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History Taking in Stroke Patient Pagan Pambudi from. Handbook of Stroke

History Taking in Stroke Patient

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Page 1: History Taking in Stroke Patient

History Takingin Stroke Patient

Pagan Pambudi

from.Handbook of Stroke

Page 2: History Taking in Stroke Patient

4 Fundamentals Question

1. Is this Vascular or Non vascular2. If vascular, ischaemic or

haemorrhagics3. if hemorrhagic where is the

lession, if ischaemic what is the artery involved

4. What is the underlying mechanism

Page 3: History Taking in Stroke Patient

Vascular vs Non vascular

• Acute and rapid onset

• Distinguish:– TIA < 24 h– RIND 24 h – 3

weeks– Complete Stroke

> 24 h– Progresive >

worsening

• Chronic• If acut consider

Todd paralysis an hemiparesis after seizure

Page 4: History Taking in Stroke Patient

Ischaemic or hemorrhagic

Ischaemic• Gradual onset• no in activity• headache,

vomiting, decrease of conciousness, seizure (uncommon)

Haemorrhagic• Abrupt, complete

deficit at onset• in activity• Headache,

vomiting, decrease of conciousness, seizure common

Page 5: History Taking in Stroke Patient

If haemorrhagic , Where is the lession

• Epidural– history of trauma

• Subdural– history of trauma– old people– lucid interval, mental status

detoriation

• Subarachnoid– severe headache

Page 6: History Taking in Stroke Patient

If haemorrhagic , Where is the lession

• ICH– Supratentorial lobar– supratentorial deep

• basal ganglia. capsula interna• thalamus

– Brainstem– Cerebellar

• IVH

Page 7: History Taking in Stroke Patient

If Ischaemic, what is the artery involved

• Anterior Circulation– hemiparesis– defect of high cortical

function: aphasia, apraxia, anosognosia, agnosia

– Seizure– hemianopsia– vertigo is uncomon– cranial nerve

involvement supranuclear

• Posterior Circulation– hemiparesis– vertigo, ataxia,

dizzines is common– bulbar palsy– diplopia– decrease of

conciousness– tend to progresive

Page 8: History Taking in Stroke Patient

What is Underlying Mechanism

• Ischaemics– Heart

• aritmia, valve disease, ischaemic disease, etc

– Large vessel• ateroschlerotics disease, Takayasu disease

– Small vessel• infection, imunological

– Hematologic• hypercoagulation state, polisitemia vera

Page 9: History Taking in Stroke Patient

What is Underlying Mechanism

• Hemorrhagic– EDH

• trauma

– SDH• trauma, tear in bridging vein (old people)

– SAH• AVM, aneurism, trauma, ICH, IVH

– ICH• Hipertension, AVM, Aneurism, Amyloid

angiopathy, Charcot Boucard microaneurism, Neoplam, Drugs, hematologic disease

Page 10: History Taking in Stroke Patient

What is Underlying Mechanism

• IVH– Hipertension, ICH extension,

neoplasm, drugs, hematologic diorder

Page 11: History Taking in Stroke Patient

Neurological Common Complaint

• Decrease of conciousness• Headache• Vertigo and Dizzines• Visual disturbance• Motor paralyze• Sensory distrubance• Seizure• Movement and gait disturbance• Cognitif impairment

Page 12: History Taking in Stroke Patient

Decrease of conciousness

• akut atau pelan• Bedakan dengan sinkop• Penurunan kesadaran pada stroke

bisa– Stroke Perdarahan– Stroke infark yang:

• luas (misal emboli 1 hemisfer dengan edema serebri berat)

• infark brainstem

Page 13: History Taking in Stroke Patient

Nyeri kepala

• Bedakan akut atau kronik progresif• Lokasi nyeri kepala• SAH sering keluhan hanya nyeri

kepala yang hebat, Sentinel headache (Px bisa tahu persis saat serangan nyeri)

• Hilang-timbul AVM, aneurisma

Page 14: History Taking in Stroke Patient

Vertigo

• Central– not severe– autonomic

symptoms rare– nystagmus

vertical and rotatory

– continous– tinitus uncomon

• Perifer– severe– autonomic

symptoms prominent

– nystagmus horizontal or rotatory

– paroxysmal– tinitus common

Page 15: History Taking in Stroke Patient

Visual disturbance

• Visual Loss– unilateral:

• acut: vascular eg Amaurosis Fugax• subacut: inflamation• chronic: compresion e.g optic nerve

meningioma

Page 16: History Taking in Stroke Patient

Visual Disturbance

• Bilateral Visual Loss– complete:

• large chiasmal lession, bilateral optic pathway and cortices disturbance

– Episodic• posterior circulation disorder

– Intermittent• demyelinating

– Gradual• neoplasm, aneurism

Page 17: History Taking in Stroke Patient

Diplopia

• Binokular diplopia– kelemahan otot ekstraokular– neurological

• Monokular diplopia– ocular problems

• untuk mengetahui bila ada diplopia, tutup satu mata membaik berarti misalignment misal parese n III, tetap diplopia problem ocular

Page 18: History Taking in Stroke Patient

Motor paralyze

• Can be– hemiparese/plegia– paraparese (lesi parasagital)– double hemiparese/plegia bedakan

dengan tetraparese pada double hemiparese ada keterlibatan saraf kranial

– Pure motor paralyze dapat terjadi pada infark lakunar

Page 19: History Taking in Stroke Patient

Sensory

• Hipesthesia• Rasa nyeri, panas thalamic

lesion• Sensory seizure: tingling,

parestesia sensory hallucination lesi parietal

• sensory disturbance of the face onion distribution lesi di tractus spinalis n V

Page 20: History Taking in Stroke Patient

Speech

• disartria– cortical– subcortical– cerebellar– brainstem

• dysfonia– parese plica voklais

Page 21: History Taking in Stroke Patient

Seizure vs Sinkop

Seizure• Aura +• Gerakan-gerakan

saat serangan• Post ictal lama• ngompol, BAB,

ejakulasi +

Sinkop• Aura –• Saat serangan

lunglia tidak ada aktivitas

• Cepat bangun• tidak ada

ngompol, BAB, ejakulasi

Page 22: History Taking in Stroke Patient

Seizure

• First time seizure in adult– usually organic

• structural– CVA: hemoragic, emboli– infection: meningensefalitis, cerebral abscess– neoplasm

• Metabolic– non ketotic hiperglicemia– hiponatremia, hipocalcemia– alcohol, benzodiazepine and opiates

withdrawal. neuroleptic overdosage, teofilin, antidepresan trisiklik

Page 23: History Taking in Stroke Patient

Cognitif impairment

dominant hemisphere

• aphasia• Gertzman

syndrome• alexia• Speech apraxia

Non dominat• Constructional

aphasia• Anosonogsia• Prosopagnosia