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Dr A.A.

Ayu Meidiary, SpS


Department of Neurology,
Sanglah General Hospital ,
Udayana University Denpasar
Movement disorder is neurologic
syndromes (hypokinetic disorder or
hyperkinetic disorder), not associated to
weakness (paresis) or spastisitas.

Hypokinetic disorder are characterized by


impairment voluntary movement ;
- Slowly movement ( bradikinesia )
- No movement ( akinesia)
Parkinsonism is an example.
Hyperkinetic disorder are characterized by
involuntary movement present as a variety of
clinical syndromes including chorea, athetosis,
ballismus, dystonia, tremor, tics and myoclonus.
The mayority of movement disorder result
from diseases that affect the basal Ganglia.
The component of basal ganglia
Circuit of basal ganglia
Neurotransmitter

The smallest part of movement disorder


result from diseases that affect
extrapiramidal system other than Basal
ganglia.
Parkinson syndromes/Parkinsonism are
characterized by resting tremor, cogwheel
rigidity, bradikinesia and postural instability due
to reduce of dopamin level with various
aetiologies.

Parkinsons disease/Idiopathic Parkinsonism


The part of Parkinsonism whose pathologically
characterized by degeneration of pigmented
neuromelanin cells in the pars compacta region of the
substansia nigra and Lewy bodies in the pigmented
brainstem neuron .
I.Idiopathic Parkinsonism
1. Parkinson s disease
2. Juvenile Parkinson s disease
II.Symptomatic Parkinsonism
1. Infectious and post infectious
Post encephalitic ( encephalitic lethargica)
Other encephalitides
2. Toxins: MPTP, CO, Mn, Mg, Etanol, cyanide.
3. Drug-Induced Parkinsonism;
neuroleptic/antipsycotic, tetrabenazine,
reserpine, phenothiazines, alfa-metil-dopa ,
lithium, flunarizin, sinarisin.

4. Vascular (atherosclerotic,Binswangers)
5. Cerebral trauma
6. etc
III. Parkinsonism Plus (Multiple system
degeneration)
1. Progresive Supra Nuclear Palsy
2. Multiple System Atrophy; striatonigral
degeneration, Shy-Drager Syndrome,
Olivopontocerebellar Degeneration,
Parkinsonism Amyotrophy Syndrome.
3. Corticobasal ganglionic degeneration.
4. Demensia syndromes; Parkinsonism-demensia
ALS (Guam) complexs, Diffuse Lewy bodies
disease, Jacob Creutzfeldt disease, Alzheimer
disease.

5. Normal Pressure Hydrocephalus.


6. Hereditary disorder ; Wilson s disease,
Hellevorden-Spatz disease, Huntington disease.
The aetiology remains unknown.
Risk factor :

1. Increase with age. Infrequently in age < 30 years


old. Tipically, onset is between the of 55 and 60
years .
2. Race : caucasian >>> Asia & Africa
3. Genetics.
4. Environments ; Toxic :
MPTP , CO , Organophosphonates
Herbicide & pesticide
Infection.
5. Craniocerebral trauma
6. Emotional stress
Pathology: The changes concentrate on the
substansia nigra. The substansia nigra shows
aloss of at least 50% of the its melanin
containing cells, maximally in the pars
compacta. Alongside these changes is found
a characteristic cytoplasmic inclusion, the
Iewy body.
Degeneration of that cells cause the
decrease of dopamin level Parkinson s
disease
1. Neostriatum (Putamen & Caudate
nucleus)
2. Globus pallidus (GP)
Interna Globus pallidus (Gpi)
External Globus pallidus ( Gpe)
3. Substansia Nigra (SN) pars compacta &
reticulata.
4. SubthalamicNucleus (STN)
5. The ventro lateral (VL) nucleus of the
thalami
Dopamine (DA) : Neurotransmitter of
nigrostriatal pathway and striatinigral
pathway.
Glutamat (Glut) :

Excitatory neurotransmitter
Neurotransmitter project from cortex to
striatum, project from thalamus to cortex
and project from cortex to medula spinalis.
Neurotransmitter project from STN to GPE
and GPI.
GABA :
Inhibitory neurotransmitter
Neurotransmitter project from all basal ganglia
nucleus except STN
Acetylcholine (AK):
Neurotransmitter project from peduncule pontis
nucleus to striatum
1. Imbalance theory of direct pathway and indirect
pathway
2. Imbalance theory of dopaminergic-cholinergic
neuron
General :
Symtom begin on one side at onset.
Resting tremor
No the other deficit Neurologis
Laboratorium and radiology finding in normal
limit.
The progression of diseease is slowly.
Respond to levodopa tratment.
Tremor :
It is a rest tremor. It decrease or disappears
with movement. It disappears with sleep.
Frequency of tremor among 4 to 6 Hz
Typically tremor begins in one upper limb with
involvement of the corresponding lower limb
approximately 2 years later.
Occasionally, the disease produces tremor at
the jaw, lip, or tongue. Rarely it affects the head
or voice.
Rigidity : Cogwheel phenomenon
Bradykinesia
Facial impassivity produces a fixed expression
Infrequent blinking
Speech volume becomes reduced
Micrographia
A change in walking speed

Loss of postural reflexes


The posture becomes stoped and patient have increasing
difficulty in maintaining posture when pushess suddenly
either backward or forwards
1. Stage one:
Signs and symptoms on one side only
Symptoms mild
Symptoms inconvelent but not dissabling
Usually presents with tremor of one limb
Friends have nother changes in posture, Iocomotion and
facial expression
2. Stage two:
Symptoms are bilateral
Minimal dissability
Posture and gait affected
3. Stage three
Significant slowing of body movement
Early impairment of equilibrium on walking or
standing
Generalized dysfunction that is moderately severe
4. Stage four
Severe symptoms
Can still walk to a limited extent
Rigidity and bradykinesia
No longer able to live alone
Tremor may be less than earlier stages
5. Stage five
- Cachectic stage
- Invalidism complete
- Cannot stand or walk
- Requires constant nursing care
1. Possible : found one of cardinal clinical features
symptom.

2. Probable : Combination two of the cardinal clinical


features or one of the three first symptom whose
asymmetrically.

3. Definite : Combination three of the cardinal clinical


features or found two symptom whose one of them
asymmetrically
Hypokinesia :
- Secondary muscle atrofi/weaknes
- Joint contractur
- Deformity : kyphosis, scoliosis
Cognitive disturbances : aphasia , agnosia, etc
Autonomic disturbances : urinary incontinence,

constipation
Mood disturbances : depression
Adverse effect of drug
Essential tremor

Symptomatic Parkinsonism

Parkinsonism Plus
Indication : in order to role out other
disease

Head CT Scan , MRI , PET


General suport

Medication :
- Algorithm of Management
- Notice :
* Individualize medication regimen
* Responsiveness to treatment
* Adverse effect of drug
Surgery Unilateral Thalamotomy,
pallidotomy, Foetal substansia nigra
transplant , deep brain stimulation.

Medical Rehabilitaation :
- Physiotherapy
- Occupation therapy
- Speech therapy
- Psycotherapy
- Social therapy
Recent development in therapeutical strategies
increase quality of life and longevity in PD
patients.
Life expectancy still below normal
expectations due to complications such as
choking , pneumonia, and falls.
The progression of symptoms no way to

predict ; - may take over 20 years.


- in some people , however, the disease
progress more quickly.
Parkinsonism is a clinical syndromes, that is
characterized by varying degree of bradykinesia
, resting tremor, rigidity and postural instability,
because of reduction of striatal dopaminergic
transmission with multiple etiologies.
Parkinsonds (PD) is subdivision of parkinsonism.
The pathological hallmark of PD are
degeneration of the dopaminergic cells of the
substansia nigra pars compacta and lewy bodies
in pigmented brainstem neurons.
The pathophysiology of PD including
imbalance theory of direct-indirect pathway
and and imbalance theory of dopaminergic-
cholinergic neuron.
Four primary sign of PD are bradykinesia,

rigidity, resting tremor and postural instability.


The progression of PD are measure by Hoenh

and Yahr Staging of Parkinsonds


Diagnostic criterion (Hughes criterion) of PD
including possible PD, probable PD, and
definite PD.
Management of PD including general support,

medication, surgery, medical rehabilitation.


The course of PD are varied for an individual

person. The complications such as choking,


pneumonia and falls might occur that can lead
to significant comorbidity or death.
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In Simposium New Consept in The Managementof Parkinsons
disease. Jakarta. Hal 1 19
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Saraf.2003. Konsensus Tata laksana Penyakit Parkinson. Hal 8 33
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