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Overview of Treatment of Advancing Parkinson’s Disease

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1 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

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3 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”

4 Epidemiology 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

5 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

6 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)

7 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)

8 Nigral – Striatal Changes
=Motor Symptoms Normal Parkinson’s disease Substantia nigra PET scan showing striatal fluorodopa uptake of a normal brain versus PD Parkinson’s Disease is a Dopamine Deficiency Disorder Idiopathic PD is associated with the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc). Since dopamine is closely involved in regulating the activity of the basal ganglia, loss of dopamine innervation causes dysregulation of movement control. The cardinal symptoms of PD are resting tremor, rigidity, bradykinesia and postural instability. Importantly, there is a strong correlation between the level of parkinsonian disability and the severity of dopamine loss. Positron Emission Tomography (PET) scans, using radioactively labelled dopamine (fluorodopa), can assess the integrity of dopaminergic neurons. They can also help to identify patients with early PD and monitor disease progression in patients with established PD. After having made a diagnosis of PD, important decisions then have to be made about its subsequent management. Brooks. Neurology 1993; 43: S6–16. Marsden. J Neurol Neurosurg Psychiatry 1994; 57: 672–681. Lang & Lozano. N Engl J Med 1998; 339: 1044–1053. Gross pathology of the mid brain showing a normal brain versus PD Brooks 1993 Marsden 1994 Lang & Lozano 1998 8

9 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

10 Current Hypothesis of PD Timeline
Clinical Onset 20 year prodrome 20 year disease stage Hoehn & Yahr stage Symptoms: Hyposmia Constipation Bladder disorder -20y Sleep disorder, Obesity, Depression -10y I Unilateral Tremor, Rigidity, Akinesia 0 II Bilateral disease III Poor balance +10y IV Falls, Dependency, Cognitive decline V Chair/bed- bound Dementia +20y Pathology: Enteric plexus; Olfactory bulb; CN X Coeruleus, Caudal raphe & magnocellular RF Substantia nigra; Amygdala (CN) Meynert’s n; PPN Temporal lobe: TEC, CA-2 plexus; Intralaminar thalamic Nuclei Prefrontal cortex: tertiary sensory association areas Secondary, then primary motor & sensory areas Sympathetic nervous system 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.

11 CLASSIFICATION / RECOGNITION OF PD
PD or “PD Plus” “TYPICAL” VS “ATYPICAL” 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 EVOLVING CONCEPTS: SEVERAL DISEASES OR DIFFERENT PRESENTATIONS OF SAME DISEASE? TREMOR-PREDOMINANT PIGD PDD AKINETIC YOPD

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13 TOTAL APPROACH TO TREATMENT

14 Medication Treatments
In early PD, any medication chosen will likely provide some benefit However: the treatment path chosen early may 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

15 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

16 Levodopa 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

17 L-dopa-Associated Motor Complications
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

18 With permission from R. Hauser
In Advanced Parkinson’s Disease, Brain Dopamine Levels Reflect Plasma Levodopa Levels In Advanced PD, Brain Dopamine Levels Reflect Plasma Levodopa Levels This schematic shows the theoretical impact of pulsatile plasma levodopa levels on striatal dopamine levels over the course of the disease. As discussed, it is increasingly believed that the way in which dopamine receptors are stimulated by levodopa is a key factor in the development of motor complications. During the early stages of PD, there are sufficient striatal terminals available to take up and store dopamine for later release, buffering the pulsatile levodopa levels that result from standard oral levodopa therapy, and so preventing the dopamine receptors from exposure to excessive or inadequate dopaminergic stimulation. However, as PD advances, the progressive neurodegeneration of striatal terminals results in a reduced striatal dopamine storage capacity and this buffering capacity is lost. As a consequence, dopamine receptors now become exposed to pulsatile, intermittent dopaminergic stimulation. It is now theorized that dopaminergic therapies that deliver more continuous dopaminergic stimulation (CDS) provide a way of avoiding the oscillations in striatal dopaminergic delivery. Mouradian et al. Ann Neurol 1990; 27:18 –23. Olanow et al. Neurology 2000; 55 (Suppl 4): S72–S77. Stocchi et al. Brain 2002; 125: 2058–2066. Olanow et al. Neurology 2001; 56: S1–S86. Mouradian et al 1990 Olanow et al 2000 Stocchi et al 2002 With permission from R. Hauser 41

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20 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

21 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

22 Dopamine Agonists: Caution
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 Orthostatic hypotension: Patients with Parkinson’s disease who are being treated with dopaminergic agonists ordinarily require careful monitoring for signs and symptoms of orthostatic hypotension, especially during dose escalation. Additionally, these patients appear to have an impaired capacity to respond to an orthostatic challenge. Therefore, patients should be informed of this risk. Hallucinations: Patients receiving MIRAPEX® (pramipexole dihydrochloride tablets) had a higher rate of hallucinations compared to patients receiving placebo in both the early and advanced double-blind trials. The risk of hallucinations increases with age. Please see complete prescribing information in this CD-ROM. Reference: MIRAPEX [package insert]. Kalamazoo, MI 49001, USA: Pharmacia & Upjohn Company; 1999. 22

23 Impulse Control Disorders
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 fold increased odds of having ICD. (Gambling, sexual ICDs, shopping and binge-eating)

24 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

25 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

26 Dual Inhibition of the Two Major Levodopa Degradation Pathways
Schematic of Dual Inhibition of DDC* and COMT Enzyme Pathways Dual Inhibition of the Two Major Levodopa Degradation Pathways When administered alone, levodopa is rapidly decarboxylated to dopamine in the peripheral circulation and only 1% passes into the brain where it is required. By inhibiting the peripheral decarboxylation of levodopa, a dopa decarboxylase inhibitor (DDCI) such as carbidopa prolongs the plasma half-life of levodopa from 50 minutes to 1.5 hours. However, even with this inhibition, still only about 10% of a given levodopa dose enters the brain. Dual inhibition of both the DDC and COMT pathways has been shown to: Prolong levodopa’s elimination half-life in PD patients from 1.3 to 2.4 hours. Increase levodopa plasma bioavailability (area under the concentration–time curve; AUC) between 35–40%. Importantly, this dual inhibition is believed to result in an approximately 30–50% reduction in the variability of levodopa plasma levels. Nutt et al. Neurology 1994; 44: 913–919. Gordin et al. Adv Neurol 2002; 91: 237–250. Stalevo [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corp; 2003. 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 Gordin et al 2002 Stalevo PI, 2003

27 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

28 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

29 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

30 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

31 Surgical Therapies Deep Brain Stimulation
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

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34 Global Presentation of PD
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

35 Nonmotor Symptoms in PD
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 Dr Lew: bullets hopefully clarified HRQOL = health-related quality of life Schrag A, et al. J Neurol Neurosurg Psychiatry. 2000;69: Chaudhuri KR, et al. Lancet Neurol. 2006;5:

36 NON-MOTOR SYMPTOMS Seen in Early & Late PD
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 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

37 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

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39 Cognitive Decline (Cognitive changes, psychosis, behavior changes most common reason for institutionalization in PD) 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)

40 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 40

41 Non-Motor Symptoms Seen Early and Late PD
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

42 Orthostasis Drink 16 oz of water first thing in the am.
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) 42

43 GI Dysmotility / Constipation
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

44 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

45 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

46 Nonmotor Symptoms in PD
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

47 GU Dysfunction 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. 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!

48 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

49 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!!

50 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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52 The James Parkinson’s Tulip April is PD Awareness Month!


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