1. Medical Diagnosis
1.1. Diagnosis is difficult, and requires prolonged observation of signs and symptoms
1.1.1. No single definiitive test
1.1.2. Handwriting samples, speech analysis, interview questions, physical examination
1.1.3. A diagnosis is typically made when at least two of the four cardinal features of PD are present
1.1.3.1. Rigidity
1.1.3.2. Bradykinesia
1.1.3.3. Tremor
1.1.3.3.1. Clinical Course
1.1.3.4. Postural instability
2. Medical Management
2.1. Pharmacological Management
2.1.1. Should be constant to prevent peaks and valleys
2.1.2. Starting early helps slow the progression
2.1.3. Levodopa/Carbidopa
2.1.3.1. Sinemet, gold standard
2.1.3.2. Helps metabolize dopamine in the brain
2.1.3.3. End-of-dose deterioration
2.1.3.4. Akathisia: motor restlessness
2.1.4. Dopamine Agonists
2.1.4.1. Stimulate postsynaptic dopamine receptors
2.1.4.2. Used when there is a decline in response to Sinemet
2.1.5. Anticholinergics
2.1.5.1. Block cholinergic function, have the most benefit moderating tremor and dystonia
2.1.6. Monoamine Oxidase B Inhibitors
2.1.6.1. Helps to prevent degredation of dopamine in the brain, enhances level of dopamine
2.1.7. Optimal performance is at peak dosage, optimal time for PT
2.2. Nutritional Management
2.2.1. High protein diet can block the effectiveness of L-dopa
2.2.1.1. A high-calorie, low-protein diet is recommended
2.2.2. Occupational training for functional tasks like eating may be needed
2.3. Deep Brain Stimulation
2.3.1. Implantation of electrodes into the brain, blocking nerve signals causing symptoms
2.3.1.1. Suppression of the subthalamic nucleus
3. Framework for Rehabilitation
3.1. Therapeutic Care Continuum
3.1.1. Early
3.1.1.1. Functional and independent with minimal impairments
3.1.1.2. Benefits of early PT are improving fitness levels and delaying or preventing direct impairments
3.1.2. Middle
3.1.2.1. Usually independent in ADLs and gait, but impairments become more obvious
3.1.2.1.1. Exercise has been show to improve motor function and performance
3.1.3. Late
3.1.3.1. Patients are dependent in many or most ADLs and most are wheelchair ridden
3.1.3.1.1. Environmental and support changes are needed to help patient function
4. Physical Therapy Examination and Evaluation
4.1. Cognitive Function
4.1.1. MoCA
4.2. Psychosocial Function
4.2.1. Depression, anxiety, stress, social implications of decline of function and progression of disease
4.2.2. Geriatric Depression Scale, Beck Depression Inventory
4.3. Sensory Function
4.3.1. Aching, cramping, numbness, tingling
4.3.2. MSK aches and pains
4.3.3. Changes in smell
4.3.4. Decreased visual acuity, visual fields, loss of color discrimination, pursuits, accomodation, tracking
4.4. Musculoskeletal Function
4.4.1. Posture
4.4.1.1. Flexed and stooped posture
4.4.2. Plumb lines and photography are used to document changes
4.4.3. Joint flexibility: ROM
4.4.3.1. Loss in hip and knee extension, DF, shoulder flexion, elbow extension, spine and neck extension, axial rotation
4.4.4. MMTs
4.5. Motor Function
4.5.1. Rigidity
4.5.1.1. Asymmetrical early on, present on both sides of a joint, examine also for facial mobility
4.5.2. Tremor
4.5.2.1. Initially, tremor at rest
4.5.2.2. Action tremor
4.5.2.2.1. Difficulty with functional skills, ADLs
4.5.2.3. Stress can increase tremor
4.5.3. Freezing of gait
4.5.3.1. Worsened by stress and anxiety
4.5.4. Bradykinesia
4.5.4.1. Slowed movements
4.5.4.1.1. TImed tests for RAMs can be used to observe effects
4.5.5. Hypokinesia
4.5.5.1. Decrease in amplitude
4.5.6. Akinesia
4.5.6.1. No movement
4.5.7. Fatigue
4.5.7.1. Decline in motor functions + rigidity lead to an increase in fatigue
4.6. Autonomic Function
4.6.1. Excessive drooling, sweating, greasy skin, abnormalities in thermoregulation
4.6.2. Reduced cardiorespiratory function
4.6.2.1. Measured with RR, FEV1/FVC, TLC, MIF
4.6.3. Orthostatic hypotension
4.7. Integumentary Integrity
4.7.1. Oily skin, bruising, skin breakdown, incontinence
4.7.2. Pressure relieving strategies must be taught, especially later in the progression due prolonged sedentary positions
4.8. Functional Status
4.8.1. BADL
4.8.2. IADL
4.8.3. 5xSTS
4.8.3.1. 20s
4.8.4. Profile PD
4.8.4.1. Rates (0-4) the difficulty of bodily function and cognitive tasks
4.9. Globe Health Measures
4.9.1. Assess the ability to perform a variety of routine tasks across a variety of populations
4.9.2. PDQ-39
4.9.3. PDSI
5. Patient, Family, and Caregiver Education
5.1. Patient and family must be educated on disease progression, availbale resources (social, mechanical, etc.), medications, orthotics and devices, psychosocial help, preventative measures, community resources, and course of physical therapy
6. New Info
6.1. Hypomimia (masked facial expressions) can have significant social consequences for PD patients.
6.2. Postural deformity and vestibular deficits lead to more sedentary lifestyle, leading to decreased BMD, leading to osteoporosis, fractures, decrease in QoL, and mortality
6.3. Paucity: excess of movement, tremors
6.4. A high protein diet can block the effectiveness of L-dopa, which can inhibit effective motor proformance
7. Incidence
7.1. PD affects ~1 million Americans and 7-10 million people worldwide. More than 2% of people older than 65 have PD.
7.1.1. The prevalence is ex[ected to rise due to the aging population.
7.2. The average onset is 50-60 years.
7.3. Men are affected 1.2-1.5x more than women.
8. Etiology
8.1. Parkinson's Disease
8.1.1. Most common parkinsonism, 78% of cases
8.1.2. Refers to the cases where the cause is unknown or genetically determined
8.1.3. Two groups: postural instability gait disturbed (PIGD) and tremor dominant
8.2. Secondary Parkinsonism
8.2.1. Results from viruses, toxins, tumors, etc.
8.2.2. Postencephalitic Parkinsonism
8.2.2.1. A slow virus (from the influenza epidemics in 1917-1926) infects the brain and causes the onset of parkinsonian symptoms many years later (this type is not seen anymore).
8.2.3. Toxic Parkinsonism
8.2.3.1. People who are exposed to certain environmental toxins (pesticides and industrial chemicals) can exhibit parkinsonian symptoms.
8.2.4. Drug-Induced Parkinsonism (DIP)
8.2.4.1. A selection of drugs that interfere with the dopaminergic mechanisms can produce symptoms that mimic PD. Withdrawal usually resolves symptoms within a few weeks.
8.2.4.1.1. Neuroleptic drugs (chloropromazine, haloperidol, thioridazine, and thiothixene)
8.2.4.1.2. Antidepressants (amitriptyline, amoxapine, and trazodone)
8.2.4.1.3. Antihypertensive drugs (methyldopa and reserpine)
8.3. Parkinson-Plus Syndromes
8.3.1. Conditions that mimic PD, but are caused by other neuro disorders
8.3.2. A group of disorders interfere with the substantia nigra and can produce parkinsonian symptoms.
8.3.2.1. Striatonigral degeneration, Shy-Drager syndrome, progressive supranuclear palsy, multi-infarct vascular disease, Alzheimer's, diffuse Lewy body disease, juvenile Huntington's disease, etc.
8.3.3. Early on, these conditions present similarly to PD, but over time, other diagnostic symptoms appear (such as cognitive impairment in Alzheimer's). These conditions also do not improve with the administration of levodopa therapy.
8.4. Parkinsonism: a group of disorders with primary disturbances in the dopamine systems of the basal ganglia.
9. Pathophysiology
9.1. The basal ganglia are a group of subcortical nuclei that engage in multiple circuits (or loops), some of whihc are motor.
9.1.1. The direct motor loop goes from the cortexx-->putamen-->globus pallidus-->VL nucleus of thalamus-->back to cortex
9.1.1.1. This activates the cortex in a positive feedback loop and assists in the initiation of voluntary movement.
9.1.2. The indirect loop helps to decrease thalamocortical activation
9.1.3. The superior colliculi assist in regulation of saccadic eye movement.
9.1.4. The reticular formation helps in trunk and limb musculature, as well as arousal.
9.1.5. Other circuits are involved with memory and cognitive functions.
9.2. PD is the degenration of the dopaminergic neurons in the basal ganglia that produce dopamine.
9.2.1. Over time, there is a continuing presence of Leewy bodies.
10. Stages of Parkinson's Disease
10.1. Stage 1: lesion found in the medulla oblongata
10.2. Stage 2: lesions in the caudal ralphe nuclei, reticular nucleus, and coeruleus-subcoeruleus complex
10.3. Stage 3: involvement of the nigrostriatal system
10.4. Stage 4: lesion in the cortex
10.5. Stage 5: lesions involve the sensory association areas of prefrontal cortex
10.6. Stage 6: sensory association areas of the neocortex and premotor areas
11. Clinical Presentation
11.1. Primary Motor Symptoms
11.1.1. Rigidity
11.1.1.1. Hallmark of PD
11.1.1.2. Cogwheel rigidity: jerky, ratchet-like resistance to passive motion
11.1.1.2.1. Tremor co-exists
11.1.1.3. Lead pipe rigidity: sustained resistance to passive movement with no fluctuations, often asymmetrical
11.1.1.3.1. Affects proximal muscles first
11.1.2. Bradykinesia
11.1.2.1. Slowness of movement, made worse by weakness, tremor, and rigidity
11.1.2.1.1. Can also be affected by pradyphrenia (slowness of thought)
11.1.2.2. One of the most disabling parts of PD
11.1.2.3. Freezing of gait (FOG): can be triggered when a patient is confronted by competing stimuli (deer in the headlights), and can be overcome using tricks (dropping a tissue initiates a stepping response).
11.1.2.4. Hypokinesia: slowed and reduced movements
11.1.2.4.1. Micrographia: handwriting that starts out strong but becomes smaller as writing proceeds
11.1.3. Tremor
11.1.3.1. Involuntary shaking and oscillating movements resulting from contractions of opposing muscles
11.1.3.1.1. 70% of patients experience a slight unilateral tremor of the hand or foot
11.1.3.1.2. Aggrevated by emotional or physical stress
11.1.4. Postural Instability
11.1.4.1. As PD progresses, patients have increasing difficulty controlling their COM, increasing postural instability
11.1.4.1.1. Patients also have difficulty balancing in self-initiated movements and in perturbed movements
11.1.4.2. Increasing visual and vestibular issues also contribute to balance deficits
11.1.4.2.1. Some patients have an inability to percieve upright position
11.1.4.3. Postural deformity leads to more sedentary lifestyle, leading to decreased BMD, leading to osteoporosis, fractures, decrease in QoL, and mortality
11.2. Secondary Motor Symptoms
11.2.1. Muscle Performance
11.2.1.1. Strength reduction is present in patients with PD
11.2.1.2. Torque production is decreased at all speeds
11.2.1.2.1. Leads to activity limitations and muscle weakness
11.2.1.3. It is theorized this is due to a decrease in dopamine
11.2.1.4. Asynchronization
11.2.1.4.1. Inability to smoothly increase firing rate
11.2.2. Motor Function
11.2.2.1. The striatum of the basal ganglia recieve impulses from all cortical areas, which travel throughout the thalamus, and are concerned with motor planning
11.2.2.1.1. There are motor planning deficits in PD, which involve a loss of regulatory control of voluntary and automatic movement responses
11.2.3. Gait
11.2.3.1. Gait disturbances are common in late-onset or advanced PD
11.2.3.1.1. Festinating gait pattern: progressive increase in speed with a shortening of stride
11.3. Nonmotor Symptoms
11.3.1. Sensory
11.3.1.1. There is no primary sensory loss in PD
11.3.1.2. 50% of experience parathesias and pain, including numbness, tingling, cold, aching, and burning pain
11.3.1.2.1. This is liekly die to PD's effect on central nociception
11.3.1.2.2. Symptoms are intermittnet, and vary in location and intensity
11.3.1.3. Some of these symptoms of discomfort and pain are from postural stress syndrome
11.3.1.3.1. This is ssecondary to faulty posture, ligament strain, lack and movement, and rigidity of muscle
11.3.1.4. Olfactory dysfunction is common, with a loss of the sense of smell
11.3.1.4.1. These symptoms may take years to show up
11.3.1.4.2. Anticholinergic drugs can cause visual disturbances
11.3.2. Dysphagia
11.3.2.1. Impaired swallowing is present in up to 95% of patients, resulting from rigidity
11.3.2.1.1. Impaired tongue control, chewing, delayed swallowing, and peristalsis can all be present
11.3.2.1.2. Sialorrhea (excessive drooling) is common as well, which can be a social hinderance
11.3.3. Speech disorders
11.3.3.1. Hypokinetic dysarthria: decreased voice volume, monotine speech, or distorted articulation
11.3.3.2. Degraded vocal quality, hoarseness
11.3.3.3. Reduced vital capacity can lead to reduced air expended during speech and even mutism (not speaking at all)
11.3.4. Cognitive function
11.3.4.1. PD dementia occurs in 20-40% of patients, with older individuals having a higher risk
11.3.4.2. Bradyphrenia: slowed thinking
11.3.4.2.1. Early and non-specific feature seen in PD
11.3.5. Depression and anxiety
11.3.5.1. Up to 40% of PD patients are diagnosed with major depression
11.3.5.2. Hypomimia: reduction in facial expressions
11.3.5.2.1. Gives the appearance of depression
11.3.5.3. Dysthymic disorder: chronic depression and dysphoric mood
11.3.5.3.1. Results in poor appetite, overeating, insomnia, hypersomnia, low energy, low self-espeem, poor concentration
11.3.5.4. Anxiety and panic attachs are common in 38% of PD patients, as well as OCD
11.3.6. Autonomic dysfunction
11.3.6.1. This is a direct manifesttaion of PD, due to the presence of Lewy bodies
11.3.6.1.1. Seborrhea, seborrheic dermatitis and slow pupillary responses are common
11.3.6.2. GI dysfunction
11.3.6.2.1. Poor motility, changes in appetite, inadequate hydration, constipation, weight loss
11.3.6.3. Urinary dysfunction
11.3.6.3.1. Incontinence, urinary frequency, urgency, nocturia
11.3.6.4. Sympathetic denervation of the heart
11.3.6.4.1. Orthostatic hypotension
11.3.6.5. Airway obstruction, restrictive lung dysfunction
11.3.6.5.1. Lower FVC, FEV1, higher RV, venous pooling, edema
11.3.7. Sleep disorders
11.3.7.1. Excessive daytime somnolence (sleepiness)
11.3.7.2. Insomnia (disturbed sleep pattern)
12. Physical Therapy Intervention
12.1. Motor Learning Strategies
12.1.1. Motor learning deficits lead to slower learning rates, reduced efficiency
12.1.1.1. Long and complex morements can be broken down into parts, then progressed into more complex over time
12.1.1.2. Varied practice, open environment, block practice, random practice, external cues
12.2. Exercise Training
12.2.1. Helps to improve motor function, neuroprotective effects
12.2.2. Relaxation techniques: rocking, rhythmic rotational movements, diaphragmatic breathing
12.2.3. Flexibility: ROM, stretching (D2 pattern in UE, D1 in LE), positional stretching
12.2.3.1. 2-3 days/week, 4 reps for 30-60s
12.3. Pulmonary Rehabilitation
12.3.1. Diaphragmatic breathing
12.3.2. Improving trunk extension will help with breathing pattern
12.3.3. Vibrating and shaking can help to clear secretions
12.3.4. Resistance training
12.3.4.1. Coordinate breathing with UE movement
12.4. Balance Training
12.4.1. Education, postual alignment, weight shifting, dynamic stability
12.4.2. Learning is task specific, mimic what they may encounter
12.5. Locomotor Training
12.5.1. Metronomes, "walk tall", "walk fast", use floor markers to improve step and stride length
12.5.2. Treadmill training with harness
12.6. Spinal Orthotics
12.6.1. Used in patients with spinal deformities
12.7. Functional Training
12.7.1. Rhythmic rotation, bridging, rolling
12.7.2. Quadruped, kneeling, half-kneeling
12.7.3. Sitting
12.7.3.1. Weight shiting, trunk rotation, PNF, educate on off-loading
12.7.4. STS
12.7.4.1. Difficult for patients, 5xSTS
12.7.4.1.1. Strengthen hip and knee extensors through partial squats at sink
12.8. Speech Therapy
12.8.1. Breathy, monotone soft voice is what patient perceives as normal
12.8.1.1. SLP will aid in speech therapy
12.9. Aerobic Exercise
12.9.1. Work out at 60-80% of HRmax and monitor vitals and RPE throughout
12.9.2. Walking, ergometry
12.9.2.1. Start small, work up endurance, intermittent exercise
12.9.2.1.1. Long duration OR more frequent exercise when lower intensoty is required
12.10. Group and Home Exercises
12.10.1. Patients can benefit from the social interaction, camraderie, and support group exercise offers
13. Psychosocial Issues
13.1. PD affects all aspects of life for both the patient, as well as the family
13.1.1. This can significantly take a toll on everyone's mental health
13.1.2. Social isolation is a common coping mechanism for PD patients