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Disease?
Described by James Parkinson in 1817
as Shaking palsy & Paralysis agitans.
Parkinsons disease is a progressive
(TRAP)
Etiology
Parkinsons disease(primary parkinsonism) is
idiopathic.
Secondary parkinsonism results from a number of
different causes such as Postinfectious,
pharmacological, Metabolic and parkinson-plus
syndromes.
Genetic link in a small number of Parkinson cases.
Larger genetic link is found in young-onset
Parkinson disease.
Research has shown a link between PD and
growing up in a rural areamay be due to
pesticides, insecticide use, and/or well water.
Pathophysiology
Parkinson disease is associated with
degeneration of dopaminergic neurons in the
Substantia Nigra (SNpc).
Depletion of Dopamine leads to motor
disturbance such as:
Reduction in initiating movts.(Patient wants
to move but cannot), Tremor and Rigidity due
to loss of inhibitory influences within the BG.
When 80% of dopaminergic neurons are
degenerated, the signs of disease become
clinically evident.
Pathophysiology
Onset is 60 yrs.
5-10% of cases occur under the age of
females.
Clinical Manifestations
o Fundamental Features
Rigidity.
Akinesia and Bradykinesia.
Tremor.
Postural Instability.
Clinical Manifestations
o Secondary Impairments or complications
Poverty of Movements.
Fatigue.
Masked Face.
Gait disturbance.
Swallowing and Communication Dysfunction.
Cognitive and Behavioral Dysfunction.
Autonomic Dysfunction.
Cardiopulmonary Dysfunction.
Visual and Sensorimotor Disturbance.
Musculoskeletal Changes.
Clinical Manifestations
o RIGIDITY
An increase in muscle tone leading to a
Control.
Bradykinesia: Slowness and difficulty maintaining
movts.
Hpokinesia: reduction in the speed, range, and
amplitude of movements.
Results in difficulty of Motor planning, performing
movements.
Automatic movements are impaired e.g. loss of reciprocal
Smiling on command.
Clinical Manifestations
o GAIT DISTURBANCE
Gait pattern: decrease stride length, loss of
reciprocal arm swing , loss of normal heel-
toe progression, lengthened stance phase
and double support and shortened single-
limb support.
Festinating gait: Small shuffling steps with
progressive increase in speed.
Propulsive and Retropulsive gait.
Taking multiple small steps to turn or
change direction.
Clinical Manifestations
o MUSCULOSKELETAL CHANGES
Contractures of contractile and non-
contractile tissues.
Contractures of hip and knee flexors, hip
rotators and adductors, plantarflexors,
dorsal spine and neck flexor,
shoulder adductors and internal
rotator and elbow flexors.
Kyphosis and Scoliosis.
Osteoporosis.
Clinical Manifestations
o Swallowing and communication
Dysphagia: Due to rigidity, reduced
mobility and restricted ROM. (Oral,
Pharyngeal and esophageal phases of
swallowing are affected)
Dysarthria: Decrease voice volume,
monotone and monopitch speech,
distorted articulation and uncontrolled
speech rate.
Mutism: Whispering in advanced cases.
Clinical Manifestations
o Behavioral Dysfunction
Dementia: (Approx. 1/3 of PD patients)
Memory impairment, loss of thinking,
reasoning and judgment.
Bradyphrenia: Slowness of thought
processes with lack of concentration and
attention.
Depression: (25-40%) Apathy, passivity,
loss of ambition or enthusiasm, change in
appetite, lack of sleep and dependency.
Clinical Manifestations
o Autonomic Disorder
Urinary frequency, urgency and
nocturia.
Reproductive Disorder: Impotence
GIT Disturbance: Decrease digestion
and constipation.
Excessive perspiration.
Thermoregulatory abnormalities.
Greasy skin
Clinical Manifestations
o Cardiopulmonary Dysfunction
Orthostatic hypotension (may cause
movements.
Paresthesias (numbness and tingling)
Not a cure
0 No signs of disease
1 Unilateral disease
1.5 Unilateral disease with axial involvement
2 Bilateral disease without postural instability
2.5 Early signs of postural instability (recovery on
the pull test)
3 Bilateral disease with postural instability,
physically independent
4 Severe disability, but still able to stand or walk
unassisted
5 Confinement to wheelchair or bed
Assessment
oSCHWAB AND ENGLAND ACTIVITIES OF DAILY LIVING (ADL)
100% - completely independent. Able to do all activities without slowness,
difficulty, or impairment
90% - completely independent. Able to do all activities with some slowness,
four times as long for some. May take large part of day for chores
60% - some dependency. Can do most activities, but very slowly and with
everything
40% - very dependent. Can assist with all chores but few alone
30% - with effort, now and then does a few chores alone or begins alone.
Modified bathroom
Full bathroom and bedroom on first floor
Lift chair
physically tiring.
Introduce techniques for enhancing
voice volume.
Treatment
ADLs
Patients generally wake in an off state.
waking.
Wait until meds take effect before engaging in
challenging ADLs.
Home modifications
Shower seat
Rugs/carpet/furniture
Clothing considerations
Treatment
Leisure
Spectator sports
Deep breathing & relaxation sessions (at home
or in community)
Activities which are not physically demanding
Explore ways to adapt activities enjoyed prior to
disease onset.
Education
Allow extra time for school work
Decrease class load
Handwriting adaptive devices
Aide for typing/note-taking
Treatment
Keep journal of symptoms
Educate patient and family/care partner on
management
Assistance with health care management
Discuss options for care of children/pets
Work
Educate & inform co-workers
Explore work-at-home options
Adapt job requirements as disease progresses