inhibitors (e.g. Rasagiline)- reduce levodopa degradation and thus to increase and prolong its effect in striatal dopaminergic neurotransmission
- Carbidopa is given along with levodopa (Co-careldopa) as it reduces the breakdown of levodopa peripherally, leading to a better therapeutic effect.
- Vitamin D supplements
- Physical Therapy → exercise, occupational therapy, speech therapy
- Avoid antipsychotics as they worsen symptoms.
What are some causes of secondary parksinson’s disease?
Primary Parkinsonism is due to classic idiopathic Parkinson’s disease and includes sporadic and familial cases. The classic idiopathic Parkinson’s disease makes up about 75-80% of cases of Parkinsonism.
Secondary parkinsonism could be due to many known causes such as:
- Neuroleptic therapy (e.g. for schizophrenia)
- Vascular insults (e.g. in the basal ganglia)
- MPTP toxin from illicit drug contamination
- Post-encephalitis
- Repeated head injury
- Manganese or copper toxicity (Wilson’s disease)
- HIV
Summarise the epidemiology of Parkinson’s disease
Very COMMON
Prevalence: 1-2% of > 60 yrs
Mean age of onset: 57 yrs
