Transcript Treatment of Advanced 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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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”
Epidemiology
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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
Etiolotgy
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ETIOLOGY IS UNKNOWN
RISK FACTORS SUSPECTED:
– GENETICS +
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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
–
–
–
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Protein alteration
Cell clearing dysfunction
Chemical transport dysfunction
Different genes in different populations
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)
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)
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
Substantia nigra
Brooks 1993
Marsden 1994
Lang & Lozano 1998
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
Current Hypothesis of PD
Timeline
Clinical
Onset
Hoehn & Yahr
stage
Symptoms:
Hyposmia
Constipation
Bladder disorder
Sleep disorder,
Obesity,
Depression
I
Unilateral
Tremor, Rigidity,
Akinesia
-10y
0
-20y
Pathology:
II
Bilateral
disease
III
Poor
balance
+10y
IV
Falls,
Dependency,
Cognitive
decline
V
Chair/bedbound
Dementia
+20y
1
2
3
4
5
6
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.
CLASSIFICATION / RECOGNITION OF
PD
PD or “PD Plus”
“TYPICAL” VS “ATYPICAL”
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PRECLINICAL:
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–
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PREMOTOR:
–
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EVOLVING CONCEPTS:
– SEVERAL DISEASES OR
DIFFERENT
PRESENTATIONS OF SAME
DISEASE?
– TREMORPREDOMINANT
– PIGD
– PDD
– AKINETIC
– YOPD
SUBTLE AND VARIOUS FEATURES OCCUR
FOR YEARS
MOTOR:
–
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“PARS (Parkinson’s At Risk Syndrome) –
genetic “at risk”
Biomarker (ytd)+, but – symptoms
CLASSIC MOTOR FEATURES OCCUR
ADVANCING DISEASE:
– COGNITIVE CHANGES
– SWALLOWING CHANGES
– ADVANCED POSTURAL
INSTABILITY
– NON-MOTOR ISSUES
– MEDICATION
COMPLICATIONS
TOTAL APPROACH TO
TREATMENT
MEDICATION
MOOD
EXERCISE
TOTAL
TREATMENT
NUTRITION
HYDRATION
ACTIVITIES
SLEEP
Medication Treatments
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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:
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–
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–
–
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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
ADVANCING DISEASE TREATMENT
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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 / NONDOPAMINERGIC SYMPTOMS
Levodopa
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L-3,4dihydroxyphenylalanine
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 /
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(DATATOP study data, Ahlskog et
al, 2001))
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Motor complications can
cause significant
disability and impact
QoL (Marras et al 2003)
Dopamine Dysregulation
Syndrome
L-dopa-Associated Motor Complications
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– delayed gastric emptying
– dietary protein competes for aa
carriers in the gut that also
transport l-dopa
– short plasma half-life
MOTOR
COMPLICATIONS
INCLUDE:
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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:
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
In Advanced Parkinson’s Disease, Brain
Dopamine Levels Reflect Plasma Levodopa Levels
Mouradian et al
1990 from R. Hauser
With permission
Olanow et al 2000
Stocchi et al 2002
41
Dopamine Agonists
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Much longer T1/2 than levodopa
Delay development of motor fluctuations in
de-novo patients
– Ropinirole 056
(dyskinesia 20% vs 45%),
(dyskinesia 25% vs 54%), PELMOPET
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CALM-PD
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
Dopamine Agonists
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Ergots: not recommended due to fibrotic complications
Ropinirole (Requip / Requip XL)
– Start 0.25mg tid and titrate to 3mg tid as minimal therapeutic
dose
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Pramipexole (Mirapex / Mirapex ER)
– Start 0.125mg tid and titrate to 0.5mg tid as initial therapeutic
goal
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Rotigotine (Neupro)
– Transdermal patch: start 2mg patch initially and titrate if no
response, to 4mg or 6mg patch
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Apomorphine (Apokyn)
– For advanced PD only as rescue medicine
– Subcutaneous injection
Dopamine Agonists: Caution
Ankle / leg edema
 Orthostatic Hypotension*
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– 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
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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
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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
Impulse Control Disorders
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Dopamine agonist medications
have been associated with the
development of Compulsive
behaviors such as gambling
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It is recommended to screen
for these before starting
therapy and at each visit once
on therapy
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Typically reverses with
discontinuation of medicine
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Weintraub et al, 2010
(Arch. Neuro) did a xsectional 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)
MAOB-Inhibitors
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Selegeline (Eldepryl, Deprenyl)
– Inhibits catabolism of dopamine
– Amphetamine metabolites
– Dose 5mg – 10mg per day (usually before noon)
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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
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Rasageline (Azilect)
– Approved for mono- and adjunctive tx
– About 10X more potent than selegeline (oral)
– Dose 0.5mg – 1mg once daily
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

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
COMT-Inhibitors
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WHAT THEY ARE NOT!
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Enhance levels of exogenous levodopa
Tolcapone (Tasmar)
– Not symptomatically effective alone (use ONLY with levodopa)
– Not indicated for early PD, indicated for Advanced PD with
EODWO
– Has “black box warning”
– Associated with fatal liver failure
– Monitoring needed
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Entacapone (Comtan, Stalevo)
– Taken with each dose of levodopa
– Increases availability of levodopa in the plasma
– Only peripheral action
Amantadine
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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
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Anticholinergics
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Earliest class of agents for PD
– Belladonna used for centuries
– 1940s trihexyphenidyl created
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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
Apomorphine – Rescue Therapy
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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
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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
Surgical Therapies

Ablative – permanent lesioning
– Thalamotomy
– Pallidotomy
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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
Global Presentation of PD
MOTOR
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RIGIDITY
BRADYKINESIA
TREMOR
POSTURAL INSTABILITY*
POSTURAL CHANGES
SPEECH CHANGES*
DECREASED DEXTERITY
HYPOMIMIA
FESTINATING/FREEZING
GAIT*
DYSTONIA
MICROGRAPHIA
DYSPHAGIA*
*LIKELY NON-DOPAMINERGIC FEATURES
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NON-MOTOR*
CONSTIPATION
ANOSMIA
GERD
DEPRESSION/ ANXIETY
APATHY
COGNITIVE CHANGES
SLEEP DISTURBANCES
SEBORRHEIC DERMATITIS
BLADDER URGENCY /
FREQUENCY
SWEATING SPELLS
HYPOTENSION
SEXUAL DYSFUNCTION
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
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.
NON-MOTOR SYMPTOMS
Seen in Early & Late PD
MOOD DISTURBANCE
Depression
May be present up to 5-10 years
prior to PD diagnosis
 10% of general population
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50-60% in PD
– 5%-25% major
– 10%-30% minor
– Suicidal ideation common, suicide
is not
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SSRIs, SNRIs, Tricyclics,
Buproprion
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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
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
Cognitive Decline
(Cognitive changes, psychosis, behavior
changes most common reason for institutionalization in PD)
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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)
Hallucinations and Paranoia
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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
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
Orthostasis
– Autonomic dysregulation
– PD meds, antihypertensives, 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)
GI Dysmotility / Constipation
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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
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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
Dysphagia
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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
Drooling (sialorrhea)
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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
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 wearingoff 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. Melanoma2-7x higher risk in PD
∙ Annual screening
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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
GU Dysfunction
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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!
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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.
Falls in PD
Meta-analysis of several studies of falls in PD
(Pickerington et al. Mov Dis 2007)
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Incidence of falls significant even in early PD
(Kerr et al.2010)

Turning in PD is hazardous and associated with imbalance and FOG

– showed very high fall rate (46%) with injury rate from 25% - 78%
– Best predictor was prior fall within previous year
– 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
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!!
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
The James Parkinson’s Tulip
April is PD Awareness Month!