The document defines various terms related to strokes, including stroke, TIA, progressive stroke, completed stroke, and hemorrhagic vs ischemic stroke. It discusses the epidemiology, risk factors, types, clinical features, investigations, and differential diagnosis of strokes. Specifically, it provides details on the clinical presentations and neurological deficits associated with occlusion of different arteries in the anterior and posterior circulations. It also outlines the objectives and modalities used to investigate a potential stroke, including non-invasive tests like CT, MRI, and Doppler ultrasound and invasive tests like angiography.

1. Ashwin Haridas
Asem Ali Ashraf
Adam Ebrahim

2. Definitions
 Stroke
 Clinical syndrome of rapid onset of focal deficits of
brain function lasting more than 24 hours or leading to
death
 Transient Ischemic attack (TIA)
 Clinical syndrome of rapid onset of focal deficits of
brain function which resolves within 24 hours
 Amaurosis fugax

3. Definitions
 Progressive Stroke
 A stroke in which the focal neurological deficits worsen
with time
 Also called stroke in evolution
 Completed Stroke
 A stroke in which the focal neurological deficits persist
and do not worsen with time

4. Epidemiology
 Third most common cause of death after cancer and
ischeamic heart disease
 Most common cause of severe physical disability
 Prevalence of stroke in India is about 1.54 per 1000
 Death rate is about 0.6 per 1000
 Incidence and prevalence of stroke is on the rise due
to increasing adoption of unhealthy lifestyle & an
increasing life expectancy

5. Stroke Risk Factors
 Fixed
 Age
 Gender (Male>Female)
 Race (Afro-
Caribbean>Asian>Euro
pean)
 Heredity
 Previous vascular event
eg. MI, peripheral
embolism
 High fibinogen
 Modifiable
 Hypertension
 Heart disease (Atrial
fibrillation,
endocarditis)
 Diabetes mellitus
 Hyperlipidaemia
 Smoking
 Excess alcohol
consumption
 Oral contraceptives

6. Anterior Circulation
Posterior Circulation

7. Middle Cerebral Artery

8. Anterior Cerebral Artery

9. Posterior Cerebral Artery

10. Types of Stroke
 Ischemic
 Hemorrhagic

11. Ischemic Stroke
 80% of strokes
 Arterial occlusion of an intracranial vessel leads to
hypoperfusion of the brain region it supplies
 Two etiological types
 Thrombotic
 Embolic

12. Etiology of ischemic stroke
 Thrombotic
 Lacunar stroke
 Large vessel thrombosis
 Hypercoagulable
disorders
 Embolic
 Artery to artery
 Carotid bifurcation
 Aortic arch
 Cardioembolic
 Atrial fibrillation
 Myocardial infarction
 Mural thrombus
 Bacterial endocarditis
 Mitral stenosis
 Paradoxical embolus

13. Thrombotic Stroke
 Atherosclerosis is the most common pathology
leading to thrombotic occlusion of blood vessels
 Hypercoagulable disorders – uncommon cause
 Antiphospholipid syndrome
 Sickle cell anemia
 Polycythemia vera
 Homocysteinemia
 Vasculitis: PAN, Wegener’s granulomatosis, giant cell
arteritis

14.  Lacunar stroke
 Accounts for 20% of all strokes
 Results from occlusion of small deep penetrating
arteries of the brain
 Pathology: lipohyalinosis & microatheroma
 Thrombosis leads to small infarcts known as lacunes
 Clinically manifested as lacunar syndromes
Thrombotic Stroke

15. Embolic Stroke
 Cardioembolic stroke
 Embolus from the heart gets lodged in intracranial vessels
 MCA most commonly affected
 Atrial fibrillation is the most common cause
 Others: MI, prosthetic valves, rheumatic heart disease
 Artery to artery embolism
 Thrombus formed on atherosclerotic plaques gets embolized
to intracranial vessels
 Carotid bifurcation atherosclerosis is the most common
source
 Others: aortic arch, vertebral arteries etc.

16. Etiology of ischemic stroke

17.  Blood supply to the brain is autoregulated
 Blood flow
 If zero leads to death of brain tissue within 4-10min
 <16-18ml/100g tissue/min infarction within an hour
 Ischemia leads to development of an ischemic core
and an ischemic penumbra
Pathophysiology of Ischemic Stroke

19. Ischemic Penumbra
 Tissue surrounding the core region of
infarction which is ischemic but
reversibly dysfunctional
 Maintained by collaterals
 Can be salvaged if reperfused in time
 Primary goal of revascuralization
therapies

20. ATP depletion
Hypoperfusion
Failure of Na+
/K+
ATPase membrane ionic pump
Calcium entry
Glutamate release
Activation of lipid peroxidases, proteases & NO synthase
Destruction of intracellular organelles, cell
membrane & release of free radicals
Free fatty acid release
Activation of pro-coagulant
pathways
Liquefactive necrosis
Thrombus/embolus
Membrane depolarization & cytotoxic cellular
edema

21. Hemorrhagic Stroke
 Two types
 Intracerebral
hemorrhage(ICH)
 Subarachnoid
hemorrhage(SAH)
 Higher mortality rates
when compared to
ischemic stroke

22. Intracerebral Hemorrhage
• Result of chronic hypertension
• Small arteries are damaged due to hypertension
• In advanced stages vessel wall is disrupted and leads
to leakage
• Other causes: amyloid angiopathy, anticoagulant
therapy, cavernous hemangioma, cocaine,
amphetamines

23. Subarachnoid Hemorrhage
 Most common cause is rupture of saccular or Berry
aneurysms
 Other causes include arteriovenous malformations,
angiomas, mycotic aneurysmal rupture etc.
 Associated with extremely severe headache

24. Pathophysiology Of Hemorrhagic Stroke
 Explosive entry of blood into the brain parenchyma
structurally disrupts neurons
 White matter fibre tracts are split
 Immediate cessation of neuronal function
 Expanding hemorrhage can act as a mass lesion and
cause further progression of neurological deficits
 Large hemorrhages can cause transtentorial coning
and rapid death

25. CLINICAL FEATURES

26. History
 Ask for onset and progression of neurological
symptoms – completed stroke or stroke in evolution
 History of previous TIAs & amaurosis fugax
 History of hypertension & diabetes mellitus
 History of heart conditions like arrhythmias, RHD &
prosthetic valves

27.  History of seizures & migraine
 History of anticoagulant therapy
 History of oral contraceptive use
 History of any hypercoagulable disorders like sickle
cell anemia & polycythemia vera
 Substance abuse: cocaine, amphetamines
History

28. Examination of a stroke patient
 The neurological examination is highly
variable and depends on the location of the
vascular lesion.
 Skin: look for xanthelasma,rashes
(arteritis,splinter haemorrhages,livedo
reticularis),limb ischemia(DVT)
 Eyes:look for diabetic changes,retinal
emboli,hypertensive changes,arcus
senilis(refer to ophthalmologist)

29. Examination of a stroke patient
 CVS: hyper/hypotension, abnormal
rhythm(atrial fibrillation),murmurs(valvular
anomaly),raised JVP(heart failure),peripheral
pulses and bruits(generalised arteriopathy)
 Respiratory system: pulmonary edema,
infection
 Abdomen: urinary retention
 Locomotor system: injuries sustained during
collapse with stroke, comorbities which
influence functional abilities.

30. General feature
 Most cerebrovascular diseases are manifest by the
abrupt onset of a focal neurologic deficit, as if the
patient was "struck by the hand of God.”
 The clinical manifestations of stroke are highly
variable because of the complex anatomy of the brain
and its vasculature.

31. ‘HAND OF GOD’

32. CLINICAL CLASSIFICATION

34. Stroke Syndromes
 Stroke syndromes are divided into: (1) large-vessel
stroke within the anterior circulation
 (2) large-vessel stroke within the posterior
circulation,and
 (3) small-vessel disease of either vascular bed.

35. Stroke Within the Anterior
Circulation
 The internal carotid artery and its branches comprise
the anterior circulation of the brain i.e the anterior
and middle cerebral arteries

36. Middle cerebral artery
 Signs and symptoms: Structures involved
 Paralysis of the contralateral face, arm, and leg; sensory
impairment over the same area: Somatic motor area
 Motor aphasia: Motor speech area of the dominant
hemisphere
 Central aphasia:Central, suprasylvian speech area and
parietooccipital cortex of the dominant hemisphere
 Conduction aphasia: Central speech area (parietal
operculum)

37. Cont….
 Homonymous hemianopia (often homonymous inferior
quadrantanopia): Optic radiation deep to second temporal
convolution
 Paralysis of conjugate gaze to the opposite side: Frontal
contraversive eye field or projecting fibers
 Central aphasia:Central, suprasylvian speech area and
parietooccipital cortex of the dominant hemisphere
 Conduction aphasia: Central speech area (parietal
operculum)
 Homonymous hemianopia (often homonymous inferior
quadrantanopia): Optic radiation deep to second temporal
convolution

38. Cont..
 Apractognosia(agnosia +apraxia) of the nondominant
hemisphere:Nondominant parietal lobe (area corresponding to
speech area in dominant hemisphere); loss of topographic
memory is usually due to a nondominant lesion, occasionally to
a dominant one.
 Apraxia is a neurological disorder characterized by loss of the
ability to execute or carry out learned purposeful movements,
despite having the desire and the physical ability to perform
the movements. It is a disorder of motor planning.
 Agnosia (a-gnosis, "non-knowledge", or loss of knowledge) is
a loss of ability to recognize objects, persons, sounds, shapes,
or smells while the specific sense is not defective nor is there
any significant memory loss

39. Deficits Due To ACA Occlussion
 Occlusion of the anterior cerebral artery may result in the
following defects:
 If stroke occurs prior to the anterior communicating artery it
is usually well tolerated secondary to collateral circulation
 Paralysis of the contralateral foot and leg
 Sensory loss in the contralateral foot and leg
 Left sided strokes may develop transcortical motor aphasia
 Gait apraxia
 Urinary incontinence which usually occurs with bilateral
damage in the acute phase

40. Internal Carotid Artery
 The clinical picture of internal carotid occlusion
varies depending on whether the cause of ischemia is
propagated thrombus, embolism, or low flow. The
cortex supplied by the MCA territory is affected most
often. With a competent circle of Willis, occlusion
may go unnoticed.

41. Internal Carotid Artery
 If the thrombus propagates up the internal carotid
artery into the MCA or embolizes it, symptoms are
identical to proximal MCA occlusion.
 Sometimes there is massive infarction of the entire
deep white matter and cortical surface.

42. Internal Carotid Artery
 When the origins of both the ACA and MCA are
occluded at the top of the carotid artery, abulia or
stupor occurs with hemiplegia, hemianesthesia,
and aphasia or anosognosia. When the PCA arises
from the internal carotid artery (a configuration
called a fetal posterior cerebral artery), it may also
become occluded and give rise to symptoms
referable to its peripheral territory

43. Internal Carotid Artery
 In addition to supplying the ipsilateral brain, the
internal carotid artery perfuses the optic nerve and
retina via the ophthalmic artery. In ~25% of
symptomatic internal carotid disease, recurrent
transient monocular blindness (amaurosis fugax)
warns of the lesion. Patients typically describe a
horizontal shade that sweeps down or up across the
field of vision

44. Internal Carotid Artery
 A high-pitched prolonged carotid bruit fading into
diastole is often associated with tightly stenotic
lesions. As the stenosis grows tighter and flow distal
to the stenosis becomes reduced, the bruit becomes
fainter and may disappear when occlusion is
imminent.

45. Posterior Circulation
 DYSARTHRIA & FACIAL NUMBNESS
 ATAXIA & HORNER’S SYNDROME
 FACIAL WEAKNESS(LMN)
 HEMIPARESIS
 HEMISENSORY LOSS
 HEMIANOPIA
 LOSS OF CONSCIOSNESS
 DIPLOPIA, VERTIGO, VOMITING

46. CLASSICAL PRESENTATIONS
THROMBOTIC
 H/O TIA
 STROKE IN
EVOLUTION
 USUALLY HAPPENS
EARLY MORNING
EMBOLIC
 PATIENTS WITH KNOWN
HEART DISEASE LIKE IHD,
VALVULAR HEART DISEASE
 RAPID RECOVERY
HAEMORRHAGIC
 STROKE IN
HYPERTENSIVE
PATIENTS
 ASSOCIATED WITH
EMOTIONAL
EXCITEMENT
 HEADACHE & VOMITING

47. DIFFERENTIAL DIAGNOSIS
 SPACE OCCUPYING LESION(TUMOR)
 SEIZURE
 MIGRAINE
 SUBDURAL HAEMATOMA
 METABOLIC DISTURBANCE LIKE
HYPOGLYCAEMIA

48. Hypoglycemia
 That transient hypoglycemia may produce a
stroke like picture with hemiplegia and
aphasia has been known for years.
 The wide use of bedside rapid laboratory
testing for glucose now makes this easily
detectable and treatable. The hemiplegia
may resolve immediately with the
administration of intravenous glucose but
resolution over a hours is also reported

49. Space Occupying Lesions
 Subacute or chronic duration of symptoms, however
some patients may present with acutely probably due
to bleeding into a tumour
 Associated with deep seated bursting headache,
projectile vomiting due raised ICT

50. SEIZURES AND POST ICTAL STATES
 Traditional thought is that these postictal
symptoms are manifestations of seizure-induced
alterations in neuronal function that are
reversible; structural neuronal alterations are not
present. The postictal weakness or Todd’s
paralysis usually follows partial motor seizures but
may follow generalized seizures as well. Duration
is usually brief but may last 48 hours

51. MIGRAINE
 Migraine may actually precipitate a stroke, but there is
also a variant of migraine, hemiplegic migraine, where
unilateral hemiparesis outlasts the headache. This is
difficult if not impossible to diagnose correctly at first
presentation when it must be regarded as a diagnosis of
exclusion; only with recurrent, stereotypic attacks can this
be suspected. Cases with alternating hemiplegia have been
reported. At times this disorder has been shown to be
familial.

52. SUMMARY
 Rapid onset focal deficit of brain function confirms
stroke
 Onset and progression will decide the aetiology
 Precise history of deficit will decide the site of lesion

54. INVESTIGATION OBJECTIVES
 To confirm the vascular nature of the lesion
 The pathological type of the vascular lesion
 The underlying vascular disease
 Risk factors present

55. INVESTIGATION MODALITIES:
BRAIN
NON-INVASIVE
 CT Scan
 MRI Scan
 MR Angiography
 Doppler Ultrasound
 EEG
 PET
 SPECT
INVASIVE
 Lumbar Puncture
 Contrast Angiography
(Cerebral Arteriography)
 CT Angiography

56. PATHOLOGICAL TYPES
STROKE
HAEMORRHAGIC ISCHAEMIC

57. CT SCAN
 Mandatory initial investigation
 Haemorrhage appears instantly as a hyperdense area
 Infarct appears as a hypodense area
 Infarct may not appear before 48 hrs
 MRI may be done instead but ct scan is more sensitive for
detecting haemorrhage
 Diffusion weighted MRI is good for identifying ischaemic
lesion

59. ISCHAEMIC LESION

60. STROKE PATIENT
CT SCAN/MRI
VASCULAR NATURE
CONFIRMED
HAEMORRHAGE ISCHAEMIA
Cont’d…

61. SEARCH FOR SOURCE
CEREBRAL
ARTERIOGRAPHY
MRA/CTA DOPPLER PET/SPECT
SEARCH FOR SOURCE
Cont’d…

63. Carotid Artery Ultrasound Showing a Completely
Calcified Atherosclerotic Plaque

65. 3-D reconstruction of CT angiogram showing stenosis at the
carotid bifurcation

66. Intra-arterial angiography showing arteriovenous
malformation

67. MR angiogram showing giant aneurysm at
the middle cerebral artery bifurcation

68. NORMAL CT SCAN
HAEMORRHAGE
SUSPECTED
LUMBAR PUNCTURE
CSF WITH BLOOD/
XANTHOCHROMIA
HAEMORRHAGE CONFIRMED

69. UNDERLYING DISEASE
 Cerebral vasculature
 Abnormalities like aneurysms or
 AV malformations
 Cerebral angiography
 Vascular imaging – MRA/CTA or doppler (non invasive)

70. CARDIOVASCULAR
Like MI, atrial fibrillation, valvular diseases etc.
 Electrocardiogram
 Chest X-Ray
 Echocardiography
 Transesophageal ultrasound
 Holter monitoring(paroxysmal nocturnal arrhythmia)
 Blood cultures
UNDERLYING DISEASE

71. UNDERLYING DISEASE
 Serum lipids for hyperlipidemia
 ANA for SLE
 MR Angiography for arterial dissection
 Lupus anticoagulant for antiphospholipid antibody
syndrome
 ESR, CRP, ANCA for vasculitis
 PT, aPTT, Platelet count for bleeding disorders
 Proteins C & S for hypercoagulability

72. TREATMENT OBJECTIVES
1. MINIMIZE VOLUME OF BRAIN IRREVERSIBLY
DAMAGED
2. PREVENT COMPLICATIONS
3. REHABILITATION
4. REDUCE RISK OF RECCURENCE

73. MANAGEMENT OF A TRANSIENT
ISCHAEMIC ATTACK (TIA)
MEDICAL MANAGEMENT
(if diffuse atherosclerotic disease or poor operative
candidates)
 Stop smoking
 Concurrent medical problems to be addressed:
 Emboli from heart and other parts of cardiovascular
system
(a) anti coagulants: Heparin(IV), Warfarin(oral)
(b) anti platelet drugs: Aspirin(oral), Ticlopidine
 Diabetes, Hypertension, Hyperlipidemia

74. MANAGEMENT OF A TRANSIENT
ISCHAEMIC ATTACK(TIA) – Cont’d
SURGICAL MANAGEMENT
 CAROTID AND CEREBRAL ARTERIOGRAPHY
STENOSIS
Mild to Moderate Severe
Regular Follow Up
Carotid Endarterectomy
 All above can be done only if there is relatively little atherosclerosis
elsewhere in cerebrovascular system.

75. MANAGEMENT OF AN ACUTE
EPISODE OF STROKE
 AIRWAY - Maintain airway, prevent aspiration, keep nil per oral
 BREATHING - Maintain oxygen saturation > 97%
- Supplementary oxygen
 CIRCULATION - Adequacy of pulse and BP
- Fluid, Anti Arrhythmics, Ionotropes
 HYDRATION - Prevent dehydration ; give adequate fluids
- Parenteral or via nasogastric tube
 NUTRITION - Nutritional supplements and Nasogatric feeding
 MEDICATION - Administer medication also by routes other than
oral

76. MANAGEMENT OF AN ACUTE
EPISODE OF STROKE Cont’d
 BLOOD PRESSURE - unless indicated (heart or renal
failure,hypertensive encephalopathy or aortic dissection) it should
not be lowered for the fear of expansion of infarct.
Ischaemic stroke - maintain 180/110 mm Hg
Haemorrhagic stroke – keep MAP <115 mm Hg
 BLOOD GLUCOSE - INSULIN to treat hyperglycaemia(can increase
infarct size)
- maintain < 200mg%
 TEMPERATURE - early use of antipyretics
 PRESSURE AREAS – To prevent occurrence of decubitus ulcers
 INCONTINENCE

77. EARLY MANAGEMENT

79. ISCHAEMIC STROKE
 THROMBOLYTICS and REVASCULARISATION -
- tPA (alteplase)-0.9mg/kg(max 90mg)
10% of dose – initial IV bolus
remainder infused over one hour
- to be used < 3 hrs of onset of symptoms
(for maximum efficacy)
- haemorrhage to be ruled out
 NEUROPROTECTIVE AGENTS

80. ANTI PLATELET THERAPY
 Asprin, Clopidogrel
- act by inhibiting platelet aggregation and adhesion.
- aspirin 300mg single dose to be given immediately
following diagnosis.
- if alteplase given it can be with held for 24 hrs.
- later aspirin at a dose of 75 mg in combination with
clopidogrel 75 mg daily for about one year duration.

81. ANTI COAGULANTS
 HEPARINS , WARFARIN
-heparins act by accelerating the inhibition of factor II
and factor X of coagulation cascade
-warfarin antagonises vitamin K to prevent activation of
clotting factors
-decrease risk of recurrence and venous thromboembolism
-intra cranial haemorrhage to be excluded before therapy
-more useful if stroke is evolving

82. ANTI COAGULANTS - Cont’d
 HYPEROSMOLAR AGENTS
- reduce cerebral oedema
- 20% mannitol IV – 100ml TID
- oral glycerol if swallow is normal
 Concurrent medical problems such as atrial fibrillations to
be tackled
 OTHERS:
- PENTOXYPHYLLINE (hemorrheology modifier)
to be used within 12 hrs
-NEUROPROTECTIVE AGENTS

83. HAEMORRHAGIC STROKE
 Control of hypertension
 Control coagulation abnormalities (esp due to oral
anticoagulants)
 Surgical decompression
 Surgery for aneurysms and arterio-venous malformations
 Anti platelet
Anti platelet and anti coagulants
anti coagulants are contraindicated

84. REHABILITATION
 PHYSIOTHERAPY - as early as
possible
- initially passive moments
- later active movements
- in every case early mobilization
- prevents contractures, spasticity
and atrophy
 OCCUPATIONAL THERAPY

85. REHABILITATION - Cont’d
 SPEECH THERAPY
 IMPROVE QUALITY OF LIFE
WITH MOTOR AIDS
-leg brace, toe spring , cane ,
walking stick

86. STROKE UNITS –
A MULTIDISCIPLINARY APPROACH
 Immediate resuscitation , prevent complications
and recurrence
 Emergency 24 hr evaluation and comprehensive
care
 Improves neurological outcome
 Reduces mortality
 1000 patients admitted to stroke units saves the
lives of atleast 5o patients at end of 6 months

87. SECONDARY PREVENTION
 Blood pressure control
 Diabetes Management
 Lipid Management
 Smoking Cessation
 Alcohol Moderation
 Weight
Reduction/Physical
Activity
 Carotid Artery
Interventions
 Anti platelet agents /
Anti coagulants
 Statins
 Diuretics +/- ACE
inhibitors

88. COMPLICATIONS
 Due to cortical brain injury(immediate)
- Epilepsy/seizures
- Cerebral oedema
 Residual deficits from stroke
- Paralysis
- Aphasia

89. COMPLICATIONS – Cont’d
 Due to immobility
- Chest infections
- Pressure sores
- Deep vein thrombosis /
pulmonary embolism
- Painful shoulder
- Urinary infection/constipation
- Depression and anxiety

90. PROGNOSIS
ISCHAEMIC STROKE
 Mortality rate in first 30 days is 8-12%
 Can vary depending upon size, location, symptoms of
stroke
 Time that elapses from the event to medical intervention
 First 3 hrs after stroke - GOLDEN PERIOD

91. PROGNOSIS – Cont’d
INTRACEREBRAL HAEMORRHAGE
 Mortality rate in first 30 days is almost 50%
 Site and extent of hematoma also plays a role in
determining the prognosis
 Hamorrhagic strokes have a poor prognosis
compared to ischaemic type .