Parkinson's Disease - Epidemiology & Pathophysiology Flashcards
Epidemiology of PD:
PD is a progressive, degenerative neurological disorder that causes severe movement difficulties
Results in resting tremor, bradykinesia, rigidity and impaired reflexes as well as cognitive problems
One of the most common neurological diseases of individuals over the age of 50 [median onset - 56]
Most common neurodegenerative disorder, affecting >1% of individuals older than 60years worldwide
Much higher prevalence in Caucasians than African or Asian populations, even within ‘western’ countries
Pathophysiology of PD:
Primarily affects the basal ganglia, which controls complex motor planning
Basal ganglia linked to other motor and sensory areas, as well as cognitive and motivational areas, so nonmotor disabilities common.
Substantial Nigeria often most affected, so the nigrostriatal tract degenerates
‘Striatal’ refers to the fibre projections to globus pallidus and putamen in corpus striatum - one part of the basal ganglia
Primary pathological event is the degeneration of dopamine release cells, so nervous transmission is affected or halted, particularly in caudate nucleus, putamen and substantial nigra
Cause of damage to substantia nigra unknown
Autonomic dysfunction sometimes associated with lesions in the hypothalamus, dorsal nucleus of vagus nerve, or disturbed metabolism of catecholamines
Causes/Aetiology of PD:
Not know how idiopathic PD [IPD] is caused:
- evidence both for and against genetic and environmental causes
- some evidence for mitochondrial dysfunctions or free radical toxicity in brain tissue
- no definitive recognisable risk factors exist for development of IPD
Only diagnosed through symptoms
Classification of PD: 3 categories
- Idiopathic Parkinson’s disease [IPD] means ‘appearing spontaneously or from unknown cause” = 75-90% of all cases
- Secondary Parkinsonism displays similar symptoms to IPD but damage to the substantia nigra ‘basal ganglia’ is identified= includes postencephaltic, drug-induced, toxic, traumatic, metabolic and neoplastic [new growth] causes
- Parkinsonism plus syndromes - due to multiple system degeneration or atrophies; includes inheritable degenerative diseases that cause Parkinson’s related symptoms
How can the clinical symptoms of IPD be classified?
- Tremor predominant
- Postural instability-gait deficiency
- Akinetic rigidity predominant
May also differentiate based on mental status, clinical course or age of onset, e.g.
- juvenile [<40y.o]
- 40-75 y.o
- > 75 y.o.
Classification - Hoehn and Yahr staging of PD = 5 stages
Stage 1 = signs and symptoms on one side only, symptoms mild and inconvenient but not disabling, usually presents with tremor of one limb, friends have noticed changes in posture, locomotion and facial expression
Stage 2 = symptoms bilateral, minimal disability, posture and gain affected
Stage 3 = significant slowing of body movements, early impairment of equilibrium on walking and standing, generalised dysfunction that’s moderately severe
Stage 4 = severe symptoms, limited walking, rigidity and bradykinesia, cant live alone, tremor may have lessened.
Stage 5 = cachectic stage, invalidism complete, cant stand or walk, nursing care
Classification - Unified Parkinson’s disease Rating Scale [UPDRS] + Schwann and England Activities of Daily Living Scale
Allows the longitudinal rating of patients capabilities:
- mentation, behaviour and mood
- activities of daily living
- motor performance
- complications of therapy
Interview plus clinical observation
Rating between 0-100% on capacity to carry out daily tasks
Functional Consequences : Motor problems
Gait and balance deficits: difficulty getting out of bed, car or chair
Decreased step length and foot clearance, loss of heel-toe pattern, increased shuffling
Posture flexed forward so faster steps and difficulty in stopping
Loss of natural arm pattern
‘Freezing’ during walking
Slow turning
Difficulty getting dressed, writing, speech
Balance deficits, so increased falls when perturbed
Rigidity reduces movement at joints, especially the vertebrae
Difficulty rolling side-to-side, difficulty getting out of bed, car, or chair
Bradykinesia - slow movements
Functional Consequences : Non-motor problems
Much increased risk of dementia - significant effect of QoL
~Autonomic Dysfunction: drooling, constipation, urinary problems, orthostatic hypotension [sudden & short lived drop in BP], erectile dysfunction, dysphagia, excessive sweating, hypohydrosis [lack of sweating]
~Neuropsychiatric problems: hallucinations, delusions, cognitive decline, dementia and depression
~Sleep disorders: difficulty falling or staying asleep, restless leg syndrome, R.E.M. Sleep disorders
~ sensory disorders: pain, difficulty staying still, loss of smell
Pharmacology: What is the main drug used in PD?
It’s the primary therapeutic intervention
Many side effects, including GI upset, othostatic hypertension [dizziness], brady-tachycardia, arrhythmia, dry mouth, blurred vision, headaches, ataxia, cognitive disturbances
Exercise program needs to be flexible
Main drug - Levodopa [L-dopa]
L-dopa had major side effects; dyskinesia, dystopias, and end-of-dose wearing off, or ‘off time’
Frequently appears 5-7years after therapy starts
Pharmacology - L-dopa
Form of dopamine that can cross the blood-brain barrier, replenishes dopamine Side effects include: - dyskinesia [incl muscle spasms] - low BP - Arrhythmia - GI problems - Nausea - hair loss -sleep disorders, confusion, anxiety -hallucinations
Medical/surgical treatments
Neuroablation or lesion made in areas of the brain [thalamus or globus pallidus]; thalamotomy to reduce tremor and pallidotomy to decrease rigidity, bradykinesia, tremor, spasms and off state dystonias
Stem cell transplants to promote dopamine-releasing cells - ongoing not yet successful
Deep brain stimulation [DBS] is most common procedure to treat symptoms: high frequency stimulation mimics the lesions
Removeable and able to specifically test for best effects
Decrease in ‘off’ time meds and improvements in ‘on’ time dyskinesias
Performance Testing: Neurological exam
Rigidity, tremor, bradykinesia and postural reflexes
Rigidity - grasp on or both wrists and shake hand/s up and down to observe looseness and ease of movement, patient to remain passive
Passively flexing and extending joints in upper and lower limbs
Neck and trunk in all planes should be examined passively
Remember rigidity not velocity-specific
Resting tremor: rest hands in lap, recite sentence or count backwards, tremor becomes obvious
Hands similar to rolling pill between fingers; uncommon that postural or intention tremor present in later stages of disease
Postural tremor excited by holding limbs against gravity, arms outstreched, slow oscillation seen
Intention tremor elicited by moving limb voluntarily, as in picking up a cup or water and bringing to mouth to drink
Bradykinesia: sit with both hands on lap, then ask them to supinate and pronate as fast as possible for at least 30 seconds
If bradykinesia, movement with break down after a few seconds
Postural reflexes: patient stands with back to examiner with eyes open, examiner reaches over shoulder and pulls backwards firmly
Patient may 1) stay in place, 2)step back but recover quickly, 3)fall back and require assistance, 4)not attempt to recover
Exercise Testing: Dynamic balance test, Gait observation, strength tests
Balance, gait, mobility, ROM and manual muscle testing required
~dynamic balance test: sitting and standing, functional reach, berg balance scale
~gait observation: stride length and frequency, heel-toe, obstacle avoidance, turn time
~strength tests: done by dynamometers and isokinetic equipment
Exercise Prescription - Aerobic
Level walking surfaces, such as a track advised
Anecdotal reports that swimming and aquatics enables tham to move more easily
HR variability may be greater in IPD
Performance significantly better when on medication
