The document discusses the approach to transient ischemic attack (TIA) and stroke. It provides definitions of TIA and acute stroke, and classifications of stroke. It also reviews epidemiological data on stroke from Malaysia, clinical features of different types of stroke, etiologies, investigations and management of acute ischemic stroke.

1. Approach to TIA/Stroke
Dr Ahmad Shahir Mawardi
Neurology Registrar
Neurology Department
Hospital Kuala Lumpur
23rd September 2015

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

3. Do you know...

4. 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).

5. Malaysia's data

6. • 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

7. • 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

8. Malaysia's data

10. 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”.

11. 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”.

12. 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

13. 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

14. Classification
Purpose:
1.Immediate stroke supportive care and rehabilitation,
2.Prognostic purposes
3.Guides cost effective investigations
4.Aids decisions for therapy and secondary stroke
prevention strategies.
5.Setting up stroke registries/ data banks/
epidemiological studies.

15. 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

17. • NO cortical sign
• 5 subtypes
1.Pure motor
2.Pure sensory
3.Ataxic Hemiparesis
4.Dysarthria-clumsy hand syndrome
5.Mixed motor sensory
Lacunar infarction

18. Cortical signs
• Aphasia
• Neglect (may be spatial, sensory, visual,
auditory)
• Alteration of consciousness
• Visual field cut

19. • Common site (2PITC):
– Putamen 37%
– Thalamus 14%
– Caudate 10%
– Pons 16%
– Int capsule, post limb 10%
• less common ant limbs,
cerebellum
Lacunar infarction

20. Time course of lacunar infarction
Percentage
offunction%
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21. 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?

22. • 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

23. “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

32. Brain and its functional territories

35. MCA infarction
• motor & sensory deficit
(Face>UL>LL)
• homonymous hemianopia
• Gaze preference
• Dominant hemisphere:
– aphasia
• Non dominant hemisphere
– neglect

36. ACA infarction
• Motor +/- Sensory deficit
(LL>> Face, UL)
• Primitive reflexes
– grasp, sucking
reflexes
• Gait apraxia
• Abulia

37. PCA infarction
• Homonymous hemianopia
• visual hallucination
• alexia without agraphia
• cranial nerve lesion (III nerve)
• motor deficit (cerebral
peduncle, midbrain)

38. Vertebrobasilar
• Lower brainstem lesion
• Crossed motor & sensory
deficit
• Coma
• Dizziness, Hiccup
• Cerebellar signs
**bilateral = Basilar artery

39. 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

40. 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

41. Investigations
1. Confirm the diagnosis
2. Determine the stroke mechanism
3. Risk stratification and prognostication
4. Identify potentially treatable large obstructive
lesions of the cerebrovascular circulation

42. • ON ADMISSION
– FBC, RP, LFT, RBS, Coag*
• NEXT DAY
– FBS, FSL
• OPTIONAL TESTS
– VDRL, Autoimmune, Thrombophilia, LA,
Homocystein, CRP
• ECG/Holter/ECHO/Imaging
Investigations

43. Young stroke
• Valvular heart disease
• Vascular malformations
• Premature
atherosclerosis
• Arteritis
• Coagulopathy : APS,
protein C defiency
• Moyamoya, Takayasu
disease
• Amyloid angiopathy
• Migraine
• Mitochondrial disease

44. Imaging (I)
CXR
madatory
•Cardiomegaly
•Aspiration
CT brain
•Ischaemic vs haemorrhage
•Confirms site of lesion, cause of lesion, extent of brain affected

45. Imaging (II)
ECHO suspected cardioembolism, assess cardiac function
MRI
Sensitive
Useful tool to select patients for thrombolysis where available
Carotid duplex extracranial vessel disease
TCD
Identifies intracranial vessel disease with prognostic and
therapeutic implications
MRA
Non invasive tool to assess intra- and extra-cerebral circulation
Objective 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

46. Early CT changes
• “Dot sign”
• loss of grey-white differentiation

48. Management
• General
• Specific (Reperfusion therapy)
– rTPA, mechanical thrombectomy
• Primary prevention
• Secondary prevention

49. Acute Mx of Ischaemic Stroke (General)

50. Acute Mx of Ischaemic Stroke (General)

51. Acute Mx of Ischaemic Stroke (General)

52. Thank you

53. Question 1
A 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 brain
B. order for CT Angiogram
C. order for CT perfusion C
D. start thrombolysis
E. Echocardiogram c

54. Question 2
What is the contraindication of IV
Alteplase in acute stroke?
A. BP > 180/90 mmHg
B. Major surgery within 3 months
C. Hypodensity > 1/3 of the cerebral
hemisphere
D. INR > 1.2
E. Age > 80
c

55. 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

56. 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

57. 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