Cerebrovascular diseases like stroke are a major cause of death and disability in the US. There are two main types of stroke - ischemic caused by blockage of an artery and hemorrhagic caused by bleeding. Risk factors include age, hypertension, diabetes, smoking, prior stroke or TIA. Diagnosis involves brain imaging like CT or MRI. Treatment depends on type and severity but may include thrombolysis, anticoagulation, antiplatelet drugs, managing risk factors, and rehabilitation. Preventing stroke requires risk factor modification and treatments like antiplatelet drugs.

1. Stroke

2. Cerebrovascular Diseases
• Cerebrovascular diseases include some of the most
common and devastating disorders:
ischemic stroke, hemorrhagic stroke, and
cerebrovascular anomalies such as intracranial
aneurysms and arteriovenous malformations (AVMs).
• They cause ~200,000 deaths each year in the United
States and are a major cause of disability
• Third leading cause of death in the U.S
• Incidence increases with age
• Mortality from stroke increases with age
• The prevalence and incidence of stroke is also on the rise
in developing countries

3. ………….CVD
• A stroke, or cerebrovascular accident, is defined by this
abrupt onset of a neurologic deficit that is attributable to a
focal vascular cause AND the neurologic signs and
symptoms last for >24 h.
the definition of stroke is clinical, and laboratory studies
including brain imaging are used to support the diagnosis.
• Cerebral ischemia is caused by reduction of blood flow
longer than several seconds
• Transient Ischemic Attack (TIA) –all neurologic signs and
symptoms resolve within 24 h
– typically lasts for 5-15 minutes.
– blood flow is quickly restored brain tissue recovers fully

4. …………………Cont’d
• Infarction – absence of blood flow more than a few
minutes
• Generalized reduction in cerebral blood flow
causes syncope and if prolonged
–watershed/borederzone infarctions
–Global hypoxia-ischemia
–Hypoxic –ischemic encephalopathy

6. ………….cont’d
• Patients at risk should be brought to ER if they develop
–Loss of sensory/motor function ,
–Change in vision, gait, ability to speak or
understand,
–Severe headache
• Immediate CT Scan should be done
• there are no reliable clinical findings that conclusively
separate ischemia from hemorrhage,
• A more depressed level of consciousness, higher
initial blood pressure, or worsening of symptoms
after onset favor hemorrhage, and a deficit that remits
suggests ischemia

7. Stroke Risk Factors
NONMODIFIABLE
– age
– Gender
– Race/ethnicity
– family history
– genetics
• MODIFIABLE
 Arterial hypertension-3-4x
 TIA
 Prior stroke
 Asymptomatic carotid stenosis
 Carotid disease
 DM-2-4x
 Dyslipidemia
 Smoking -2-3x
 Excessive alcohol
 high homocystein
 Obesity

8. Differential Diagnosis
• Seizure
• Tumors
• Migraine
• Metabolic encephalopathies

9. Ischemic Stroke
• About 85% of all strokes
• Occurs when a cerebral artery is blocked by a
clot or other foreign matter
• Causes ischemia (inadequate blood supply to
tissue)
• Progresses to infarction (death of tissues)
• Classified as:
– Embolic Stroke
– Thrombotic Stroke

10. Pathophysiology of Ischemic Stroke
– Acute vascular occlusion with subsequent reduction in blood
flow to region supplied
– Severity depends on collaterals, site and vascular anatomy
– 100% reduction of flow causes infarction in 4-10 mins
– If blood flow is restored prior to a significant amount of
cell death, the patient may experience only transient
symptoms, i.e., a TIA
Ischemic Penumbra
– Tissue surrounding the core region of infarction is
ischemic but reversibly dysfunctional
– Viability of brain tissue is preserved if perfusion is restored
within a critical time period (2 to 4 hours?)
– saving the ischemic penumbra is the goal of
revascularization therapies

11. ……………………..Ischemic
• Focal cerebral infarction occurs via two distinct
pathways:
1. a necrotic pathway
in which cellular cytoskeletal breakdown is rapid, due
principally to energy failure of the cell;
Ischemia produces necrosis by starving neurons of glucose
Release of free radical, glutamate(if excess it is neurotoxic)
2. an apoptotic pathway
in which cells become programmed to die

12. Conditions influencing progression and extent of
ischemic injury
 Rate & duration of the ischemic event
 Collateral circulation in the involved area of the brain
 Systemic circulation & arterial blood pressure
 Coagulation abnormalities
 Temperature – fever
 Glucose - hyperglycemia

13. ………..ischemic
• Embolic
– The occlusion is caused by an embolus (solid, liquid, or
gaseous mass) carried to a blood vessel from another
area
– Most common emboli are blood clots
– Risk factors for blood clots include Atrial Fibrillation and
diseased or damaged carotid or vertebral arteries
– Rare causes of emboli include air, tumor tissue, and fat
– Occurs suddenly & may rarely be accompanied by
headache

14. CARDIOEMBOLIC STROKE
• 20% of all ischemic strokes
• Emolization of thrombotic material
• Causes TIA / Stroke
• Sudden, maximum deficit at the onset
• Common sites
–MCA or one of the branches
–PCA
–ACA( infrequently)
• Small vessel / large infarcts
• Cardiac diseases associated are
AF, MI, IE
prosthatic valve,
rheumatic heart disease,
ischemic cardiomayopathy,
MVP

15. ……isch
Atrial Fibrillation
• The commonest cause of Cardioembolic stroke
• Annual risk of stroke –5%
• High risk
–Age > 60 yrs
–HTN, DM,
–Poor LV Function, CHF, Dilated chambers
–Thyrotoxicosis,
–Previous TIA / Stroke , MS , Prosthetic Valves

16. ………….cardioembolic
• Recent MI
– recent Transmural MI involving the anteroapical wall of the
ventricle is associated with a higher risk of stroke
– Prophylactic anticoagulation has been shown to decrease
the risk
• Paradoxical embolization
– occurs in 15% of the general population
– DVT, fat or tumor emboli, IV air, amniotic fluid,
• Bacterial endocarditis
– causes multifocal infarct and hemorrhage into the
infarct
– Usually associated with brain abscess and mycotic
aneurysm

17. Artery-Artery embolic stroke
– Carotid bifurcation
– Aortic Arch
– Common carotid
– Internal carotid
– Vertebral, Basilar arteries
– Arterial Dissection

18. ………………Ischemic
Thrombotic
– The occlusion is caused by a cerebral thrombus; a
blood clot which develops gradually in a
previously diseased artery and obstructs it
Large Vessel thrombosis
Small Vessel thrombosis ( lacunar stroke)
– Caused by atherosclerosis:
• atheromatous plaque deposits form on the inner walls
of arteries, resulting in narrowing and reduction of
blood flow
• platelets adhere to the roughened surface of the
plaque deposit and a blood clot is created

19. 3. Uncommon Causes
• Hypercoagulable States
• Venous Sinus thrombosis
• Fibromuscular dysplasia
• Vasculitis
–Systemic
–Primary CNS
–Meningitis
• Cardiogenic
• SAH vasospasm
• Drugs
• Eclampsia

20. Transient Ischemic Attacks (TIAs)
• Temporary interruption of blood supply to brain
• Carotid artery disease a common cause
• Stroke-like neurological deficit symptoms
– abrupt onset
– Symptoms resolve in less than 24 hours, usually within
minutes.
– No long-term effects, but high stroke risk
- One third of TIA patients will suffer an acute stroke
• The risk of stroke after a TIA is ~10–15% in the first 3 months,
with most events occurring in the first 2 days

22. Imaging Studies in Stroke
CT SCAN
– Preferred standard initial modality in all acute strokes
– Better than MRI for detection of Acute blood
– Can identify other ICSOL mimickers of stroke
Disadvantages
Infarcts missed / not reliably seen in the first 24-48 hrs
Misses small cortical infarcts
Misses posterior fossa infarcts b/c of bone artifact
MRI
– Shows location and extent of infarction in all areas
– Less sensitive for acute blood
– More expensive, time consuming, not readily available
– Outside the acute period →more useful
 MRI perfusion studies, Diffusion weighted image,MR angiography
Cerebral Angiography

23. Management of Ischemic Stroke
• The first goal is to prevent or reverse brain injury
• ABC of life
• Immediate Imaging (Perform an emergency noncontrast head CT scan)
• Ischemic Stroke diagnosed…………..
1. Medical Support
2. Thrombolysis
3. Anticoagulation
4. Antiplatelet agents
5. Neuroprotection

24. Medical Support
• Optimize cerebral perfusion to the penumbra
• Prevent/Treat complications of bedridden pts
• Infections, DVT, PE
Blood Pressure Mx
• BP Should be lowered only if
 Malignant HTN
 >220/130
 Thrombolytic planned(< 185/110)
• B blockers ( esmolol, labetolol)
• Rx fever
• Maintain serum glucose < 200 mg/dl
Raised ICP
• 5-10% have significant edema---Peak at 2nd -3rd day
• Esp. Close monitoring of Cerebellar infarction !!!
• Standard Mx
• Craniotomy, hemicraniectomy

25. Thrombolysis
• Thrombolysis
• benefit for rtPA given within 3 hrs, but with increased
risk of bleeding
• Risk of bleeding is higher …
–Larger infarct, longer duration, and higher dose
Indications
• Onset < 3 hrs
• CT shows no ICH, No edema >1/3 MCA territory
• Age >18 yrs
• Consent

26. …………………..cont’d
Anti-Platelet Agents
– ASA is the only drug studied
– studies revealed ASA reduced both recurrence and
mortality minimally
– Safe and beneficial
Anti-Coagulation
• Role in Thrombotic stroke is uncertain
• Role in embolic stroke
 Useful both for primary and secondary prevention and established
embolic stroke

27. Rehabilitation
• Improves neurologic outcome and reduces
mortality
• Occupational, physical, speech therapy
• Prevention of Complications of immobility
• Physical therapy can recruit unused neural
pathways

28. Prevention of stroke
Primary Prevention
• Risk factor modification and Rx
• Cardiac illnesses
• Anti - Platelet Agents
– Can prevent TIA , Stroke
– Inhibit formation of intraarterial platelet aggregates, thrombus
formation and embolization
– ASA, Clopidogrel, ASA+ dipyridamole
– Ticolopidine
– FDA Recommendation -- 50- 325 mgs of ASA daily
• Most anti-platelets reduce risk of vascular events in pts at risk.
• Relative risk reduction for stroke 25- 30 % , and for all vascular events 25
%.
• Anti- coagulation for those with cardiac illness ( eg. AF, MI, Prosthetic
Valves )

29. Intracranial Hemorrhage
• ICH is caused by bleeding directly into or around the
brain
• Spontaneous rupture of deep, small penetrating artery
• Commonest Sites
• Putamen, Thalamus, Pons, Cerebellum
• it produces neurologic symptoms by producing
a mass effect on neural structures,
from the toxic effects of blood itself, or
by increasing intracranial pressure
• Most common type of ICH
• Account for about 10% of all stokes
• Associated with 50% of case fatality

30. ……………ICH
• CAUSES
– HTN
– TRAUMA,
– CEREBRAL AMYLOID ANG
• RISK
– advanced age
– heavy alcohol consumption
– cocaine use
• Most hypertensive IPH develop within 30-90/min

31. Clinical feature
Symptoms
– Almost always in awake & some times stressed pt
– Abrupt onset of focal neurologic deficit typically worsen over 30-90min
– Diminished level of consciousness
– Headache & vomiting
– Seizure uncommon
SIGNS
– Putamen → contralateral hemi paresis
– Thalamic → contralateral hemiplegia, prominent sensory deficit ,typical
ocular disturbances
– Pontine → deep coma with quadriplegia, pin point pupils
– Cerebellar → develop over several hours occipital headache ,repeated
vomiting, ataxia of gait & dizziness or vertigo

32. IMAGING
• CT→ the most reliable
→ after 2wks value decreases mimic infarct
• MRI ,CT angiog
when the cause of ICH is uncertain
if pts presented >1-2 wks after onset
younger non hypertensive and
hematoma is unusual site for HTN

33. MANEGEMENT
• ABC of life
• CONTROL BP elevation treat if SBP>180
DBP>105
• TREATMENT of ↑ ICP with manitol or ventriculostomy
• SURGERY
– indicated for cerebellar hematomas >3cm
PROGNOSIS
– worst with supratentorial hematoma >60ml
– extension into the ventricular system

34. Subarachnoid Hemorrhage
• Characterized by extravasations of blood into the spaces
covering the CNS that are filled with CSF
• Excluding head trauma, the most common cause of SAH is
rupture of saccular aneurysm ~ 80% of cases, others are
vascular anomaly and extension from 1ry ICH
• Incidence accounts for 2-5% of all new strokes
• Affects 21,000-33,000 popn each yr in US
• Aggregate world wide incidence is ~ 10.5 cases/100,000
person/yr
• Incidence increases with age: mean age at presentation is
55yrs
• Risk for women is 1.6x that of men
• Risk for blacks is 2.1 x that of whites

35. • Average case fatality rate is 51% and accounts
for 5% of deaths from stroke
• Most deaths occur within 2wks after the ictus,
10% before pt receives medical attention, 24%
within 24 hrs after the event
• Aneurysm size and sites are important in predicting risk of
rupture.
– those > 7mm in diameter and those at top of
Basilar artery and at origin of Post. Communicating
artery are at high risk of rupture

36. ……………SHA
• Causes
• Saccular aneurysm
• Trauma
• AVM
• Extension from an intraparenchymal
hmmge

37. Clinical Manifestation
• Unruptured Aneurysm--- ASxic
• Sudden transient loss of consciousness: ½ pts
• Sudden severe headache ~ 45% pts
• Nausea, vomiting, neck pain and photophobia
• Focal Signs
• P/E
– Retinal hamorrhage
– Meningismus
– Focal neurologic deficit may occur

38. Diagnosis
• CT: a good quality CT will reveal SAH in 100% of
cases within 12 hr after onset of Sxs and in > 93%
within 24 hr.
• Can also demonstrate intraparenchymal hematoma,
hydrocephalus and cerebral edema
• Can locate the underlying aneurysm.
• Most reliable test for predicting cerebral vasospasm
and poor outcome
Sensitivity drops to 50% at 7days
• LP: should be performed in any pt with suspected SAH

39. Complications
• Rebleeding
• Hydrocephalus
• Vasospasm
• Hyponatremia
• Seizure
 Seen in up to 1/3rd of pts
 May lead to rebleeding
 Prophylactic anticonvulsant mandatory

40. Management of SAH
• Surgical management
– Clipping
– Coil
• Medical
– ABC
– BP control, maintain adequate cerebral perfusion
– ICH Mx ( Medical, Surgical )
– Definitive Mx (repair) of aneurysm
– Quiet room, sedation, laxatives, analgesics
– Prophylactic phenytoin
– Steriods- for head/neck pain, otherwise not beneficial
– Preventing rebleeding, Managing vasospasm, hydrocephalus, and
hyponatremia
– Preventing pulmonary embolism