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By this definition ,TIA, which lasts <24 hours, and patients with stroke
symptoms caused by subdural hemorrhage, tumors, poisoning, or trauma are
excluded.
1.WHO MONICA Project Investigators. The World Health Organization MONICA Project (Monitoring trends and determinants in
cardiovascular disease). J Clin Epidemiol 41, 105-114. 1988
Epidemiology
Global Epidemiology of Stroke
• Annually, 15 million worldwide suffer a stroke-5 million die and 5 million
are permanently disabled [2]
• WHO estimates a stroke occurs every 5 seconds [3]
• Stroke related disability is the sixth most common cause of reduced
DALYs[2]
• Accounts for 10% of all deaths worldwide[2]
2.Grysiewicz RA, Thomas K, Pandey DK. Epidemiology of Ischemic and Hemorrhagic Stroke:
Incidence,Prevalence, Mortality, and Risk Factors. Neurol Clin. 2008 Nov;26(4):871-95, vii.
3.Donnan GA, Fisher M, Macleod M, et al. Stroke. Lancet 2008;371(9624):1612–23.
Global Epidemiology of Stroke
• Globally, stroke is the second leading cause of death [4]
• In the United States, a stroke occurs approximately every 40
seconds; that translates into 2160 strokes per day.[2]
• 1 out of 16 Americans dies as a consequence of stroke [5].
• Total cost of stroke has been estimated at $65.5 billion in 2008.
4.Bogousslavsky J, Aarli J, Kimura J. Stroke: time for a global campaign? Cerebrovasc Dis 2003;16(2):111–3.
5. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statisticsd2008 update: a report from the American
Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008;117(4):e25–146.
Global Epidemiology of Stroke
Incidence:
• Varies from 240 per 100,000 in Dijon, France to 600 per 100,000 in
Novosibirsk, Russia [3]
• Framingham Heart Study (FHS) estimates for 1990 to 2004 was 5.3 in
men and 5.1 in women[6]
Prevalence:
• Varies from 1.6% to 6% [5]
Recurrence of Stroke:
• 2% at 7 days, 4% at 30 days,12% at 1 year, and 29% at 5 years after initial
cerebral ischemia [7].
Case fatality and mortality:
• Rochester Epidemiologic Project: Risk for death after first ischemic strok
7% at 7 days, 14% at 30 days, 27% at 1 year, and 53% at 5 years [7].
6. Carandang R, Seshadri S, Beuser A, et al. Trends in incidence, lifetime risk, severity, and 30-day mortality of stroke over the past
50 years. JAMA 2006;296(24):2939–46.
7. Petty GW, Brown RD Jr, Whisnant JP, et al. Survival and recurrence after first cerebral infarction: a population-based study in
Rochester, Minnesota, 1975 through 1989. Neurology 1998;50(1):208–16.
Stroke in India
Stroke Morbidity and Mortality in India
• Prevalence 55.6 per 100,000 all ages (Dalal 2007)
• 0.63 million deaths (WHO 2005)
• 1.44-1.64 million cases of new acute strokes every year (WHO
2005, Murthy 2007)
• 6,398,000 DALYs (WHO 2009)
• 12% of strokes occur in the population aged <40 years (Shah +
Mathur 2006)
• 28-30 day case fatality ranges from 18-41% (Dalal et al 2008,
Das et al 2007)
Stroke in India
• Prevalence : 84-262/100,000 in rural and 334-424/100,000 in
urban areas.(WHO 2008)
9. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE 3rd. Classification of
subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org
10172 in Acute Stroke Treatment. Stroke. 1993 Jan;24(1):35-41.
Classification of Stroke Subtypes
Stroke Data Bank Subtype (NINDS) Classification [10]
Derived from the Harvard Stroke Registry classification, the National
Institute of Neurological Disorders and Stroke (NINDS) Stroke Data Bank
recognised -
1. Atherothrombosis
2. Tandem arterial pathology
3. Cardiac Embolism
4. Lacune
5. Unusual Cause
6. Infarction of undetermined cause
7. Parenchymatous haemorrhage
8. Subarachnoid Hemorrhage
10. Amarenco P, Bogousslavsky J, Caplan LR, Donnan GA, Hennerici MG. Classification of stroke subtypes. Cerebrovasc
Dis. 2009;27(5):493-501. Epub 2009 Apr 3.
The Oxford Community Stroke Project
classification
(OCSP/ Bamford / Oxford classification)
Based on symptoms -
1.Total anterior circulation stroke (TAC)
2. Partial anterior circulation stroke (PAC)
3.Lacunar stroke (LAC)
4. Posterior circulation stroke (POC)
The type of stroke is then coded by adding a final letter to the above:
• I – for infarct (e.g. TACI)
• H – for haemorrhage (e.g. TACH)
• S – for syndrome; intermediate pathogenesis, prior to imaging (e.g. TACS)
These four entities predict the extent of the stroke, the area of the brain
affected, the underlying cause, and the prognosis.
11. Bamford J, Sandercock PA, Dennis MS, Burn J, Warlow CP: Classification and
natural history of clinically identifiable subtypes of brain infarction. Lancet 1991;
337: 1521– 1526.
SSS-TOAST Classification
12. Ay, H, Benner, T, Arsava, EM. A computerized algorithm for etiologic classification of ischemic stroke: the
Causative Classification of Stroke System. Stroke 2007; 38:2979 .
Causative Classification System (CCS)
Automated version of the SSS-TOAST (Arsava et
al,Neurology 75 October 5, 2010) (https://ccs.mgh.harvard.edu)
Etiopathology
Etiology of Ischemic Stroke
A. Thrombosis Large intracranial
Large extracranial vessels vessels
• Atherosclerosis • Atherosclerosis
• Dissection • Dissection
• Takayasu arteritis • Arteritis/vasculitis
• Giant cell arteritis • Noninflammatory
• Fibromuscular vasculopathy
dysplasia • Moyamoya
syndrome
• Vasoconstriction
Small vessel disease
• Lipohyalinosis ( due to hypertension) and fibrinoid degeneration
• Atheroma formation at their origin or in the parent large artery
B.Cardioaortic embolic stroke
1. Cardiac sources definite - 2. Cardiac sources possible
antithrombotic therapy generally Mitral annular calcification
used
Left atrial thrombus Patent foramen ovale
Left ventricular thrombus Atrial septal aneurysm
Atrial fibrillation Atrial septal aneurysm with
Sustained atrial flutter patent foramen ovale
Recent myocardial infarction (within 1 Left ventricular aneurysm
month) without thrombus
Rheumatic mitral or aortic valve disease Isolated left atrial smoke (no
Bioprosthetic and mechanical heart valve mitral stenosis or atrial
Chronic myocardial infarction with fibrillation)
ejection fraction <28 percent Mitral valve strands
Symptomatic heart failure with ejection
fraction <30 percent
Dilated cardiomyopathy
derangement.
Consequences of reduction in blood flow
during stroke
• Brain contains little or no energy stores and relies on blood for their delivery.
• During stroke, reduction of blood flow to brain results in a deprivation of glucose and
oxygen .
• Central core irreversibly damaged and necrosis if ischemia is long enough. (Infarct)
• Cells which receive oxygen and glucose by diffusion from collaterals are viable.
(Penumbra)
Mechanisms of ischemic cell injury and
death
• Depletion of ATP
• Changes in ionic concentrations of sodium, potassium, and calcium
• Increased lactate
• Oxygen free radicals
• Intracellular accumulation of water, Activation of proteolytic
processes
• Excitatory glutamate at synapses---- NMDA) receptor----
depolarization----calcium influx
• Nitric oxide
• Inflammatory pathway
• Necrosis and apoptosis
Investigations in Ischemic Stroke
Vital signs
Blood pressure
• MAP usually elevated in acute stroke.
• Represents response to maintain brain perfusion.
• Decision to treat requires balance between severe increases in blood
pressure, and decline in neurologic functioning with decreased BP.
Breathing
• Raised ICP (ICH/vertebrobasilar ischemia/ bihemispheric ischemia) -
decreased respiratory drive /muscular airway obstruction.
• Hypoventilation (increase in PCO2) - cerebral vasodilation -further elevates
ICP.
• Intubation- to restore adequate ventilation and protect airway.
• Especially in vomiting with increased ICP
Fever
• Worsens brain ischemia
•
History and Physical
Examination
Distinguish between stroke and stroke mimics
• Migraine
• Head trauma
• Brain tumor
• Todd's palsy (paresis, aphasia, neglect, etc. after a seizure
episode)
• Functional deficit (conversion reaction)
• Systemic infection
• Toxic-metabolic disturbances (hypoglycemia, acute renal
failure, hepatic insufficiency, exogenous drug intoxication)
(Ask for use of insulin/OHA/ seizure disorder/ drug overdose or
abuse/ medications/ recent trauma/hysteria.)
Clinical Course: Embolic strokes
Occur suddenly; deficits maximal at onset & Rapid recovery
Multiple embolic events with different clinical symptoms (initially weakness, followed by
paresthesias).
Clinical Course: Thrombotic Stroke
Symptoms fluctuate; Stepwise / stuttering progression &
some periods of improvement
Clinical Course: Lacunar Stroke
• Symptoms develop over short time, hours or at most few days
• large artery-related ischemia can evolve over longer period.
• stuttering course may ensue
Clinical course : Intracerebral
hemorrhage
• Does not improve
during the early period
• Rapid downhill course
• Progresses in minutes/
few hours
• Aneurysmal SAH
develops in an instant.
Focal brain dysfunction
is less common.
Physical examination
• Absent pulses (inferior extremity, radial, or carotid) - favors atherosclerosis with
thrombosis
• Sudden onset of cold, blue limb- favors embolism.
• Occlusion of common carotid artery in the neck neck with bruit -occlusive
extracranial disease
• Temporal arteritis- temporal arteries irregular and with dilatation, tender, pulseless
• Cardiac findings(especially atrial fibrillation, murmurs,cardiac enlargement) - favor
cardiac-origin embolism.
• Carotid artery occlusion –iris speckled, ipsilateral pupil dilated and poorly reactive,
retinal ischemia
• Fundus - cholesterol crystal, white platelet-fibrin, or red clot emboli. Subhyaloid
hemorrhage in brain or subarachnoid hemorrhage.
What Is a Minimal Diagnostic
Evaluation?
• Blood pressure
• H/o chronic blood pressure- lowering treatment
• Tobacco smoking (current or stopped within the previous 6
months)
• Diabetes mellitus
• Weight, Height, Waist circumference
• Physical exercise versus sedentary lifestyle
• Family h/o vascular disease
• H/o coronary intervention, acute coronary syndrome or
myocardial infarction, atrial fibrillation.
• Noncontrast brain CT or brain MRI
• Electrocardiogram
• Complete blood count including platelets
• Cardiac enzymes and troponin
• Electrolytes, urea nitrogen, creatinine
• Serum glucose
• Prothrombin time and international normalized ratio (INR), Partial
thromboplastin time
• Oxygen saturation
• Lipid profile
• Assessment of extracranial arteries (Carotid ultrasound examination or MRA/
CT angiography/X-ray angiography).
• Assessment of intracranial arteries (Transcranial Doppler/ MRA/CT
angiography/or X-ray angiography/high-resolution MRI).
Appropriate in selected patients
• Liver function tests
• Toxicology screen
• Blood alcohol level
• Pregnancy test in women of child-bearing potential
• Arterial blood gas if hypoxia is suspected
• Lumbar puncture if subarachnoid hemorrhage is suspected and
head CT scan is negative for blood
• Electroencephalogram if seizures are suspected
Algorithm for imaging management of acute stroke
patients (Kunst & Schaefer, 2011)
• The score divides the middle cerebral artery (MCA) territory into 10
regions of interest.
• 3 points - Subcortical structures (1 each for caudate, LN, IC)
• 7 points – Allotted to MCA cortex
3 points - M1. M2, M3 regions (Axial CT cut at BG level)
1 points - insular cortex
3 points - M4, M5, and M6 regions (CT cut just rostral to BG)
• 1 point is subtracted for an area showing EIC, such as focal swelling or
parenchymal hypoattenuation, for each of the defined regions.
• Therefore, a normal CT scan has an ASPECTS value 10 points.
Utility of ASPECTS
• The median ASPECTS value was 8; a value of < 7 was associated with a
sharp increase in dependence and death at three months.
Lacunar stroke,
Brainstem stroke, or
• Limitations
• Less sensitive than DWI in Hyperacute infarcton
• Lack of specificity for acute hemorrhage.
Diffusion-Weighted Imaging
(DWI)
• Principle:
In stroke, cytotoxic edema → movement of water molecules
into the IC compartment → Restricted movement of water
molecules → Appears as Hyperintense signal on DWI
• DWI is also subject to signal alteration from gross patient motion, tissue
vibration, and cardiac-related motions, and so the term apparent diffusion
coefficient (ADC) has been coined.
• ADC values
• low within hours after the stroke continue to decline for the next few
days.
• Remain reduced for first 4 to 5 days after stroke
• Pseudonormalization between 7 -10 days
• After this the ADC subsequently rises in the lesion (i.e., the ADC map
shows hyperintensity) beyond 10 days
• These agents remain in the intravascular space when the BBB is intact,
inducing a local magnetic field gradient in the capillary bed.
• A transient increase in signal is observed as the agent moves out into the
tissue .
DWI-PWI Mismatch
• Several studies have shown that the perfusion deficit (measured as a
prolonged MTT or TTP delay) is initially larger in the acute setting .
• It appears that in 70% to 80% of patients imaged within the first 6 hours of
stroke, measured PWI deficits > DWI deficit.
Evolution Of Infarct with
PWI deficit> DWI deficit
A - 1 hour
B - 3 days
post-ictus
Ultrasound Methods
Carotid and vertebral duplex
Color flow guided duplex ultrasound is well established as a noninvasive examination
to evaluate extracranial atherosclerotic disease.
Transcranial Doppler
• Uses low frequency (2 MHz) pulsed sound to penetrate bony windows and
visualize intracranial vessels of the circle of Willis.
• Noninvasive means of assessing the patency of intracranial vessels.
• Able to detect intracranial stenosis, identify collateral pathways, detect emboli on a
real-time basis, and monitor reperfusion after thrombolysis
• Major drawbacks include examiner-dependence, poor patient windows , and low
sensitivity in the vertebrobasilar system.
Bernard TJ, Goldenberg NA. Pediatric Arterial Ischemic Stroke. Hematol Oncol Clin
N Am 24 (2010) 167–180
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