Parkinson's Disease
Dr. Kleyn
Department of Geriatric Medicine
SVCMC
History

James Parkinson

1817, England

Shaking palsy

Paralysis agitans

“Involuntary tremulous motion, with
lessened muscular power, in parts not in
action and even when supported; with a
propensity to bend the trunk forward, and
to pass from a walking to a running pace,
the senses and intellects being uninjured.”
Introduction
Parkinson’s disease is a chronic
neurodegenerative movement disorder
affecting voluntary and emotional
movements and most commonly seen in
the elderly, but is also found in the young
and inexorably progresses leading to
significant disability.
Epidemiology
Primarily a disease of the elderly
 Mean age 55, Range 20 - 80 years
 Juvenile parkinsonism- Less than 20 years
 M/F = 3:2
 Prevalence increases with age

Aging and Parkinson’s disease
Exponential fall
Linear fall
Anatomy-Basal Ganglia
Internal
capsule
Putamen
Globus
pallidus
Caudate
Nucleus
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY

DA
SUBSTANTIA NIGRA
GLOBUS, PARS RETICULATA
A
C
H
GABA
STRIATUM
CAUDATE, PUTAMEN
Chemical Balance in Corpus Striatum

Excitatory
Cholinergic
pathway
BALANCE
 Inhibitory
Dopaminergic
pathway
Chemical Balance in Corpus Striatum
 Excitatory
Cholinergic
pathway
Imbalance
 Inhibitory
Dopaminergic
pathway
Parkinson’s disease - Pathophysiology
Pathology - Lewy Bodies

Eosinophilic
hyaline inclusion
bodies
 Spherical dense
hyaline core with
a clear halo
 Mechanism of
formation
unknown
Pathology
Lewy body dementia
Parkinson’s disease
Pathology-Parkinson’s disease
MIDBRAIN
Classification and Etiology
Idiopathic Parkinson’s disease
 Parkinson-like syndromes


Drug induced parkinsonism
 Hypoxia
 Tumor
 Trauma
 Vascular:Multiinfarct
 Toxin:Mn, CO, MPTP and cyanide
 Post-encephalitic parkinsonism (von Economo’s
encephalitis)
 Normal pressure hydrocephalus
 Wilson’s disease, Hutington’s disease
Classification and Etiology

Medications that can cause parkinsonian
symptoms, but not PD itself, include the following:
o
o
o
o

Metoclopramide
Domperidone
Reserpine-containing antihypertensives
Neuroleptics
Some evidence also indicates that certain
environmental factors (including smoking and
coffee drinking) may actually have protective
associations.
Clinical features of Idiopatic Parkinson’s
disease.
Major features
Minor features


Resting tremor in hands,
arms, legs, jaw, and face
 Bradykinesia
 Rigidity- cogwheel or
lead-pipe







Bradyphrenia
Speech abnormalities
Depression
Dysautonomia
Dystonia
Constipation
Hallucinations
Dysphagia
Parkinson’s disease Symptomatology
Parkinson’s disease -Symptomatology
Tremor dominant
Tremor:
 Rest
 Fixed frequency 3-6 Hz
 Not a feature of old age
 Pill-rolling
 Usually starts in one limb, and then to
other limbs
 Rarely starts in lower limbs
 Intermittent for many years
 They usually disappear briefly during
movement and do not occur during
sleep.
 Tremors can also eventually occur in the
head, lips, tongue, and feet. In younger
patients tremor is usually predominant
and often suggests a less aggressive
form of the disease.
Parkinson’s disease-Symptomatology
Rigidity
 Striatal hand: Ulnar deviation, MCP
flexion, IP extension
 Striatal
 Sitting
toe: Big toe dorsiflexion
en bloc: Collapses into a chair on
attempting to sit down
Parkinson’s disease-Symptomatology
Posture
 Kyphosis
 Flexed elbows, knees
and hips
 Hands held in front of
body
 Trunk bent forward
 Head bowed
Parkinson’s disease-Symptomatology
Bradykinesia

Slowness of motion (bradykinesia) is one of the classic
symptoms of Parkinson's disease.
Hypomimia- “masked facies”,expressionless face, blinking
 Speech abnormalities Hypophonia: soft voice
 Aprosody of speech: monotonous and lack of inflection
 Tachyphemia: do not separate syllables together, running
words together
 Patients may eventually develop a stooped posture and a slow,
shuffling walk. The gait can be erratic and unsteady.
Parkinson’s disease-Symptomatology
Motor fluctuations

Freezing phenomenon- Sudden, transient inability

to perform active movements, lasting no more than a
few seconds
Start hesitation
Turn hesitation
Target hesitation
Palilalia (speaking)
Apraxia of eyelid opening
Writing

Kinesia paradoxica-Despite severe rigidity and





bradykinesia, they may rise suddenly and move
normally
Parkinson’s disease-Symptomatology
“Today is a sunny day in Toronto"
Loop drawing:
Amplitude
Interloop distance
“Micrographia”
Parkinson’s disease-Symptomatology







Festinating gait
Drooling of saliva
Dysphagia
Constipation
Dementia
Depression
Orthostatic
hypotension

Low resting blood
pressure
HTN
Normotensive
 Sweating
abnormalitiesexcessive
perspiration
 Blepharospasm/
keratitis
Movement Disorders






Parkinson’s disease
Hutington’s disease
Multiple system atrophy
Motor neuron disease
Cortical basal ganglionic
degeneration
Patients with PD may develop
a stooped posture and a slow,
shuffling walk. The gait can be
erratic and unsteady.
Movement Disorders

“Off”phase
Movement Disorders

“On” phase
Diagnosis
There are currently no blood or laboratory tests that
have been proven to help in diagnosing PD. Therefore
the diagnosis is based on medical history and a
neurological examination. The disease can be difficult
to diagnose accurately.
Doctors may sometimes request imaging studies (i.e.
MRI’s or brain scans) or laboratory tests in order to
rule out other diseases.
Differential diagnosis of Parkinson’s diseases.
N e u ro lo g ic d is o rd e r
M u ltip le s y s te m a tro p h y
E s s e n tia l tre m o r
H u n tin g to n ’s d is e a s e s
T o x in -in d u c e d
p a rk in s o n is m
D ru g -in d u c e d
p a rk in s o n is m
C o rtic a l b a s a l g a n g lio n ic
d e g e n e ra tio n
F e a tu re s
P ro m in e n t d y s a u to n o m ia
C e re b e lla r d y s p h a n c tio n o r
p e rip h . n e u ro p a th y .
K in e tic tre m o r p lu s in s ta b ility .
F a m ily h is to ry .
Y o u n g e r p a tie n t,fa m ily H x ,
n o tre m o r.
E x p o s u re to C O , c y a n id e , M n ,
M P T P , m e th a n o l o r la c q u e r
th in e r.
A n tid o p a m in e rg ic e x p o s u re
B ila te ra l o n s e t. R e v e rs ib ility .
A lie n lim b ,d y s to n ia ,m y o c lo n u s ,
p a rie ta l s e n s o ry lo s s .
Parkinson’s disease - Management
Nonpharmacologic Management
S u pp o rt
P at ient
A ssess em oti o n al n eeds
P e e r su p p o rt
G ro u p su p p o rt(dise a se sta g e a pp ro p ria te
P ro fe ssio n al co u n se lling
L e g a l/fin a n cia l co u n se lling
O ccu p a tio n al co u n se lling
(e a rly d ise a se )
Fam ily
Nonpharmacologic Management
E x e rc is e
E d u c a tio n
A s s e s s e x e rc is e c a p ac ity a n d lim ita tio ns
T ra in in g
A e ro b i c
S tre n g h th e n in g
S tre tc h in g
N o n w e ig h t b e a rin g
R e g u la r,fo c u s s e d e x e rc ise
Nonpharmacologic Management
N u t r it io n
O b t a in d ie t a r y h is t o ry
E d u c a te a b o u t b a la n c e d d ie t
N u t r it io n a l c o u n s e llin g
Drugs for Parkinson’s disease
A m a n ta d in e
W e ll to le ra te d , p o s s ib le a n k le
e d e m a o r liv e d o re tic u la ris
A n tic h o lin e rg ic s
G o o d fo r tre m o r
A v o id in p a tie n ts a g e 6 5 a n d o ld e r
S id e e ffe c ts in c lu d e d ys k in e s ia ,
c h o re a , d y s to n ia
C o n tro v e rs ia l n e u ro p ro te c tiv e
a g e n t. M in im a l s ym p to m . b e n e fit
H e lp fu l w ith s u p e rim p o s e d
re s tle s s le g s sy n d ro m e
C a rb id o p a /L e v a d o p a
S e le g ilin e
B ro m o c rip tin e
S e le c tiv e C O M T
in h ib ito r
A d ju n c tiv e th e ra p y ; in c re a s e s
b io a v a ila b ility o f le v a d o p a ; s id e
e ffe c ts in c lu d e d ia rrh e a ,
d y s k in e s ia
The Management of Parkinson’s disease
P a rk in so n's d ise a se
N o n P h a rm a c o lo g ic
P h a rm ac o lo g ic
E d u c a tion
N e uro p ro te ction
? S e le g ilin e
S u pp o rt
F u n c tion a l im pa irm e nt
Yes
E x e rc ise
NO
? A n tic h olin e rg ics
N u trition
? A m a nta d ine
D o p a m in e A g o n ists
L e vod o pa
Dose
Dose
C o m b in e d the ra py
D o p a m ine a g o n ist
+
L e vod o pa
+ /C O M T in h ib itor
S u rg ic al th e rap y if un a c c e pta b le c o n trol
w ith m e d ic a l th e ra py
Surgical Therapy- Deep brain stimulation

When symptoms are
uncontrollable with
medical therapy
 None ablative method is
used
 Transpalntation of fetal
nigral cells
 Thalamotomy
Parkinson’s disease - Imaging
Predicted developments
Research into the causes of Parkinson’s diseases are
likely to show that multiple genetic and environmental
factors are involved
 Disease of early onset is more likely to be genetic
 New drugs acting on both dopaminergic and nondopaminergic transmitter systems will become available
over the next 10 years
 Clinical trials of new drugs with neuroprotective and
neurorescue properties are in progress

Research
At no time in the past have the basic and clinical
sciences applied to Parkinson’s disease been so
active.
Future progress in understanding the causation
and pathogenesis of the disorder will permit the
development of new treatments that will slow, halt,
or even reverse the currently progressive course
of Parkinson’s disease.