Understanding Parkinson's Disease: Maximizing Function from the Clinic to Home

Transcription

1 Understanding Parkinson's Disease: Maximizing Function from the Clinic to Home Date: Saturday, October 1, 2016 Time: 7:45 AM - 3:45 PM Session ID & Location: 5D: MtgRm7 CEU Eligibility: 0.40 Presented by: Christina M. Durrough, PT, DPT, NCS Session Description: This session is designed to provide a comprehensive overview of Parkinson s disease. The speaker will discuss the neurophysiology of Parkinson s disease in order to explain symptoms and signs observed in the clinic, as well as medical management and its impact on physical therapy. Emphasis will be placed on reviewing the literature pertaining to neuroplasticity driven by high intensity exercise. Lecture and lab portions of the session will address evidence-based physical therapy outcome measures and interventions for patients across all stages of Parkinson s disease. Specific case studies will be examined to allow attendees to apply topics addressed in the session to facilitate translation of session content to daily practice. Upon completion of the course, participants will be able to: Describe the implications of dopaminergic cell death on the physiology of the basal ganglia Identify various environmental and genetic risk factors for Parkinson s disease Recognize the expected signs and symptoms of idiopathic Parkinson s disease, secondary Parkinsonism, and Parkinson-plus syndromes Discuss medical (pharmacological and surgical) interventions for Parkinson s disease and their impact on rehabilitation Select, administer, and interpret evidence-based outcome measures to be used in the management of individuals with Parkinson s disease Select and perform appropriate evidence-based interventions for individuals of various functional levels Presenter Bio(s): Christina Durrough, PT, DPT, NCS is a physical therapist at Vanderbilt Pi Beta Phi Rehabilitation Institute outpatient neurologic clinic. She is actively involved in the Parkinson s disease community in Nashville. Additionally, she participates in research and teaching opportunities. She is a co-founder of an online continuing education platform called Rehab Knowledge Advantage. She received her Doctorate of Physical Therapy at Ohio State University and completed the Neurologic Clinical Residency at Vanderbilt and Belmont University.

2 Maximizing Function from the Clinic to Home Pre- and Post-Test Christina M. Durrough, PT, DPT, NCS PTAG and TPTA INSIGHT 2016 October 1, Approximately what percentage of dopaminergic neurons are lost before the onset of physical signs of Parkinson s disease? a. 0-20% b % c % d % 2. What is the gold standard medication for treating Parkinson s disease? a. Mirapex b. Rasagiline c. Selegiline d. Sinemet 3. Which of the following is not considered a cardinal sign of Parkinson s disease? a. Postural instability b. Rigidity c. Akinesia d. Freezing/festinating gait 4. True or False: A patient obtains a score of 24/28 on the Mini-BESTest. According to scoring guidelines, this patient is considered a high falls risk. a. True b. False 5. What is the most common psychiatric symptom in Parkinson s disease? a. Poor concentration b. Apathy c. Axiety d. Depression 6. Which of the following are disease-modifying components in the management of Parkinson s disease? a. Pharmacological agents b. Deep brain stimulation surgery c. Exercise d. Both A and C

3 Understanding Parkinson s Disease: Maximizing Function from the Clinic to Home Christina M. Durrough, PT, DPT, NCS PTAG and TPTA INSIGHT 2016 October 1, 2016 Objectives Describe the implications of dopaminergic cell death on the physiology of the basal ganglia Identify various environmental and genetic risk factors for Parkinson s disease Recognize the expected signs and symptoms of idiopathic Parkinson s disease, secondary Parkinsonism, and Parkinson-plus syndromes Discuss medical (pharmacological and surgical) interventions for Parkinson s disease and their impact on rehabilitation Select, administer, and interpret evidence-based outcome measures to be used in the management of individuals with Parkinson s disease Select and perform appropriate evidence-based interventions for individuals of various functional levels Overview Background: neuro-anatomy, pathophysiology, demographics Clinical manifestations and classifications of Parkinson s disease Management of Parkinson s disease Outcome measures Evidence-based physical and occupational therapy interventions Future of physical therapy Christina M. Durrough, PT, DPT, NCS 1

4 History of Parkinson s Disease First described by James Parkinson in 1817 An Essay on the Shaking Palsy Michael J. Fox Foundation Founded in 2000 Has raised more than $450 million for Parkinson s disease research to date Neuro-anatomy and Physiology of the Basal Ganglia Christina M. Durrough, PT, DPT, NCS 2

5 Parkinson s Disease Defined A chronic, progressive central nervous system disorder that results from death of dopamine-producing cells in the substantia nigra (part of the basal ganglia) Second most common neurodegenerative condition Alzheimer s disease is most common Basal Ganglia Components [location] Caudate [cerebrum] Putamen [cerebrum] Globus pallidus (internus and externus) [cerebrum] Subthalamic nucleus [diencephalon] Substantia nigra (pars compacta and pars reticulata) [midbrain] - Photo Credit - neurophysiology.wikispaces.com/basal+ganglia+ii - Photo Credit - Blumenfeld. Figure Christina M. Durrough, PT, DPT, NCS 3

6 Terminology Striatum = caudate + putamen Lentiform nucleus = globus pallidus + putamen - Photo Credit - neurophysiology.wikispaces.com/basal+ganglia+ii Function Regulates movement via control of sequencing, muscle tone, and muscle force Communicates with motor planning areas of the cerebral cortex via the thalamus Influences lower motor neurons via connections with the pedunculopontinenucleus of the midbrain Neurotransmitters Gamma-aminobutyric acid (GABA) [inhibitory] Glutamate [excitatory] Dopamine [both inhibitory and excitatory] Christina M. Durrough, PT, DPT, NCS 4

7 Pathways Direct pathway Indirect pathway Pathways Direct pathway Facilitates movement In the absence of modulation from the basal ganglia, the thalamus exerts excitatory influence on the motor cortex and increases movement. Motor Cortex + + Movement Thalamus Christina M. Durrough, PT, DPT, NCS 5

8 At rest, the globus pallidus internus (GPi) inhibits the excitatory signals from the thalamus by releasing GABA. Motor Cortex + Movement + Striatum Globus Pallidus (internus) Thalamus Substantia Nigra Subthalamic Nucleus To initiate movement, the motor cortex sends an excitatory signal to the striatum. Motor Cortex + Movement + + Striatum Globus Pallidus (internus) Thalamus Substantia Nigra Subthalamic Nucleus In turn, the striatum increases neurotransmitter release GABA inhibits the GPi. Motor Cortex + Movement + + Striatum Globus Pallidus (internus) Thalamus Substantia Nigra Subthalamic Nucleus Christina M. Durrough, PT, DPT, NCS 6

9 Inhibition of the GPi s release of GABA leads to dis-inhibition of the thalamus and results in increased motor activity. Motor Cortex + Movement + + Striatum Globus Pallidus (internus) Dis-inhibition Thalamus Substantia Nigra Subthalamic Nucleus Nigrostriatal Impact: The subthalamic nucleus excites the substantia nigra, which sends dopamine to the striatum. + Motor Cortex + + Movement Striatum Globus Pallidus (internus) Dis-inhibition Thalamus + Dopamine + Substantia Nigra + Subthalamic Nucleus Nigrostriatal Impact: In the direct pathway, dopamine acts as an excitatory neurotransmitter by binding to D1 receptors. + Motor Cortex + + Movement Striatum D1 receptors Globus Pallidus (internus) Dis-inhibition Thalamus + Dopamine + Substantia Nigra + Subthalamic Nucleus Christina M. Durrough, PT, DPT, NCS 7

10 Nigrostriatal Impact: Dopamine further excites the striatum, ultimately leading to greater dis-inhibition of the thalamus and increased motor activity. + Motor Cortex + + Movement Striatum D1 receptors Globus Pallidus (internus) Dis-inhibition Thalamus + Dopamine + Substantia Nigra + Subthalamic Nucleus Pathways Direct pathway Facilitates movement Dopamine has excitatory effect more movement Pathways Indirect pathway Suppresses movement Christina M. Durrough, PT, DPT, NCS 8

11 At rest, the globus pallidus externus (GPe) inhibits the excitatory signals from the subthalamic nucleus to the GPi. Motor Cortex + Movement + Striatum Globus Pallidus (internus) Thalamus + Substantia Nigra Globus Pallidus (externus) Subthalamic Nucleus To initiate the indirect pathway, the motor cortex sends and excitatory signal to the striatum. Motor Cortex + Movement + + Striatum Globus Pallidus (internus) Thalamus + Substantia Nigra Globus Pallidus (externus) Subthalamic Nucleus In turn, the striatum increases neurotransmitter release GABA inhibits the globus pallidus externus. Motor Cortex + Movement + + Striatum Globus Pallidus (internus) + Thalamus Substantia Nigra Globus Pallidus (externus) Subthalamic Nucleus Christina M. Durrough, PT, DPT, NCS 9

12 Inhibition of the GPe s release of GABA leads to dis-inhibition of the subthalamic nucleus and increased excitatory signals to the GPi. + Motor Cortex + + Movement Striatum Globus Pallidus (internus) + Thalamus Substantia Nigra Globus Pallidus (externus) Dis-inhibition Subthalamic Nucleus Excitation of the GPi results in increased release of GABA to the thalamus and further reduced motor activity. Motor Cortex + Movement + + Striatum Globus Pallidus (internus) + Thalamus Substantia Nigra Globus Pallidus (externus) Dis-inhibition Subthalamic Nucleus Nigrostriatal Impact: The subthalamic nucleus excites the substantia nigra, which sends dopamine to the striatum. + Motor Cortex Movement Striatum Dopamine Substantia Nigra Globus Pallidus (internus) Globus Pallidus (externus) + + Dis-inhibition Thalamus Subthalamic Nucleus Christina M. Durrough, PT, DPT, NCS 10

13 Nigrostriatal Impact: In the indirect pathway, dopamine acts as an inhibitory neurotransmitter by binding to D2 receptors. + Motor Cortex Movement Striatum D2 receptors Dopamine Substantia Nigra Globus Pallidus (internus) Globus Pallidus (externus) + + Dis-inhibition Thalamus Subthalamic Nucleus Nigrostriatal Impact: Dopamine inhibits the striatum, ultimately leading to reduced inhibition of the thalamus and increased motor activity. + Motor Cortex + + Movement Striatum D2 receptors Dopamine Substantia Nigra Globus Pallidus (internus) Globus Pallidus (externus) + + Less Dis-inhibition Thalamus Subthalamic Nucleus Pathways Indirect pathway Suppresses movement Dopamine has inhibitory effect more movement Christina M. Durrough, PT, DPT, NCS 11

14 Pathways Direct pathway Indirect pathway Dopamine Voluntary Movement Pathophysiology of Parkinson s Disease Dopamine Loss in PD Loss of dopaminergic neurons in the substantia nigra pars compacta leads to Parkinsonian symptoms 60-80% loss of dopaminergic neurons occurs before onset of physical signs [Cheng HC, et al ] Christina M. Durrough, PT, DPT, NCS 12

15 Effect on Basal Ganglia Pathways Direct pathway Less dopamine results in decreased facilitation of motor output Effect on Basal Ganglia Pathways Indirect pathway Less dopamine results in increased inhibition of (decreased) motor output Effect on Basal Ganglia Pathways Direct pathway Indirect pathway Less dopamine Less voluntary movement Christina M. Durrough, PT, DPT, NCS 13

16 Epidemiology Prevalence (worldwide by age) PER 100,000 2,000 1,800 1,600 1,400 1,200 1, ,903 1, AGE RANGE [Pringsheim N, et al ] Epidemiology Summary Age: sharp increase in prevalence/incidence with increasing age 0.3% in entire population, 1% in people over 60 years of age, up to 4% in highest age groups Ethnicity: Caucasians more affected than African Americans and Asians Sex: men slightly more affected than women [de Lau LM, Breteler MM ] [Dahodwala N, et al ] [Pringsheim N, et al ] Christina M. Durrough, PT, DPT, NCS 14

17 Etiology Etiology of Parkinson s Disease Sporadic (cause typically unknown) 90% of cases Genetic (monogenetic mutations) 10% of cases [de Lau LM, Breteler MM ] Etiology of Sporadic PD Cellular mechanisms Oxidative stress Accumulation of toxic proteins Mitochondrial malfunction Inadequate neurotrophic factors (GDNF) Inflammatory glia [Dauer W, Przedborski S ] Christina M. Durrough, PT, DPT, NCS 15

18 Environmental Factors in PD Occupational exposures Tobacco, coffee, and alcohol Dietary factors [de Lau LM, Breteler MM ] Environmental Factors in PD Occupational exposures Exposure to pesticides and herbicides (plantation workers, farmers) Exposure to heavy metals (welders) [de Lau LM, Breteler MM ] Environmental Factors in PD Tobacco, coffee, and alcohol Smoking: inverse association Active component (hypothesized): nicotine may be neuroprotective Coffee: inverse association Active component: caffeine Improves motor deficits in a mouse model of PD Alcohol: possible inverse association (inconsistent results) [de Lau LM, Breteler MM ] Christina M. Durrough, PT, DPT, NCS 16

19 Environmental Factors in PD Dietary factors Antioxidants (vitamins E and C): may neutralize free radicals to reduce oxidative stress (no confirmation in the literature) Unsaturated fatty acids: inverse association Dairy/milk products: positive association (mechanism unclear) Dietary iron: possible positive association (inconsistent results) [de Lau LM, Breteler MM ] Etiology of Parkinson s Disease Sporadic (cause typically unknown) 90% of cases Genetic (monogenetic mutations) 10% of cases [de Lau LM, Breteler MM ] Genetic Factors in PD Causative genes Susceptibility genes [de Lau LM, Breteler MM ] Christina M. Durrough, PT, DPT, NCS 17

20 Genetic Factors in PD Causative genes Monogenetic mutations account for approximately 10% of cases 12 genes currently identified Somewhat atypical presentation Young onset (before age of 50), dystonia, early dementia [de Lau LM, Breteler MM ] Genetic Factors in PD Susceptibility genes Parkinson s disease may result from complex interactions between environmental and genetic factors Certain genes may increase susceptibility to PD Further research warranted [de Lau LM, Breteler MM ] Overview Background: neuro-anatomy, pathophysiology, demographics Clinical manifestations and classifications of Parkinson s disease Management of Parkinson s disease Outcome measures Evidence-based physical and occupational therapy interventions Future of physical therapy Christina M. Durrough, PT, DPT, NCS 18

21 Clinical Manifestations Clinical Manifestations of PD Cardinal signs Other signs and symptoms Cardinal Signs Tremor Rigidity Akinesia/bradykinesia Postural instability Christina M. Durrough, PT, DPT, NCS 19

22 Cardinal Signs Tremor Resting tremor that subsides with action Present in 70% of individuals at diagnosis Begins unilaterally, usually affecting one hand or foot Can be exacerbated by stress or excitement [Parkinson s Disease Foundation] Cardinal Signs Rigidity Hypertonia characterized by resistance through the entire range of motion regardless of velocity May be cogwheel or lead pipe Cogwheel: resistance followed by giving way in step-like movements Lead pipe: constant resistance Initially affects proximal musculature and extends distally Can cause decreased range of motion, slowness, fatigue, and pain [Parkinson s Disease Foundation] Cardinal Signs Akinesia/bradykinesia Akinesia: loss or impairment of voluntary movement Bradykinesia: slowness of movement Impairs ability to initiate and execute movements Hypokinesia common [Parkinson s Disease Foundation] Christina M. Durrough, PT, DPT, NCS 20

23 Cardinal Signs Postural instability Impairments in reactive and anticipatory balance reactions Posterior losses of balance common (retropulsion) Anterior losses of balance due to festination and forward flexed posture [Parkinson s Disease Foundation] Clinical Manifestations of PD Cardinal signs Other signs and symptoms Other motor signs and symptoms Non-motor signs and symptoms Other Motor Signs and Symptoms Freezing of gait Forward flexed posture Incoordination (gross and fine) Hypomimia Dystonia Dysarthria Christina M. Durrough, PT, DPT, NCS 21

24 Freezing of Gait Two theories 1. Loss of automaticity Basal ganglia controls automatic, well-learned movements Acts as an internal cue to enable movement sequences to be carried out implicitly, automatically, and without attention Therefore, in Parkinson s disease, movement arrests when not performed in an explicit, conscious, and attentional manner 2. Optic flow Rapidly moving targets in peripheral visual fields are able to bypass the affected basal ganglia Disruption of optic flow results in freezing Freezing of Gait Typically occurs when something changes the flow of walking Initiation Turning Surface changes Thresholds Crowded areas Non-Motor Signs and Symptoms May precede onset of motor symptoms by years Most common pre-motor symptoms: Loss of sense of smell (olfaction) Sleep disturbances (REM behavior disorder) Mood disorders Dysautonomia (orthostatic hypotension) Constipation [LohleM, et al ] Christina M. Durrough, PT, DPT, NCS 22

25 Non-Motor Signs and Symptoms Depression Dysphagia Hypophonia Fatigue Generalized stiffness Micrographia Sialorrhea Cognitive dysfunction Executive function Motivation Memory Attention Dementia (later stages of PD) [LohleM, et al ] Non-Motor Signs and Symptoms Dementia with Lewy bodies Misfolded alpha-synuclein proteins (Lewy bodies) area hallmark of PD Progressive dementia characterized by deficits in attention and executive function Memory impairment may not be evident in early stages Fluctuating cognition Visual hallucinations [Vekrellis K, et al ] Classifications of Parkinson s Disease Christina M. Durrough, PT, DPT, NCS 23

26 Classifications of Parkinson s Disease Primary parkinsonism/idiopathic Parkinson s disease Secondary parkinsonism Parkinson-plus syndromes Primary Parkinsonism/Idiopathic PD Approximately 85% of all Parkinson s cases Unilateral onset that progresses slowly Primary Parkinsonism/Idiopathic PD Sub-types Tremor dominant Postural instability/gait disturbance [Zetusky WJ, et al ] Christina M. Durrough, PT, DPT, NCS 24

27 Primary Parkinsonism/Idiopathic PD Sub-types Tremor dominant Earlier age at onset More often family history of Parkinsonism Relative preservation of mental status Slower progression More favorable prognosis [Zetusky WJ, et al ] Primary Parkinsonism/Idiopathic PD Sub-types Postural instability/gait disturbance More rapid progression More severe cognitive dysfunction Poorer prognosis Two variants Postural instability with falling (PIF) Freezing of gait (FOG) [Factor SA, et al ] [Marras C, et al ] [Zetusky WJ, et al ] Primary Parkinsonism/Idiopathic PD Sub-types Postural instability/gait disturbance Postural Instability with Falling Depression Inversely associated with APOEε4 allele (protective effect) Freezing of Gait Psychotic symptoms Inversely associated with CYP2D6*4 allele (protective effect) Longer duration of disease Differing non-motor features and genetic predictors suggest these are pathophysiologically distinct variants, which has implications for identifying therapeutic targets and predicting outcomes. [Factor SA, et al ] Christina M. Durrough, PT, DPT, NCS 25

28 Diagnostic Criteria Clinical diagnosis Definitive diagnosis only possible at autopsy Presence of at least 2/4 cardinal signs Absence of secondary causes CT or MRI to rule out other diagnoses Positive response to levodopa [Massano J, Bhatia KP ] Classifications of Parkinson s Disease Primary parkinsonism/idiopathic Parkinson s disease Secondary parkinsonism Parkinson-plus syndromes Secondary Parkinsonism Vascular parkinsonism Drug-induced parkinsonism Infection Toxins Christina M. Durrough, PT, DPT, NCS 26

29 Secondary Parkinsonism Vascular parkinsonism Caused by one or more small strokes Lower extremities and gait more affected Rest tremor uncommon Other signs of stroke may be present (hemiparesis, spasticity) Scarce response to levodopa [Massano J, Bhatia KP ] Secondary Parkinsonism Drug-induced parkinsonism Neuroleptic/anti-psychotic medications Symmetrical presentation Orolingual dyskinesia, tardive dyskinesia, or akathisia may be present Ceasing medication typically reverses symptoms Could take up to two years [Drug-induced Parkinsonism ] [Massano J, Bhatia KP ] Secondary Parkinsonism Infection Encephalitis, influenza, HIV, meningitis [Jang H, et al ] Christina M. Durrough, PT, DPT, NCS 27

30 Secondary Parkinsonism Toxins Carbon monoxide Heavy metals: manganese (welders), copper, lead Mercury (tremor) MPTP (animal models of PD, recreational drug) Toluene (solvent in paint thinners, adhesives, etc.) Classifications of Parkinson s Disease Primary parkinsonism/idiopathic Parkinson s disease Secondary parkinsonism Parkinson-plus syndromes Parkinson-Plus Syndromes Progressive supranuclear palsy (PSP) Multiple system atrophy (MSA) Corticobasalganglionicdegeneration (CBGD) Christina M. Durrough, PT, DPT, NCS 28

31 Parkinson-Plus Syndromes Progressive supranuclear palsy (PSP) Early postural instability and falls Vertical gaze paresis Difficulty controlling eyelids ( PSP stare ) Median survival time from onset: 5.3 years [Bower JH, et al ] Parkinson-Plus Syndromes Multiple system atrophy (MSA) Parkinsonian symptoms, along with autonomic dysfunction and cerebellar dysfunction Median survival time from onset: 8.5 years [Bower JH, et al ] Parkinson-Plus Syndromes Corticobasalganglionicdegeneration (CBGD) Focal rigidity Marked dystonia (usually in one arm) Limb apraxia Alien hand syndrome Parkinsonian symptoms Median survival time from onset: 6-8 years [Association for Frontotemporal Degeneration] Christina M. Durrough, PT, DPT, NCS 29

32 Prognostic Factors Prognosis Median survival time from motor onset (idiopathic PD): 15.8 years Typically a slow, variable rate of progression Pneumonia is most common cause of death [Forsaa EB, et al ] Negative Prognostic Factors Greater baseline impairment Early cognitive disturbance Older age Lack of tremor at onset (PIGD) [Marras C, et al ] Christina M. Durrough, PT, DPT, NCS 30

33 Positive Prognostic Factors Less baseline impairment Younger age onset Tremor dominant sub-type Lack of cognitive impairment Staging and Progression of Parkinson s Disease Hoehn and Yahr Most widely accepted scale for describing the progression of symptoms in Parkinson s disease Developed in 1967 with 5 stages Revised and expanded in 2004 to include 7 stages Christina M. Durrough, PT, DPT, NCS 31

34 Modified Hoehn and Yahr Scale Stage 0 No signs of disease. 1 Unilateral symptoms only. 1.5 Unilateral and axial involvement. Description 2 Bilateral symptoms. No impairment of balance. 2.5 Mild bilateral disease with recovery on pull test. 3 Balance impairment. Mild to moderate disease. Physically independent. 4 Severe disability, but still able to stand or walk unassisted. 5 Needing a wheelchair or bedridden unless assisted. Hoehn and Yahr Analyzed Strengths Wide utilization and acceptance High correlations with some standardized scales of motor impairment, disability, and quality of life Limitations Mixing of impairment and disability Non-linearity Heavy weighting of postural instability as the primary index of disease severity Does not fully capture other motor features or non-motor symptoms [Goetz CG, et al ] Unified Parkinson s Disease Rating Scale Developed by an international panel of neurologists in the 1980s (UPDRS) Gold standard for quantifying symptoms and progression of Parkinson s disease Revised by the Movement Disorders Society in 2008 to incorporate more clinically pertinent items(mds-updrs) [Goetz CG, et al ] Christina M. Durrough, PT, DPT, NCS 32

35 UPDRS vs. MDS-UPDRS UPDRS Six parts 1. Mentation, behavior, and mood 2. Activities of daily living 3. Motor examination 4. Complications of therapy 5. Modified Hoehn and Yahr staging 6. Schwab and England Activities of Daily Living Scale MDS-UPDRS Four parts 1. Non-motor experiences of daily living 2. Motor experiences of daily living 3. Motor examination 4. Motor complications [Goetz CG, et al ] UPDRS Motor Items rated from 0 (normal) to 4 (most severe impairment) Assesses speech, facial expression, tremor, rigidity, coordination, transfers, posture, gait, postural stability, and bradykinesia [Goetz CG, et al ] UPDRS Motor Limitations for physical therapists Emphasis of responses heavily weighted to later stages of PD Does not adequately capture meaningful changes in the earlier stages of the disease [Schenkman M, et al ] Christina M. Durrough, PT, DPT, NCS 33

36 UPDRS Motor Limitations for physical therapists No uniform anchors associated with each question (i.e., a score of 2 on one item may not correlate with a score of 2 on another item) [Schenkman M, et al ] UPDRS Motor Limitations for physical therapists Scale weighted to impairments not likely to respond to PT interventions [Schenkman M, et al ] UPDRS Motor Limitations for physical therapists Extensive training recommended for reliable scoring Training material provided by the International Parkinson and Movement Disorder Society $1,500 for non-profit use $30,000 for industry use [Schenkman M, et al ] Christina M. Durrough, PT, DPT, NCS 34

37 Overview Background: neuro-anatomy, pathophysiology, demographics Clinical manifestations and classifications of Parkinson s disease Management of Parkinson s disease Outcome measures Evidence-based physical and occupational therapy interventions Future of physical therapy Therapeutic Options Pharmacology Psychological Support Surgery (deep brain stimulation) Exercise (body and voice) Pharmacological Management Christina M. Durrough, PT, DPT, NCS 35

38 Pharmacological Management Dopaminergic medications used to control the symptoms of Parkinson s disease Individual response to specific medications will change over time Requires frequent communication with medical team Adjustment of dosage, schedule, and/or changing medications Levodopa-Carbidopa (Sinemet) Gold standard Levodopa Precursor to dopamine that is able to cross the blood-brain barrier (dopamine cannot) Carbidopa DOPA decarboxylase inhibitor (DDCI) that prevents levodopa from converting into dopamine in the periphery Side effects Nausea, drowsiness, orthostatic hypotension, dyskinesia, motor fluctuations, hallucinations Levodopa-Carbidopa (Sinemet) Recommended patients take Sinemet on an empty stomach 30 minutes before or 1 hour after meals Protein can slow absorption of Sinemet Christina M. Durrough, PT, DPT, NCS 36

39 On-Off Times On times Medication effectively controlling symptoms Off times Regular and predictable decline symptom control between doses Therapeutic Window Dyskinesia On Off Time (years) Therapeutic Window Over time, the duration of target clinical response (therapeutic window) becomes shorter Dyskinesia On Off Christina M. Durrough, PT, DPT, NCS 37

40 Therapeutic Window Dyskinesia Abnormal involuntary movements that usually occur at peak dose Dyskinesia On Off Therapeutic Window Off times Lack of symptom management between doses Dyskinesia On Off Other Medications Dopamine agonists COMT inhibitors MAO type-b inhibitors Anticholinergics Amantadine Christina M. Durrough, PT, DPT, NCS 38

41 Other Medications Dopamine agonists Directly stimulate dopamine receptors Initial therapy or adjunct therapy May delay or reduce motor fluctuations and dyskinesia Not as effective as Sinemet but provides relief of symptoms with longer half-life Brand names: Mirapex, Requip, Neupro Other Medications COMT inhibitors Catechol-O-methyl transferase inhibitors Prevent peripheral degradation of levodopa May decrease off time or reduce levodopa dose necessary for clinical effect Brand names: Comtan, Tasmar Other Medications MAO type-b inhibitors Monoamine oxidase inhibitors Block breakdown of dopamine in the brain Brand names: Selegiline, Rasagiline Christina M. Durrough, PT, DPT, NCS 39

42 Other Medications Anticholinergics Reduce over-activity of acetylcholine; inhibit dopamine reuptake in the striatum Used mainly for tremors and rigidity Brand names: Artane, Cogentin Other Medications Amantadine Dopamine agonist and dopamine reuptake inhibitor Often used to treat dyskinesia Brand names: Symmetrel, Kemadrin Symptoms Unresponsive to Medications Postural instability Freezing Mental changes Autonomic nervous system dysfunction [Sethi K ] Christina M. Durrough, PT, DPT, NCS 40

43 Rehabilitation Implications Questions to ask Timing of rehabilitation Rehabilitation Implications Questions to ask How long before dose kicks in? How long does a dose last? Presence and severity of on/off times? Off times predictable? Functional implications? Rehabilitation Implications Timing of rehabilitation Patients will perform better and be more comfortable in their on time May be valuable to examine patient during both on and off times Complete re-assessments at a consistent time during medication cycle for accurate comparisons Teach strategies that may be helpful during off times [Dibble LE, et al ] Christina M. Durrough, PT, DPT, NCS 41

44 Surgical Management Deep Brain Stimulation Electrodes placed in the brain are connected by wires to an implantable pulse generator (IPG) under the skin of the chest Mechanism of action unclear (suppression or activation of cells) - Photo Credit - [Vitek JL ] Goals of Surgery Minimize off times and dyskinesia Reduce medication dosages Fewer side effects Christina M. Durrough, PT, DPT, NCS 42

45 Criteria of Surgical Candidates Idiopathic Parkinson s disease Intact cognitive function Good response to dopamine Lack of co-morbidity Realistic expectations Age of candidate Normal brain MRI Ability to tolerate awake surgery Degree of disability Difficulty performing ADLs due to motor fluctuations/dyskinesia but still functioning fairly well overall Ability to attend follow-up appointments Programming DBS [UCSF Department of Neurological Surgery ] Target Sites Site Thalamus Effect Reduces tremor but not other symptoms of PD (used more often for essential tremor) Globus pallidus internus Reduces tremor, rigidity, bradykinesia, dyskinesia Subthalamic nucleus Reduces tremor, rigidity, bradykinesia, dyskinesia Target Sites Globus pallidus internus versus subthalamic nucleus No difference in quality of life or cognition, mood, and behavior between the two sites During the most off point in the day, individuals with STN DBS performed daily tasks more independently Greater reduction in medication dosage after STN DBS [Odekerken VJJ, et al ] Christina M. Durrough, PT, DPT, NCS 43

46 Limitations of DBS Variable reduction in symptoms Postural instability not impacted Brain surgery- chance of infection Psychological Support The Shaking Palsy Involuntary tremulous motion, with lessened voluntary power, in parts not in action, and even when supported; with a propensity to bend the trunk forwards, and to pass from a walking to a running pace: the senses and intellects being uninjured. Christina M. Durrough, PT, DPT, NCS 44

47 [Weintraub D, Burn DJ ] Quintessential Neuropsychiatric Disorder Anxiety Apathy Dementia Depression Disorders of sleep and wakefulness Impulse control disorders Psychosis [Weintraub D, Burn DJ ] Dopamine s Impact on Limbic Functions Low Dopamine Depression Apathy Anhedonia Anxiety High Dopamine Euphoria/mania Impulsivity Pleasure-seeking/risktaking behavior [Blonder LX, Sleven JT ] [Nieollon A, Coquerel A ] Christina M. Durrough, PT, DPT, NCS 45

48 Depression Most common psychiatric symptom in PD Affects approximately 40% of people with PD Symptoms include: Depressed mood, diminished interest/pleasure, fatigue, sleep changes, poor concentration, change in appetite May precede onset of motor symptoms [Blonder LX, Sleven JT ] Suicide Rate? INCREASED OR DECREASED [Myslobodsky M, et al ] Caregiver Burden Caregiver burden increases with: Disability Psychiatric symptoms Particularly depression, hallucinations, and confusion Falls No difference in caregiver burden between older/younger or male/female caregivers [Schrag A, et al ] Christina M. Durrough, PT, DPT, NCS 46

49 Patient Depression Caregiver Quality of Life Patient Quality of Life and Level of Function Caregiver Burden [Schrag A, et al ] Pharmacologic Management Selective serotonin reuptake inhibitors Tricyclic antidepressants Pramipexole (dopamine agonist) sometimes Do not necessarily make motor symptoms worse [Friedman JH, Weintraub D ] Support Groups Large network of support groups for individuals with Parkinson s disease and their families/caregivers Variety of formats Large groups/small groups Patient groups/caregiver groups/mixed groups Lecture formats/informal discussions Helps with day-to-day coping Relating stories, common struggles, etc. Christina M. Durrough, PT, DPT, NCS 47

50 Exercise Health Benefits of Exercise Improved cardiovascular health Improved motor performance Improved psychological health (reduced depression) Improved sleep Decreased fatigue Improved bone health (osteoporosis prevention) Health Benefits of Exercise Neuroprotective for individuals with Parkinson s disease Only disease-modifying component in the management of Parkinson s disease Pharmacology Psychological Support Surgery (deep brain stimulation) Exercise (body and voice) Christina M. Durrough, PT, DPT, NCS 48

51 Animal Models Early disease Moderate disease Severe disease Early Disease Study 1 4 groups (1) saline, (2) saline plus exercise, (3) MPTP, (4) MPTP plus exercise Exercise: treadmill running x 28 days beginning day 5 post-lesion Results Improved balance in both exercise groups Increased stimulus-evoked release and decreased decay of dopamine in the dorsal striatum of MPTP plus exercise mice only Increased striatal dopamine in saline plus exercise versus saline only mice No differences in MPTP mice [Petzinger GM, et al ] Early Disease Study 2 Rats received a unilateral lesion before being randomized into 4 groups (1) lesioned plus no cast, (2) lesioned plus cast on post-operative days 1-7 [early cast], (3) lesioned plus casts on post-operative days 7-13 [late casts], (4) lesioned plus casts on post-operative days 3-9 [intermediate casts] 3 sham groups (1) sham and no casts, (2) sham and casts on post-operative days 1-7, (3) sham and casts on post-operative days 7-13 [Tillerson JL, et al ] Christina M. Durrough, PT, DPT, NCS 49

52 Early Disease Study 2 Rats placed in cages with playmates casted animals forced to rely on impaired forelimb for exploration and movement Results Uncasted animals had chronic behavioral deficits and no neurochemical protection against the loss of striatal dopamine Early forced use spared behavioral function and striatal dopamine levels even with removal of cast after 7 days (no different than sham controls) Reduced behavioral deficits during forced-use but gradually worsened asymmetry over time with intermediate casting Persistent behavioral deficits with late casting Degree of forelimb asymmetry was correlated with level of dopamine depletion [Tillerson JL, et al ] Early Disease Study 2 Conclusions Exercise may delay or prevent Parkinson s disease in healthy individuals Exercise may slow disease progression and motor deterioration in early Parkinson s disease [Tillerson JL, et al ] Moderate Disease Mice with moderate neurodegeneration (chronic Parkinsonism) participated in treadmill exercise x 18 weeks Functional outcomes Markedly improved balance and coordination Cellular outcomes Significant deterrence in loss of neuronal dopamine-producing cells Improved mitochondrial function Increase in brain region-specific levels of brain-derived and glial cell line-derived neurotrophic factors [Lau YS ] Christina M. Durrough, PT, DPT, NCS 50

53 Severe Disease Mice with severe neurodegeneration participated in treadmill exercise x 12 weeks Functional outcomes Restoration of gait pattern consistency and step length (matching that of non-lesioned mice) No improvement in cognitive learning deficits (water maze) Improved balance Cellular outcomes No significant increase in striatal dopamine levels [Pothakos K, et al ] Translating Animal Research to Humans Studies of high intensity and forced-use exercise High Intensity Exercise in Early PD Individuals with early PD (Hoehn and Yahr stages 1 and 2) randomized to high intensity, low intensity, or zero intensity (education) exercise 24 sessions over 8 weeks (treadmill training) [Fisher BE, et al ] Christina M. Durrough, PT, DPT, NCS 51

54 High Intensity Exercise in Early PD Results High intensity exercise resulted in post-exercise increases in gait speed, step and stride length, and hip and ankle joint excursion during self-selected and fast gait, and improved weight distribution during sit-to-stand transfers Inconsistent improvements in low and zero intensity groups More normal corticomotor excitability in high intensity group [Fisher BE, et al ] High Intensity Exercise in Early PD Corticomotor excitability assessed via cortical silent period (CSP) durations in response to single-pulse transcranial magnetic stimulation (TMS) Shortened CSP durations are one of the most consistent and widely reproduced TMS findings among people with PD High intensity exercise group demonstrated lengthening in CSP (more normal corticomotor excitability) [Fisher BE, et al ] Forced Use Cycling 10 individuals with mild to moderate PD randomly assigned to complete 8 weeks of forced exercise or voluntary exercise Forced exercise (FE): pedaled at a rate 30% greater than their preferred voluntary rate Voluntary exercise (VE): pedaled at preferred rate [Ridgel AL, et al ] Christina M. Durrough, PT, DPT, NCS 52

55 Forced Use Cycling Results Aerobic fitness improved for both groups UPDRS (motor): 35% improvement after FE, no change after VE Functional bimanual dexterity task: improvement after FE, no change after VE Rigidity and bradykinesia: improvements maintained 4 weeks after FE cessation [Ridgel AL, et al ] Forced Use Cycling Conclusions Aerobic fitness can be improved in patients with PD following both VE and FE Only FE results in significant improvements in motor function and bimanual dexterity [Ridgel AL, et al ] Forced Use Cycling Proposed mechanism FE leads to a shift in motor control strategy, from feedback to a greater reliance on feedforward processes, which suggests FE may be altering central motor control processes [Ridgel AL, et al ] Christina M. Durrough, PT, DPT, NCS 53

56 Forced Use Cycling Functional MRI showing activation patterns in the bilateral putamen, globus pallidus, thalamus, primary motor, and supplementary motor areas Post-exercise off medication Off medication On medication [Alberts JL, et al ] Forced Use Cycling Significant correlation between FE and medication for regions of the basal ganglia and cortex FE and medication utilize similar pathways to produce symptomatic relief [Alberts JL, et al ] High Intensity Exercise Revisited Effects of intensive exercise early in the disease Individuals newly diagnosed with PD (N=40) randomly assigned to multidisciplinary intensive rehabilitation or control group (only medications) Intensive rehabilitation consisted of two 4-week bouts of inpatient rehabilitation at baseline and 1 year [Frazzitta G, et al ] Christina M. Durrough, PT, DPT, NCS 54

57 High Intensity Exercise Revisited Outcome measures UPDRS, Six-Minute Walk Test, Timed Up and Go, PD Disability Scale, levodopa equivalents [Frazzitta G, et al ] High Intensity Exercise Revisited Results (motor tests) Intervention group: UPDRS, Timed Up and Go, PD Disability Scale at better at 2 years than baseline Control group: no changes in any outcome measures [Frazzitta G, et al ] High Intensity Exercise Revisited Results (medications) Percentages of patients in monotherapy Intervention Control Baseline 100% 100% 6 months 100% 40% 1 year 100% 20% 18 months 89% 20% 2 years 75% 20% [Frazzitta G, et al ] Christina M. Durrough, PT, DPT, NCS 55

58 CONTROLS INTENSIVE REHABILITATION P= vs. BASELINE P=0.89 vs. BASELINE [Frazzitta G, et al ] Conclusions Exercise-dependent plasticity Increases in synaptic strength and neurotransmission potentiation of functional circuitry in PD Exercise is a pivotal element of motor learning Sufficient capacity for motor learning in PD, although rate and performance is reduced compared to controls [Abbruzzese G, et al ] Conclusions No consensus about optimal approach Heterogeneity of interventions in the literature Patient-centered, goal-based plans of care Practice variables to be considered across interventions Intensity, specificity, complexity [Abbruzzese G, et al ] Christina M. Durrough, PT, DPT, NCS 56

59 Physical Therapy Examination Physical Therapy Examination Medical history/chart review Subjective interview Impairment testing Movement analysis Standardized outcome measures Physical Therapy Examination Medical history/chart review Gather pertinent medical history to begin forming hypotheses regarding movement patterns Date of diagnosis, co-morbidities, falls history (maybe) Christina M. Durrough, PT, DPT, NCS 57

60 Physical Therapy Examination Subjective interview Patient and family report Specific activity limitations and participation restrictions Falls history What conditions? Current/previous exercise Goals for therapy Physical Therapy Examination Impairment testing Posture Balance Coordination Static Sensation Dynamic Strength Reactive Anticipatory Range of motion Tone Physical Therapy Examination Movement analysis Transfers Bed mobility Gait Activities of daily living Christina M. Durrough, PT, DPT, NCS 58

61 Physical Therapy Examination Standardized outcome measures Overview Background: neuro-anatomy, pathophysiology, demographics Clinical manifestations and classifications of Parkinson s disease Management of Parkinson s disease Outcome measures Evidence-based physical and occupational therapy interventions Future of physical therapy Benefits of Utilizing Outcome Measures Establishes baseline status as a means to quantify change in function Provides information about effectiveness of the care plan as part of periodic re-examination For patients as a cohort: provides the opportunity to collectively compare care to determine an intervention s effectiveness Providers: provides a common language to evaluate the success of physical therapy interventions, thereby providing a basis for comparing outcomes related to an intervention across clinics [APTA Combined Sections Meeting ] Christina M. Durrough, PT, DPT, NCS 59

62 PD-EDGE Task Force EDGE = Evidence Database to Guide Effectiveness Objectives 1. Evaluate the various outcome measures that have been utilized within clinical care and across research studies for people with Parkinson s disease 2. Determine a core set of outcome measures that could be utilized by clinicians across the continuum of care and for clinicians and researchers across the stages of disease progression 3. Present these core measures through clinical cases crossing disease stages with recommendations to support their use to measure change, as well as guide clinical decision making [APTA Combined Sections Meeting ] Highly Recommended Measures Body Structure and Function MDS-UPDRS revised (part 3) MDS-UPDRS (part 1) Montreal Cognitive Assessment Activity Six-Minute Walk Test 10-Meter Walk Test Mini-BESTest Functional Gait Assessment 5 Times Sit to Stand 9 Hole Peg Test Participation PDQ-8 or PDQ-39 Recommended Measures for Specific Conditions Freezing of Gait: Freezing of Gait Questionnaire Fatigue: Parkinson s Fatigue Scale Fear of Falling: Activities-Specific Balance Confidence Scale (ABC) Dual Task: Timed Up and Go Cognitive [APTA Combined Sections Meeting ] Highly Recommended Measures Selected outcome measures are included in handouts Durrough and Flemming 2016 Christina M. Durrough, PT, DPT, NCS 60

63 Determining Falls Risk A variety of functional measures have been shown to be valid and reliable in assessing risk for falls in Parkinson s disease Dibble and colleagues (2008) stated that it was unlikely that any one measure may effectively capture falls risk in PD Use multiple functional measures to decrease false negative findings and more accurately predict the probability of falls PD-EDGE Task Force recommends use of the Mini-BESTest as the primary measure [Dibble LE, et al ] BESTest Balance Evaluation Systems Test Comprehensive balance assessment Assesses Biomechanical constraints (center of gravity alignment) Stability constraints (functional reach forward/lateral) Transitions anticipatory postural adjustment (SLS, sit-to-stand) Reactive postural response (compensatory stepping) Sensory orientation (mctsib) Stability in gait (includes Timed Up and Go, gait speed) Mini-BESTest 14-item scale developed using psychometric techniques to improve the BESTest Each item scored minutes to administer Contains items belonging evenly to 4/6 sections of the BESTest If assistance is required, score 0; if assistive device is needed, score 1 point lower [Franchignoni F, et al ] Christina M. Durrough, PT, DPT, NCS 61

64 Mini-BESTest Maximum score = 28 Falls risk cut-off (varies) = 19, 20, 23 Minimal clinically important difference = 4 Overview Background: neuro-anatomy, pathophysiology, demographics Clinical manifestations and classifications of Parkinson s disease Management of Parkinson s disease Outcome measures Evidence-based physical and occupational therapy interventions Future of physical therapy Goals of PT/OT Slow progression of disability Optimize participation in home, work, and recreational activities Optimize independence and safety with performance of functional tasks (gait, balance, transfers, bed mobility, ADLs) Preserve or improve physical capacity (strength, range of motion, endurance) Prevent falls Christina M. Durrough, PT, DPT, NCS 62

65 [Clarke CE, et al ] [Clarke CE, et al ] Clarke CE, et al Design: multi-center randomized controlled trial set in the United Kingdom PT/OT versus no therapy Participants: 762 individuals with mild to moderate PD Outcome measures: Nottingham Extended Activities of Daily Living Scale, PDQ-39, adverse events, caregiver quality of life Intervention: average of 4 visits over an 8-week period Results: NEADL and adverse events: no difference between therapy vs. no therapy PDQ-39 and caregiver quality of life: small differences in favor of therapy [Clarke CE, et al ] Christina M. Durrough, PT, DPT, NCS 63

66 Clarke CE, et al Study limitations Low dosage of PT Median 4 visits (i.e., half of participants received fewer than 4 sessions) Choice of outcome measures NEADL has not been validated for use in PD Ceiling effect in mild to moderate PD Lack of follow-up/home exercise program [Schenkman M, et al ] Schenkman M, et al Design: randomized controlled trial Flexibility/balance/function exercise (FBF) versus aerobic exercise (AE) versus home-based exercise (control) Participants: 121 individuals with mild to moderate PD Outcome measures: Continuous-Scale Physical Functional Performance, Functional Reach Test, walking economy, UPDRS (ADL and motor), PDQ-39 [Schenkman M, et al ] Christina M. Durrough, PT, DPT, NCS 64

67 Schenkman M, et al Interventions FBF: individualized spinal and extremity flexibility exercsies followed by group balance/functional training- 3x/week x 4 months, then 1x/month x 12 months AE: treadmill, bike, or elliptical- 3x/week x 4 months, then 1x/month x 12 months Control: National Parkinson Foundation Fitness Counts program [Schenkman M, et al ] Schenkman M, et al Results CS-PFP: FBF>AE and control Walking economy: AE>FBF and control UPDRS (ADL): FBF>control Conclusions Both FBF and AE programs may be important for people with earlyand mid-stage PD [Schenkman M, et al ] What do these aerobic, balance, flexibility, and functional exercise programs look like? Christina M. Durrough, PT, DPT, NCS 65

68 PT/OT Interventions Certification programs/protocols Other interventions and strategies Certification Programs/Protocols LSVT BIG Parkinson Wellness Recovery Rock Steady Boxing LSVT BIG Lee Silverman Voice Treatment Initially speech therapy program (LSVT LOUD) Focus on hypophonia Clinical success sparked interest in physical implications Christina M. Durrough, PT, DPT, NCS 66

69 LSVT BIG Standardized, research-based, specific protocol Intense program designed to address PD-specific challenges of bradykinesia/hypokinesia and kinesthetic awareness (sensory deficit) [Fox C, et al ] LSVT BIG Proposed mechanism of hypokinesia Impaired selfperception Small movements Deficits in internal cue Reduced amplitude of motor output [Fox C, et al ] LSVT BIG Target candidates Individuals presenting with hypokinesia/bradykinesia I don t realize I am moving small [Fox C, et al ] Christina M. Durrough, PT, DPT, NCS 67

70 LSVT BIG Proposed effects of LSVT BIG Target: Large amplitude Result: Increased amplitude of movement Mode: Intensive, high effort exercise Calibration: Improved selfperception, internal cues [Fox C, et al ] LSVT BIG Delivery method One-on-one sessions with certified physical or occupational therapist 4 consecutive days per week for 4 weeks Daily carry-over assignments and daily homework [Fox C, et al ] LSVT BIG Treatment sessions Maximal Daily Exercises Functional Component Tasks Walking BIG Hierarchy Tasks [Fox C, et al ] Christina M. Durrough, PT, DPT, NCS 68

71 LSVT BIG Maximal Daily Exercises [Fox C, et al ] LSVT BIG Maximal Daily Exercises Can be modified up or down to meet patient needs Easier Use support surface for standing portions Fewer repetitions More difficult Step onto unstable surfaces Add large amplitude sub-movements to exercises More repetitions LSVT BIG Evidence The Berlin LSVT BIG study 60 patients with mild to moderate PD randomized to 3 groups (1) LSVT BIG, (2) Nordic walking group training, (3) unsupervised home exercise Results UPDRS, TUG, gait speed: BIG > Nordic walking and home exercise PDQ-39: no difference between groups [Ebersbach G, et al ] Christina M. Durrough, PT, DPT, NCS 69

72 Parkinson Wellness Recovery (PWR) Founded by Becky Farley (also designed LSVT protocol) It is a comprehensive neuroplasticity-principled program that integrates the latest research on Parkinson disease and Rehabilitation, Exercise, and Wellness This type of research-based integrated exercise and wellness programming is necessary to counteract the inactivity, motor deterioration, and symptoms of PD. [ Parkinson Wellness Recovery (PWR) PWR!4Life Comprehensive approach including exercise ( coach to re-assess every 6 months), non-motor management, medication management [ Parkinson Wellness Recovery (PWR) Exercise Progressive aerobic training PWR! Moves targeting amplitude PWR! Up, PWR! Rock, PWR! Twist, PWR! Step All able to be performed in supine, prone, quadruped, sitting, and standing [ Christina M. Durrough, PT, DPT, NCS 70

73 [ Parkinson Wellness Recovery (PWR) Concepts of exercise High physical effort Cognitive engagement Attentional focus Emotional engagement [ Parkinson Wellness Recovery (PWR) Certification at PWR! Workshop required Christina M. Durrough, PT, DPT, NCS 71

74 Rock Steady Boxing Founded in Indianapolis in 2006 Group exercise model for individuals at all levels of Parkinson s disease Garnered national recognition with CBS Sunday Morning special Evidence for Boxing Six-subject case series sessions in a 12-week period Boxing drills, stretching, strengthening, and endurance exercise Outcome measures: Functional Reach, Berg Balance Scale, ABC Scale, TUG, Six-Minute Walk Test, gait speed, gait kinematics, UPDRS, PD Quality of Life Scale [Combs SA, et al ] Evidence for Boxing Results 6/6 participants showed improvements on at least 5/12 outcome measures 5/6 participants improved in every outcome category (balance, gait disability, quality of life) 6 th participant did not continue training during follow-up period [Combs SA, et al ] Christina M. Durrough, PT, DPT, NCS 72

75 Evidence for Boxing Conclusions Short- and long-term improvements in balance, gait, activities of daily living, and quality of life after a boxing training program Individuals with mild PD showed improvements earlier than those with moderate to severe PD Boxing training program feasible and safe [Combs SA, et al ] PT/OT Interventions Certification programs/protocols Other interventions and strategies Other Interventions Christina M. Durrough, PT, DPT, NCS 73

76 Modes of Delivery Individual PT/OT sessions Group exercise classes Home exercise programs Modes of Delivery Comparison of the three modes of delivery Individual treatment shows greatest improvements in balance and function Group classes show greatest improvement in gait Home program shows the least improvement across all outcomes [King LA, et al ] Aerobic Exercise Individuals with Parkinson s disease have decreased cardiovascular function Reach maximal aerobic capacity at significantly lower exercise levels than age-matched peers [Schenkman M, et al ] Christina M. Durrough, PT, DPT, NCS 74

77 Aerobic Exercise Aerobic exercise is safe and feasible for individuals with PD Aerobic training can improve cardiorespiratory fitness and movement economy of individuals with PD [Schenkman M, et al ] Aerobic Exercise No one form of aerobic exercise has been shown to be superior Identify an activity the patient enjoys to maximize compliance Aerobic Exercise Exercise Modes Progressions Regressions - Walking, swimming, cycling, boxing, dancing, tennis, etc. - Walking faster - Jogging - Cycling faster - Plyometric exercises - Stationary/recumbent cycle - Arm bike - Body-weight support treadmill training - Walking with assistive devices Christina M. Durrough, PT, DPT, NCS 75

78 Aerobic Exercise American College of Sports Medicine recommendations At least 150 minutes of moderate intensity exercise per week Moderate intensity exercise: minutes, 5 days/week Vigorous intensity exercise: minutes, 3 days/week One continuous session or multiple shorter sessions (at least 10 minutes in duration) [Garber CE, et al ] Aerobic Exercise Use an RPE scale for determining intensity Heart rate may be blunted by medications and/or autonomic dysfunction in PD [Garber CE, et al ] Aerobic Exercise Additional benefits? Executive function Preliminary evidence that aerobic exercise improves executive functioning in individuals with PD who have cognitive impairments Quality of life Improvements noted on the PDQ-39 following an aerobic conditioning program [Tabak R, et al ] Christina M. Durrough, PT, DPT, NCS 76

79 Treadmill Training Several review articles available, including a 2015 Cochrane review [Mehrholz J, et al ] [Herman T, et al ] Treadmill Training Summary of short- and long-term outcomes Safe and feasible Improved gait parameters (speed, stride length, distance, symmetry, joint excursion, etc.) Improved balance and motor performance (Berg, SOT, UPDRS) Improved quality of life Reduced fatigue [Mehrholz J, et al ] [Herman T, et al ] Treadmill Training Exercise Modes Progressions Regressions - Treadmill walking - Increase speed - Incline - No UE support - Slow speed - Body-weight support - UE support - Manual assistance Christina M. Durrough, PT, DPT, NCS 77

80 Dancing Why dance? Music provides external cues Learning specific movement strategies Example: correct weight-shifting when stepping backward Balance challenges Internal and external perturbations Strength, flexibility, and cardiovascular components Engaging, social, and fun motivation [Earhart GM ] Dancing Which dances? Style: tango versus waltz/foxtrot Tango slightly superior (but both beneficial) Partner vs. no partner Equal physical improvements in both conditions Partnered participants expressed more enjoyment and interest in continuing [Hackney ME, Earhart GM ] [Hackney ME, Earhart GM ] Dancing Candidates Most studies involving individuals with mild or moderate PD One case study of an individual with severe PD (H&Y IV) showed promising results [Hackney ME, Earhart GM ] Christina M. Durrough, PT, DPT, NCS 78

81 Dancing Settings and duration Improvements in clinical environments and group classes Short- and long-term benefits [Duncan RP, Earhart GM ] Dancing Exercise Modes Progressions Regressions - Dancing - Tango, waltz/foxtrot, etc. - Partner/no partner - Faster, more dynamic - More complex patterns - Less partner support - Slower dances - Simple steps - More partner support Tai Chi A martial art involving slow controlled movement and the maintenance of various postures Shown to improve postural stability, reduce falls, improve motor function (UPDRS), and improve quality of life Inconsistent effects on gait parameters [Yang Y, et al ] [Hackney ME, Earhart GM ] [Li F, et al ] [Lee MS, et al ] Christina M. Durrough, PT, DPT, NCS 79

82 Tai Chi Movements Hold a Ball (stepping sideways: left and right) Part the Wild Horse s Mane (stepping diagonally forward: left and right) Single Whip (stepping sideways: left and right) Wave Hands Like Clouds (stepping sideways: left and right) Repulse Monkey (stepping diagonally forward: left and right) Brush Knees (stepping diagonally forward: left and right) Fair Lady Works the Shuttles (stepping diagonally forward: left and right) Grasp the Peacock s Tail (stepping diagonally forward: left and right) [Li F, et al ] Balance Training Challenging balance programs have been shown to improve postural stability and reduce falls in individuals with PD Exercise programs not specifically addressing balance show little to no effect on postural stability [Sparrow D, et al ] [Klamroth S, et al ] [Sparrow D, et al ] Christina M. Durrough, PT, DPT, NCS 80

83 Flexibility Individuals with Parkinson s disease can improve spinal flexibility [Schenkman M, et al ] Flexibility Axial range of motion goals Cervical rotation, trunk extension, trunk rotation, anterior pelvic tilt Upper and lower extremity muscles to stretch Ankle plantarflexors, knee flexors, hip flexors, pectoralis major and minor, elbow flexors, finger flexors Strengthening Resistance training has been shown to be safe for individuals with PD Improved muscle volume, muscle force, and mobility (gait, stair negotiation) following high-intensity resistance training program [Dibble LE, et al ] Christina M. Durrough, PT, DPT, NCS 81

84 Strengthening Muscles to strengthen Hip extensors, hip abductors, knee extensors, ankle plantarflexors, trunk extensors Dual-Task Training Adding a cognitive task to mobility tasks has been shown to amplify gait variability and may contribute to fall risk May be amenable to interventions, especially in the early-mid stages of PD [Fritz NE, et al ] Dual-Task Training Effects of dual-task training in PD Single-task gait: improvements in speed, stride length, and endurance Balance: conflicting results Dual-task ability: short- and long-term improvements in dual-task gait and balance [Fritz NE, et al ] Christina M. Durrough, PT, DPT, NCS 82

85 Dual-Task Training Examples of dual-task activities Serial counting Naming items in categories Recalling a story Providing directions between two locations Strategy Training How Strategies Work Replaces lost internal cueing mechanism with an external cueing mechanism Bypasses the dysfunctional basal ganglia pathway via cortical, cerebellar, or brainstem pathways to normalize movement Relies on an external trigger to improve motor output Shifts the learning mode toward the explicit end of the implicitexplicit continuum Cueing may be used as a motor learning tool Christina M. Durrough, PT, DPT, NCS 83

86 Types of Strategies 1. Cognitive strategies Consciously thinking about the desired movement 2. Cueing strategies External stimulus drives movement Goals of Strategies Early stages of PD: aid in motor learning Later stages of PD: compensations to improve function When to Use Strategies May be beneficial during performance of all functional mobility, activities of daily living, and self-care For the purposes of this presentation, focus will be on gait and freezing of gait Christina M. Durrough, PT, DPT, NCS 84

87 Types of Cues Auditory Visual Tactile Verbal Attention Combination Types of Cues Auditory Rhythmic auditory stimulation Metronome, music, etc. Higher beats per minute facilitates increased gait speed Lower beats per minute facilitates decreased cadence Consider if high cadence/short step length contributes to freezing Fairly consistent findings in the literature that rhythmic auditory stimulation improves gait among individuals with PD A small feasibility study indicates possible decreases in freezing and falls [Thaut MH, AbiruM ] [Martin T, et al ] Types of Cues Visual Stepping to a target Lasers Imaginary targets (step over object) Context-specific cues Horizontal lines improve optic flow Christina M. Durrough, PT, DPT, NCS 85