1. PARKINSON’S DISEASE
&
COMPLICATIONS OF THIS DISORDER

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

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)

10. CLINICAL MANIFESTATION

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.

17. ETIOLOGY
 Unknown
 Theories
 Accelerated aging
 Genetic susceptibility
 Environmental Factors
 Oxidative stress

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

23. 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

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

26. 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

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

29. FUTURE MANAGEMENT
 Neural transplantation
 dopamine-producing
cells, ex. fetal nigral
cells.
Gene therapy

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

33. COGNITIVE ASSESSMENT
 Memory difficulties: 11-29% of PD patients
 Benign forgetfulness
 Delirium
 Alzheimer’s disease
 Other dementias
 Evaluation
 Brain imaging
 Lumbar puncture
 EEG
 Blood work for thyroid profile, vitamin B12, serology, chemistry
panel

34. 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

35. ANXIETY/RESTLESSNESS
 Primary anxiety
disorder: treat with
benzodiazepines
 Associated with “off-
periods” or low-
levopoda levels:
adjust levopoda
dosing
 Restless Leg
Syndrome:

36. SLEEP DISORDERS
 Insomnia
 careful history
 difficulty with sleep initiation
 treat depression
 REM-behavioral disorder: clonazepam
 Excessive daytime sleepiness
 correct poor sleep at night
 discontinue anticholinergics, amantadine
 reduce dopamine agonist, levopoda dosages if possible

37. ORTHOSTATIC HYPOTENSION
 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

38. URINARY INCONTINENCE/FREQUENCY
 Rule out urinary tract infection
 Bladder evaluation
 Urinary frequency

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

42. PROBLEMS THAT MAY RESPOND TO
NONPHARMACOLOGICAL APPROACHES
 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

43. REHABILITATION IMPAIRMENTS
Gait disturbance
 Decreased stride length,
cadence, velocity.
Festination
 Stooped flexed posture
 Cautious gait(fear of
falling)
 Impaired balance

44. REHABILITATION MANAGEMENT
Rehabilitation &
interventions are
directed at the main
causes of
impairments.
Multidisciplinary
approach:PT,OT,ST,RT,
Neuropsych

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?