Kstrapiramidal Syndrome: Pembimbing: Dr. Sigit Hari Nursjamsu, Sp. S Dr. Intan Nurswida, Sp. S Dr. Nella Lusti W., Sp. S

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EKSTRAPIRAMIDAL

SYNDROME

Pembimbing :
dr. Sigit Hari Nursjamsu, Sp. S
dr. Intan Nurswida, Sp. S
dr. Nella Lusti W., Sp. S

Oleh:
Amira Tauhida
201720401011107
Definition

Extrapiramidal syndrome is a reaction of antipsikotik therapy


tipical group

Inhibition of transmision dopaminergic in ganglia basalis


Disruption transmision in korpus striatum
Epidemiology
Extrapiramidal Syndrome

Acute Dystonia Around 10% patient

Akhatisia

Tardive dyskinesia Around 20-30% patient

Sindrom female:male = 2:1


parkinsonisme
Etiology
Pathofisiology
• Extrapiramidal component  korpus striatum, globus palidus,
talamik nucleus, nukleus subtalamikus, subtansia nigra, formatio
retikularis brain steam, serebelum and korteks motorik addition
area 4, area 6 dan area 8

• The component connect by akson

• Compose line circle (striatal sirkuit)


• Data from neokorteks give to korpus striatum / globus plaidus
/ thalamus

• The data processed

• Feedback to motorik korteks


Clinical Evaluation
• Acute dystonic reaction
• Parkinsonism
• Akathisia
• Tardive Dyskinesia
Acute Dystonic Reaction
• Dystonic - movement dissorder cause elongated muscle
contraction, twisting, abnormal posture of body, neck, face,
extremitas
• Misdiagnose: cerebral palsy
Drug-induced dystonia:

• levodopa,

• agonis dopamin,

• obat antipsikotik,

• antikonvulsan,

• SSRI
Parkinsonism
• Rigiditas  increase muscle tone, passive movement when

rest

As the result of excessive activity motor descenden from

brainsteam

• Type 1: agonis muscle and antagonis muscle together 

increase resistance of pasive movement  ‘lead-pipe’

• Type 2: resistance on interval regule  ‘cogwheel rigidity’


• Bradikinesia  absence of motorik volunteer activity :

(1) Decrease of motorik activity basic

(2) Slow movement so difficulity to begin

(3) Weaknesss of amplitudo movement repetitif

(4) Disturbance movement continued


• Tremor  ritmic movement (4-8 movement/secong)  distal
extremity

• Upper extremity move first than lower ekstremity

• Tremor on Parkinson suppressed with inisiasi volunter


movement

• many patient become tremor intensional


Akathisia
• Subjective  patient complain because can not rest, sleep
disturbance, consentration disturbance

• The symptomp description restless  doctor give antipsikotik

• objektive  restlessness  marching, shuffling


Tardive
Dyskinesia
• Face and tongue  chew movement, face expresion not
natural, dan fast movement extremity , like convulsion, dan
choreiform (dance)
• Upregulation of D2 receptor  hypothesis pathophysiology
Therapy Acute Dystonic
Levodopa-carbidopa
Trihexyphenidyl
(1 tab 25/100mg
(6-80 mg/day )
3x1)

Benztropine
(4-8 mg/day)
Therapy Acute Dystonic
Reduce muscle
spasme

Benztropine (IM)
atau Toxin botulinum
diphenhydramin serotype A & B
e

anti-parkinsonisme drug
Improvement during 20-30
minute
Can be repeat in 30 menit
Theapy Parkinsonism

THP 130
mg/day The last dose given
6 hours before
sleep

If the symptom can


not be controled 
amantadine
Therapy Akathisia

Reduce Muscle Relaxan


antipsikotik  propanolol
dose 30-8 mg/day

katekolaminergik
(amantadine ,
clozapine dan
diazepam iv)
Therapy Tardive Dyskinesia
• Change tipikal antipsikotik be atipikal antipsikotik

• Atipikal group  olanapine, quetiapine, risperidone,


ziprasidone
Differential Diagnose
• Drug withdrawal syndrome
• Parkinson disease
• Tetanus
• Disorders of primary extrapyramidal motion
• Distonia primer
• Hutington
• Khorea sidenham
Complication
• Movement disorders when walking can cause the patient to
fall and fraktur
• Dystonia laring can cause asfiksia and dead
• Complication of anticolinergic can cause dry mouth, blurred
vision, memory disorder, constipation, retensi urin
• Amantadine: can cause eksaserbation psikotik symptoms
Prognosis
• Acute extrapiramidal: dubia ad bonam
• Chronic extrapiramdal: dubia ad malam
THANK YOU
Jalur Dopaminergik di otak
Sintesis DA
Tyrosine ekstraseluler  tyrosine pump  intraseluler

Intraseluler:

• Tyrosine  TOH  Dopa  DDC  Dopamine

• Dopamine  transporter monoamine vesicular  vesikel


sinaptik
Terminasi kerja DA
• Ekstraseluler  COMT enzyme

• Intraseluler  MAO-A dan MAO-B  pada mitokondria di


neuron presinaptik dan sel glia
Dopamine Receptor
• DAT = dopamine transporter  presinaps

• Fungsi: clearing excess dopamine out of synaptic cleft 


VMAT2  vesikel sinaptik

• D2 autoreceptor  presinaps  = GATE-KEEPER

• Reseptor Post-sinaptik  D1 – D5
Dopaminergic Pathway
• Mesolimbic

• Mesocortical

• Nigrostriatal

• Tuberoinfundibular
VTA di brainstem  nucleus accumbens di ventral striatum
- Emotional behavior
- Hyperactivity  halusinasi dan waham = positive symptoms
VTA  dorsolateral prefrontal cortex
- Negative symptoms and cognitive symptom
VTA  ventromedial prefrontal cortex
- Negative symptoms and affective symptoms
Substantia nigra  basal ganglia di striatum
- Bagian dari sistem saraf ekstrapiramidal
- Regulasi pergerakan
- Loss of DA neuron  increase Ach activity
 extrapyramidal dysfunction
- Hiperaktivitas  gangguan hiperkinetik,
chore, diskinesia, tic
- Blokade  diskinesia tardive
Hypothalamus  anterior pituitary
- Regulates prolactin secretion
- DA  inhibition
- Postpartum  aktivitas menurun
- Blokade  galactorrhea, amenorrhea,
disfungsi seksual

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