Download Parkinson’s Disease

Parkinson’s Disease
Hannah H Florida,MD
Parkinson’s Disease
Originally described by
James Parkinson in 1817
and characterized as
Shaking Palsy.
Chronic slowly prog,
neurodegenerative disease
of the Basal Ganglia (BG).
Basic path-lack of
dopamine-producing cells
in the BG.
Background
 MC movement disorder
 1-2% > 65 y/o
 15% between ages of 65 and 74
 Cardinal signs/Classic Triad:
– tremor, bradykinesia, and rigidity.
 Dx: 2/3
 Onset: insidious, unilateral progressing to
B/L
Tremor
 Resting
 MC presenting
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symptom
Dxtic but not required
Pill-rolling motion
of hand at 3-5 Hz
Suppressed by activity,
sleep, concentration
Intensified by stress,
fatigue
Most begin unilaterally
Bradykinesia
 Required for dx
 Most disabling Sx
 Slowness/paucity of movement/motion
 Affects facial muscle>> masked face
 Inability to change direction while
walking/dif walking around obstacle
 Causes gait/postural abnormality
 Clumsy or weak limb maybe early sign
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Rigidity
 refers to an increase in resistance to passive movement
about a joint; either osclillating (cogwheel) or smooth (lead
pipe). Rigidity usually is tested by flexing and extending
the patient's relaxed wrist.
 Cogwheeling
– Racheting through the ROM due to subtle tremor
superimposed on the rigidity
 Lead pipe
– Smooth resistance to passive movement that is
independent of velocity (in contradistinction to
spasticity, which is velocity dependent)
– Lead pipe tone can be made more obvious with
voluntary movement or mental task in the c/l limb.
Postural Instability
 4th cardinal sign, but it emerges late in the disease,
usually after 8 years or more
 Imbalance and loss of righting reflexes. Its
emergence is an important milestone, because it is
poorly amenable to treatment and a common
source of disability in late disease.
– Assumption by patient of a stooped-forward posture
– Presence, usually, of a festinating gait pattern
(stumbling forward); however, retropulsion also can
occur
– Decreased arm swing during ambulatory activity
History
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Stiffness and slowed movements
Tremor or shaking at rest
Difficulty getting out of a chair or rolling over in bed
Frequent falls or tripping
Difficulty walking
Memory loss
Shifting forward of posture into a stoop
Speech changes (eg, whispering, rapid speech)
Smaller handwriting
Slowness in performing activities of daily living (ADL)
Sialorrhea
Decreased sense of smell
Clinical Manifestation
Physical Exam
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Painful dystonia, usually occurring in the early morning
Rapid, monotonous, low-volume speech
Hypokinetic dysarthria
Dysphagia
Masklike facies
Depression
– Can affect up to 50% of patients
– Suicide risk
 Akathisia (inability to sit still)
 Seborrheic dermatitis, usually of the face and scalp
 Olfactory dysfunction (hyposmia), which may be present
prior to motor symptoms and often is not recognized by the
patient
Physical Exam
 Autonomic Dysfunction
– Slowed enteric motility and constipation
– Urinary retention and incontinence
– Orthostatic hypotension
 Patients may experience freezing when
starting to walk (start-hesitation), during
turning, or while crossing a threshold, such
as going through a doorway
Physical Exam
 Dementia generally occurs late in PD and
affects 15-30% of patients. Short-term
memory and visuospatial function may be
impaired, but aphasia is not present.
Cognitive dysfunction within a year of
onset of motor features suggests a diagnosis
of Lewy body disease, a disease closely
related to PD and marked by the presence of
significant cortical Lewy bodies.
Classification of Parkinson’s
Syndrome(PS)/Parkisonism
 Idiopathic PD – 85% of all PS cases
 Drug induced Parkinsonism – 7-9%
 Parkinson-Plus Syndrome
– MSA (SDS,SND,OPCD) – 2.5%
– PSP – 1.5%
 Vascular Parkinson syndrome -3%
 Toxin-induced –rare
 Recurrent Head trauma-rare
Idiopathic PD
 D/O of the Basal Ganglia (BG)
 loss of dopamine producing cells in the substantia
nigra (SN) and locus ceruleus (LC)
 Degeneration of nigrostriatal pathway (SN to
corpus striatum)
 Sx manifest if + decreased dopamine content by >
50%)
 Loss of inhibitory input to the cholinergic system>
> excess excitatory output
 Imbalance of cholinergic input in the striatum
Basal Ganglia
 The basal ganglia are
a group of nuclei in
the brain associated
with motor functions.
 Nuclei: caudate,
putamen substantia
nigra, subthalamic,
globus pallidum
Basal Ganglia
 motor circuit modulates
cortical output
 Signals from the cerebral
cortex are processed
through the basal gangliathalamocortical motor circuit
and return to the same area
via a feedback pathway.
 Output from the motor circuit
is directed through the
internal globus pallidus
(GPi) and the substantia
nigra pars reticulata (SNr).
 inhibitory output is directed
to the thalamocortical
pathway and suppresses
movement.
Pathophysiology
 Loss of pigmented
dopaminergic neurons
in the substantia nigra
 Approximately 60-80%
of dopaminergic
neurons are lost before
the motor signs of PD
emerge.
 The presence of Lewy
bodies.
Lewy Bodies
Lewy bodies are concentric,
eosinophilic, cytoplasmic
inclusions with peripheral
halos and dense cores.
Present within pigmented
neurons of substantia
nigra.
Characteristic of PD but
not pathognomonic
Epidemiology/ M&M
 Male to female ratio = 3:2
 Prevalence = 160/100,000
 Incidence = 20/100,000 per year /general
population
 Morbidity=progressive
– more rapid in MSA and PSP
 Mortality=mean survival after onset @ 15 yrs
– PD survival >MSA,PSP
– MC cause of death:pulmonary
infection/aspiration,UTI,PE,Cx of falls/fractures
Etiology
 Unknown
 Theories
– Accelerated aging
– Genetic susceptibility
– Environmental Factors
– Oxidative stress
Accelerated Aging
– Normal aging is associated with clinical
features that may resemble PD.
– Aging is associated with a decline of
pigmented neurons in the substantia nigra
and with decreased levels of striatal
dopamine and dopa decarboxylase.
– Some authorities believe that PD may
result from the effects of aging
superimposed on an insult to the
nigrostriatal system earlier in life.
Etiology Unclear
Genetic susceptibility
- Twin studies
inconclusive
– Genetic factors play a
greater role with early
onset PD
– Increased incidence of a
family history PD
observed (16% vs 4% of
control)
– Accounts to <5% of PD
cases.
 Environmental
factors
– use of pesticides,
– living in a rural
environment
– consumption of well
water
– exposure to herbicides
– proximity to industrial
plants or quarries
Oxidative Stress
– Free radical damage,
resulting from
dopamine's oxidative
metabolism, plays a
role in the
development or
progression of PD.
– Dopamine oxidation
via MAO result in
formation of
hydrogen peroxide.
– Hydrogen peroxide
normally cleared by
glutathione
– Hydrogen peroxide
reactions with ferrous
ions, resulting in
formation of hydroxyl
radical.
- hydroxyl radicals can
cause damage to lipids,
DNA, amino acids
– PD associated with:
increased dopamine
turnover, decreased
protective mechanisms
(glutathione),
increased iron (a prooxidation molecule),
evidence of
increased lipid
peroxidation.
Etiology Unclear
 Head Trauma
 the risk of developing
Parkinsonism
increases eightfold for
patients who have had
head trauma requiring
hospitalization.
 11-fold for patients
who have experienced
severe head injury.
 Dementia Pugilistica
Clues Suggesting Atypical
Parkinsonism
 Early onset of, or rapidly progressing
dementia
 Rapidly progressive course
 Supranuclear gaze palsy
 UMN signs
 Cerebellar signs-dysmetria, ataxia
 Early urinary incontinence
 Early symptomatic postural hypotension
Parkinson’s Syndrome
 Parkinson’s Disease
– Survival approximates
US population when
treated
– Slow progressive onset
of asymmetric
bradykinesia
– Excellent sustained
Levodopa response
– Onset with either
classic pill-rolling
tremor or rigidity
 Parkinson-Plus syndromes
– Shorter survival, more
frequent complications
– Early instability
– Rapid disease
progression
– Poor response to
Levodopa
– Pyramidal and
cerebellar signs
– Early dysarthria,
dysphasia
Parkinson-Plus Syndrome
 PSP
– Supranuclear downgaze palsy, square wave
jerks
– Upright posture/frequent falls
– Pseudobulbar emotionality
– Furrowed brows/stare
 Corticobasal degeneration
– cognitive impairment
– Unilat, coarse tremor,limb apraxia/limb
dystonia-myoclonus/alien limb
Parkinson-Plus Syndrome
 MSA
– Cerebellar ataxia, pyramidal
weakness,autonomic failure, nocturnal stridor
• Shy-Drager syndrome
– Autonomic insufficiency- orthostasis, impotence
• Striatonigral degeneration
– Tremor less prominent
• Olivopontocerebellar atrophy
– Cerebellar ataxia, dysarthria
Differential Diagnosis
 Diffuse Lewy body disease
– Early onset dementia
– Delusions/hallucinations
– Agitation
 Alzheimer’s disease
– Dementia primary clinical sx
– Rest tremor rare
Differential Diagnosis
 Hereditary disorders associated with
parkinsonism
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Wilson’s disease
Huntington’s disease
Dentatorubro-pallidoluysian atrophy(DRPLA)
Machado-Joseph diseaseor spinal cebellar
ataxia (SCA-3)
Differential Diagnosis
 Secondary Parkinsonism
– Drug – induced
– Toxin – induced
– Metabolic
– Structural lesions (vascular parkisonism, etc)
– Hydrocephalus
– Infections
Drug-Induced Parkinsonism
 Antipsychotics/neuroleptics
– Haldol, chlorpromazine, thioridazine,
resperidone, olanzapine
 Antiemetics- MC drugs causing PS
– Metoclopramide,prochlorperazine
 Dopamine depletors
– methyldopa, reserpine containing anti-HTN
 Combination drugs- know components
– Triavil (amitriptyline + perphenazine)
Metabolic/Infectious Causes
 Metabolic
– Often reversible
– Hypo or
hyperthyroidism
– Hypo or
hyperparathyroidism
– Liver failure
– Central pontine
myelinolysis - rapid
correction of
hyponatremia
 Infectious
– Post-encephalitis
– Creutzfeld-Jakob
disease– Infectious masses
compressing SN/BG
– HIV
Toxin-Induced Parkinsonism
 MPTP
 Cyanide
 Iron
 Manganese
 Carbon disulfide/monoxide
 Pesticides/organic solvents
 Lead
 methanol
Vascular Parkinsonism
 Abrupt onset, usually unilateral
 Step-wise or no progression
 Other signs-
hemiparesis,aphasia,hyperreflexia
 Infarcts on neuroimaging helpful in
confirming dx
Hydrocephalus –induced
Parkinsonism
 Can be communicating or obstructive
 NPH-idiopathic
 Clinical triad
– Parkisonism/gait disorder
– Urinary/fecal incontinence
– dementia
PD vs Essential Tremor
ET should be tremor with no other
signs of parkinsonism
Both can have kinetic and rest
component
Cogwheel rigidity can be found in
ET
Treatment Options
– Preventive = no definite one available
– Symtomatic
• Pharmacological
• Surgical
– Non-motor management
– Restorative-experimental only
• Transplantation
• Neurotrophic factors
– Nonpharmacologic approaches
• PT/OT/ST
Drug Classes in PD
 Dopaminergic agents
– Levodopa (LD)
– Dopaminergic Agonists- Bromocriptine,
Ropinirole, Pramipexole
 COMT inhibitors
– Tolcapone, Entacapone
– LD + Entacapone (Stalevo)
 MAO-B inhibitors- Selegiline (Eldepryl)
 Anticholinergics
– Trihexyphenidyl, Benztropine
 Antivirals-Amantadine
Medical Management Algorithm
Surgical Management
 Candidates for ablative
surgery or deep brain
stimuation
– disabling medication-resistant
tremor
–
levodopa-responsive patients
with medication-resistant
disabling motor fluctuations
and/or levodopa-induced
dyskinesia.
– no significant cognitive
impairment, mood or
behavioral disturbances
– No other factors that may
increase the risk of surgery.
Surgical Management
 Ablative
– Thalamotomy
• Relieves tremors
– Pallidotomy
• Improves cardinal
signs
– Subthalamotomy
• Improves cardinal
signs
• Motor fluctuations,
dyskinesia
Surgical Management
 Ablative
complications
– Speech
impairments
– Cognitive
deficits
– Dysphasia
Surgical Management
 Deep drain stimulation
– Thalamic
• Dec. tremor in 90% of
pt
• No effect on cardinal
signs
– Pallidal
• Improves cardinal
signs, dyskinesia
– Subthalamic
• Improves cardinal
signs, dyskinesia, motor
fluctuations
Future Management
 Neural
transplantation
– dopamineproducing cells,
ex. fetal nigral
cells.
Gene therapy
Managing Early Complications
:Altered Mental States
 Confusion,sedation,dizziness,hallucinations,
delusions
 Reduce /eliminate CNS-active drugs of
lesser priority
– Anticholinergics
– Amantadine
– Hypnotics
- Sedatives
- Muscle relaxant
- Urinary antispasmodics
 Reduce dosage of DA,COMT inhibitor or
LD
Late Complications
 Motor
– fluctuations, dyskinesias,dystonia,freezing,falls
 Behavioral/neuropsychological
– Depression,sleep d/o, psychosis
 Autonomic
– OH, hyperhidrosis ,constipation, impotence,
urinary incontinence or retention
Stages in Decline of response to
Levodopa (LD)
 I: Pt not aware of effect of individual dose
 II: Mid afternoon loss of benefit
 III: Loss of sleep benefit; early morning
akinesia, possible foot dystonia
 IV: regular “wearing off” q 4 hrs at first,
shortens with time
 V: Frequent wearing off, abrupt on-off,
unpredictable dose response
LD Response Fluctuations
• Peripheral causes:
– delayed gastric emptying
– dietary protein
– short plasma half-life
• Central causes:
– pulsating delivery to striatal receptors
– impaired storage capacity
– alteration of DA receptor
Off- Period Dystonia
 Appears when LD dose is low esp in early
AM
 w/ or w/o parkinsonism
 Dose adjustments, add ons:
– More frequent LD dosing to avoid low plasma
levels
– Add DA, COMT inhibitor, MAO-B inhibitor
Wearing Off
 Regular and predictable decline in response
2-4 hrs after LD dose
 Most common motor fluctuation
 Dose adjustment, ad-ons:
– Change to LD-CR, or increase LD freq
– Reduce LD, add DA or COMT inhibitor
On-off Response
• Sudden and unpredictable off periods unrelated to
dosing schedule
• One of the hardest features to manage
• Dose adjustments, add-ins:
– Reduce LD, add DA
Freezing and Falls
• Freezing
– motoric block; at initiation of gait, turning, narrow spaces
– use auditory(marching steps to the beat of a metronome),
visual, proprioceptive cues ( mental rehearsal and
imaging)
• Falls
– Physical therapy evaluation
– Cane, scooter, wheelchair may be necessary
Cognitive Assessment
• Memory difficulties: 11-29% of PD patients
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Benign forgetfulness
Delirium
Alzheimer’s disease
Other dementias
• Evaluation
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Brain imaging
Lumbar puncture
EEG
Blood work for thyroid profile, vitamin B12, serology,
chemistry panel
Psychosis
• Features
– Vivid dreams/nightmares, disorientation, hallucinations,
delusional thought
• Simplify medical regimen
– Stop unnecessary non-PD meds
– Stop: anticholinergic drugs, amantadine, selegiline,
dopamine agonists, COMT inhibitors
• Change from CR to standard carbidopa/levodopa
• Try atypical antipsychotic agents
• Try low-potency traditional antipsychotic agents
Depression
• Reported in 30-90% of PD patients
• Difficult to discern from vegetative symptoms
• Depression may be related to a deficit in
serotonergic neurotransmission or to decreased
cortical levels of norepinephrine and dopamine.
• Usually responds quickly to medications
– Selective serotonin re-uptake inhibitors
– Tricyclic Antidepressants
• If ECT needed, will transiently improve PD
symptoms
Anxiety/Restlessness
• Primary anxiety disorder: treat with benzodiazepines
– Associated with “off-periods” or low-levopoda levels: adjust
levopoda dosing
• Restless Leg Syndrome: benzodiazepines, narcotics, levopoda,
dopamine agonists
Sleep Disorders
• Insomnia
– careful history
– difficulty with sleep initiation: tricyclic agents, benzodiazepines,
diphenhydramine, chloral hydrate
– treat depression
– REM-behavioral disorder: clonazepam
• Excessive daytime sleepiness
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correct poor sleep at night
discontinue anticholinergics, amantadine
reduce dopamine agonist, levopoda dosages if possible
selegeline, caffeine, methylphenidate 5-20 mgs/d
Orthostatic Hypotension
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Tilt table training for severe cases
Taper anti-hypertensive agents
Taper non-PD drugs
Increase salt intake
Elevate HOB, arising slowly, isometric exercises
Compression stockings, abdl binders
Fludrocortisone (0.1-0.4mg/d)
Midodrine (2.5-20mg/d)
Urinary Incontinence/Frequency
• Rule out urinary tract infection
• Bladder evaluation for
– detrusor hyperactivity
• *oxybutinin 5-30mg/d, propanthaline 7.5-15mg/d
– detrusor hypoactivity
– *phenoxybenzamine; prazosin
• Urinary frequency
– avoid fluid pooling in feet
– DDAVP inhaler, tolterodine tartrate 2mg hs to 2mg tid
Impaired GI Motility
 Constipation
 Vomiting
 Impaired absorption
 Treatment Options
– small frequent meals
– increased fiber/bulking agents
– stool softeners and suppositories
Sexual Dysfunction
• Medical screening
– Depression, anxiety, iatrogenic causes: S/E of SSRIs
• Endocrinologic evaluation
– Prolactin, testosterone, lutenizing hormone, thyroid screen
• Individual variation in effect of PD
• Some patients have short-lived hypersexuality with
dopaminergic drugs
• Urologic evaluation
– Erectile dysfunction• SE of alpha and beta – adrenergic blockers,
anxiolytics, digoxin, cimetidine
– Yohimbine, sildenafil
Nausea
• Levodopa-related: take with meals, add carbidopa,
add domperidone
• Other anti-PD medications: same.
– If no improvement: withdraw newest agent, re-initiate at
minimal doses, slowly increase
Excessive Sweating
• Usually levodopa related, and may be seen at peak
or trough dose drug levels
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reduce levodopa
add dopamine agonist or COMT inhibitor
add carbidopa
add Beta-blocker
Problems That May Respond to
Nonpharmacological Approaches
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Motor, mobility,balance, posture, gait
ADL difficulties
Speech : hypophonia, sialorrhea,dysphagia
Inadequate nutrition
Sleep disturbance
Autonomic dysfunction:
– OH, delayed gastric emptying, constipation,bladder
dysfunction
• Sexual dysfunction
• Depression, Anxiety
Rehabilitation Impairments
 Gait disturbance
• Decreased stride
length, cadence,
velocity.
Festination
• Stooped flexed
posture
• Cautious gait(fear
of falling)
• Impaired balance
Rehabilitation Management
 Rehabilitation
interventions are
directed at the
main causes of
impairments.
 Multidisciplinary
approach:PT,OT,
ST,D,RT,Neurop
sych
Rationale for rehabilitation
 While rehabilitation services are often given to the patient with
Parkinson disease, this occurrence is more based on common practice
rather than clear research design. There is a paucity of well-designed
research studies looking at specific rehabilitation techniques. The
existing literature is both sparse and fraught with confounding
variables such as changes in medication regimens. A recent review
examined 11 studies involving various physical therapy techniques in
Parkinson disease. The authors found insufficient evidence to support
or refute the efficacy of any form of physical therapy over another
form. Furthermore, there was insufficient evidence found to support
the efficacy of any therapy compared with no therapy. Perhaps the best
designed study was a prospective randomized crossover investigation
of 4 weeks of outpatient physical therapy, in which medication
changes were not allowed. This study demonstrated significant
improvement in activities of daily living and motor function but no
improvement in tremor, mentation, and mood. These improvements
returned to baseline 6 months after termination of the intervention.
Long-term rehabilitation programs have been advocated, but the
stability of the benefits gained in these programs has not been
demonstrated.
Cardiopulmonary Impairment
– The patient's flexed posture can lead to kyphosis, cause
a reduction in pulmonary capacity, and produce a
restrictive lung disease pattern.
– Breathing exercises, postural reeducation, and trunk
exercises may be helpful.
– Institution of a general conditioning program can
increase the patient's endurance.
– If pulmonary function progressively worsens, assisted
coughing techniques, incentive spirometry, and
respiratory therapy intervention may be required.
Rehabilitation
Hoehn and Yahr Rating scale
 divided into five
 Stage III = disease that
stages
 Stage 0 = no visible
disease;
 Stage I = disease that
involves only one side
of the body;
 Stage II = disease that
involves both sides of
the body. but does not
impair balance:
impairs balance or
walking;
 Stage IV = disease
that markedly impairs
balance or walking:
and
 Stage V = disease that
results in complete
immobility.
Rehabilitation
Hoehn and Yahr Rating scale
 Stages 0-II are mild
disease;
 Stage III is moderate
disease;
 Stages IV and V are
marked or advanced
disease. There are
gray areas between
the successive
stages.
Treatment Plan
– Maintain or increase
ROM in all joints
– Efforts to improve
postural control and
standing balance
– Prevent disuse atrophy
and muscle weakness
– Improve motor
function and mobility
Treatment Plan
– Improve gait pattern
– Improve speech,
breathing patterns
chest expansion,
mobility
– Maintain functional
independence in adl’s
– Assist in psychological
adjustment to new
lifestyle
– Upper extremity fine
motor skills
– Functional transfers
– Swallowing evaluation
– Cognitive evaluation
– Recreational therapy
– Psychosocial
intervention
– Dietary/Nutrition
– Pt/Family trainingeducation
Physical Therapy: Goal
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Maintain or increase activity level
Decrease rigidity and bradykinesia
Facilitate movement and flexibility; optimize gait
Maximize gross motor coordination and balance
Maximize independence, safety, function
Physical Therapy
 Relaxation techniques
 Gentle ROM and
stretching techniques
 Exaggerated or
patterned movements
– High stepping,wt
shifting,repitetion,
visual &verbal cues
 Back extension
exercises and pelvic
tilt
Physical Therapy
 Static and dynamic postural controls emphazing whole
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body movements sitting and standing
Stationary bike training to help reciprocal movements
Exercise: walking(1+mile/day),swimming,golf,dancing
Use of assistive devices, mobility aids, orthotics
Family training and home program
– Proper and energy conservation techniques
– After 6 mths benefit of therapy if not coninued will be gone
Occupational Therapy: Goals
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•
•
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Maximize independence, safety, function
Improve endurance, reduce energy expenditure
Training in use Adaptive Equipments
Improve body image, self-esteem, psychosocial
adjustment
• Facilitate active movement
• Maximize fine motor coordination
• Increase trunk flexibility and upright posture
Occupational Therapy
• Patient and
caregiver education
– goals of program
– transfers, task
simplification,
positioning, etc.
• Home exercise
program
• Home and
workplace
modifications
• Patient and
caregiver education
– goals of program
– transfers, task
simplification,
positioning, etc.
• Home exercise
program
• Home and
workplace
modifications
Speech Therapy
 Swallowing evaluation
including modified
barium swallow
 Cognitive evaluation
 Articulatory speech
training for dysarthria
 Early therapy esp
effective
 Teaching
conpensatory
strategies for safer
swallow
Dysphagia

The videofluoroscopic swallowing- gold
standard for dx
 oral-phase:prolonged chewing, excessive
postswallow residuals, poor bolus control,
and repetitive tongue motions.
 pharyngeal phase: vallecular and piriform
pooling, delayed triggering of the swallow
reflex, and delayed laryngeal elevation
 insufficient evidence to support or refute the
utility of dysphagia training
Techniques to Improve Speech
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Increase loudness
Face the listener directly
Emphasize key words
Use short sentences
imagery
Range-of-motion exercises for muscle of speech
Breathing exercises, breath control
Phonatory-respiratory effort model /Lee Silverman
Voice Tx=“think loud, think shout approach”
Management of Swallowing
Difficulty and Sialorrhea
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Do not rush
Eat soft foods, small bites of food
Swallow only well-chewed food
Empty mouth before next bite
Chin down positioning
Family should learn Heimlich maneuver
Be aware of saliva accumulation and swallow often
Verbal prompting
Clinicians might also choose to administer
antiparkinsonian medications prior to meals, so that
maximal benefit of drugs occurs during mastication.
Dysphagia
– If swallowing difficulties do not respond to
conservative interventions by the speech therapist, more
aggressive treatment may be required.
– Such aggressive management can include invasive
procedures, such as nasogastric or gastrostomy feeding
tube placement.
– Discussion should be initiated early on in the disease
course to ascertain the patient's wishes about a feeding
tube, in case dementia develops and the patient lacks
the capacity for decision making when a feeding tube
becomes medically indicated.
Recreational Therapy
 identifying previous recreational interests
 new interests can be identified and explored
 social and recreational pursuits
social and recreational pursuits
Community Resources
• Social worker intervention:
– Social Security office
– Medicare, Medicaid
• In-home programs
– Meals on Wheels, home visiting, etc.
Nutritional Risk Factors
•
•
•
•
•
•
•
Inactivity
Food preparation problems
Dyskinesia and feeding problems
Chewing and swallowing problems
Increased metabolic needs
Medication-related dietary restrictions
Drug side effects: anorexia, nausea, vomiting,
constipation
• Depression and dementia
Dietary Recommendations
• Eat a balance diet, including
all food groups
• Consume sufficient calories
to maintain weight
• Consume adequate fiber and
fluids to avoid constipation
• Take vitamin D and calcium
to prevent osteoporosis
• Reduce protein to minimum
daily allowance
– concentrate in evening
meal
Consultations
 Consult with a neurologist for (1) initiation and
management of medical therapy, (2) access to clinical
medication trials if patient desires, and (3) management of
side effects of L-dopa therapy.
 Consultation with a neurosurgeon may be indicated for a
surgical opinion in patients who are resistant to standard
medical therapy or who develop significant complications
secondary to L-dopa therapy.
 Consult with a psychiatrist for management of depression
in patients who do not respond to typical treatment options,
such as the use of selective serotonin reuptake inhibitors
(SSRIs), or who show evidence of contemplating suicide.
Prognosis/Complications
 Poor Prognostic
indicators
– Old age of
onset
– Early cognitive
deficits
– Lack of tremor
 Complications
– Underlying medical
illness (eg, sepsis,
pneumonia, fecal
impaction, urinary
tract infection)
should be suspected
in a PD patient with
a rapid deterioration
or new PD
symptoms
Miscellaneous Concerns
• Seborrheic dermatitis
– shampoos or lotions with ketoconazole, selenium,
pyrithione zinc
• Driving
– assess regularly for reaction speed, judgment, mental
status
– retake driver’s test
Education, Support and
Counseling
• Patient/caregiver education: newsletters, Web
resources
• Support groups: patient, caregivers
– may be appropriate to wait for disability progression
– early-onset patients may desire separate group
• Counseling
– both patient and caregiver/family; assess needs separately
– anxiety, grief, guilt, anger, isolation, depression
U.S. Support Groups
•
•
•
•
•
•
•
•
•
•
•
•
National Parkinson Foundation, Inc.
TEL: (305) 547-6666
www.parkinson.org
Parkinson’s Disease Foundation
TEL: (312) 733-1893 (Chicago)
TEL: (800) 457-6676 (New York)
www.pdf.org
The American Parkinson’s Disease Assoc., Inc.
TEL: (800) 223-2732 or (718) 981-8001
www.apdparkinson.com
The Bachman-Strauss Dystonia & Parkinson Foundation, Inc.
TEL: (212) 241-5614
References
 http://www.braddomtext.com
 PM&R Board Review by Sara Cuccurullo
 http://www.mdvu.org/library/slides/pd.asp(wemove.com)
 http://www.emedicine.com/pmr/topic99.htm
 http://www.emedicine.com/NEURO/topic304.htm