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Overview of Treatment of Advancing Parkinson’s Disease

Overview of Treatment of Advancing Parkinson’s Disease. Karen M. Thomas, DO Diplomate, ABPN Associate Professor of Clinical Neurology, EVMS Director, Movement Disorders Program Sentara Neurology Specialists Virginia Beach, VA. WHAT IS PARKINSON’S DISEASE?.

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Overview of Treatment of Advancing Parkinson’s Disease

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  1. Overview ofTreatment of Advancing Parkinson’s Disease Karen M. Thomas, DO Diplomate, ABPN Associate Professor of Clinical Neurology, EVMS Director, Movement Disorders Program Sentara Neurology Specialists Virginia Beach, VA

  2. WHAT IS PARKINSON’S DISEASE? • CLASSIC DEFINITION: A NEURODEGENERATIVE SYNDROME WITH THE HALLMARK FEATURES OF MOTOR IMPAIRMENT CAUSING: • BRADYKINESIA (slowness of movement) • TREMOR (resting > action) • RIGIDITY (stiffness) • POSTURAL INSTABILITY (impairment of postural / balance reflexes) • DIAGNOSIS IS BASED ON FINDING THESE CARDINAL FEATURES (X 200 YEARS!!) ON CLINICAL EXAMINATION AND A SUPPORTIVE HISTORY • EVOLVING CONCEPTS: • MANY OTHER FEATURES OCCUR, SEVERAL PREDATE THE MOTOR SYMPTOMS BY YEARS • PRESENTATION HIGHLY VARIABLE ACROSS PD POPULATION • NUMEROUS GENETIC ASPECTS NOW IDENTIFIED • MORE THAN JUST A “DOPAMINE DISORDER”

  3. AGE RELATED ~1 - 2% of age 65 and older ~30 % of PD in 50 and under age group ~10% of PD in 40 and under age group INCIDENCE /PREVALENCE INCREASES WITH AGE FOUND THROUGHOUT THE WORLD 1 – 1.5 MILLION IN U.S. 60,000 new cases diagnosed each year Epidemiology

  4. Etiolotgy • ETIOLOGY IS UNKNOWN • RISK FACTORS SUSPECTED: • GENETICS + • RURAL LIVING / FARMING • PESTICIDE EXPOSURE • HEAVY METAL EXPOSURE • NONSMOKER • EARLY MENOPAUSE OR OTHER HORMONAL CONTRIBUTIONS • EVOLVING CONCEPTS: • AT-RISK GENES WITH RECOGNITION OF ROLE OF GENE & IT’S INTERACTION WITH ENVIRONMENTAL FACTORS • Protein alteration • Cell clearing dysfunction • Chemical transport dysfunction • Different genes in different populations

  5. Pathology FORMATION OF LEWY BODIES AND OTHER ACCUMULATIONS (AD PATHOLOGY, TAU) LOSS OF CELLS AND NEUROTRANSMITTERS SUCH AS DOPAMINE DOPAMINERGIC CELLS ARE LOST IN THE SUBSTANTIA NIGRA / BASAL GANGLIA AND OTHER AREAS, WHICH CAUSES MOTOR SYMPTOMS PROCESS OF CELL AND NEUROCHEMICAL LOSS CONTINUES THROUGHOUT DISEASE AND IS BELIEVED TO BE A PROCESS OF CELLULAR SPREAD THAT CAUSE CHANGES TO OCCUR IN MANY AREAS INCLUDING BG, BASAL FOREBRAIN (ACh), DORSAL MOTOR NUCLEUS X, MESOPONTINE, HYPOTHALAMIC, UPPER BRAINSTEM (5HT), LC (NE)

  6. Lewy Bodies are filamentous • cytoplasmic inclusions that are considered • the pathological hallmark of PD and • contain aggregated proteins including • - synuclein and ubiquitin • MECHANISMS CONSIDERED: • REDUCED PROTEOSOMAL ACTIVITY • (IMPAIRED CLEARING OF DAMAGED PROTEINS) • MITOCHONDRIAL DYSFUNCTION • (INHIBITION OF COMPLEX I OF THE ELECTRON TRANSPORT CHAIN) • OXIDATIVE STRESS • INFLAMMATION • (PD BRAINS HAVE MARKED GLIAL ACTIVATION)

  7. Substantia nigra Nigral – Striatal Changes =Motor Symptoms Normal Parkinson’s disease PET scan showing striatal fluorodopa uptake of a normal brain versus PD Gross pathology of the mid brain showing a normal brain versus PD Brooks 1993 Marsden 1994 Lang & Lozano 1998

  8. Braak Staging based on LB Pathology Stage 3 Symptomatic motor features Braak stages I–IV in idiopathic Parkinson’s disease. In stage I olfactory and medullary areas (black). The two processes converge in stage III (red) on the medial temporal lobes and then spread widely into the neocortex. Braak et al. 2004, Cell Tissue Res

  9. ClinicalOnset IUnilateralTremor, Rigidity,Akinesia0 IIBilateraldisease IIIPoorbalance+10y IVFalls,Dependency,Cognitivedecline VChair/bed- boundDementia+20y Sleep disorder,Obesity,Depression-10y HyposmiaConstipationBladder disorder-20y Symptoms: 1 2 3 4 5 6 Enteric plexus;Olfactory bulb;CN X Coeruleus,Caudal raphe &magnocellularRF Substantia nigra;Amygdala (CN)Meynert’s n;PPN Temporal lobe: TEC,CA-2 plexus;Intralaminar thalamicNuclei Prefrontalcortex: tertiarysensoryassociationareas Secondary, thenprimary motor & sensory areas Pathology: Sympatheticnervoussystem Current Hypothesis of PD Timeline 20 year prodrome 20 year disease stage Hoehn & Yahrstage Braak stage CN X = motor component of cranial nerve X; RF = reticular formation; CN = central subnucleus of the amygdala;Meynert’s n = basal nucleus of Meynert; PPN = pedunculopontine tegmental nucleus; TEC = transentorhinal cortex; CA2 = second section of the Ammon’s horn Hawkes CH, et al. Parkinsonism Relat Disord. 2010;16(2):79-84.

  10. EVOLVING CONCEPTS: SEVERAL DISEASES OR DIFFERENT PRESENTATIONS OF SAME DISEASE? TREMOR-PREDOMINANT PIGD PDD AKINETIC YOPD PRECLINICAL: “PARS (Parkinson’s At Risk Syndrome) – genetic “at risk” Biomarker (ytd)+, but – symptoms PREMOTOR: SUBTLE AND VARIOUS FEATURES OCCUR FOR YEARS MOTOR: CLASSIC MOTOR FEATURES OCCUR ADVANCING DISEASE: COGNITIVE CHANGES SWALLOWING CHANGES ADVANCED POSTURAL INSTABILITY NON-MOTOR ISSUES MEDICATION COMPLICATIONS CLASSIFICATION / RECOGNITION OF PD • PD or “PD Plus” • “TYPICAL” VS “ATYPICAL”

  11. TOTAL APPROACH TO TREATMENT

  12. Medication Treatments • In early PD, any medication chosen will likely provide some benefit • However: the treatment path chosen earlymay change the course of symptoms later • Things to consider before choosing treatment: • Age of patient • Baseline Functionality • Social and Family activities • Cognitive Baseline • Degree of impairment from current symptoms • INITIAL MEDICATION: • YOUNGER PT AT RISK OF LEVODOPA COMPLICATIONS, START WITH SOMETHING ELSE • OLDER PT AT RISK OF SIDE EFFECTS FROM MOST MEDS, START LEVODOPA

  13. ADVANCING DISEASE TREATMENT • ADDITIONAL MEDS, MULTIDRUG TX • SAME MEDS, MORE FREQUENT, SMALL ADJUSTMENTS • LESS of “WHAT” & MORE of “HOW” • TIMING BECOMES IMPORTANT • MORE RISK OF SIDE EFFECTS • SENSITIVITY TO PLASMA LEVELS • RECEPTOR CHANGES • MORE PROMINENT NON-MOTOR / NON-DOPAMINERGIC SYMPTOMS

  14. L-3,4-dihydroxyphenylalanine Metabolic precursor to dopamine Approved by FDA in 1970 Combined with dopa decarboxylase inhibitor in 1973 Carbidopa/Levodopa, Sinemet, Sinemet CR, Parcopa, Stalevo Remains superior in tx of motor symptoms Associated with development of motor complications of therapy within 5 years of initiation in 40%- 50% of pts (Marsden 1994 / (DATATOP study data, Ahlskog et al, 2001)) Motor complications can cause significant disability and impact QoL (Marras et al 2003) Dopamine Dysregulation Syndrome Levodopa

  15. MOTOR COMPLICATIONS INCLUDE: Single wearing off times End-of –dose wearing off Delayed-on / no-on Unpredictable off times Peak-dose dyskinesia/dystonia Off-dose dystonia/dyskinesia Diphasic dyskinesia Peripheral causes: delayed gastric emptying dietary protein competes for aa carriers in the gut that also transport l-dopa short plasma half-life Central causes: pulsatile delivery to striatal receptors, dysregulation of striatal MSNs (Chase et al 1993) alteration of DA receptors (through alteration in signal transduction that regulate gene expression (Canales et al 2000) impaired storage capacity Therefore, optimal delivery technique of L-dopa still remains elusive L-dopa-Associated Motor Complications

  16. InAdvanced Parkinson’s Disease, BrainDopamine Levels Reflect Plasma Levodopa Levels Mouradian et al 1990 Olanow et al 2000 Stocchi et al 2002 With permission from R. Hauser 41

  17. Dopamine Agonists • Much longer T1/2 than levodopa • Delay development of motor fluctuations in de-novo patients • Ropinirole 056 (dyskinesia 20% vs 45%), CALM-PD (dyskinesia 25% vs 54%), PELMOPET • Effective as monotherapy but less potent in treating motor symptoms than levodopa is • Initially developed as adjunctive to L-dopa so had established role in reducing motor symptoms (initially ergots) and reducing cumulative dose of L-dopa • Now recognized to have specific side effects as class

  18. Dopamine Agonists • Ergots: not recommended due to fibrotic complications • Ropinirole (Requip / Requip XL) • Start 0.25mg tid and titrate to 3mg tid as minimal therapeutic dose • Pramipexole (Mirapex / Mirapex ER) • Start 0.125mg tid and titrate to 0.5mg tid as initial therapeutic goal • Rotigotine (Neupro) • Transdermal patch: start 2mg patch initially and titrate if no response, to 4mg or 6mg patch • Apomorphine (Apokyn) • For advanced PD only as rescue medicine • Subcutaneous injection

  19. Ankle / leg edema Orthostatic Hypotension* Patients treated with dopamine agonists ordinarily require careful monitoring for signs and symptoms of orthostatic hypotension, especially during dose escalation and in advanced PD Patients should be informed of this risk Hallucinations* Observed more frequently in patients taking dopamine agonists in both early and advanced double-blind trials The elderly (>70) are at higher risk of hallucinations and cognitive decline Sleep Attacks Patients taking dopamine agonists have reported falling asleep while engaging in activities of daily living, including the operation of a motor vehicle, which sometimes resulted in accidents Many of these patients reported somnolence while taking dopamine agonists, but did not perceive any warning signs prior to falling asleep Dopamine Agonists: Caution

  20. Dopamine agonist medications have been associated with the development of Compulsive behaviors such as gambling It is recommended to screen for these before starting therapy and at each visit once on therapy Typically reverses with discontinuation of medicine Weintraub et al, 2010 (Arch. Neuro) did a x-sectional study of 3090 pts and found: 13.6% had ICDs DA tx associated with a 2-3.5 fold increased odds of having ICD. (Gambling, sexual ICDs, shopping and binge-eating) Impulse Control Disorders

  21. MAOB-Inhibitors • Selegeline (Eldepryl, Deprenyl) • Inhibits catabolism of dopamine • Amphetamine metabolites • Dose 5mg – 10mg per day (usually before noon) • Zydis Selegeline (Zelapar) • Same as selegeline but absorbed through oral mucosa so bypasses gut metabolism (less amphetamine) • Approved for adjunctive tx of levodopa • Faster to CNS, faster action • Dose 1.25mg – 2.5mg once daily • Rasageline (Azilect) • Approved for mono- and adjunctive tx • About 10X more potent than selegeline (oral) • Dose 0.5mg – 1mg once daily

  22. MAOB-Inhibitors • Monoamines = neurotransmitters dopamine, norepinephrine, 5HT • MAOs intracellular enzymes throughout body • MAO – B selective inhibitors used in PD (MAO-B ~ 70% of brain MAO) • Disease-modifying effect in agents with propargyl structures (selegeline, rasageline) • SE: insomnia, HA, gastrointestinal upset, hallucinations, orthostasis • Contraindicated with meperidine • Caution with SSRI / SNRI (serotonin syndrome)- though risk is extremely small

  23. Dual Inhibition of the Two Major Levodopa Degradation Pathways Schematic of Dual Inhibition of DDC* and COMT Enzyme Pathways With dual inhibition, significantly more levodopa reaches the brain, with a 35–40% increase in bioavailability and a 30–50% reduction in plasma variability Nutt et al 1994. Gordin et al 2002 Stalevo PI, 2003

  24. COMT-Inhibitors • WHAT THEY ARE NOT! • Not symptomatically effective alone (use ONLY with levodopa) • Not indicated for early PD, indicated for Advanced PD with EODWO • Enhance levels of exogenous levodopa • Tolcapone (Tasmar) • Has “black box warning” • Associated with fatal liver failure • Monitoring needed • Entacapone (Comtan, Stalevo) • Taken with each dose of levodopa • Increases availability of levodopa in the plasma • Only peripheral action

  25. Amantadine • Antiviral agent • Several mechanisms of action • Anticholinergic • Dopamine release enhancement • Anti-glutamatergic (NMDA) • Generally well tolerated in younger population • Effective in tremor-predominant PD • Side effects: confusion, hallucinations, dry mouth, blurred vision. Idiosyncratic reactions: livedo reticularis and ankle edema • Dosing usually 100mg bid-tid, max dose 500 – 600mg/ day • Antidyskinetic Property due to anti-glutamate (NMDA antagonist) activity, make it useful in advanced PD in fluctuators with dyskinesias

  26. Anticholinergics • Earliest class of agents for PD • Belladonna used for centuries • 1940s trihexyphenidyl created • Little use in advanced disease • Trihexyphenidyl, Benztropine • Effective PD tremor therapy • Side effects can be prominent: Confusion, hallucinations, dry mouth, constipation, blurred vision, orthostasis, urinary retention • Increased risk with use in elderly or if cognitive problems at baseline

  27. Apomorphine – Rescue Therapy • Apokyn (2mg-6mg per dose) • D1/D2 agonist • Older dopamine agonist • Very short T1/2 • Rescue for unpredictable or predictable significant off times. • Very effective, rapid onset • Associated with significant GI side effects • Nausea and vomiting • Must pre-treat with antiemetic (trimethobenzamide, domperidone) • Orthostatic hypotension • Initial titration should be in physician’s office • Subcutaneous administration difficult for some patients • Yawning, Increased libido, priapism

  28. Ablative – permanent lesioning Thalamotomy Pallidotomy Deep Brain Stimulation Reversible implantation of electrodes into specific nuclei targets Thalamus (VIm), Globus pallidus internus, Subthalamic nucleus Not for everyone! Choosing the right candidate is a process that should include at least: Initial evaluation to determine diagnosis of Idiopathic PD Levodopa challenge Cognitive testing, Neuropsychological testing General health evaluation as surgical candidate Initial counseling and establishment of goals of surgery, with acknowledged patient understanding Surgical Therapies

  29. MOTOR RIGIDITY BRADYKINESIA TREMOR POSTURAL INSTABILITY* POSTURAL CHANGES SPEECH CHANGES* DECREASED DEXTERITY HYPOMIMIA FESTINATING/FREEZING GAIT* DYSTONIA MICROGRAPHIA DYSPHAGIA* *LIKELY NON-DOPAMINERGIC FEATURES NON-MOTOR* CONSTIPATION ANOSMIA GERD DEPRESSION/ ANXIETY APATHY COGNITIVE CHANGES SLEEP DISTURBANCES SEBORRHEIC DERMATITIS BLADDER URGENCY / FREQUENCY SWEATING SPELLS HYPOTENSION SEXUAL DYSFUNCTION Global Presentation of PD

  30. Despite emphasis on managing motor symptoms in clinical practice, evidence suggests Non-Motor Symptoms may have a greater influence on: HRQOL Institutionalization Health economics In advancing PD Nonmotor Symptoms in PD HRQOL = health-related quality of life Schrag A, et al. J Neurol Neurosurg Psychiatry. 2000;69:308-312. Chaudhuri KR, et al. Lancet Neurol. 2006;5:235-245.

  31. NON-MOTOR SYMPTOMSSeen in Early & Late PD MOOD DISTURBANCE Depression • May be present up to 5-10 years prior to PD diagnosis • 10% of general population • 50-60% in PD • 5%-25% major • 10%-30% minor • Suicidal ideation common, suicide is not • SSRIs, SNRIs, Tricyclics, Buproprion • Newer medications found more beneficial Anxiety 40% of patients with PD • May be “off” anxiety (concept of NON-MOTOR FLUCTUATIONS) • Move levodopa dosing closer together or add another medication (eg, entacapone or rasagiline) • Treat with anti-anxiety medication (Escitalopram, Sertraline, Duloxetine and Venlafaxine

  32. Nonmotor Symptoms in PD Other Neuropsychiatric • Anhedonia (inability to experience pleasure) • Apathy- • different than depression • Assoc. with cognitive impairment • Pseudo Bulbar Affect – • emotional lability • 5%-10% in PD but under-recognized • Nudexta • Frontal executive dysfunction • Planning, Working memory (spatial, goal pursuit), Distractibility • Bradyphrenia (slowed thought processes) • Dementia • Psychosis

  33. Affects several cognitive domains Lewy Bodies & Alzheimer’s pathology present Long-term disease dementia occurs in up to 80% of PD Even early PD can cause cognitive deficits Non-demented PD pts can have MCI (25%) and this increases risk of eventual dementia Dementia within 3-5 years = PDD Rivastigmine patch (Exelon patch) 4.6–9.2 mg daily Galantamine (Razadyne ER) 8–16 mg daily Addition of Memantine (Namenda) 5–10 mg 1–2x daily Non-medication approaches to improve memory (games) Cognitive Decline(Cognitive changes, psychosis, behavior changes most common reason for institutionalization in PD)

  34. Hallucinations and Paranoia • Reduce or discontinue dopamine agonists • Check dose timing of Amantadine. May need to discontinue • May need to reduce or stop MAO-B inhibitors • Reduce levodopa or switch formulation • Add acetylcholinesterase inhibitor (eg, Donepezil, Rivastigmine) • Quetiapine (Seroquel) • Clozapine

  35. SLEEP Fragmentation Initial and terminal insomnia Reduced sleep efficiency Reduced slow wave sleep REMBD Reduced rapid REM sleep Nocturnal akinesia/tremor Restless leg syndrome (RLS) OSA REMBD –Now considered an early early feature of PD Tx: clonazepam quetiepine Insomnia Valerian root Chamomile Melatonin Diphenhydramine Trazadone, Ambien Daytime Fatigue Activity / Exercise Caffeine Rarely – Stimulants Sleep Study should be considered Non-Motor SymptomsSeen Early and Late PD

  36. Autonomic dysregulation PD meds, anti-hypertensives, tricyclic antidepressants, and poor salt and fluid intake can worsen this. Conservative measures: s: 1. Increase salt intake 2. Drink “sports/electrolyte” beverage (eg, Gatorade or similar) 3. Raise head of bed 6 inches 4. Compression hose/Jobst stockings 5. Take time getting up from chair or bed, do leg / ankle pumps 6. Eat small frequent meals Drink 16 oz of water first thing in the am. Drink caffeine in the am and after lunch Add fludrocortisone (Florinef) or midodrine (ProAmatine) SSRIs (paroxetine) Pyridostigmine (little evidence) Orthostasis

  37. Delayed gastric emptying Results in food remaining in stomach for a longer period of time than normal Symptoms: nausea, vomiting, bloating, feeling full Treatment: Medications motility agents (domperidone, amitiza) diet modifications (small, frequent meals, lemon water) GERD can lead to infection and pneumonia Avoid large meals and high fat meals Fewer than 3 bowel movements per week Caused by PD, PD medications, lack of fluids and fiber, decreaseda activity Risk of fecal impaction Treatments include: increased fluid intake-6-8 cups of water or juice a day Juices starting with a “P”-Prune, pear, plum or peach Fiber supplement such as Metamucil or Citrucel Flax seed, almonds Increase fiber intake-25 grams of fiber daily Stool softeners such as pericolace or colace Miralax GI Dysmotility / Constipation

  38. Dysphagia • 50% of patients with PD have swallowing problems • Causes: 1. PD causes motor impairment of oral and swallowing muscles. 2. Poor dentition 3. Dry mouth • Diagnosis: barium swallow or endoscopy • Complications: Aspiration pneumonia, weight loss, malnutrition, choking, coughing or drooling • Treatment: Speech therapy for strengthening exercises • Diet modifications • Feeding tube

  39. Drooling (sialorrhea) • Greatest contributor is not overproduction of saliva but from slowing of the automatic swallowing reflex. • Treatments: • Mindfule Swallowing • Facial exercises / Posture exercises • Chewing gum • 1% atropine eye drops under the tongue • Oral anticholinergics such as robinul • Botulinim toxin

  40. Skin Changes: Seborrhea dermatitis-oily, flaky or inflamed skin ● Rx shampoos or lotions containing selenium, ketoconazole or corticosteriods ∙ Excessive sweating (can be a wearing-off phenomenon) ∙ Adjust Sinemet, lukewarm showers, wear lightweight clothing in warm weather, increase fluids, and in severe cases Rx meds (propranolol,gabapentin,) ∙ Too little perspiration-usually side effect of medication ∙ Decrease dose of anticholinergic ∙ Skin Cancer of all types esp. Melanoma-2-7x higher risk in PD ∙ Annual screening Sensory Changes: Hyposmia / Anosmia Decrease or loss of sense of smell) – one of the earliest features of PD, may occur decades prior to motor symptoms Decreased sense of taste (not all, sweet preserved) Pain is reported in up to 1/3 of PD patients, with variability in type Peripheral Neuropathy Small studies, percentage uncertain Visual changes Impaired visual contrast Nonmotor Symptoms in PD

  41. ED in males, vaginal dryness, and loss of libido PD can cause this due to lack of dopamine PD meds are not associated except for anticholinergics Hypersexuality secondary to medications Treatment: urological or gynecological exam to rule out non-PD problem PDIs are safe Can’t treat unless you know, Can’t know unless you ask! Urinary frequency, urgency, incontinence, incomplete emptying, hesitancy, enuresis Treatments: Medications: oxybutynin, Tolterodine, Solifenacin, Darifenacin Non-medication: pelvic floor exercises, decrease liquids before bed, avoid caffeinated drinks, wear pads at night, wear easily removable clothing, regular toileting. GU Dysfunction

  42. Falls in PD • Meta-analysis of several studies of falls in PD (Pickerington et al. Mov Dis 2007) • showed very high fall rate (46%) with injury rate from 25% - 78% • Best predictor was prior fall within previous year • Incidence of falls significant even in early PD (Kerr et al.2010) • Turning in PD is hazardous and associated with imbalance and FOG • Responds to auditory cueing ( Willems et al. Mov Dis 2007) • Tinetti Mobility Scale validated for inter / intra-rater reliability and found predictive of falls in PD by Kegelmeyer and Kloos et al. (Physical Therapy, 2007) • AAN Practice Parameter on Falls (EBR) (Thurman et al. Neurology 2008) • Clinical metrics predictive of falls = Timed Up & Go test and the Tinetti Mobility Scale • Falling / Postural instability / Balance problems are NOT responsive to PD medications

  43. MULTIDISCIPLINARY APPROACH • Requires a PD Treatment TEAM! • The Patient • Movement Disorders Neurologist • Nurse Practitioner • Medical Assistant • PCP • Physical Therapist • Speech Therapist / Occupational Therapist • Psychologist / Counselor • Carepartners EACH TEAM MEMBER HAS A DIFFERENT BUT VITAL ROLE!!

  44. Non-Medication Therapies • Physical therapy (LSVT- BIG, PWR) • Balance / Gait – focused • Posture, flexibility • Core, COG • Amplitude • Speech therapy • LSVT, Facial exercises, Breathing exercises, Singing, Swallowing techniques • Occupational therapy • ADLs, Home safety, Dexterity • Others: • Manual Medicine • Tai Chi • Music therapy • Encourages rhythmic movements, coordinating multiple movements • Art therapy • Encourages both large and small amplitude movements, stress relief, emotional expression • Recreational therapy • Massage, acupuncture

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