6

MOVEMENT
DISORDER
Basjiruddin Ahmad
Department of Neurology
Andalas University
Padang

MOVEMENT DISORDER
GENERAL OVERVIEW

A. HYPERKINESIA
TREMOR
Chorea
Dystonia
Athetosis
Tics
B. HYPOKINESIA
Parkinsonism
Spasticity
Drop attack

A. HYPERKINESIA

TREMOR : rhytmical involuntary oscilations

(mengayun) around a fixed point occur at rest
outstretching (postural), during anxiety,
caffeine, drugs
On action (intention) :
Cerebral

dysfunction
Drugs (phenitoin)
Stroke
Trauma

TREMOR

Essential tremor : retlatively

benign,
embarrasing disorder, familial, sporadic forms,
aggravated (diperburuk) by stress,excitement

Dystonic tremor :
involuntary torsion
movement, affected muscle group, movement
ussually slow

Resting tremor (Parkinsonism)

Exaggerated (lebay) physiologic tremor : Small

amplitude, high frequency

 ESSENTIAL TREMOR

Upper extremity tremor with posture and/or

action

Bilateral, usually roughly symmetric

Tremor may produce disability

No clear association with other diseases or

disorders

 ESSENTIAL

TREMOR

contd.

TREATMENT

Primodone

Propanolol 10-20 mg/day and other Beta

blockers

Tremors of some patients are quite

responsive to alcohol, and patients may selfmedicate

A. HYPERKINESIA

Tremor

CHOREA

Dystonia

Athetosis

Tics

CHOREA

Excessive spontaneous movements , rapid,

arrhytmic movements of muscle group
The movement are often incorporated into
deliberate (sengaja/tenang) movements by the
patient to camouflage their disorder
Irreguler, brief (singkat), and aburpt non
stereotype (non repetitive)
Distal predominance
Facial grimacing (menyeringai)

CHOREA

contd.

CAUSES :

Medications
Haldol,

other antipsychotics
Reglan is an important cause of tardive dyskinesia
(iatrogen otot wjah, leher, antipsiko lama, bisa
permanen)

Huntingtons disease

Hemibalism (diskinesia brat 1 sisi tbuh utama

extrmtas atas)

Post-infection

CHOREA
1. Chorea sydenham
2. Huntington disease
1. Chorea sydenham
Acute movement
Paroxismal
Uncoordinated movement
Involuntary
Emotional disturbances
Diminish while sleeping and increase by stress
5-15 th/slm hamil, kaitan demam reumatik, bs
ngenai sluruh aktvts mtorik

CHOREA

contd.

2. Huntington disease : is a neurodegenerative disease

charactized by progresive choreoathetosis,
psychological changes (mental)
Pengulangan triplet autosom dom, progres kronik
Clinical appearance
Choreatic
Cognitive dysfunction
Gait (berjalan) disorder (dan keseimbangan krn lesi
frontalis)
Clumsiness (kecanggungan)
Speech disorder
Bladder and bowel incontinence
Sexual dysfunction

CHOREA contd.

TREATMENT

Valproic acid : 15-20 mg/kg/days

Carbamazepine : 10-15 mg/kg/days

Corticosteroid

Dopaminergic blocker :
Halloperidol : 3 -40 mg/days
Primazole

A. HYPERKINESIA
Tremor
Chorea

DYSTONIA
Athetosis
Tics

DYSTONIA

Dystonia is a slow, purpose, involuntary movements

affecting muscle groups of face, limb, trunk
Agonist and antagonist
Clinical findings :
Repetitive

twisting (bongkok) and squeezing (menekan)

movements
Fixed posture

Caused :
Idiopathic (most cases)
Drug related :
Antipsychotics

and Reglan

A. HYPERKINESIA
Tremor
Chorea
Dystonia

ATHETOSIS
Tics

ATHETOSIS (memelintir, berkelok tngan)

A movement charactherized by slow, writhing

(menggeliat) of groups of muscle
More pronounce in the distal extremities
Associated with weakness and rigidity
Aggravated by stress
Disappears during sleep
Athetosis is slower than chorea and may
occur together

A. HYPERKINESIA
Tremor
Chorea
Dystonia
Athetosis

TICS

TICS

Definition : brief, sudden, irresistible,

inapposite (tdk tpat), reccurent movement
These movements are either isolated or
represent an act for a particular purpose
For a time tics can be suppresed or inhibited
Patients often feel actively in performing a
tic
Tics can be tiggered by environmental
stimuli, exciting events or life event

B. HYPOKINESIA

PARKINSON
Spasticity
Drop attack

PARKINSONS DISEASE

Parkinsons disease is a chronic

neurodegenerative disease associated with
substantial morbidity, increased mortality,
and high economic burden (beban)

Parkinsons results from the degeneration of

dopamine-producing nerve cells in the brain,
specifically in the substantia nigra.

PARKINSON DISEASE

contd.

EPIDEMIOLOGY

The most common movement disorder affecting 1

2 % of the general population over the age of 65
years.

Prevalence rate in men are slightly higher than in

women

Age onset usually between 50-70 years

Rarely in people less than 30 years old

Incidence is 20 every 100.000 population

PARKINSON DISEASE

contd....

RISK FACTORS

Age - the most important risk factor

Positive family history
Male gender
Environmental exposure: Herbicide and
pesticide exposure, metals (manganese,
iron), well water (sumur bnyk mineral) ,
farming, rural residence, wood pulp mills
(pabrik/gilingan); and steel alloy industries
Race
Life experiences (trauma, emotional
stress, personality traits such as shyness
and depressiveness)?
An inverse correlation between cigarette
smoking and caffeine intake in case-

PATHOPHYSIOLOGY

The etiology of parkinson disease is not yet clear

Its widely believed that genetic and enviromental factor

induce neuronal death

The most common pathological feature is degeneration of

dopaminergic neurons in pars compacta of substansia
nigra

The lost of dopaminergic neuron decreased activity of

thalamus,thus reducing excitatory input to motor cortex
and initiate involuntary movement

The presence of lewy bodies is another classic

pathological finding in parkinson disease

CLINICAL FEATURES

Four cardinal symptoms:

Resting tremor
Bradykinesia (generalized
slowness of movements)
Muscle rigidity
Postural instability

CLINICAL FEATURES

Resting tremor: most common first symptom, usually

asymmetric and most evident in one hand with the arm
at rest.
Shaking or trembling (gigil) in the hand, arm, leg, face,
and it spreads, sometimes affecting only one side of the
body.

contd.

Worsen when the muscles are relaxed or individual is stressed

Dissapears during sleep or during intentionally moved

Bradykinesia: spontaneus and automatic movement are

lost and all movement becomes extremely slow. Diffiulty
with daily activities such as writing, shaving, using a
knife and fork and opening buttons
Decreased blinking, masked facies, slowed chewing and
swallowing.

CLINICAL FEATURES

contd....

Rigidity: muscle tone increased in both flexor and

extensor muscles providing a constant resistance to
passive movements of the joints
Stooped posture, anteroflexed head, and flexed
knees and elbows.

Postural instability: due to loss of postural

reflexes. balance and coordination become
impaired.
Patients tend to lean forward or backward, and to
develop a stooped posture. Walking with quick and
small steps.

ADDITIONAL CLINICAL FEATURES

Dysfunction of the autonomic nervous system:

impaired gastrointestinal motility, bladder dysfunction,
excessive head and neck sweating, and orthostatic
hypotension.

Depression: mild to moderate depression in 50% of

patients.

Cognitive impairment: mild cognitive decline including

impaired visual-spatial perception and attention
Slowness in execution of motor tasks
At least 1/3 become demented during the course of the
disease.

OTHER SYMPTOMS

Difficulty swallowing or chewing

Urinary problems
Constipation
Irregular sleep
Short breathing

NON-MOTOR FEATURES OF PD :

Include :
mental

health problems
depression
psychotic symptoms
dementia
sleep disturbance
falls
autonomic disturbance

PARKINSON DISEASE

contd.

DIAGNOSIS

No specific test or marker for PD

Diagnosis is made on clinical ground

Depends on the presence of at least two of the

three major signs : tremor at rest, rigidity,
and bradykinesia.

Bradykinesia is tested by determining how

quickly the person can tap the finger and
thumb together.

Clinical criteria for diagnosis (by Hughes)

Possible

Alt least one of TRAP symptoms (tremor, rigiditas,

akinesia, postur tak stabil)

Probable

Combining 2 major symptoms (including postural

instability) or 1 of 3 asymetrical cardinal signs

Definite

Combining 3 of 4 major symptoms or 2 symptoms with

another asymetrical symptom (3 cardinal signs)

TREATMENT

The goal of therapy is to reverse functional

disability, abolition of all symtoms and signs is
not currently possible even with high dose of
medication

Treatment highly individualized

no universal first choice drug therapy

choice of adjuvant drug should take into account

clinical and lifestyle characteristics

patient preference

TREATMENT contd.

1.

Supporting treatment

Explanation to the patient, giving support,

and and occupational counseling

education for the patient, in order obtain

general picture of the disease

Emotional support and professsional

counseling

Training in accordance with their physical

condicions

TREATMENT contd.
2.

Medication
.

Anticholinergic : benztropine mesylate 1-8 mg/day

thyhexyphenidil 3 -6 mg/ day

NMDA antagonist : amantadine (symetrel) 100-300mg/day

Dopaminergic : carbidopa+levodopa 10/100mg, 25/100mg,

25/250 mg

Dopamine agonist : bromocryptine 5-40mg/day

pramipexole 1,5-4,5 mg/day
ropinirole 0,75-2,4mg/day

COMT inhibitors : entacapone 200 mg/day

MAO-B inhibitors : selegiline 5 mg/day

TREATMENT contd.

2.

Operative treatment
. Deep

2.

brain Stimulation

Rehabilitation treatment: physic, occupation, speech,

psychotherapy

SUGGESTED ACTIONS

make sure there are enough

physiotherapists
occupational

therapists
speech and language therapists

PD patients should have regular access to

monitoring and alteration of medication

a continuing point of contact
a reliable source of information

COMPLICATION OF PARKINSON DISEASE

Complication of long-term levodopa therapy
Dyskinesia
Freezing
Falls
Response fluctuations
Behavioral / psychiatric disorder
Dementia
Depression
Psycoses

REFERENCE
1.

Waters CH. Diagnosis and maanagement of Parkinsons disease, second edition.

Caddo, Professional Communications nc; 1999: 31-71.

2.

Basjiruddin A. Management of lates Parkinsons disease. In: Sjahrir H, dkk (eds).

Parkinsons disease and other movement disordres. Medan; 2007: 124-43.

3.

Wolters EC, Bosboom JLW. Parkinsons disease. In: Wolters et al (eds).

Parkinsonism and related disorders. Amsterdam, VU University Press; 2007:143155.

4.

Parkinsons: Clinical features and differential diagnosis. Fahn S, Jankovic J.

Principles and practice of movement disorders. Philadelphia, Churchill Livingstone
Elsevier; 2007: 79-96.

5.

Benazzouz A. Parkinsons disease and implication of basal ganglia in its

pathoophysiology. Egypt, June 2009.

6.

NHS National Institu for Health and Clinical Excellence. Parkinsons disease.June,
2006

7.

Jakala P. Parkinsons disease, finland, 2008

THANK YOU