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Parkinson’s Disease
Historical Perspective
First described by British
doctor James Parkinson
Identified its major
symptoms and called it
“the shaking palsy”
Research progressed
slowly until the 1960’s
60’s linked the disease to
the loss of cells that
produce dopamine
Initial Symptoms
First signs can be
mistaken for another
condition.
Can be considered by
the patient as a
normal part of the
aging process.
Persistent mild fatigue
Handwriting might
become “shaky”
Person might feel
unbalanced or have
difficulty performing
sit-to-stands
Agitation, irritability,
& depression
Lack of affect
(masked face
phenom)
Initial symptoms can
go on for years
Movement Disorders
Hand tremors
Muscles associated
with movement all
Typically involves a
have opposing
rhythmic back-andmuscles - when one is
forth motion of the
activated, the other is
thumb at 3 bpm.
relaxed.
Most evident when
Brain’s signals in PD
the limb is at rest or
patients become
under stress
confused causing both
Patients report rigidity
sets
of
muscles
to
or resistance to
remain engaged and
movement
contracted.
Movement Disorders cont’d
Spontaneous
movements can
become progressively
slower and may
actually cease.
This is known as
bradykinesia
Impaired balance and
coordination (known
as postural instability)
Causes PD pt.’s to
lean unnaturally
backward or forward
Common to see
someone with head
down, stooped stance
Movement Disorders cont’d
Become vulnerable to
falls
Those who tend to
lean backward have to
step step backward
first before they begin
walking (known as
retropulsion)
Some develop a midstride halting which
creates a risk for falls.
Most common gait
characteristics are
short, quick steps.
Can appear as if they
are scrambling
forward to keep their
balance.
Secondary Symptoms
Depression
Emotional Changes
(Irritable, pessimistic,
fearful, become
dependent or isolated)
Memory Loss (slower
thought processes)
Swallowing
Difficulties
Speech Problems
Bladder/Bowel Prob’s
Excessive sweating
Sleep Disturbance
Causes
Basal Ganglia and
Dopamine is
Substantia Nigra cell
responsible for the
death or dysfunction
transmission of
signals associated
These neurons
with smooth,
produce the
controlled, muscular
neurotransmitter
activity from the
(neuro-chemical)
substantia nigra to the
dopamine
corpus striatum
Causes cont’d
PD “occurs” when
these neurons die or
fail to function
properly.
Without enough
dopamine, neurons in
the corpus striatum do
not function in the
usual coordinated
manner.
The result is an
inability to direct or
control the body’s
movements normally.
Typical PD pt. has an
80% reduction of
dopamine producing
cells.
Theories about cell death
Nerve cells are
Damage is normally
damaged by free
controlled by other
radicals - unstable
chemicals called
molecules generated
antioxidants.
by normal chemical
Not understood yet
reactions.
what mechanistic
Free radicals lack one
event prevents this
electron and attempt
“checks and balances”
to replace it by
reacting with nearby
procedure to take
molecules in a process
place.
called oxidation.
Theories about cell death cont’d
Toxins destroy
Genetic factors
dopamine producing
1/5th of PD pt.s have
neurons.
at least 1 relative with
Exposure to pesticides
parkinsonian
or a toxic substance in
symptoms
the food supply.
Investigating the
Not proven
theory that the roots
conclusively.
of PD are in a facet of
DNA.
Incidence
500,000 Americans
have the diagnosis of
PD
50,000 new cases
each year (in the U.S.
alone)
Numbers are higher
because of dismissal
of symptoms or
misdiagnosis.
Not gender-specific
Avg. age of onset is
60 yrs. Old
Estimated that 5-10%
of pt.s experience
symptoms before the
age of 40.
Diagnosis
Neuropsychological
tests
CAT (computerized
tomography)
MRI (magnetic
resonance)
These are used to rule
out other diagnosis
Side effects of
medications
Multiple Strokes
Progressive
Supranuclear Palsy
Shy-Drager
Syndrome
Wilsons Disease
Treatment
Cure does not exist
Tx is usually
comprised of
medications and
therapies that relieve
symptoms.
Levodopa (Sinemet)
First used in the
1960’s
Delays the onset of
symptoms for 75% of
PD pt.s
Used to make
dopamine, which
itself cannot be
injected into the body
because it cannot pass
the blood-brain
barrier.
Treatment cont’d
When Levodopa is
combined with
Carbidopa, L-dopa
holds back the
conversion of
levodopa into
dopamine until it
reaches the brain.
Effective in treating
bradykinesia and
rigidity
Less effective in
reducing tremor
Often ineffective in
relieving problems
related to balance.
Levodopa Side Effects
Nausea
Vomiting
Low Blood Pressure
Restlessness
Twitching, nodding,
jerking (large doses)
Lower dosage limits
the side effects but
symptoms then
reoccur.
Long-term use
diminishes
effectiveness
Taking frequently but
in smaller amounts is
an occasionally
effective solution.
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