Intro to Parkinson's disease Flashcards
(29 cards)
How does smoking/drinking affect PD?
-seems to be protective for PD
What are the characteristics of PD?
- unilateral disease
- symptoms start unilaterally then spread to the other side as the disease progresses
- one side tends to be more affected than the other
- people who live in the country side more likely to get it
- People in the medical profession at increased risk
- 2nd most common neurodegenerative disease
- Mean age of onset=65 years
- Men are 1.5times more likely to get it
What are the symptoms associated with PD?
- Forward tilt of trunk
- Rigidity and trembling of head & extremities
- Reduced arm swinging
- Shuffling gait with small steps
- Bradykinesia
Outline the pathophysiology of PD
-Loss of dopamine neurons from substantia nigra
(so the black lines disappear)
-substantia nigra is a basal ganglia structure which is therefore part of the mid brain
-PD does NOT start in the non-dopinergic areas (EXTRANIGRAL)- IT IS SPECIFICALLY THE DOPAMINERGIC AREAS OF THE SN.
What is the function of the basal ganglia
- Motor control region
- Target of dopamine neurons
- Control of voluntary movements
Parkinson’s patients tend to have Lewy bodies. What are they?
- typical inclusion in their motor neurones (in substantia nigra)
- They are mainly composed of a protein called alpha synuclein. This protein accumulates throughout the brain and causes neuronal damage which then causes the symptoms
Outline the two separate PD pathologies
- ) Early cell loss
- Ventrolateral nigra
- Pre SMA cortex - ) Early alpha synuclein
- Brainstem
- Forebrain
Which neurochemical pathways are affected in PD?
- Dopamine
- Norepinephrine
- Serotonin
- Acetylcholine
What are the risk factors for PD
- head injury
- pesticide exposure
- family history of PD
What are the major clinical manifestations of PD?
- Cardinal features:tremor,rigidity,akinesia
- Other motor features: gait& equilibrium,dysarthria, fix postures
- Non-motor features: hyposmia (reduced ability to smell),depression, sleep alterations,cognitive impairment
What is unique about the tremor observed in PD
it is at REST
What are the 3 S’s observed in the motor symptoms in PD?
- Shaking
- Slowness
- Stiffness
What is an important non-motor syndrome involving REM in PD
- Rem sleep behaviour disorder (RBD)
- Very specific for PD
- can occur in some other diseases
- acting out dreams in REM
- may lead to physical injury to patient/partner
- Associated with PD,synucleinopaty, narcolepsy, brainstem structural lesions
- 40% risk of parkinsonian disorder or dementia after 5 years
Outline olfactory dysfunction in PD
- 70-100% of pts
- usually preserved in PARK2 (early onset genetic PD). psp/cbd, Vascular and drug induced parkinsonism, Mild OD in MSA & AD
- Recommended for PD vs PSP
What is DaTSCAN used for?
- SPECT imaging of membrane dopamine transporters
- Detects degeneration of dopaminergic nigrostriatal pathway eg presynaptic parkinsonian syndromes
- A scan
What are the motor symptoms of PD?
-resting tremor
-rigidity
-bradykinesia
-freezing
dyskinesia
-postural instability
-dystonia
-constipation
-bladder dysfunction
-daytime somnolence
define dystonia
-A movement disorder in which the patients muscles contract uncontrollably
What is freezing of gait?
- phenomena in which people are ‘stuck to the floor’ and find it difficult to initiate their movement/gait
- If you give them a visible cue eg lines on the floor they find it easier to initiate their movement
- typical of PD but not every pt will have it
- can also have freezing of the voice/freezing of other movements
What does pulsatile delivery of traditional levodopa lead to?
Pulsatile stiumlation of dopamine receptors
At what point can we diagnose PD
once people develop motor symptoms
- The motor symptoms are related to a loss of dopamine-only occurs when the pathology of PD reaches the mesencephalon (mid-brain) so it takes a while before we can actually detect the symptoms
- so people probs have PD few years before they came into clinic from motor symptoms
What happens to gastric absorption in PD?
- It is slowed
- and there is medication overload
List the CDS treatment options for pts inadequately treated with traditional oral therapies
- Duodenal carbidopa/levodopa gel infusion
- Subcutaneous apomorphine infusion
- Transermal Rotigotine ( dopamine agonist; leave the patch for about 24hrs; gives a stable level of DA in the blood; associated with less dyskinesia/less motor complications)
outline the use of subcutaneous apomorphine infusion
- DA agonist
- Looks like DA but stimulates the DA receptors
- comes in a fluid; attached to a pump which pumps the fluid with the apomorphine under the skin
- small needle; allows for absorption of the fluid by the skin
- stable level of DA so preventing the motor
- symptoms but addresses the dyskinesia
- Intra-jejunal levodopa infusion is similar system to the above
Outline duodopa infusion therapy
- Levodopa/carbidopa in gel suspension
- 100ml cassette
- PEG with duodenal tube
- Ambulatory pump
- Morning bolus dose
- Continuous maintenance infusion over 16hr
