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Description
Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately dopamine-producing (“dopaminergic”) neurons in a specific area of the brain called substantia nigra (1).
PD is a progressive disorder of the central nervous system (CNS) with both motor and nonmotor symptoms.
Motor symptoms include the cardinal features of rigidity, bradykinesia, tremor, and postural instability.
Nonmotor symptoms (NMSs) may precede the onset of motor symptoms by several years. These early premotor symptoms can include loss of sense of smell (anosmia), constipation, rapid eye movement (REM) sleep behavior disorder, depression, anxiety, and orthostatic hypotension.
Other nonmotor symptoms include excessive daytime sleepiness, fatigue, pain, altered bladder function, erectile dysfunction, excessive saliva, integumentary changes, difficulty speaking and swallowing, apathy, and cognitive problems (reduced concentration, and attention, slowed thinking, confusion, and in some cases dementia).
Onset is insidious with a slow rate of progression (2).
Incidence
PD is the second most common neurodegenerative disorder and affects an estimated 1 million Americans and an estimated 7 to 10 million people worldwide.
More than 2% of people older than 65 years of age have PD, second only to Alzheimer's disease among neurodegenerative disorders.
The average age of onset is 50 to 60 years. Young-onset PD is classified as beginning between 21 and 50 years of age, and juvenile-onset PD affects individuals less than 21 years of age.
Men are affected 1.2 to 1.5 times more frequently than women, but this varies across the globe (2).
Etiology
The term parkinsonism is a generic term used to describe a group of bradykinetic syndromes with primary disturbances in the dopamine system of basal ganglia (BG).
Secondary parkinsonism results from a number of different identifiable causes, including viruses, toxins, drugs, and tumors.
The term atypical parkinsonism (Parkinson Plus Syndrome) refers to those conditions that mimic PD in some aspects, but these symptoms are caused by other neurodegenerative disorders (2).
Pathophysiology
The BG is a network of subcortical nuclei consisting of the caudate nucleus, the putamen, the globus pallidus, and the subthalamic nucleus along with the substantia nigra.
The caudate and the putamen together are called the striatum.
The direct motor loop through the BG consists of signals transmitted from the cortex to putamen to globus pallidus, to ventrolateral (VL) nucleus of the thalamus, and back to the cortex (supplementary motor area). This VL-SMA connection is excitatory and facilitates the discharge of cells in the SMA.
The BG thus serves to activate the cortex via a positive-feedback loop and assists in the initiation of voluntary movement. Inhibition of the thalamus by the BG is thought to underlie the hypokinesia seen in PD.
An indirect loop through the BG involves the subthalamic nucleus, the globus pallidus interna, and substantia nigra pars reticulata to the superior colliculus and midbrain tegmentum.
This indirect loop serves to decrease thalamocortical activation. The BG projection to the superior colliculus assists in the regulation of saccadic eye movements. The BG projection to the reticular formation assists in the regulation of trunk and limb musculature, sleep and wakefulness, and arousal (2).
Clinical Presentation
Cardinal Motor Symptoms
Rigidity
Cogwheel: is a jerky, ratchet-like resistance to passive movement as muscles alternately tense and relax.
Lead pipe: is a sustained resistance to passive movement in all directions, with no fluctuations.
Bradykinesia
Akinesia: refers to the poverty of spontaneous movement. May include the absence of associate movements such as arm swing during walking or freezing of gait.
Hypokinesia: refers to slowed and reduced movements.
Tremor
Resting tremor: as it is present at rest, suppressed briefly with voluntary movement and disappears with sleep.
Postural Instability
The ability to achieve, maintain and regain balance during posture and movement are all components of postural control that are impaired in individuals with PD, resulting in postural instability.
Festination
Unintentionally rapid short steps.
Freezing of Gait
Trembling of the legs and transient inability to effectively step, or absence of leg movements/akinesia, described as being "stick to the ground").
Stress and increased cognitive load, dual tasking, changing direction, and changing surfaces can all contribute to festination and freezing of gait episodes (2).
Image is from O'Sullivan Physical Rehabilitation. 7th Edition.
Clinical Course
Hoehn and Yahr Classification of Disability Scale
An estimate of the stage and severity of the disease can be made using a staging scale. The most widely used scale in clinical practice and research trials is the Hoehn and Yahr (2).
Image is from O'Sullivan Physical Rehabilitation. 7th Edition.
Pharmacological Management
Carbidopa/Levodopa (Sinemet) is the gold standard drug therapy for PD. It is a dopamine precursor that is metabolized to dopamine in the brain.
Other medications include Dopamine agonists, COMT inhibitors, MAO-B inhibitors, Anticholinergics, Amantadine, Norepinephrine Precursors, Cholinesterase Inhibitors, and Atypical Antipsychotics (2).
Outcome Measures
MoCA, Mini-BEST, Parkinson Fatigue Scale, MDS-UPDRS, NMSQuest, NMSS, PDQ-39 or PDQ-8, NFOG-Q, 6 MWT, 10 MWT, 9-hole Peg Test, ABC scale, Berg Balance Scale, DGI, Functional Reach, FGA, 5xSTS, TUG, TUG + Cognitive (2).
Exercise Interventions
Flexibility training
AROM
PROM
Resistance training
Specific areas of weakness are targeted, such as the antigravity extensor muscles.
Relaxation techniques
Gentle rocking
Breathing
Functional training
Bed mobility skills
Sit to stands
Standing activities
Rotation
Balance training
Tandem
SL
Perturbations
Nintendo Wii balance board
Locomotor training
Reciprocal arm swing with vertical poles
Big steps
Use auditory cues
Music
Targets to reach for
Motor-Cognitive Dual-Task training (3)
LSVT LOUD
Lee Silverman Voice Treatment
Stimulates muscles of larynx & speech through systemic series of exercises.
One goal: Speak LOUD!
Treatment parameters:
High intensity, high effort
60 min sessions x 4 sessions/week (3)
LSVT BIG
Same principles as LSVT LOUD
Principles of Neuroplasticity
Forced use
High intensity
Repetition
Complexity
Feedback/motivation
Retraining strategy
Improve amplitude of limb & body movement
Sensory recalibration (3)
Treatment Focus
Improved self-perception/monitoring "calibration"
To accurately target normal
Increase the amplitude of movement
Increase size & speed of movements (3)
LSVT Exercise Protocol
Maximal Daily Task Exercises
7 Multidirectional movements
Constant, repetitive with high effort.
Multidirectional with large amplitude & definitive start/stop.
Calibrate -retrain sensory perception.
Endurance, balance & strengthening benefits.
3-5 Functional Movements
Over learn familiar commonly used & salient everyday movements.
Encourages compliance & carryover.
Bed mobility, sit to stand, sit & reach, walk & turn.
Hierarchical Tasks
Purpose
Bring amplitude rescaling into everyday living.
Context-specific and complex activities.
Emotionally salient and patient-driven.
Examples: car transfers, reaching into cupboards, writing, chores, donning/doffing shoes and socks (3).
Images from Parkinson's Disease: Evidence-Based Practice PowerPoint
PWR Moves
Real-world carryover
Allow for adaptability
Large amplitude & high effort (3)
Images from Parkinson's Disease: Evidence-Based Practice PowerPoint
Rock Steady Boxing
Non-profit organization gives people with Parkinson's disease hope by improving their quality of life through a non-contact boxing based fitness curriculum.
Addresses:
Agility
Strength
Speed
Muscular Endurance
Hand-eye coordination
Footwork (3)
Board Style Question
A 65-year old male is referred to a PT by his orthopedist for treatment of bilateral adhesive capsulitis. The patient reports that his arms feel very stiff and he has trouble raising them. The therapist performed a full examination. During the examination, the therapist noted the patient's posture was kyphotic and rounded shoulders. PROM was within functional limits in both shoulders with stiffness and cogwheeling. Bilateral GH joint mobility was WNL. Strength was grossly 4/5 for all musculature. The sensation was intact in bilateral UE's. What should the PT do NEXT?
Apply a thermal modality to bilateral anterior shoulders in preparation for stretching the stiff shoulders.
Perform grad I and II posterior glenohumeral joint mobilizations to reduce the forward shoulder posture.
Contact the patient's orthopedist to discuss the findings of the examination.
Provide the patient with some simple self-stretches he can do daily to improve his kyphotic posture.
Correct Answer: C
The physical therapist should recognize the signs of Parkinson’s as a possible reason for the patient’s complaints of shoulder stiffness. There was no limitation of motion and no capsular pattern to support a diagnosis of adhesive capsulitis, yet there was cogwheeling upon PROM. In addition, it is rare to have bilateral adhesive capsulitis. It is likely a more systemic issue. The patient also has a kyphotic posture, which may or may not be related to the onset of Parkinson’s; however, this patient needs to be examined by a neurologist before the physical therapist begins treatment. The therapist should discuss the findings with the orthopedist and refer the patient back to his doctor for follow-up.
Answer A: At this time the main concern is that the patient may have been misdiagnosed and is showing signs of Parkinson’s disease. The patient has full range of motion in his shoulders and does not need stretching of the shoulders.
Answer B: At this time the main concern is that the patient may have been misdiagnosed and is showing signs of Parkinson’s disease. Therefore, addressing the forward
shoulder posture is not a priority.
Answer D: At this time the main concern is that the patient may have been misdiagnosed and is showing signs of Parkinson’s disease. Daily postural stretching is a good
idea for anyone with poor posture; however, this patient needs to be examined by a neurologist before the physical therapist begins treatment.
References
www.parkinson.org
Physical Rehabilitation. 7th Edition. Susan B. O'Sullivan PT, EdD. Thomas J. Schmitz PT, PhD. George Fulk PT, Ph.D. ISBN-13: 978-0-8036-6162-2
Meghan Malley PT, DPT, Parkinson's Disease: Evidence-Based Practice PowerPoint.
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