Approach to TIA/Stroke

Dr Ahmad Shahir MawardiNeurology Registrar

Neurology DepartmentHospital Kuala Lumpur23rd September 2015

Outline• Overview/Introduction• Definition• Classification of stroke• Identifying TIA/ acute stroke• Aetiology• Investigations• Management of acute stroke (superficial)

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Epidemiology• Annually 15 million people worldwide

suffer a stroke– 5 million die– 5 million are left permanently disabled.

• Top 4 leading causes of death in ASEAN countries,– death rate :

• 10.9/100 000 (Thailand)• 54.2/100 000 (Singapore).

Malaysia's data

• In Kelantan, 158 stroke patients were admitted to HUSM between January 1997 and December 1998.– 56·3% ischemic stroke– 36·1% primary intracerebral hemorrhage– 7·6% subarachnoid hemorrhage.

• 246 stroke patients admitted to Penang Hospital from December 1998 to November 1999– 74·8% ischemic stroke – 25·2% hemorrhagic stroke

Malaysia's data

• 163 ischemic stroke patients were admitted to HUKM from June 2000 until January 2001– 62·6% lacunar infarct – 26·4% middle cerebral infarct – 11·0% other manifestations – The mortality rate: 11·7%, with a mean age of 62·2 years

• UMMC 83 ischemic stroke patients were admitted between June 2000 and November 2000– hyperhomocysteinemia was found to be a risk factor for ischemic stroke

(odds ratio 5·3) – Depression was reported in (66%) 3-6 months poststroke

• It has been reported that six new stroke cases occur in Malaysia every hour

Malaysia's data

Malaysia's data

Stroke • A Clinical syndrome characterized by rapidly

developing clinical symptoms and/or signs of focal, and at times global, loss of cerebral function, with symptoms lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin”.

Transient Ischaemic Attack• A clinical syndrome characterized by an acute loss of

focal cerebral or monocular function with symptoms lasting less than 24 hours and which is thought to be due to inadequate cerebral or ocular blood supply as a result of arterial thrombosis or embolism”.

Acute Stroke • Sudden non-convulsive, focal neurological

deficit resulting from vascular disease

• Could be divided into: » Acute ischemia infarction » Intraparenchymal hemorrhage» Subarachnoid hemorrhage

**a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention

Transient Ischemic Attack• Old definition - (Clinically-based)

– brief episode of neurologic dysfunction < 24 hours resulting from focal temporary cerebral ischemia

• New definition - (Tissue-based)– transient episode of neurologic dysfunction

caused by focal brain, spinal cord, or retinal ischemia, without acute infarction*

**a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention

Classification

Purpose:

1. Immediate stroke supportive care and rehabilitation, 2.Prognostic purposes3.Guides cost effective investigations 4.Aids decisions for therapy and secondary stroke

prevention strategies. 5.Setting up stroke registries/ data banks/

epidemiological studies.

1. WHO classification: hemorrhagic (intraparenchymal, subarachnoid), ischemic or Transient Ischemic Attack TIA.

2. Oxfordshire Community Stroke Project (OCSP) classification for ischemic stroke – TACI, PACI, POCI, LACI), and unclassified.

3. Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification – large artery, small vessels, cardioembolic, stroke of determined cause, stroke of undetermined cause

4. Location of stroke – right hemisphere, left hemisphere, brainstem, cerebellar.

Classification

• NO cortical sign

• 5 subtypes1.Pure motor2.Pure sensory3.Ataxic Hemiparesis4.Dysarthria-clumsy hand syndrome5.Mixed motor sensory

Lacunar infarction

Cortical signs

• Aphasia• Neglect (may be spatial, sensory, visual,

auditory)• Alteration of consciousness• Visual field cut

• Common site (2PITC):– Putamen 37%– Thalamus 14%– Caudate 10%– Pons 16%– Int capsule, post limb 10%

• less common ant limbs, cerebellum

Lacunar infarction

Time course of lacunar infarctionP

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Diagnosis/ Identifying • Stroke is a clinical diagnosis

• History is of utmost importance– obtain information from the patient, family members, friends, or

witnesses.

• The diagnosis should provide answers to the following questions:1. What is the neurological deficit?2. Where is the lesion?3. What is the lesion?4. Why has the lesion occurred?5. What are the potential complications and prognosis?

• The signs and symptoms of a stroke depend on the type, location and the extent of the affected brain tissue.

• Sudden or rapid onset within minutes to an hour. – however, a stepwise or gradual worsening or waxing and waning

symptoms.

• 1/3 of all strokes occur during night sleep– Further imaging is needed to detect mismatch of penumbra

and infarcted area

Diagnosis/ Identifying

“Wake-up” stroke

• It is not uncommon that patient presented with hemiparesis upon waking up

• Further imaging is needed to detect mismatch of penumbra and infarcted area

Brain and its functional territories

MCA infarction • motor & sensory deficit

(Face>UL>LL)

• homonymous hemianopia

• Gaze preference

• Dominant hemisphere:

– aphasia

• Non dominant hemisphere

– neglect

ACA infarction • Motor +/- Sensory deficit

(LL>> Face, UL)• Primitive reflexes

– grasp, sucking reflexes

• Gait apraxia• Abulia

PCA infarction • Homonymous hemianopia• visual hallucination • alexia without agraphia• cranial nerve lesion (III nerve)• motor deficit (cerebral

peduncle, midbrain)

Vertebrobasilar• Lower brainstem lesion

• Crossed motor & sensory deficit

• Coma

• Dizziness, Hiccup

• Cerebellar signs

**bilateral = Basilar artery

1. Atherothromboembolism (50%)

2. Intracranial small vessel disease (penetrating artery disease) (25%)

3. Cardiogenic embolism (20%)

4. Others – arterial dissection, trauma, vasculitis (primary/secondary),

metabolic disorders, congenital disorders – less common causes such as migraine, pregnancy, oral

contraceptives, etc.

Etiology

Stroke Mimicker

Psychogenic Lack of objective cranial nerve findings, neurological findings in a nonvascular distribution, inconsistent examination

Seizures History of seizures, witnessed seizure activity, postictal period

Hypoglycemia History of diabetes, low serum glucose, decreased level of consciousness

Migraine with aura

History of similar events, preceding aura, headache

Hypertensive encephalopathy

Headache, delirium, significant hypertension, cortical blindness, cerebral edema, seizure

Wernicke’s encephalopathy

History of alcohol abuse, ataxia, ophthalmoplegia, confusion

CNS abscess History of drug abuse, endocarditis, medical device implant with fever

CNS tumor Gradual progression of symptoms, other primary malignancy, seizure at onset

Drug toxicity Lithium, phenytoin, carbamazepine

Investigations

1. Confirm the diagnosis2. Determine the stroke mechanism3. Risk stratification and prognostication4. Identify potentially treatable large obstructive

lesions of the cerebrovascular circulation

• ON ADMISSION– FBC, RP, LFT, RBS, Coag*

• NEXT DAY– FBS, FSL

• OPTIONAL TESTS– VDRL, Autoimmune, Thrombophilia, LA,

Homocystein, CRP

• ECG/Holter/ECHO/Imaging

Investigations

Young stroke • Valvular heart disease

• Vascular malformations

• Premature atherosclerosis

• Arteritis

• Coagulopathy : APS, protein C defiency

• Moyamoya, Takayasu disease

• Amyloid angiopathy

• Migraine

• Mitochondrial disease

Imaging (I)

CXRmadatory•Cardiomegaly•Aspiration

CT brain•Ischaemic vs haemorrhage•Confirms site of lesion, cause of lesion, extent of brain affected

Imaging (II)ECHO suspected cardioembolism, assess cardiac function

MRI SensitiveUseful tool to select patients for thrombolysis where available

Carotid duplex extracranial vessel disease

TCDIdentifies intracranial vessel disease with prognostic andtherapeutic implications

MRANon invasive tool to assess intra- and extra-cerebral circulationObjective assessment of vessel stenosis

CT angiography Non invasive tool to assess intra- and extra-cerebral circulation.

MR venography In suspected cerebral venous thrombosis

Contrast angiogram Gold standard assessment of cerebral vasculature

Early CT changes

• “Dot sign” • loss of grey-white differentiation

Management

• General• Specific (Reperfusion therapy)

– rTPA, mechanical thrombectomy• Primary prevention• Secondary prevention

Acute Mx of Ischaemic Stroke (General)

Acute Mx of Ischaemic Stroke (General)

Acute Mx of Ischaemic Stroke (General)

Thank you

Question 1A 50 year-old man presents to you with right-sided hemiparesis upon waking up in the morning. Urgent CT brain shows early changes over the left MCA territory. What is your next step?A. order for MRI brainB. order for CT AngiogramC. order for CT perfusion CD. start thrombolysisE. Echocardiogram c

Question 2

What is the contraindication of IV Alteplase in acute stroke? A. BP > 180/90 mmHgB. Major surgery within 3 months C. Hypodensity > 1/3 of the cerebral hemisphereD. INR > 1.2E. Age > 80 c

Question 3• Which of the following is TRUE regarding NIHSS assessment?

A. While assessing question 1b, 2 point should be given if the patient has severe dysarthria or is intubated

B. For sensory assessment, 1 point is given for quadriplegic patient

C. Limb ataxia should not be scored if the patient has dense hemiplegia

D. Best language cannot be assessed in intubated patient

E. No points should be given for visual assessment if the patient was blind before the stroke c

Question 4• Which of the following is NOT early changes of infarction on CT brain?

• A. Hypodensity

• B. Loss of sulcus

• C. Loss of insular ribbon

• D. Dot’s sign

• E. Poor grey-white differentiation A

Question 5• Regarding clinical features of stroke

• A. lower limb weakness is worse than upper limb weakness in MCA infarction

• B. Abulia in a common presentation in posterior circulation infarction

• C. Cortical signs are present in lacunar infarction

• D. The common sites of lacunar infarction include basal ganglia, internal capsule, thalamus, cerebellum and pons

• E. Visual neglect is a feature of posterior circulation infarction

D