This presentation describes the different types of stroke.

1. STROKE
CLASSIFICATION
STROKE FOUNDATION: PRABAHO

2. CLASSIFICATION
Stroke is classified into the following subtypes-
Thrombotic
Embolic
Ischaemicstroke
Intracerebralhaemorrhage
Subarachnoidhaemorrhage
Haemorrhagicstroke

4. Stroke type Clinical course Risk factors Other clues
Intracerebral
hemorrhage
Gradual onset and progression during
minutes or hours in most patients but
may present abruptly with maximal
deficit at onset.
Hypertension, trauma, bleeding diatheses,
illicit drugs (eg, amphetamines,
cocaine), vascular malformations. More
common in Black people and Asian people
than in White people.
May be precipitated by sex
or other physical activity.
Patient may have reduced
alertness.
Subarachnoi
hemorrhage
Abrupt onset of sudden, severe
headache. Focal brain dysfunction less
common than with other types.
Smoking, hypertension, moderate to heavy
alcohol use, genetic susceptibility (eg,
polycystic kidney disease, family history
of subarachnoid hemorrhage) and
sympathomimetic drugs (eg, cocaine)
May be precipitated by sex
or other physical activity.
Patient may have reduced
alertness.
Ischemic
(thrombotic)
Stuttering progression with periods of
improvement. Lacunes develop over
hours or at most a few days; large artery
ischemia may evolve over longer periods.
Atherosclerotic risk factors (age, smoking,
diabetes mellitus, etc). Males affected more
commonly than females. May have history
of TIA.
May have neck bruit.
Ischemic
(embolic)
Sudden onset with deficit maximal at
onset. Clinical findings may improve
quickly.
Atherosclerotic risk factors as
listed above. Males affected more
commonly than females. History of heart
disease (valvular, atrial fibrillation,
endocarditis).
Can be precipitated by
getting up at night to urinate
or sudden coughing or
sneezing.

5. CLASSIFICATION SYSTEMS FOR ISCHEMIC
STROKE
TOAST classification —
• The TOAST classification scheme for ischemic stroke is widely
used and has good interobserver agreement.
• The TOAST system attempts to classify ischemic strokes
according to the major pathophysiologic mechanisms that are
recognized as the cause of most ischemic strokes

6. It assigns ischemic strokes to five subtypes-
Large-artery atherosclerosis
Cardioembolism
Small-vessel occlusion
Stroke of other determined etiology
Stroke of undetermined etiology
Two or more causes identified
Negative evaluation
Incomplete evaluation

7. LIMITATIONS OF TOAST CLASSIFICATION
• advances in stroke evaluation and diagnostic imaging have allowed more
frequent identification of potential vascular and cardiac causes of stroke
• These advances could cause an increasing proportion of ischemic strokes to be
classified as "undetermined“ if the strict definition of this category (cases with two
or more potential causes) is applied.

8. • As a result, an evidenced-based modification of the TOAST criteria called SSS-
TOAST was developed
• The SSS-TOAST system divides each of the original TOAST subtypes into three
subcategories as "evident," "probable," or "possible" based upon the weight of
diagnostic evidence as determined by predefined clinical and imaging criteria
• SSS-TOAST called the Causative Classification System (CCS)

9. CAUSATIVE CLASSIFICATION SYSTEM (CCS) OF
ISCHEMIC STROKE ETIOLOGY
Large artery atherosclerosis
• Evident
1. Either occlusive or stenotic (≥50 percent diameter reduction or <50 percent
diameter reduction with plaque ulceration or thrombosis) vascular disease
judged to be caused by atherosclerosis in the clinically relevant extracranial or
intracranial arteries, and
2. The absence of acute infarction in vascular territories other than the stenotic or
occluded artery

10. • Probable
1. History of ≥1 transient monocular blindness (TMB), TIA, or stroke from the territory
of index artery affected by atherosclerosis within the last month, or
2. Evidence of near-occlusive stenosis or nonchronic complete occlusion judged to be
caused by atherosclerosis in the clinically relevant extracranial or intracranial
arteries (except for the vertebral arteries), or
3. The presence of ipsilateral and unilateral internal watershed infarctions or multiple,
temporally separate, infarctions exclusively within the territory of the affected artery

11. • Possible
1. The presence of an atherosclerotic plaque protruding into the lumen and
causing mild stenosis (<50 percent) in the absence of any detectable plaque
ulceration or thrombosis in a clinically relevant extracranial or intracranial artery
and history of ≥2 TMB, TIA, or stroke from the territory of index artery affected
by atherosclerosis, at least one event within the last month, or
2. Evidence for evident large artery atherosclerosis in the absence of complete
diagnostic investigation for other mechanisms

12. Cardio-aortic embolism
• Evident
1. The presence of a high-risk cardiac source of cerebral embolism

13. • Probable
1. Evidence of systemic embolism, or
2. The presence of multiple acute infarctions that have occurred closely related in
time within both right and left anterior or both anterior and posterior
circulations in the absence of occlusion or near-occlusive stenosis of all relevant
vessels. Other diseases that can cause multifocal ischemic brain injury such as
vasculitides, vasculopathies, and hemostatic or hemodynamic disturbances
must not be present.

14. • Possible
1. The presence of a cardiac condition with low or uncertain primary risk of
cerebral embolism, or
2. Evidence for evident cardio-aortic embolism in the absence of complete
diagnostic investigation for other mechanisms

15. Small artery occlusion
• Evident
1. Imaging evidence of a single and clinically relevant acute infarction <20 mm in
greatest diameter within the territory of basal or brainstem penetrating arteries
in the absence of any other pathology in the parent artery at the site of the
origin of the penetrating artery (focal atheroma, parent vessel dissection,
vasculitis, vasospasm, etc)

16. • Probable
1. The presence of stereotypic lacunar transient ischemic attacks within the past
week, or
2. The presence of a classical lacunar syndrome

17. • Possible
1. Presenting with a classical lacunar syndrome in the absence of imaging that is
sensitive enough to detect small infarctions, or
2. Evidence for evident small artery occlusion in the absence of complete
diagnostic investigation for other mechanisms

18. Other causes
• Evident
1. The presence of a specific disease process that involves clinically appropriate
brain arteries

19. • Probable
1. A specific disease process that has occurred in clear and close temporal or spatial
relationship to the onset of brain infarction such as arterial dissection, cardiac or
arterial surgery, and cardiovascular interventions
• Possible
1. Evidence for an evident other cause in the absence of complete diagnostic
investigation for mechanisms listed above

20. Undetermined causes
• Unknown (no evident, probable, or possible criteria for the causes above)
1. Cryptogenic embolism: Angiographic evidence of abrupt cut-off consistent
with a blood clot within otherwise angiographically normal looking intracranial
arteries, or Imaging evidence of complete recanalization of previously occluded
artery, or The presence of multiple acute infarctions that have occurred closely
related in time without detectable abnormality in the relevant vessels

21. • Unclassified
1. The presence of >1 evident mechanism in which there is either probable
evidence for each, or no probable evidence to be able to establish a single
cause

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