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1.stroke epidemiology and stroke syndromes dr trilochan shrivastava
1. STROKE EPIDEMIOLOGY AND STROKE
SYNDROMES
Dr. Trilochan Srivastava
MD, DM (Neurology)
Fellowship in Cerebrovascular Intervention
Professor
Department of Neurology
SMS Medical College, Jaipur
2. STROKES ACCOUNT FOR 10% OF ALL-CAUSE MORTALITY
Other causes
27%
Cancer
12%
Stroke
10%
Accidents
9%
Respiratory infections 7%
HIV/AIDS 5%
chronic obstructive pulmonary
disease 5%
Perinatal causes
Diarrhoea
Tuberculosis
3%3%
4%
2%
Malaria
Coronary heart
disease
13%
Stroke is the 3rd leading cause of death and the 1st cause of severe morbidity
worldwide
(~ 3 ‰ of population/year, 600 hemiplegic/100.000 people)
3. 10% of strokes are fatal
~35% will die within the 1st year (~20% within the 1st month)
~30% will experience a new & often more serious stroke within the
next 5 years (~10% within the 1st year)
~30% of survivors becomes handicapped and/or develops
vascular Dementia
«cross» cardiovascular risk!
After a stroke: x2 or x3 risk for myocardial infarction
In ~10% of patients with myocardial infarction, stroke will
occur within the next 5 years
Epidemiological data with clinical significance
* Framingham Heart Study; American Heart Association, Heart and Stroke Facts statistical update,
Lees KR, et al. BMJ 2000;320:991–994; Hankey GJ, Warlow CP. Lancet 1999;354:1457–1463
4. Incidence – Mortality of
ischemic & hemorrhagic Stroke
The majority of strokes is ischemic
Ischemic
strokes
Hemorragic
strokes
Mortality1stmonth
%
5. MEAN AGE OF STROKE INCIDENCE,
PREVALENCE AND MORTALITY
6. STROKE EPIDEMIOLOGY IN INDIA
The estimated adjusted
prevalence rate of
stroke range, 84-
262/100,000 in rural and
334-424/ 100,000 in
urban areas.
The incidence rate is
119-145/100,000 based
on the recent population
based studies.
7. STROKE STATISTICS IN INDIA
Most important cause of Disability
Stroke is the No. 3 cause of death (#1 – Heart Disease, #2 –
Cancer)
Prevalence 55.6 per 100,000 all ages (Dalal 2007)
1.44-1.64 million cases of new acute strokes every year
(WHO 2005, Murthy 2007)
0.63 million deaths (WHO 2005)
28-30 day case fatality ranges from 18-41% (Dalal et al
2008, Das et al 2007)
By 2015, India report 1.6 million cases of stroke annually, at
least one-third of whom disabled
10. STROKE STATISTICS
Every 3.1 minutes someone dies of a stroke
Stroke risk increases with age
12% of strokes occur in the population aged <40
years (Shah + Mathur 2006)
For each decade after age 55, the risk of stroke
doubles.
72% of all strokes occur in people over the age
of 65
12. RISK OF RECURRENCE IN PATIENTS WITH PREVIOUS
TRANSIENT ISCHEMIC ATTACK (TIA) OR STROKE
After TIA After Stroke
30 days* 4 - 8% 3 - 10%
1 year 12 - 13% 10 - 14%
5 years 24 - 29% 25 - 40%
* Early recurrence: cardioembolism & stroke from extracranial atherosclerosis
13. RISK FACTORS
Non-modifiable:
Age : Doubling of strokes’ frequency for every 10 years after 55
yrs of age
Gender: Men x 1,4 increased risk ; >75 yrs same risk in both
gender
Family history of stroke (inheritance)
History of stroke or myocardial infraction
14. MAJOR MODIFIABLE RISK FACTORS
Hypertension: the most potent risk factor (60% of stroke, in mild x2 increase
of risk & in severe x7)
Diabetes: elevated risk x4 , even more when hypertension coexists
Dyslipidaemia: Hypercholesterolaemia > 240 mg/dl
correlation with stroke mortality
Smoking: possibility of stroke x2
cessation reduces the risk (50%) during the 1st year
Risk for embolic events:
- Atrial fibrillation, myocardial infarction-arterial wall clot
- Εndocarditis, artificial valves, cardiac surgery
- carotid stenotic disease
15. OTHER MODIFIABLE RISK FACTORS
Obesity, high fat and sodium diet
Insulin resistance
Decreased physical activity (walking for 30 min per day)
Increased alcohol consumption (>2 drinks per day)
Heart disease : CD,CHF
Patent foramen ovale (paradoxical embolism)
Arteriopathy : Inflammatory vessel damage caused by infectious diseases
(syphilis, chlamydia, Η.p), collagen disease angiitis (SLE, polyarteritis
nodosa), antiphospholypidemic syndrome
Migraine
Hypotheroidism
Sleep apnoea syndrome
Drug use
17. CEREBROVASCULAR DISEASE
Ischemic stroke
Hemorrhagic stroke
Cerebrovascular anomalies such as intracranial
aneurysms and arteriovenous malformations
(AVMs)
18. STROKE
Definition:
abrupt onset of a neurologic deficit that is
attributable to a focal vascular cause last > 24
hrs
Transient ischemic attack (TIA) - all neurologic
signs and symptoms resolve within 24 h regardless
of whether there is imaging evidence of new
permanent brain injury
19. DEFINITION OF TERMS
Thrombosis: inappropriate clotting
Embolism: migration of clots
Ischemia: loss of blood supply in a tissue due to
impeded arterial flow or reduced venous drainage
Infarction: cell death
20. HEMORRHAGIC STROKE
HT
Hemorrhage are
classified by location
Bleeding into subdural
and epidural spaces
is principally produced
by trauma
SAHs are produced by
trauma and rupture of
intracranial aneurysms
22. APPROACH TO THE PATIENT
Rapid evaluation is essential for use of
time sensitive treatments such as
thrombolysis
Important clues pointing to stroke:
Hemiparesis
Changes in vision
Changes in gait
Disturbance in the ability to speak or
understand
Sudden severe headache
23. ISCHEMIC STROKE
Acute occlusion of an intracranial vessel causing
reduction in blood flow to the brain region
The magnitude of flow reduction is a function of
collateral blood flow
24. CAUSES OF ISCHEMIC STROKE
Carotid /Intracranial
Atherosclerosis
Embolism: CAD, AF
30% of strokes remain
unexplained despite
extensive evaluation
25. CARDIOEMBOLIC STROKE
Responsible for 20% of all
ischemic strokes
Embolism of thrombotic
material forming on the
atrial or ventricular wall or
the left heart valves
Thrombi then detach and
embolize into the arterial
circulation
Embolic strokes tend to be
sudden in onset, with
maximum neurologic
deficit at once
26. CARDIOEMBOLIC STROKE CAUSES:
Rheumatic heart
disease
Non-rheumatic AF
MI
Prosthetic valves
Ischemic
cardiomyopathy
27. CAROTID ATHEROSCLEROSIS
10% of all ischemic
strokes
frequently within the
common carotid
bifurcation and proximal
internal carotid artery
RISK FACTORS:
Male gender, older age,
smoking, hypertension,
diabetes, and
hypercholesterolemia
28. OTHER CAUSES OF STROKE
Intracranial Atherosclerosis
Dissection of Internal Carotid Artery
Hypercoagulability
Venous sinus thrombosis
Fibromuscular dysplasia
Vasculitis
Drugs (amphetamines, cocaine,
phenylpropanolamine)
29. TRANSIENT ISCHEMIC ATTACK (TIA)
Episodes of stroke symptoms that last briefly
Duration < 24 hrs
May arise from emboli to the brain or from in situ
thrombosis
Amaurosis fugax – transient monocular blindness
occurs from emboli to the central retinal artery of
the eye
30. TRANSIENT ISCHEMIC ATTACK (TIA)
Risk of stroke after a TIA is ~10-15% in the first 3
months with most events occurring in the first 2
days
Acute antiplatelet therapy is effective and
recommended
33. STROKE WITHIN THE ANTERIOR CIRCULATION
Middle Cerebral Artery
Anterior Cerebral Artery
Anterior Choroidal Arteries
Internal Carotid Artery
Common Carotid Artery
34. MIDDLE CEREBRAL ARTERY
Occlusion of the
proximal MCA or one of
its major branches is
most often due to an
embolus rather than
intracranial
atherothrombosis
35. MIDDLE CEREBRAL ARTERY
The proximal MCA (M1 segment) supplies the following:
Basal Ganglion
Putamen
Outer globus pallidus
Posterior limb of the internal capsule
Corona radiata
Most of the caudate nucleus
36. MCA
In the sylvian fissure,
the MCA divides into
the superior and
inferior divisions (M2
branches)
Superior division
supplies
Frontal and superior
parietal cortex
Inferior division
supplies
Inferior parietal and
temporal cortex
37. MIDDLE CEREBRAL ARTERY
Entire MCA is occluded at its origin :
contralateral hemiplegia, hemianesthesia
homonymous hemianopia, gaze preference to
the ipsilateral side
Dysarthria is common because of facial
weakness
Global aphasia
38. MIDDLE CEREBRAL ARTERY: PARTIAL
SYNDROMES
Brachial syndrome : embolic occlusion of a single
branch include hand, or arm and hand, weakness
alone
Frontal Opercular Syndrome: facial weakness with
nonfluent (Broca) aphasia, with or without arm
weakness
Lacunar stroke within internal capsule - pure motor
stroke or sensory-motor stroke contralateral to the
lesion
40. ANTERIOR CEREBRAL ARTERY
Paralysis of opposite foot and leg: Motor
leg area
A lesser degree of paresis of opposite arm
Urinary incontinence: Sensorimotor area in
paracentral lobule
43. STROKE WITHIN THE POSTERIOR
CIRCULATION
Result from atheroma
formation or emboli that
lodge at the top of the
basilar artery
May also be caused by
dissection of the
vertebral artery
44. POSTERIOR CEREBRAL ARTERY
(1) P1 syndrome: midbrain,
subthalamic, and thalamic
signs, which are due to
disease of the proximal P1
segment of the PCA or its
penetrating branches
(2) P2 syndrome: cortical
temporal and occipital
lobe signs, due to
occlusion of the P2 segment
distal to the junction of the
PCA with the posterior
communicating artery.
45. POSTERIOR CEREBRAL ARTERY
P1 Syndromes
third nerve palsy with
contralateral ataxia
(Claude's syndrome) or
with contralateral
hemiplegia (Weber's
syndrome)
contralateral
hemiballismus (if
subthalamic nucleus is
involved)
thalamic Déjerine-
Roussy syndrome -
contralateral
hemisensory loss
followed later by an
agonizing, searing or
burning pain in the
affected areas
46. POSTERIOR CEREBRAL ARTERY
P2 Syndromes
Occulsion of the PCA causes
infarction of the medial
temporal and occipital lobes
Contralateral homonymous
hemianopia with macula
sparing is the usual
manifestation
acute disturbance in memory
(hippocampus)
peduncular hallucinosis -
visual hallucinations of
brightly colored scenes and
objects
infarction in the distal PCAs
produces cortical blindness
(blindness with preserved
PLR)
Anton's syndrome – unaware
of blindness and in denial
47. BASILAR ARTERY
Atheromatous lesions are
most frequent in the
proximal basilar and the
distal vertebral segments
Complete basilar occlusion
“locked-in" state of
preserved consciousness
with quadriplegia and
cranial nerve signs
suggests complete pontine
and lower midbrain
infarction
48. BASILAR ARTERY
Occlusion of the superior
cerebellar artery results in
Ipsilateral cerebellar ataxia,
nausea and vomiting,
dysarthria, contralateral loss of
pain and temp sensation
Occusion of the anterior
inferior cerebellar artery
results in
Ipsilateral deafness, facial
weakness, vertigo, nausea and
vomiting, nystagmus, tinnitus
and contralateral loss of pain
and temperature sensation
49. LATERAL MEDULLARY SYNDROME
(OCCLUSION OF VERTEBRAL, POSTERIOR INFERIOR CEREBELLAR ARTERIES)
On side of lesion
Pain, numbness, impaired sensation over
one-half the face: Descending tract and nucleus
fifth nerve
Ataxia of limbs, falling to side of lesion:
Uncertain—restiform body, cerebellar
hemisphere, cerebellar fibers, spinocerebellar
tract (?)
Nystagmus, diplopia, oscillopsia, vertigo, nausea,
vomiting: Vestibular nucleus
Horner's syndrome (miosis, ptosis, decreased
sweating): Descending sympathetic tract
Dysphagia, hoarseness, paralysis of palate,
paralysis of vocal cord, diminished gag reflex:
Issuing fibers ninth and tenth nerves
Loss of taste: Nucleus and tractus solitarius
Numbness of ipsilateral arm, trunk, or leg:
Cuneate and gracile nuclei
Weakness of lower face: Genuflected upper
motor neuron fibers to ipsilateral facial nucleus
On side opposite lesion
Impaired pain and thermal sense over half the
body, sometimes face: Spinothalamic tract
50. MEDIAL MEDULLARY SYNDROME
(OCCLUSION OF VERTEBRAL ARTERY OR OF BRANCH OF VERTEBRAL OR
LOWER BASILAR ARTERY)
On side of lesion
Paralysis with atrophy of
one-half half the tongue:
Ipsilateral twelfth nerve
On side opposite lesion
Paralysis of arm and leg,
sparing face; impaired
tactile and proprioceptive
sense over one-half the
body: Contralateral
pyramidal tract and medial
lemniscus