2. 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.
3. BACKGROUND
MOSTLY known as movement disorder
1-2% > 65 y/o
15% between ages of 65 and 74
Cardinal signs;
tremor, bradykinesia, rigidity & postural instability.
Dx:2/3
Onset: unilateral progressing to B/L
4. TREMOR
Resting
. Pill-rolling motion
Suppressed by
activity, sleep,
concentration
Intensified by stress,
fatigue
Mostly begin
unilateral.
5. BRADYKINESIA
Required for dx
Most disabling Sx
Slowness 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
6. 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.
7. 4th cardinal sign, but itINSTABILITY in the
POSTURAL emerges late
disease, usually after 8 years or more
Imbalance and loss of righting reflexes.
Assumption by patient of a stooped-forward posture
Presence, usually, of a festinating gait pattern
(stumbling forward).
Decreased arm swing during ambulation
8.
9. Stiffness and slowed movements DISEASE
CONSEQUENCES OF
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)
11. PHYSICAL EXAM
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) .
Olfactory dysfunction (hyposmia), which may be present prior to
motor symptoms and often is not recognized by the patient
12. PHYSICAL
Autonomic Dysfunction EXAM
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
13. CLASSIFICATION OF PARKINSON’S
Idiopathic PD – 85% of all PS cases
Drug induced Parkinsonism – 7-9%
Parkinson-Plus Syndrome
Vascular Parkinson syndrome -3%
Toxin-induced –rare
Recurrent Head trauma-rare
14. 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
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
15. EPIDEMIOLOGY/M&M
Male to female ratio = 3:2
Prevalence = 160/100,000
Incidence = 20/100,000 per year /general population
Morbidity=progressive
Mortality=mean survival after onset @ 15 yrs
PD survival >MSA,PSP
MC cause of death: pulmonary infection/aspiration, UTI, PE,
of falls/fractures
16. Normal
Aaging is associated with clinical
CCELERATED AGING
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.
18. ETIOLOGY UNCLEAR
Environmental factors
.Genetic susceptibility use of pesticides,
- Twin studies living in a rural
inconclusive environment
Genetic factors play a consumption of well
greater role with early water
onset PD
Increased incidence of a exposure to herbicides
family history PD proximity to industrial
observed plants or quarries
19. Head Trauma TIOLOGY UNCLEAR
E increases
the risk of developing
Parkinson
. The former champion boxer
Muhammad Ali was diagnosed
with Parkinson's in 1984 at the
age of 42, and is one of the
most high-profile people
battling the condition.
20. OXIDATIVE STRESS
Free radical damage, Hydrogen peroxide reactions
with ferrous ions, resulting in
resulting from dopamine's formation of hydroxyl radical.
oxidative metabolism, - hydroxyl radicals can cause
plays a role in the damage to lipids, DNA,
amino acids
development or
PD associated with:
progression of PD. increased dopamine
Dopamine oxidation via turnover, decreased
protective mechanisms
MAO result in formation of (glutathione),
hydrogen peroxide. increased iron (a pro-
Hydrogen peroxide oxidation molecule),
evidence of increased lipid
normally cleared by peroxidation.
glutathione
21. CLUES SUGGESTING ATYPICAL PARKINSONISM
Early onset of, or rapidly progressing
dementia
Rapidly progressive course
Supranuclear gaze palsy
Cerebellar signs-dysmetria, ataxia
Early urinary incontinence.
22. PARKINSON’S SYNDROME
Parkinson’s Disease Parkinson-Plus
Survival syndromes
approximates US Shorter survival, more
population when frequent
treated complications
Slow progressive Early instability
onset of asymmetric Rapid disease
bradykinesia progression
Onset with either Poor response to
classic pill-rolling Levodopa
tremor or rigidity Pyramidal and
cerebellar signs
Early dysarthria,
dysphasia
24. 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
25. TREATMENT OPTIONS
Preventive = no definite one available
Symptomatic
Pharmacological
Surgical
Non-motor management
Restorative-experimental only
Transplantation
Neurotrophic factors
Nonpharmacologic approaches
PT/OT/ST
27. SURGICAL MANAGEMENT
Candidates for deep brain
stimulation
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.
28. Deep drain URGICAL MANAGEMENT
S 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
30. MANAGING EARLY COMPLICATIONS :ALTERED
MENTAL STATES
Confusion, sedation, dizziness, hallucinations,
delusions
Reduce /eliminate CNS-active drugs of lesser priority
Anticholinergics - Sedatives and many other
medications.
31. LATE COMPLICATIONS
Motor
fluctuations, dyskinesias,dystonia,freezing,falls
Behavioral/neuropsychological
Depression,sleep d/o, psychosis
Autonomic
OH, hyperhidrosis ,constipation, impotence, urinary
incontinence or retention
32. 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
39. IMPAIRED GI MOTILITY
Constipation
Vomiting
Impaired absorption
Treatment Options
small frequent meals
increased fiber/bulking agents
stool softeners and suppositories
40. 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
41. EXCESSIVE SWEATING
Usually levodopa related, and may be seen at peak or trough
dose drug levels
45. 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.
46. 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.
47. REHABILITATION
AND 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.
48. Maintain or increase
TREATMENT PLAN
ROM in all joints
Efforts to improve
postural control and
standing balance
Prevent disuse /atrophy
and muscle weakness
Improve motor function
and mobility
49. Improve gait TREATMENT
pattern PLAN Upper extremity fine
Improve speech, breathing motor skills
patterns chest expansion, Functional transfers
mobility
Swallowing
Maintain functional evaluation
independence in adl’s
Cognitive evaluation
Assist in psychological
Recreational therapy
adjustment to new lifestyle
Pt/Family training-
education
50. PHYSICAL THERAPY: GOAL
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
51. 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
52. PHYSICAL THERAPY
Static and dynamic postural controls emphazing whole 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
53. OCCUPATIONAL THERAPY: GOALS
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
54. Patient and caregiver education
O CCUPATIONAL
goals of program
THERAPY
transfers, task simplification,
positioning, etc.
Home exercise program
Home and workplace
modifications
55. Swallowing evaluationTHERAPY
SPEECH
including modified barium
swallow
Articulatory speech training
for dysarthria
Early therapy is effective
Teaching compensatory
strategies for safer swallow
56.
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.
57. TECHNIQUES TO IMPROVE SPEECH
Increase loudness
Face the listener directly
Emphasize key words
Use short sentences
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”
58. MANAGEMENT OF SWALLOWING DIFFICULTY
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.
59. RECREATIONAL THERAPY
identifying previous recreational interests
new interests can be identified and explored
social and recreational pursuits
social and recreational pursuits
60. COMMUNITY RESOURCES
Social worker intervention:
Social Security office
Medicare, Medicaid
In-home programs
Meals on Wheels, home visiting, etc.
61. 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
62. 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.
63. Poor PROGNOSIS/COMPLICATIONS
Prognostic Complications
indicators Underlying medical illness
( sepsis, pneumonia, fecal
Old age of impaction, urinary tract
infection) should be
onset suspected in a PD patient
Early cognitive
deficits
Lack of tremor
64. REFERENCES
Neuro Rehab Book ( PTA Program)
http://www.emedicine.com/pmr/topic99.htm
http://www.emedicine.com/NEURO/topic304.htm
ANY QUESTION?
Editor's Notes
Gait observation in linear motion, in changes of direction; if pt uses >5 steps to complete 180 degree turn, PD shld be consideredBradykinesia refers to slowness of movement but also includes a paucity of spontaneous movements and decreased amplitude of movement. Bradykinesia also is expressed as micrographia (small handwriting), decreased blink rate, and hypophonia (soft speech). hypomimia (decreased facial expression),
Cogwheeling may be appreciated in tremors not associated with an increase in tone (ie, essential tremor). Rigidity
There s sometimes confusion differentiating a parkinsonian tremor from ET.ET shld have tremor alone, no other signs of parkinsonism nor any other neurologic signs such hyperreflexia,weakness,or sensory loss. Both d/o may have kinetic and rest component although traditionally pt w/ ET have more postural & kinetic tremor w/ dampening upon rest,where as PD more often have rest tremor dampens with action. In addition,ET pts may exhibit mild signs of bradykinesia & cogwheeling when examined when examined for rigidity.in the early tremor pt,the historical findings of famhx suggesting AD inheritance, a long hx of tremor w/o progression of motor difficulties & tremor response to alcohol r helpful n the dx of ET.lastly ET does not respond to antiPD drugs but may improve w/ propanolol,primidone,andbenzos
No definite preventative tx available there is however wide range of sxmatic tx including pharmacologic and surgical methods. The non motr mgt include tx of depression,OH,excessive drowsiness,& psychosis. Finally, restorative therapies such as fetal or porcine cell transplantation are n expe use & neurotrophic factors susch as GDNF & small molecules such as neuroimmunophillins are being explored Rehabilitaion part is where I’m going to focus more since neurologist are by practice the ones managing their medications. Besides it will takeperhaps another hour to discuss the pharmacologic, side effects of these meds, we certainly discuss them some other time if you like.
Briefly on medical management; Dopaminergic therapy is d cornerstonr of sxmatic mngt of PD LD replaces dopamine presynaptically while dopamine agonists act directly on receptors post synaptically. LD is administered w/ peripheral decarboxylase inhibitor either benserazide or carbidopa. The newest class r the COMT inhibitors, also increase bioavailability of LD by inhibiting peripheral or central catechol o-methyl transferase. Other agents r anticholinergics, the MAO-B inhibitors selegiline and the antiviral amantadine.Bromocriptine=parlodel, pergolide=Permax,ropinirole=requip,pramipexole=mirapexCOMT inhibitors-Tolcapone(Tasmar),Entacapone (Comtan) L-Dopa + Entacapone (Stalevo)MAO-B inhibitors- Selegiline (Eldepryl)Anticholinergics-Trihexyphenidyl(Artane),Benztropine (Cogentin)Antivirals-AmantadineL-Dopa(Sinemet), Dopamine Agonists- Bromocriptine (Parlodel), Ropinirole(Requip),Pramipexole(Mirapex)
When pts develop confusion,sedation,dizziness,halluci or delusions the simplest intervention is to reduce or eliminate sedating meds or antiPD meds of lesser priority.commonly used sedating meds includes hypnotics, sedatives,muscle relaxant,urinary antispasmodics. Low potency antiPD meds that may contribute significantly to confusion include anticholiner, amantadine and selegiline. When this option is not adequate, dosage reduction of LD, DA or COMT inhibitor m/b necessary. Drug related psychotic symptoms in early illness are often associated w/ atypical parkinsonian syndromes
Management of late stages of PD involves tx of motor response fluctuations, dyskinesias,dystonia,freezing and falls. In add, besides these motor fluctuations there r behavioral & neuropsychological concerns, such as depression, sleep d/o, & psychosis. Autonomic problems include OH, hyperhidrosis, constipation, impotence, u inc or retention.