PARKINSON DISEASE DANCE FOR PD WORKSHOP
Heather Ene, MD Associate Professor University of Colorado Denver Departments of PMR and Neurology July 2011 Normal Motor Control • Central Nervous System • Premotor, Supplementary Motor and Primary Motor Cortex • Sensory Cortex • Limbic System Structures • Basal ganglia • Thalamus • Cerebellum • Brainstem • Spinal Cord
• Lower motor and sensory neurons
• Muscle fibers Multiple Segregated Parallel Loops Basal Ganglia
• Caudate
• Putamen
• Globus Pallidus
• Subthalamic Nucleus
• Substantia Nigra Role of the Basal Ganglia • Selection and accentuation of certain motor patterns, to the exclusion of others • Center-surround concept • Preparation for movement • Scaling of speed and amplitude of movement • Motor learning • Sequencing of motor patterns • Termination of an ongoing motor program • Behavioral learning based upon reward • Part of the development of habits/motor learning • Sensory processing Concept of Parkinson Disease
• Widespread neuro-degenerative disorder • Central and peripheral nervous systems involved • Multiple neurotransmitter systems affected
• Different presenting symptoms & progression • Tremor predominant form • Postural instability gait disorder form
• Multiple genetic associations
Pathology of PD
•Cumulative loss of dopaminergic neurons in the substantia nigra compacta (SNc) is responsible for key motor features of the PD, particularly bradykinesia.
•Lewy bodies accumulate in multiple brain regions, starting in the brainstem, and affecting multiple neurotransmitter systems (Braak 2003) • May explain some of the “non-motor” features Physiology of PD Motor Symptoms*
• Conceptualized as an imbalance between excitatory and inhibitory input from the BG via the thalamus to the cortex.
• The result is excessive inhibition of the cortex.
• *particularly bradykinesia Early Symptoms
• Decreased sense of smell • Autonomic dysfunction • Constipation • Sleep disorders • Urinary frequency and urgency • Sexual dysfunction • REM d/o • Excessive daytime sleepiness • Insomnia • Mood disorders • Depression, anxiety • Shoulder pain
• Restless leg syndrome Cardinal Motor Features • 4-6 Hz rest tremor – Similar frequency “re-emergent” postural tremor
• Bradykinesia/hypokinesia – Slowness of initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions
• Rigidity
• Loss of postural reflexes – Generally occurs later in disease Clinical Diagnosis
• Presence of cardinal motor features. • Early symptoms are often unrecognized as early PD until the motor symptoms develop.
• Characteristics of symptom onset and progression.
• Response to levodopa (dopamine replacement).
• Lack of features suggesting an alternative diagnosis. • There are many Parkinson disease mimics. Motor Symptoms Non-motor Symptoms
Cognitive symptoms: executive dysfunction, Tremor, bradykinesia, rigidity, postural instability bradyphrenia, tip-of-the-tongue (word finding) phenomenon, hallucinations
Psychiatric symptoms: depression, anxiety, apathy, Hypomimia, dysarthria, dysphagia, sialorrhoea anhedonia, fatigue, impulse control disorder
Sensory symptoms: anosmia, ageusia, pain, Decreased arm swing, shuffling gait, festination, paresthesias, abnormal eye movements – difficulty difficulty arising from chair and turning in bed reading, defective eye-hand coordination, visual spatial dysfunction, impaired color discrimination
Dysautonomia: orthostatic hypotension, constipation, urinary and sexual dysfunction, Micrographia, cutting food, feeding, hygiene, slow abnormal sweating, seborrhoea activities of daily living Melanoma Weight loss
Sleep disorders: REM behavior disorder, vivid Glabellar reflex, blepharospasm, dystonia, striatal dreams, daytime drowsiness, sleep fragmentation, deformity, scoliosis, camptocormia restless legs syndrome
Adapted from Jankovic 2007 Frequent Concerns • Poorly controlled tremor
• Wearing off of medications before next dose
• Dyskinesias
• Falls/near falls
• Orthostatic hypotension (leading to falls)
• Cognitive impairment
• Anxiety
• Pain (often present, but not often mentioned) Medication Choices
• Degree of disability • Risk of medication induced motor • Age of the patient fluctuations
• Most bothersome • Cost symptoms
• Other medical conditions
• Side effect profile Pharmacological Treatment Motor Symptoms
• Dopamine replacement • MAO B Inhibitors • Levodopa/Carbidopa (Sinemet) • Selegiline (Eldepryl and Zelapar) • Dopamine agonists • Rasagiline (Azilect) • Pramipexole (Mirapex) • Ropirinole (Requip) • Rotigotine (Neupro)* • Anticholingergics • Bromocriptine (Parlodel) • Trihexyphenidyl (Artane) • Apomorphine (Apokyn) • Benztropine (Cogentin)
• COMT Inhibitors • Increased dopamine release and • Entacapone (Comtan) decreased reuptake + NMDA • Tolcapone (Tasmar) receptor blockade • Amantadine (Symmetrel) Pharmacological Treatment
COMT = catechol O-methyltransferase, MAO = monoamine oxidase Deep Brain Stimulation (DBS)
• Electrodes implanted in the subthalamic nucleus (STN) or globus pallidus internus (GPi)
• Leads are tunneled under the skin and connected to a neurostimulator placed under the clavicle.
• Hand held programmer used to adjust stimulation parameters.
• Patients have limited control.
• High-frequency stimulation used for “neuromodulation” • Mechanism of action poorly understood. • Probably decreases the excessive output of the basal ganglia upon the thalamus and allows the thalamus to excite the cortex. DBS Indications
• Advanced PD (?) • Cognitively intact
• Severe medically • Absence of significant or “refractory” tremor uncontrolled psychiatric problems • Medication-induced complications impacting quality of life • Realistic expectations
• Levodopa responsive impairments • Except tremor DBS Outcomes • Increased “on time”
• Decreased rigidity, bradykinesia, akinesia and tremor
• Decreased medication use and medication-induced dyskinesia
• Improved quality of sleep and total sleep time
• Decreased pain??? DBS Outcomes • Variable effect upon postural instability and speech impairment – can be worse!!!!!
• Possible cognitive decline - temporary or permanent
• Depression and anxiety may increase if dopaminergic medications are significantly reduced
• Impulse control problems
• Significant weight gain Restorative Surgery
• Experimental
• Gene transfer
• Stem cell transplantation Exercise
• Possible neuroprotective effects - particularly high intensity aerobic activity. • Possible pro-degenerative effects of inactivity
• Management of PD motor symptoms. • Ex. Tremor, rigidity, bradykinesia
• Management of PD nonmotor symptoms. • Ex. Depression, anxiety, sleep dysregulation, pain Skilled Therapies
• Improve strength and activity tolerance
• Teach “tricks” for overcoming or adapting to motor limitations
• Provide education patient and family on strategies to accomplish activities of daily living (ADLs)
• Access appropriate adaptive equipment and orthotics Aerobic Training for PD
• Treadmill training is associated with: • Improved overall aerobic conditioning
• Decreased energy expenditure during walking
• Improved overground gait measures, including increased speed and stride length Aerobic Training for PD
• Body Weight Supported Treadmill: • Increased speed • High repetition • Active engagement • Sensory experience of more normal gait mechanics • Multisensory cues • Task-specific training Aerobic Training for PD
• Cycling: • Improved aerobic conditioning • Forced-cycling at a high pedaling rate is associated with: • Off medications improvements in tremor, rigidity and bradykinesia • Improved upper extremity function Resistance Training
• Evidence for primary weakness, in addition to deconditioning.
• The weakness may contribute to postural instability.
• Weakness + slowness may also contribute to difficulties with sit- stand transfers, gait and stair climbing. Resistance Training
• Progressive resistance exercises are safe, well tolerated and are associated with: • Increased strength in target muscles
• Improved sit-stand transfers
• Improved balance
• Improved gait velocity and stride length Spinal Flexibility Programs
• Spinal range of motion is decreased even in early PD.
• Poor spinal flexibility is associated with decreased balance.
• Spinal flexibility can be improved with targeted exercise.
• Interventions include: • Schenkman’s Axial Mobility Program, NPF Fitness Counts Program, PD yoga classes, Tai Chi, Quigong, Dance Rhythmic Cueing
• Use of external auditory stimuli to facilitate movement initiation and continuation.
• Rhythmic pacing alone (metronomic) or embedded.
• Postulated to “circumvent disordered circuitry and entrain rhythmic motor responses”, perhaps via cerebellar connections to premotor cortex. Rhythmical Cueing
• Associated with rapid improvements: • Increased gait velocity and stride length
• Increased step cadence (number of steps/time)
• Improved lower extremity muscle activation patterns
• Improved postural instability and gait scores on UPDRS
• Modest decrease in freezing of gait (FOG) severity Visual Cueing
• Use of lines drawn ┴ to direction of gait to increase gait speed and step length.
• U-Step laser cane or laser walker for FOG. Dance • Combination of rhythmic, visual and tactile cueing
• Social contact
• Emotional response Mark Morris Dance Group Dance
• Hackney 2007: • Twenty 1 hour sessions of Argentine Tango over 13 weeks (n=9) v. structured strength and flexibility program (n=10).
• Both groups showed significant improvements in UPDRS III, a trend toward decreased FOG, and slight improvement in gait velocity.
• Tango group showed additional improvements in Berg Balance Test and a trend toward improvement in the Timed Up and Go Test. Dance • Hackney 2009 • Twenty 1 hour sessions of Argentine Tango (n=14) v. twenty 1 hour sessions of Fox Trot over 13 weeks (n=17 ) v. no intervention (n=17).
• Both dance groups showed significant improvements in the Berg Balance Scale, 6- minute walk distance, and backward stride length . • No improvement seen in controls
• Tango group showed improvement in FOG • No improvement in Fox Trot group and worsening in controls
• Controls showed sign worsening on UPDRSIII Amplitude-Specific Training
• Bradykinesia and hypokinesia are cardinal features of PD.
• Faulty sensorimotor processing leads to reduced gain in the motor command for selecting and reinforcing movement amplitude. • Part of the problem may be related to abnormal perception of the energy cost of the movement Amplitude-Specific Training
• LVST/LOUD (Lee Silverman Voice Treatment) • Consciously increasing volume
• Modification of speech patterns • Ex. use of shorter sentences
• Breathing exercises
• Range-of-motion exercises for the muscles of speech
• Significant long-term (2 years) improvements in vocal loudness and speech intelligibility
• Transfer of improvements from LVST to swallow and facial expression Amplitude-Specific Training • Training BIG • Based upon observation that speed increases with increased movement amplitude.
• Use of repetitive large amplitude full body movements, with directed attention to the feeling of “moving big”.
• May be most effective for earlier stage of PD. • Possibly due to increasing impairment of directed attention in later stages.
• Transfer of cued repetitive movement to un-cued functional tasks (reaching and gait) observed. References •
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• References • Hirsch MA HF, Hirsch HVB. From Research to Practice: Rehabilitation of Persons Living with Parkinson's Disease. Topics in Geriatric Rehabilitation 2008;24(2):92-8. • Hirsch MA, Toole T, Maitland CG, Rider RA. The effects of balance training and high-intensity resistance training on persons with idiopathic Parkinson’s disease. Arch Phys Med Rehabil. 2003;84(4):1109-1117. • Iansek R. Interdisciplinary Rehabilitation in Parkinson’s Disease. Parkinson’s Disease; Advances in Neurology. Lippincott, Williams and Wilkins. 1999;Chap 76:555-559. • Johnell O, Melton LJ, Atkinson EJ.. Fracture risk in patients with parkinsonism: a population based study in Olmstead County, Minnesota. Age Ageing 1992;21:32-38. • Kern DS and Kumar R. Deep brain stimulation. The Neurologist 2007;13:237- 252. • King LA, Horak FB. Delaying mobility disability in people with Parkinson diseases using a sensorimotor agility exercise program. Phys Ther 2009;89(4):384-393. • Lim I, van Wegen E, de Goede C, Deutekom M, Nieuwboer A, Willems A, Jones D, Rochester L, Kwakkel G. Effects of external rhythmical cueing on gait in patients with Parkinson’s disease: a systematic review. Clin Rehabil 2005;19:695-713. • Liotti M, Vogel D, Brown S Hypophonia in Parkinson’s disease: neural correlates of voice treatment revealed by PET. Neurology 2003;60:432-440. References • •
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• Ramig L, Sapir S, Countryman S, Pawlas AA, O’Brien C, Hoehn M, Thompson LL. Intensive voice treatment (LVST) for individuals with Parkinson’s disease:a two year follow up. J Neurol Neurosurg Psychiatry 2001;71:493-498. • Schenkman M, Morey M, Kuchibhalta. Spinal flexibilit and balance control among community-dwelling adults with and without Parkinson’s disease. J Gerontol MS 2000;55:M441-445. • Schenkman M, Cutson TM, Maggie K, Chandler J, Pieper CF, Ray L, Laub KC. Exercise to improve spinal flexibility and function for people with Parkinson’s Disease: a randomized, controlled trial. J Am Geriatric Soc 1998;46:1207-1216. • Sideway B, Anderson J, Danielson G, Martin L, Smith G. Effects of long-term gait training using visual cues in an individual with Parkinson Disease. Phys Ther.2006;86:186-194. • Smith AD, Zigmond MJ. Can the brain be protected through exercise? Lessons from an animal model of parkinsonism. Exp Neurol 2003;184(1):31-39. • Sutoo D, Akiyama K. Regulation of brain function by exercise. Neurobiol Disease 2003;13(1):1-14. • Tillerson J, Cohen A, Caudle M, Zigmond M, Shallert T. Forced nonuse in unilateral parkinsonian rats exacerbates injury. J Neurosci 2002;22(15):6790-6799. • Tillerson J, Cohen A, Philhower J, Miller G, Zigmond M, Shallert T. Forced limb-use effects on the behavioural and neurochemical effects of 6-hydroxydopamine. J Neurosci 2001;21(12):4427-4435. • Tillerson JL, Cohen WM, Reveron ME, Miller GW. Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson’s disease. J Neurosci 2003;119:899-911. References •
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