Parkinson's Flashcards
What is Parkinson’s Disease?
Parkinson’s disease is a neurodegenerative projection and is a progressive, adult-onset condition and is developed when neurons stop working in the basal ganlia (base of forebrain and upperbrain) and occurs in the substantia nigra.
What is the diagnosis of parkinsons disease?
Is based on medical history, physical examination and symptoms (shaking or tremor, brandkinesia, rigidity.)
What are the motor symptoms of Parkinsons disease?
Hypokinesia (lack of stimulation of cerebral cortex to initiate movement), tremor (involuntary shakiness. Resting tremor. Disappears with intentional movement), rigidity (muscle stiffness), stooped posture, expressionless face, dystonia (painful muscle cramps), bradykinesia (slow movement), akinesia (absence of voluntary movement), freezing gait, shuffling gait and smell steps and postural instability (can lead to balance problems and falls)
What are the non-motor symptoms of parkinsons disease?
Anxiety, cognitive impairment, difficulty smelling, speech and communication problems, depression and orthostatic hypotension
What is the Parkinson’s disease classification?
- Age of onset: Juvenile onset, early-on, late onset
- Clinical symptoms: Tremor predominant, akinetic- rigidity predominant and postural instability-gait difficulty predominant
- Mental status: Dementia present/ absent
- Clinical course: benign, progressive, malignant
- Disability
What is the impact of motor symptoms of movement?
Tremors: at rest or with actions
Rigidity: Starts in the neck and shoulders then spreads to trunk and extremities
Speed: Ability to move fingers, hands, arms and legs reduced (bradykinesia)
Control: To rise from a chair is lessened
Posture: Kyphosis, flexed knees and elbows and adducted shoulders
Gait: slow and shuffling (festinating steps), decreased arm swing and difficulty initiating step (start hesitation)
Postural righting/recovery reflexes: compromised and lost
Falls: more common
Freezing: become more frequent
Negotiating doorways and narrowed spaces
ADLS: execution of fine motor tasks (e.g. cutting & swallowing food; turning / rising from bed; assistance with dressing / bathing).
Handwriting (micrographia): minute / illegible handwriting.
Communication: volume & understanding of speech; loss of facial expression (hypomimia = mask-like appearance).
What are the effects of exercise training on the brain?
The effects on the brain:
Growth, development, survival and differentiation of neurons, connection between neurons in the nervous system, regulation which all go into neuroplasticity which is the ability of the brain to change and adapt, form and or reorganise synaptic connections. it also utilises glucose changes the immune system and has the ability to reduce inflammation.
What are the effects of exercise training on Parkinson’s disease?
Parkinson’s disease from the affect of exercise can improve function, fail to impact on function or reduce function.
Exercise training will be beneficial athletes there are few deleterious effects associated with it
Progressive nature of the disease, variability of symptoms and impact of medications make prediction very difficult, recommended: peak dose= 45 mins-1hour after taking medication
Autonomic nervous system dysfunction: thermal regulation (sweating patterns, altered HR (altered / blunted chronotropic response) & BP (postural hypotension).
Muscular rigidity can decrease exercise efficiency (= higher HR & VO2 response during exercise.
What is the exercise programming for Parkinson’s disease?
Aerobic (Leg and arm ergometry, rowing)/ Goals= improve/maintain work capacity, control body weight and seated if balanced is comprised/ Intensity/frequency/duration= 60-80 HR peak, 3 days/week, <60 mins/session with the time to goal being 3 months
Endurance (Short walking sessions 20-30 mins supervised)/Goals= increase work capacity. Intensity/frequency/duration= Speed dependant on individual and 4-6 sessions/week
Strength (weight machines, resistance bands, circuit training). Goals= maintain or improve strength in arms, shoulders, legs and hips and increase MVV, peak torque and power. Intensity/frequency= use light weight, 1 set of 8-12 reps increasing to 8-15 reps, 3 days week for 20-30 mins.
Stretching for Parkinson’s disease?
The muscle that tend to be tight in Parkinson’s are those that bend and rotate joints:
At least 10 minutes of stretching at a time
At least 3-4 per week: Daily is better
Hold stretches for 10-30 seconds
3-4 repetitions of each stretch.
Focus should be on: Chest wall, shoulder and elbows, hamstrings, calves, front of wrists and palms and low back and neck.
What are the reported benefits of exercise training?
1) Improved gait, balance and coordination
2) Reduced falls
3) Increased flexibility and posture
4) Reduced freezing of gait
5) Improved working memory and decision making
6) Improved attention/concentration
7) Reduced depression and anxiety
8) Improved quality of sleep and quality of living
What are the difficulties of motor learning and techniques to improve motor learning?
Difficulties with motor learning in PD:
Altered perception, cognition, reduced motivation (distributed sleep, depression, low mood), reduced activation, 2 out of 3 stages of motor learning depend on dopamine levels (cognitive, associate, autonomous), pain, hypomimia (reduced facial expression), freezing, low BP, tremor, high resting metabolic rates are common, dystonia (impairment of muscle tone) and dyskinesia (movement impairment)
Techniques to improve motor learning:
Do not overload cognitively
Do not explain “too much”
Demonstrate the movement
Shape: optimise alignment BIG, largest amplitude
Drive (muscle activation): optimise motor output with your body, voice, enthusiasm
Stabilise: repetition/reinforcement with positive feedback
Recalibrate: refrain sensory perception
Motivate/excite/infuse
Set clear goals and link it to function
Adherence
Exercise testing for PD?
Speed (10m walking test, Timed up and go). which is measured by time, gait and turns. Endpoints= Note vitals, symptoms, time, distance at rest and when stopping (TUG can help falls prediction)
Endurance (6& 12 min. walk). measured by distance or gait. Endpoints= Note vitals, symptoms, time, distance at rest and when stopping (Aerobic training may improve walking velocity
Use HR response to determine impact of medications
Seated / harness if balance is compromised)
Strength (hand grip strength test, dynamometer) measured by maximal voluntary and contraction. (Need to use EMG to determine strength deficits)
Flexibility (Goniometry) measured by the joint angles at full extension/ flexion. Endpoints= Joint angles at full flexion/extension. (Especially important to measure ROM in neck, trunk, shoulders, hip & knees)
Functional (sit to stand, push and release test, miniBEST test, TUG and lindop) which is measured by time and balance). Endpoints= If they take 3 or more steps can show balance. (Multiple attempts in the sit to stand may suggest quadriceps weakness &/or poor motor control
Strength training should target quadriceps)
Neuromuscular (Gait analysis, balance) measured by pull test, 360 degree turn, functional turn. Endpoints= level of difficulty. (Use gait analysis if functional gait training / motor intervention is necessary. Classify disability level & define existing balance deficits).
What are therapeutic options and management?
Pharmacological Therapy: Dopaminergic (e.g. Levodopa, MAO-B inhibitors, Amantadine, anticholinergics (Cannot modify or slow down the disease or protect DA neurons and loses effect over time)
Non- pharmacological therapy: Exercise, nutrition, education (physical activity has been shown to maintain quality of life and improve motor ability, reduce the levels of fatigue)
Surgical therapy: DBS (deep brain stimulation)
What are the drug treatments?
Dopaminergic- Mechanism of action: Increase dopamine levels, carbidopa inhibits breakdown of levodopa (Exercise considerations include can produce bradycardia and transient peak dose tachycardia and dyskinesia
Dopamine agonists- Mechanism of action: activate dopamine receptors in basal ganglia (Exercise considerations are that it may lower BP and exacerbate dyskinesia )
Glutamate antagonists- Mechanisms of action: Increases presynaptic release of dopamine
Anticholinergics- Mechanisms of action: Increase breakdown of acetylcholine
Monoamine oxidase type B (MAO-B) inhibitors- Mechanism of action: Inhibut breakdown of dopamine by mitochondrial oxidation of dopamine (Exercise considerations include associated with dyskinesia and mood elevation)
Catechol-O-methyltransferase (COMT) inhibitors- Mechanism of action:Inhibit breakdown of dopamine
