Parkinsonism Flashcards
What builds up in the brain leading to neuronal death?
Where does it build up?
What type of neurons are affected?
What sex is it commoner in?
Lewy bodies
Substancia nigra
Dopaminergic neurons
Male
S+S:
Onset?
Assym/symmetrical?
Insidious onset
Asymmetrical onset, stays worse on that side.
UNILATERAL onset is characteristic of Parkinson disease!
What is the Parkinsonism triad?
Tremor
Rigidity
Brady/hypokinesia
- Tremor:
- What part of body tremors?
- How is it usually described?
- When is it worse?
- What makes the tremor go away?
- Rigidity:
- What is the rigidity known as?
- What type of rigidity do you get when combined with the tremor?
- How does the person feel?
- What can you get them to do on examination that will make it more pronounced?
- Brady/hypokinesia:
- What is slowed
- Face
- What about their blinks
- Speech
- What does micrographia mean?
- How can bradykinesia be found on motor examination?
What about their gait?
Fingers/hands (can be found in legs, jaw, lips and tongue
Pill-rolling movement
Worse at rest
Voluntary movement
Hypertonia - Lead-pipe rigidity
Cogwheeling
They feel stuck
You get them to do something on contralateral side - so making a fist, painting the wall etc. ======== Slow initiation of movement Slow speed Slow amplitude
Blank face - (expressionless - looks like mask - hypomimia)
Reduced blinks
Monotone speech (later slurred or absent)
Features abnormally small, cramped handwriting or the progression to progressively smaller handwriting.
Festinant gait - shuffling, pitched forward, with reduced arm swing
Other symptoms:
Postural instability:
- What is the main feature of this?
- How is this tested?
- What is their posture like?
TRAP
– Tremor, Rigidity, Akinesia, and Postural instability
Autonomic symptoms:
- Urine
- Stool
- Skin
- Saliva
- BP - which contributes to instability and falls
WHY DO THEY NOT GET HYPERREFLEXIA?
Imbalance and tendency to fall
Pull test
Forward-leaning gait - thats why they fall
Urinary frequency and urgency Constipation Sweating Dribbling Orthostatic hypotension - contributes to instability and falls
Parkinson’s disease is characterized by degeneration of the substantia nigra, a structure in the midbrain (labeled as SN in the picture above) which is part of the basal ganglia circuitry. As mentioned above, the basal ganglia does not have direct connections to the LMN. Thus, disorders of the basal ganglia are not expected to affect the stretch reflex directly. That’s why they don’t cause hyperreflexia.
https://www.quora.com/Why-isnt-hyperreflexia-a-Parkinsons-sign-while-hypertonia-is-present
Other symptoms:
EARLY signs:
What is a sensory sign that patients may notice before symptoms even develop?
Neuropsychiatric symptoms:
- Mood
- Sleep - what type of dreams do they have?
- What type of hallucinations do they have?
- How many years post-diagnosis does it take for them to develop dementia?
What is an early motor sign in their gait?
What are some personality changes that may be noticed?
LATE signs:
Motor:
- What happens to their face?
- What about with their eyes?
Anosmia or hyposmia
Depression
Sleep - REM sleep disorder, insomnia, vivid dreams
Visual hallucinations
> 1 yr - only called Lewy body dementia if dementia comes before parkinsonism.
Lack of arm swimming
Inability to interpret sensations and hence to recognize things.
Hypomimia - low degree of facial expression
Reduced blinking
DDx:
Neurodegenerative - 2
Drugs that have anti-dopaminergic effects may induce parkinsonism (PSEUDOPARKINSONISM). What types of drugs can cause this? - 4
What metabolic disorder of the liver can cause this?
A TIA’s and CNS infections could also cause Parkinsonism.
Tremor:
- What is psychological tremor?
- What is essential tremor?
- What can make an essential tremor better?
- What is a dystonic tremor? Where does it happen?
Others:
What CVD event may cause Parkinsonism?
Wilson’s Disease
PD LBD - Dementia with LB ------ TYPICAL antipsychotics Anti-emetics (metaclopamide) CCB;s Amioadrone Lithium
High amplitude, present in all
Symmetrical, postural tremor - ALCOHOL makes better
Coarse
Irregular tremor
Often in face and neck
Multiple strokes
Diagnosis:
What type of diagnosis is it?
Pharmacological diagnosis:
- What can be done?
If a diagnosis is unclear or there is poor treatment response, what imaging can be done? - 3
A clinical diagnosis with:
- Brady/hypokinesia + Tremor, rigidity or postural instability”
Levodopa challenge test - symptoms will be relieved if it is PD
CT/MRI
DaTSCAN - a specific type of single-photon emission computed tomography (SPECT) imaging technique that helps visualize dopamine transporter levels in the brain.- CAN DISTINGUISH PD FROM AN ESSENTIAL TREMOR
DaTSCAN:
What type of scan is it?
What does it show in PD?
What does it differentiate between?
What does it not differentiate between?
SPECT
Striatal dopaminergic neuron loss
PD and drug-induced or essential tremor
Not between PD and LBD or Parkinson’s plus syndromes, as they also feature striatal dopaminergic neuron loss.
Consernative/MDT Management:
Who is involved in the MDT?
Role of a physio?
Role of an OT?
Who can help with problems with communications, swallowing or salivation?
Who else needs to be contacted?
Specialist nurse
Improves gait and balance
Help with work, family role, and ADLs
Speech and language therapist
DVLA
Medical Management:
Why is Rx often delayed in early disease?
What 2 drugs should be given if motor symptoms are affecting QoL OR they are > 65 yrs old?
What drug should be given if the motor symptoms are NOT affecting QoL OR they are <65 years old?
What drugs are given in later disease?
Symptoms are usually not causing significant impairment
Levodopa + dopa-decarboxylase inhibitor (CARBIDOPA)
Carbidopa/levodopa remains the most effective drug to treat PD. In addition to helping prevent NAUSEA carbidopa prevents levodopa from being converted into dopamine prematurely in the bloodstream, allowing more of it to get to the brain.
MAO-B inhibitor or Dopamine agonists
These drugs are used in combo + COMT inhibitors
Medical Management:
Rx for non-motor features, after considering non-pharmacological measures and reversible causes (e.g. drug side effects) first:
- Rx for psychosis?
- Rx for sleep problems:
- For daytime sleepiness - M
- For REM sleep disorder - C, - Rx for dementia?
- Rx for orthostatic hypotension - (M - vasopressor, F - steroid)
- Rx for mood disorders?
iF THE patient is <65 yrs old with just a tremor, what can be prescribed?
Anti-psychotics - Quetiapine or clozapine
Modafinil for daytime sleepiness
Clonazepam or melatonin for REM sleep disorder
Cholinesterase inhibitors - done-evil
Midodrine or fludrocortisone
SSRIs - Citalopram etc.
Anticholinergics - WARNING - can worsen psych symptoms (particularly dementia)
Surgical Management:
Deep brain stimulation is a Rx for PD. It improves motor symptoms.
What is it?
Indications?
A surgery to implant a device that sends electrical signals to brain areas responsible for body movement.
Electrodes are placed deep in the brain and are connected to a stimulator device.
Similar to a heart pacemaker, a neurostimulator uses electric pulses to regulate brain activity.
Primarily recommended for patients with severe motor symptoms who respond to levodopa treatment but are not sufficiently controlled by it (or if a decrease in dosage is necessary due to side effects)
Levodopa:
How is sometimes shortened?
Why is a bittersweet drug?
What is given with it to reduce peripheral conversion of levodopa to dopamine? Why?
What side effects does peripheral dopamine cause?
What is an alternative for levodopa?
L-DOPA
Most effective, however, also has motor complications (dyskinesia)
It also has increasing side effects as you increase the dose.
DDCI - Dopa-decarboxylase inhibitor (CARBIDOPA)
Prolonged therapeutic effect
N&V
Apomorphine
Levodopa:
Side effects - short term:
- As with all meds-
- BP
- Legs, sacrum and lungs
- Neuropsychiatric
- Sleep disturbance - how?
- What colour does their urine turn?
N&V
Postural hypotension
Oedema
Confusion, visual hallucinations, delusions etc.
Vivid dreams/nightmares
Daytime drowsiness
Red urine
