Gait disorder

(Parkinson)

DR. FERY LUVITA SARI

• Menjelaskan gangguan cara berjalan (gait disorder)
pd usila
• Menjelaskan berbagai penyebab gangguan cara
berjalan pada usila
• Patofisiologi Parkinson pd usila
• Diagnosis Parkinson pd usila
• Menjelaskan dan memberi tata laksana Parkinson pd
usila
• Komplikasi Parkinson pd usila
Help! I’ve Fallen and I Can’t Get Up!
3
 Epidemiologi
4

 Falls  penyebab tertinggi cedera (± 24 %)

 Lebih sering pada anak ˂ 5 tahun dan dewasa ≥ 65
tahun
 Merupakan 70 % penyebab kematian pada
kecelakaan ≥ 75 tahun
 Falls in Older Adults

 20% - 30% fear falling1

 35%-40% of people 65+ fall each year2
 Those who fall are 2-3 times more
likely to fall again3
 10%-20% of falls cause serious
injuries4

1. Vellas BJ, Age & Aging, 1997; Friedman SM, JAGS, 2002
2. Hornbrook, Gerontologist, 1994; Hausdorff, Arch Phys Med &
Rehab, 2001
3. Tinetti, New Eng J Med, 1988; Teno, JAGS,1990
4. Sterling, J Trauma-Inj Infection & Critical Care, 2001
 Fall Risk Factors in Older Adults

1. Chronic health
conditions
2. Physical and functional
impairments
3. Medication and
alcohol use
4. Environmental
hazards
 Etiology of falls

 Accidents / environment 37%

 Weakness, balance, gait 12%
 Drop attack 11%
 Dizziness or vertigo 8%
 Orthostatic hypotension 5%
 Acute illness, medications, vision 18%
 Unknown 8%

Rubenstein et al JAGS
1988
 Evaluasi: risiko Fall
8

A. Tes Get Up and Go

B. Pemeriksaan Kardiovaskular
C. Pemeriksaan Neurologis
1. Menilai koordinasi dan keseimbangan

2. Memeriksa kekuatan otot ekstremitas bawah

3. Memeriksa sensibilitas Proprioseptif dan getar

 Mechanisms of Fall
Contributing
Intrinsic : factors Extrinsic :
Aging, poor balance Home hazards

Occurrence of falls

No injuries
Fall Outcomes

Soft tissues Loss of Disability,

Fractures
injures, Confidence reduced
trauma quality of life
 Multiple
systems
atrophy

Progressive
PD supranuclear
palsy

Parkinsonism

Drug-induced Lewy body

parkinsonism dementia

Vascular
parkinsonism
 What Is Parkinson's
11 Disease?

 Parkinson's Disease is a clinical

syndrome caused by lesion in the
basal ganglia ,predominantly in
the substantia nigra ,that
produce deficits in motor
behavior.
 Who is Affected by
Parkinson’s Disease
12
Moh.Ali

Pop John Paul II

Michael Fox
Artis
 History
13

 In 1817 James Parkinson published a study on the “an

essay on the shaking palsy”
 In 1957 Carlsson observed similarities between
parkinsonian symptoms and the side effects of chronic
treatment with reserpine, a known monoamine depleting
drug (Yurek and Sladek 1990).
 In 1960 Ehringer and Hornykiewicz observed that
concentrations of striatal dopamine were depleted in
parkinsonian patients.
 Yurek and Sladek (1990) is "severe reduction of dopamine
in all compartments of the basal ganglia."
 14

 The disease is chronic (it persists over a long

period of time) and progressive (its
symptoms grow worse over time). It is not
contagious nor is it usually inherited-that is,
it does not pass directly from one family
member or generation to the next.
 Affects about 1 in every 250 people over 40 years old and
about 1 in every 100 people over 65 years old.
 It is slightly more common in men than in women.
 Medication can treat its symptoms, and the disorder is
not directly life-threatening.
 Mostly it is a quality of life issue.
 About half of all patients treated with drugs have no
major disabilities 10 years after the onset of the disease.

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 CAUSES OF PARKINSONISM
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 An adverse reaction to prescription drugs

 Use of illegal drugs
 Exposure to environmental toxins
 Stroke
 Thyroid and parathyroid disorders
 Repeated head trauma (for example, the trauma associated with
boxing)
 Brain tumor
 An excess of fluid around the brain (called hydrocephalus)
 Brain inflammation (encephalitis) resulting from infection
 19

 external or an internal

toxin selectively destroys

dopaminergic neurons.

 An environmental risk factor

(exposure to pesticides or a
toxin in the food supply)
 20

 Researchers believe that genetics sometimes plays a

role in the cellular breakdown. Fifteen to twenty
percent of Parkinson's patients have a close relative
who has experienced parkinsonian symptoms (such
as a tremor).
 In rare instances, Parkinson's disease may be
caused by a viral infection.
 Many researchers believe that a
combination of oxidative damage,
environmental toxins, genetic
predisposition, and accelerated aging may
ultimately be shown to cause the disease.

21
 CAUSES
22
 The exact cause of the disease
remains a mystery.
 In Parkinson's, cells that produce
dopamine begin to degenerate.
Insufficient dopamine disturbs the
balance between dopamine and
other transmitters, such as
acetylcholine
 Dopamine is a chemical messenger
responsible for transmitting signals
between the substantia nigra and
the next "relay station" of the brain,
the corpus striatum, to produce
smooth, purposeful muscle activity.
 CAUSES
23

 Loss of dopamine causes the nerve

cells of the striatum to fire out of
control, leaving patients unable to
direct or control their movements
in a normal manner.
 Studies have shown that
Parkinson's patients have a loss of
80 percent or more of dopamine-
producing cells in the substantia
nigra.
 Clinical features

slowness of movement
Bradykinesia

Stiffness or resistance of the

limb to passive movement when
the limb is relaxed
Neck, extremity
Cogwheel

Poor balance Postural

instability PD Rigidity

Shaking back and forth when the

Resting limb is relaxed
Tremor 4-6 Hz, intermitten
 Clinical features
In 3 out of 4 patients, the
tremor may affect only 1 part the tremor takes the form of a
of the body, especially during rhythmic back-and-forth
the early stages, ater it may Pill-rolling at motion of the thumb and
become more general rest forefinger at 3 beats per
second

usually begins in
a hand, although
usually disappears
during sleep or Diminished: Resting Arms/legs/
feet
sometimes a foot
or the jaw is
improves with -On action
intentional movement Tremor /jaw/tongue affected first

Present:
It is most obvious when the
hand is at rest or when a person
-At rest
is under stress -When
distracted
 Clinical features
Cogwheel
rigidity
(upper
limbs)

Increased tone
Flexed when opposite
posture Rigidity arm moves
actively

Lead pipe
rigidity
(legs)
 Clinical features
Activities once performed quickly and
easily, such as washing or dressing, may
Difficulty take several hours
initiating
movement

Poor rapid
Reduced
fine
spontaneous Bradykinesia
blinking movements
(fingers)

Facial
the slowing down and loss of immobility
spontaneous and automatic
(hypomimia)
movement
 Clinical features
can cause patients to have a stopped
Loss of posture in which the head is bowed
and the shoulders are drooped
postural
reflexes

Postural
instabili
ty
impaired balance
and coordination Difficulty
Retropulsio
making n
turns
 Changes in facial expression
30

 Reduced ability to show

facial expressions "mask"
appearance to face
 Staring
 May be unable to close
mouth
 Reduced rate of blinking
 Additional symptoms that may be
associated with this disease:
32

 Depression
 Confusion
 Dementia
 Seborrhea (skin)
 Muscle function/feeling loss
 Muscle atrophy
 Memory loss
 Drooling
 Anxiety, stress, and tension
 STAGING OF PD
Hoehn and Yahr
33

 1. Stage One
 Signs and symptoms on one side only Symptoms mild
 Symptoms inconvenient but not disabling
 Usually presents with tremor of one limb
 Friends have noticed changes in posture, locomotion and facial
expression
 STAGING OF PD
Hoehn and Yahr
34

 2. Stage Two
 Symptoms are bilateral

 Minimal disability

 Posture and gait affected

 STAGING OF PD
Hoehn and Yahr
35

 3. Stage Three
 Significant slowing of body movements
 Early impairment of equilibrium on walking or standing
 Generalized dysfunction that is moderately severe
 STAGING OF PD
Hoehn and Yahr
36

 4. Stage Four
 Severe symptoms

 Can still walk to a limited extent

 Rigidity and bradykinesia

 No longer able to stand alone

 Tremor may be less than earlier stages

 STAGING OF PD
Hoehn and Yahr
37

 5. Stage Five
Cachectic stage

Invalidism complete

Cannot stand or walk

Requires constant nursing care

 DIAGNOSIS
38

 There are no blood tests or X-rays that will confirm the

diagnosis.
 The diagnosis is made on finding 2 of the 3 cardinal
features of the disorder on neurologic exam and ruling
out other possible causes including several conditions
that can mimic Parkinson's Disease but often have
additional features (Parkinson's "Plus").
40
 Pharmacological Treatments for Parkinson’s
Disease
41
Pharmacological Example of Rationale Drawbacks (side effects)
Approach drug used

Increase the L- dopa Since there is a loss of dopaminergic neurons, After about 4 yrs most pts experience a
dopamine (Levodopa) replace the dopamine "wearing Off" phenomenon, they loose
sensitivity to the drug, may develop episodes
of immobility, alternating with episodes of
normal or involiuntary movements

Give drugs that act Bromocriptine Since there is a loss of dopaminergic neurons, These drugs are expensive, may cause
like dopamine (Parlodel) replace with drugs that act like dopamine confusion, diziness on standing, involuntary
(dopamine motion
agonists)

Decrease Artane, Parkinsonism is caused by excess stimulation of Side effects can be blurred vision, memory
acetylcholine by Cogentin extrapyramidal motor system due to imbalnce impairment
giving between dopamine and acetycholine (less
anticholinergic dopamine, greater effect of acetycholine which is
grugs excitatory). Therefore, restore balance by ecreasing
acetycholine to levels that match the decreased
dopamine

Increase the effect Selegiline Dopamine is normally broken down by the enzyme Side effects are onsomnia
of remaining (deprenyl) monamime oxidase B. If you inhibit this enzyme,
dopamine by then dopamine is not broken down as quickly, it
blocking its reamins longer in the tissue exerting its effect. In a
breakdown sense, this is physiologically equivalent to
increasing the amount of dopamine
 Surgical Therapy
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 Resurgence of stereotactic surgery with better

imaging and equipment
 Lesioning vs. long-term electrical stimulation with
implanted deep brain electrodes (DBS)
 Stereotactic Surgery
48

 Thalamotomy and thalamic DBS: only improvement of

tremor
 Pallidotomy and pallidal stimulation: main effect on
dyskinesias, but mild improvement of parkinsonism
 Subthalamic stimulation (or lesions): all features, but
technically more difficult and greater risk of bleeding
 Transplantation (fetal, genetically engineered cells,
xenografts): still experimental
 JANGAN TERBURU-BURU
49

 Sabda Rasulullah SAW :

 "Bertenang-tenang itu dari Allah dan tergopoh-
gopoh itu dari syaitan." Riwayat Baihaqi

FALL PADA LANSIA 04/03/2011

Terima Kasih