This document provides information on ischemic stroke. Some key points: - Ischemic stroke occurs when blood flow to the brain is blocked, typically by a clot. It accounts for 80% of strokes. - The brain receives blood supply from two pairs of arteries: the internal carotid arteries and vertebral arteries. Strokes can occur in the anterior or posterior circulation territories. - Clinical assessment involves determining the neurological deficits, their onset, and ruling out "stroke mimics". Scoring systems like NIHSS and ASPECTS are used to evaluate severity. - Management involves supporting vital functions, controlling risk factors like blood pressure, preventing complications, and in some cases reperfusion therapies like thrombol

1. ISCHEMIC STROKE

2. Contents
1. Neurovascular Anatomy
2. Definition
3. Terminology
4. Pathophysiology
5. Classification
6. Assessment and diagnosis
• Exclude stroke mimics
7. Related scoring system
• NIHSS
• ASPECT
• ABCD2
• MODIFIED RANKIN SCORE
8. Management
9. CT BRAIN IMAGES

3. Neurovascular Anatomy
• Brain supplied by two pairs of arteries
1.Bilateral Internal Carotid Arteries (anterior)
2.Bilateral Vertebral Arteries (posterior)
• Anterior Circulation (ICA > ACA and MCA)
1.Supplies the frontal, parietal and part of the Temporal Lobe
• Posterior Circulation (Vertebral arteries > BASILAR
ARTERY> PCA)
1.Supplies the Occipital Lobe, Cerebellum, Brainstem and part of
the Temporal Lobe
• Circle of Willis
1.Anterior and Posterior Circulation are interconnected

5. Circle of Willis
1. Anterior cerebral
artery (left and right)
2. Anterior communicating
artery
3. Internal carotid artery (left
and right)
4. Posterior cerebral
artery (left and right)
5. Posterior communicating
artery (left and right)

7. 1. ACA : medial aspect of the cerebral
hemispheres back to the parietal lobe
• Medial lenticulostriate arteries :globus
pallidus and medial portion of
the putamen
• Recurrent artery of Heubner : IC,
GP, CN etc
2. MCA : majority of the lateral surface of the
hemisphere
• Lateral lenticulostriate arteries: Lateral
portion of the putamen and external
capsule as well as the upper internal
capsule.
3. Anterior Choroidal artery : branch of ICA and
supply many deep structures eg : IC,
thalamus,optic tract ,GP, CN etc
4. PCA : posteromedial surface of the temporal
lobe and the occipital lobe

9. 1. ACA : medial aspect of the cerebral hemispheres back to
the parietal lobe
• Medial lenticulostriate arteries :globus pallidus and
medial portion of the putamen
• Recurrent artery of Heubner : IC ,GP,CN etc
2. MCA : majority of the lateral surface of the hemisphere
• Lateral lenticulostriate arteries: Lateral portion of
the putamen and external capsule as well as the
upper internal capsule.
3. Anterior Choroidal artery : branch of ICA and supply many
deep structures eg : IC, thalamus,optic tract ,GP, CN etc
4. PCA : posteromedial surface of the temporal lobe and the
occipital lobe

10. ASCENDING AND
DESCENDING TRACTS

11. DESCENDING TRACT
PYRAMIDAL TRACT
• voluntary control of the muscles and face
• Originate from MOTOR CORTEX
1. Corticospinal tracts
2. Corticobulbar tracts
EXTRAPYRAMIDAL TRACT
• Responsible for involuntary and automatic control of
all musculature egmuscle, tone, balance, posture, locomotion
• Originate from BRAIN STEM
1. Vestibulospinal
2. Reticulospinal
3. Rubrospinal
4. tectospinal

12. ASCENDING
TRACTS
DESCENDING
TRACTS

13. DEFINITION OF STROKE
•A clinical syndrome characterized by rapidly
developing clinical symptoms and/or signs of
focal, and at times global, loss of cerebral
function, with symptoms lasting more than 24
hours or leading to death.
•no apparent cause other than that of a vascular
origin

14. Core : Infarcted brain, not salvageable
Penumbra
• located around the ischemic core
• Hypoperfused brain at risk for progression to infarction, salvageable
• target of reperfusion therapy

15. Core : Infarcted brain, not salvageable
Penumbra
• located around the ischemic core
• Hypoperfused brain at risk for progression to infarction, salvageable
• target of reperfusion therapy
• PENUMBRA represented by total area of hypoperfused brain MINUS infarcted core
• Depicted by prolonged time it takes for contrast to reach and traverse areas of the brain. Most
commonly used threshold in CTP is Tmax > 6s.
MRI
CT PERFUSION

16. Transient Ischaemic Attack (TIA)
• However,a time-based definition is inadequate because there is risk
of permanent tissue infarction even when focal transient neurologic
symptoms last less than one hour.
• NEW DEFINITION : a transient episode of neurologic dysfunction
caused by focal brain, spinal cord, or retinal ischaemia, without acute
infarction.
•MEANS NO HYPODENSITY IN CT BRAIN
OLD DEFINITION (time-based)
characterized by an acute loss of focal cerebral or monocular functions with symptoms lasting less
than 24 hours and which is thought to be due to inadequate cerebral and ocular blood supply as a
result of arterial thrombosis or embolism.

18. Timing of stroke
Strokes may be classified and timed as:
I. Early hyperacute (a stroke that is 0–6 hours old) *Ideal patient for
thrombolysis/thrombectomy*
II. Late hyperacute (6–24 hours) *decision for thrombolysis based on
advanced imaging*
III. Acute (24 hours to 7 days)
IV. Subacute (1–3 weeks)
V. Chronic (more than 3 weeks)

19. Pathophysiology
LACUNAR STROKE

21. Terminology

22. Both refers to Unilateral muscle weakness
HEMIPARESIS
• Partial weakness
• Motor power 1 - 4+
HEMIPLEGIA
• Complete paralysis
• Motor power 0

23. Aphasia
• a disorder of language and Part of higher
cortical function
• Can be fluent (eg : Wernicke’s) or nonfluent
(Broca’s) aphasia
• Test by asking pt to describe the situation in
the picture and name the objects .
Dysarthria
• disorder of the motor production or
articulation of speech
• breakdown in performing the coordinated
muscular movements necessary for
speech production.
• Test by asking pt to read given words.
General rule
No matter how garbled the speech, if the patient is speaking in
correct sentences—using grammar and vocabulary—he has
dysarthria and not aphasia.

24. CLASSIFICATION
1. TOAST – Aetiological
2. OXFORD –Clinical

26. Relevant history
1. Underlying medical condition and premorbid status (RANKIN
SCORE)
2. What is the deficit?
• Weakness
• Numbness
• Slurred speech/language problem
• Visual complaint
• Loss of balance/gait
3. Onset of deficit (witnessed or awake stroke)
BEFAST >>>> ACTIVATE STROKE PROTOCOL

27. Involving
subcortical area
Involving
cortical area
Involving
cortical area

28. Higher cortical functions
The higher cortical functions include language, vision,
recognizing objects in space (visuospatial recognition), and
awareness. characteristics of higher-order functions are as
follows:
• The cerebral cortex must be involved—complex interactions
occur within the cortex and between it and other brain areas
• Both conscious and unconscious information processing
occurs

30. Homunculus

31. infarction of the
optic radiations
HEMINEGLECT
1

32. Parietal lobe involvement –MCA infarct
• prominent sign is usually a hemisensory deficit.
• can cause Gerstmann syndrome (dominant hemisphere)
1. Left/right confusion, - ask the patient to raise a specific hand
2. Finger agnosia- Inability to distinguish or identify individual fingers of the
hand
3. Acalculia (inability to do arithmetic) – Simple addition/subtraction
4. Agraphia (inability to write letters or words correctly) – write name
• and/or astereognosia (inability to recognize objects by
touch/palpation)

33. 2

34. • DUE to disease of small penetrating arteries
• Example of lacunar stroke : Internal capsule
stroke
• IC contains critical ascending and
descending tracts.
• Ascending tracts : CTS and CBT
• Located at ant part of posterior limb of IC
• Descending tracts : Third order neurons >
thalamocortical fibers
• Located at post part of posterior limb of IC
• Due to organized arrangement of these tract
in IC, lacunar infarct
• will cause specific deficit (motor or sensory)
• cause equal extent of weakness of all FACE,ARM
AND LEG due convergence of all fibres at one
place.

35. • Homonymous hemianopia
• Cortical blindness
• Ataxia
• Dizziness or vertigo
• Dysarthria
• Diplopia
• Dysphagia
As a rule, brainstem stroke causes ipsilateral cranial nerve deficits
and a contralateral hemisensory defect and/or hemiparesis.
Horner’s syndrome (lateral medullary syndrome/ Wallenberg
syndrome )
• miosis (a constricted pupil),
• ptosis (a weak, droopy eyelid),
• anhydrosis (decreased sweating),
• enophthalmos
Cerebellar signs
• Scanning speech –slow and
breaking of words
• Nystagmus
• Dysmetria : finger nose test
• Dysdiadochokinesia
• Broad stand and wide staggering
gait, fall towards lesion.
ROMBERG TEST : PROPRIOCEPTION test,
not for cerebellar function

36. Broad stand and wide staggering gait, fall towards lesion.

37. CLINICAL FEATURES

38. Spasticity
• Normal situation : descending
tract predominantly has inhibitory
input (less muscle contraction)
• In UMNL, both descending
inhibitory and excitatory input
from cortex is lost.
• However LMN still has excitatory
input from muscle spindle.
• Leading to increase in tone
Initially hypotonic ,but as time goes
on become hypertonia.

39. Hyperreflexia
• loss of net inhibitory
activity from descending
motor results in
disinhibition of spinal
reflex circuits.
• leads to exaggerated deep
tendon reflexes

40. Clonus
Due to exaggerated stretch
reflex of the gastrocnemius
and soleus
• inhibitory dampening
effect of descending
nerves on alpha and
gamma motor neurons is
removed.

41. Babinski Reflex
•Generally there is net
cortical inhibition to
dorsiflexion.
•UMNL there is
disinhibition to
dorsiflexion causes up
going plantar
extension of the large toe along with extension
and fanning of the remaining toes.

42. National Institutes
of Health Stroke
Scale (NIHSS)

43. SUMMARY

44. Involving
subcortical area
Involving
cortical area
Involving
cortical area

45. Hyperacute infarct
• Hyperdense vessel sign represents acute intraluminal thrombus,
recognised as focal or linear increased (white) density within the
artery on non-contrast CT head.
• most commonly seen in MCA
Early parenchymal signs include
subtle blurring, decreased
attenuation and swelling of the
grey-white matter junction of
affected regions.
It should be noted that deep grey
matter structures are affected
before the cortex due to
lenticulostriate arteries being end
arteries, and cytotoxic edema
occurring earlier..

46. • Loss of Insular
ribbon sign
describes the
loss of
grey/white
matter
differentiation
in the lateral
• margins of the
insular cortex,
supplied by
the insular
segment of
the MCA

47. • Obscuration of the
lentiform nucleus, also
called blurred basal
ganglia, is an
important sign of
infarction.

48. Management
1.Airway support and oxygen
supplemental oxygen if SPO2 <95%
2.Avoid infection
•Treat according to source of infection

49. Blood pressure control in AIS
• 15% reduction over 24hours if BP of ≥220/120 mm Hg
• Do not treat hypertension If SBP<220 OR DBP <120. Mild HPT is desirable
at 160-180/90-100 .This is to maintain cerebral perfusion to reduce further
ischemia.
• drugs:
• IV Labetalol 10-20mg boluses at 10 mins intervals up to 150-300mg or IVI Labetalol
• T.Captopril 6.25-12.5mg.
• Nifedipine should be avoided because of the risk of rapid decline in blood pressure.
• In special circumstances such as concomitant acute coronary event, acute
heart failure, aortic dissection, post-thrombolysis sICH, or
preeclampsia/eclampsia early reduction of bp is indicated.

50. GLUCOSE
Target 6.0-10.0 mmol/L
and ensure that
hypoglycemia is avoided.
SEIZURE
• Recommendation: New-onset
seizures in acute stroke should
be treated using short-acting
medications if they are not self-
limiting.
• Prophylactic anti-seizure meds
is not recommended.
Literature review concluded tight glucose
(4.0-7.5 mmol/L) in the first few hours of
acute ischemic stroke does not provide
mortality /morbidity benefit but
significantly increases hypoglycemic
episode.

51. Raised Intracranial Pressure
• Cerebral oedema and increased intracranial pressure largely occur with large cerebral
infarctions.
• Recommendation: Hyperventilation is an emergency measure that acts almost
immediately; a reduction of the PCO2 by 5 to 10 mmHg can lower intracranial pressure
by 25% to 30%.
• Recommendation: Mannitol (0.25 to 0.5g/kg) administered intravenously over 20
minutes lowers intracranial pressure and can be given every 6 hours.42 Maximum daily
dose is 2g/kg
• If hydrocephalus is present, drainage of cerebrospinal fluid via an intra-ventricular
catheter can rapidly lower intracranial pressure
• significant reduction in mortality when decompressive craniectomy was performed within
48 hours of malignant MCA infarction in <60 y/o pts/ .
• Hemicraniectomy and surgical decompressive therapy within 48 hours after symptom
onset is recommended to control intracranial pressure and prevent herniation among
those patients with very large infarcts of the cerebral hemisphere

52. Malignant infarct
• Usually Large MCA infarct
• caused by an embolic or thrombotic occlusion of the distal portion of the ICA or sphenoidal
segment (M1) of the MCA territory.
• Cause cerebral edema that is severe enough to produce brain tissue shifts and
herniation
• ASPECTS of ≤7 at baseline was independently associated with the development of
malignant brain edema
• Malignant MCA stroke is indicated by:
• MCA territory stroke of >50% on CT
• Perfusion deficit of >66% on CT
• Infarct volume >82 mL within 6 hours of onset (on MRI)
• Infarct volume of >145mL within 14 hours of onset (on MRI)
• https://www.ahajournals.org/doi/full/10.1161/strokeaha.111.619734

53. ASPECTS SCORE
• Determines MCA stroke severity using available CT
• A normal CT scan receives an ASPECTS of 10 points.
• An ASPECTS of ≤7 points highly correlates with negative functional outcome, determined
by Modified Rankin Scale (mRS).

54. Measures the degree of disability or dependence in the daily
activities of people who have suffered a stroke or other causes of
neurological disability.

55. NUTRITION
• Recommendation: Enteral feeding should be started within 7
days of admission (oral or tube feeding).
• was associated with an absolute reduction in risk of death/poor
outcome
• water swallowing test
• wet voice after swallowing, incomplete oral-labial closure, or
coughing reflex on swallowing indicates high risk of developing
aspiration.
• Absence of gag reflex alone does not predict risk of
aspiration.

56. • Recommendation: The recommended dose of oral
Aspirin post-stroke is 75mg to 325mg daily. (Level I,
Grade A)
• A 25% risk reduction of stroke was seen in all patients with stroke
who received Aspirin. Aspirin given within 48 hours had shown to
be beneficial in reducing recurrent stroke and deaths.
• Studies comparing the effects of different dosages of Aspirin had
failed to show any differences in stroke recurrences.
• Daily Aspirin is not recommended for primary prevention of
stroke in in view of the of bleeding which outweighs any
benefits.
ASPIRIN

57. DAPT IN TIA/MINOR STROKE
Minor stroke and HIGH RISK TIA patients
(NIHSS <5, ABCD2 >2), showed that those who
received a combination of Clopidogrel and
Aspirin had a lower risk of major ischemic events
for 3 weeks to 3 months, but a higher risk of
major hemorrhage at 90 days than those who
received Aspirin alone.

60. Who requires admission?? Who can be consider for discharge?
• LOW RISK ABCD2 0-2
• Need to include social and logistic factors
• ABCD2 score alone does not sufficiently identify the short-term risk
for stroke who can be safely discharged from the ED. (ACEP 2016)

61. Stroke in AF
• Aspirin could be considered before the initiation of OAC after an AF
patient suffers from an ischemic stroke.
• Oral anticoagulant (OAC) has been proven to be superior to no
treatment or Aspirin in patients with NVAF.
• OAC to prevent cardioembolic stroke is recommended for all NVAF
male patients with CHA2DS2-VASc score of 2 or more and female
patients with a CHA2DS2-VASc score of 3 or more.
• DOACs are preferred as compared to VKA or Aspirin in AF patients
with a previous stroke. (Level 1 Evidence , Grade A)

62. HAS-BLED score

64. • Disability outcomes (RANKIN SCORE) after acute stroke did not differ
significantly between patients assigned to a lying-flat position for 24
hours and patients assigned to a sitting-up position with the head
elevated to at least 30 degrees for 24 hours.
*85% of patient in this study having ischemic stroke.*

66. References
1. CPG ISCHEMIC STROKE 2020
2. AHA 2021 Guideline for the Prevention of Stroke in Patients With
Stroke and Transient Ischemic Attack
3. UPTODATE
4. Localization in Clinical Neurology Seventh edition Paul W. Brazis,
MD
5. Fundamentals of Neurology ,An Illustrated Guide 2nd Revised and
Updated Edition Heinrich Mattle, MD