This document provides an overview of ischaemic stroke, including its definition, risk factors, pathophysiology, clinical presentation, diagnosis and management. Key points include: - Ischaemic stroke accounts for 80% of strokes and results from focal brain infarction due to obstruction of cerebral blood flow. - Major risk factors include hypertension, atrial fibrillation, diabetes, hyperlipidemia and previous stroke or TIA. - Clinical syndromes depend on the location of brain infarction and can include motor/sensory deficits, aphasia and visual field cuts. - Diagnosis involves neuroimaging such as CT, MRI and vascular imaging to identify the cause. - Acute

1. ISCHAEMIC STROKE
Osama Ragab
Lecturer of Neurology
Tanta University
2016

2. Definition
 Stroke is defined as an episode of focal neurologic (brain, retina, spinal
cord) dysfunction (even if less than 24 hours in duration) in which the
autopsy,computedtomography(CT)brainscan,ormagneticresonance
imaging (MRI) brain scan shows features consistent with focal brain
infarctionorhemorrhage.
 Ischaemic stroke is responsible for about 80% of all strokes,
intracerebral haemorrhage for 15%, and subarachnoid haemorrhage for
5%

3. Risk Factors for Stroke
 classifiedasmodifiableandunmodifiableriskforischemicstroke
 - Nonmodifiable risk factors for stroke include older age, male gender,
ethnicity,familyhistory,andpriorhistoryofstroke.
 -Modifiableriskfactorsmaybesubdividedintolifestyleandbehavioral
riskfactorsandnon-lifestylefactors,

4.  modifiable lifestyle risk factors include cigarette
consumptionandillicitdruguse,
 Non-lifestyle risk factors include low socioeconomic
status, arterial hypertension, dyslipidemia, heart disease,
andasymptomaticcarotidarterydisease.
Risk Factors for Stroke

5. CardiaccausesofIS.
Highrisk
 AF–MS–AMI– recentIE–NVAF-dilatedcardiomyopathy.
Moderaterisk
 RemoteMI–PFO–TR–hypertrophicmyopathy-aterial
myxoma
Risk Factors for Stroke

6. AF
Risk Factors for Stroke

7.  arterialhypertension,
reductioninSBPof10to12mmHgand5to6mmHgdiastolicisassociated
witha38%reductioninstrokeincidence.
 Type2DM,
Diabetic persons with retinopathy and autonomic neuropathy have high
riskforischemicstroke.
 HightotalcholesterolandhighLDLconcentration:
patients at risk for stroke or who have had a cerebral infarction should be
treatedtoagoalLDLlevelofbelow70mg/dL.
Risk Factors for Stroke

8.  HeredityandRiskofStroke
 Nonatheroscleroticvasculopathies
 Familialatrialmyxomas,hereditarycardiomyopathies.
 DeficienciesofproteinCandSorantithrombin(AT).
 Inherited metabolic disorders that can cause stroke include
mitochondrialencephalopathyandhomocystinuria.
Risk Factors for Stroke

9. Brain blood supply

10. Brain blood supply

11. Brain blood supply

13. Pathophysiology of Cerebral
Ischemia
 Normalcerebralbloodflowatrestinthenormaladultbrainisapproximately
50to55mL/100g/min.
 Whenbloodflowdecreasesto18mL/100g/min,thebrainreachesathreshold
forelectricalfailure.
 whenbloodflowdecreasesto8mL/100g/min.Celldeathcanresult.
 Thesethresholdsmarktheupperandlowerblood-flowlimitsoftheischemic
penumbra.

14. Pathophysiology of Cerebral
Ischemia

15. Clinical Syndromes of Cerebral
Ischemia
 Transient Ischemic Attacks
TIA is a temporary and “non-marching” neurological
deficit of sudden onset; attributed to focal ischemia of
the brain, retina, or cochlea; and lasting less than 1
hours with free DW MRI.

16. ABCD2 ≥ 4 moderate to high stroke risk & in need for hospital
admission.
Clinical Syndromes of Cerebral
Ischemia

17.  MCAocclusion
 Motor&sensorydeficit (Face>UL>LL)
 homonymoushemianopia
 Gazepreference
 Dominanthemisphere:aphasia
 Nondominanthemisphere:neglect
Carotid Artery System Syndromes

18.  ACAocclusion
 Motor+/-Sensorydeficit (LL>>Face,UL)
 Primitivereflexes
 grasp,suckingreflexes
 Gaitapraxia
 Abulia,akineticmutism,paratonia
Carotid Artery System Syndromes

19.  Amaurosis fugax is the sole feature that
distinguishes the carotid artery syndrome from a
middle cerebral artery (MCA)
Carotid Artery System Syndromes

20.  Alexia with agraphia may occur with left-sided angular
gyrus involvement.
 Gerstmann syndrome, which consists of finger agnosia,
acalculia, right-left disorientation, and agraphia, may be
seen with dominant-hemisphere parietal lesions.
 Anosognosia, the denial of hemiparesis, is most commonly
associated with right hemispheric strokes.
 Nondominant infarction may cause hemi-inattention, tactile
extinction, visual extinction, anosognosia, apraxia, impaired
prosody, and (rarely) acute confusion and agitated delirium.
Carotid Artery System Syndromes

21. Lacunar Syndromes
Thefivebestrecognizedsyndromesare:
(1) pure motor hemiparesis
(2) pure sensory stroke.
(3) sensory motor stroke.
(4) ataxic hemiparesis.
(5) dysarthria–clumsy hand syndrome:

22. Vertebrobasilar System Syndromes
 PCA cclusion
 Dominant hemisphere can create the interesting
phenomenon of alexia without agraphia.
 Bilateral occipital lobe damage can lead to
cortical blindness with denial of deficits and
confabulation (Anton syndrome)
 More extensive bilateral PCA infarctions affecting
the posterior parietal lobes cause oculomotor
apraxia, optic ataxia ,and simultagnosia a
condition known as Balint syndrome .

23.  Brain stem infarction
Distubed conc level.
Crossed hemiparesis.
Lower motor cranial neuropathy.
Diplopia -dysphagia- dysartheria.
Ataxia
Horner syndrome.
Vertebrobasilar System Syndromes

24.  Top of the basilar syndrome (characterized by
visual, oculomotor, and behavioral abnormalities,
often without significant motor dysfunction)
Vertebrobasilar System Syndromes

25. Differential diagnosis
 Seizure
 Migraine
 Encephalitis- Abcess
 Gliomas
 Demylination
 Hypoglycaemia
 Conversion
 Metabolic encephalopathy

26. Workup
Neuro – imaging
 CT and CTA
 MRI – MRA
 Carotid duplex and TCD

27. CT & CTA
 HDMCA sign

28.  Insular ribbon sign
CT & CTA

29.  Sulci effacement
CT & CTA

30.  Lentiform obscuration
CT & CTA

31. CT & CTA

32. CT & CTA

33. CT & CTA

34. CT & CTA

36. MRI & MRA

37. MRI & MRA

38. MRI & MRA

39. MRI & MRA

40. MRI & MRA

41. MRI & MRA

42. TCD

43. aetiology investigtion
 Echo –cardiography.
 Extra and intracranial duplex.
 CTA & MRA.
 Lipid profile
 Coagulation profile
 ESR and vasculitic work up
 Homocystien – APLS- Anti thrombin – sickle cell

44. management
 assess the patient’s airway, breathing, and
circulation (ABCs); stabilize the patient as
necessary; and complete initial evaluation and
assessment, including imaging and laboratory
studies, within 60 minutes of patient arrival.
 The central goal of therapy in acute ischemic
stroke is to preserve tissue in the ischemic
penumbra.

45.  Oxygen supplementation
 Supplemental oxygen is recommended when the
patient has a documented oxygen requirement (ie,
oxygen saturation < 95%).
 In the small proportion of patients with stroke who
are relatively hypotensive, administration of IV fluid,
vasopressor therapy, or both may improve flow
through critical stenoses.
 Hypoglycemia and hyperglycemia
 Hypoglycemia needs to be identified and treated early
in the evaluation
management

46.  Blood pressure: optimal management of blood
pressure in acute stroke is uncertain. Blood pressure is
often elevated on admission, but tends to decrease
spontaneously during the first few days, while
existing antihypertensive therapy should be
continued.
 Cerebral autoregulation is disturbed after stroke, so
lower levels of hypertension should probably not be
treated in the acute phase, except in patients with
coexistent hypertensive encephalopathy, aortic
dissection, acute myocardial infarction or severe left
ventricular failure
management

47. Patient otherwise eligible for acute reperfusion therapy, except that BP is >185/1
mmHg
If heart rate >55 beats per minute:
– Labetalol 10–20 mg IV over 1–2 minutes; may repeat one time
or
– Metoprolol 5 mg IV over 3–5 minutes; may repeat in 5 minutes, tw
times, if necessary
or
• Nicardipine 5 mg/hr IV; titrate up by 2.5 mg/hr every 5–15 minute
maximum 5 mg/hr; when desired BP reached, adjust to maintain proper B
limits
or
• Hydralazine 5 mg IV over 1 minute; may repeat 5 mg IV bolus in
minutes
– If systolic BP still >180 mmHg, give 10 mg IV bolus every 5 minut
until target systolic BP reached
– Increase to 20 mg bolus if required
– Maximum hydralazine dose = 240 mg
or
• Other agents (e.g. enalaprilat) may be considered when appropriate
Management of BP during and after r-tPA or other acute reperfusion therapy
maintain BP at or below 180/105 mmHg:
Monitor BP every 15 minutes for 2 hours from the start of r-tPA therap
then every 30 minutes for 6 hours, and then every hour for 16 hours.
If systolic BP>180–230 mmHg or diastolic BP >105–120 mmHg:
– Labetalol 10 mg IV followed by continuous IV infusion 2–8 mg/mi

48. Fibrinolytic Therapy
ThrombolysiswithintravenousrtPA,alteplase,shouldbe
consideredinallpatientswithadefinitedisablingischemicstroke
whocanbetreatedwithin4.5hoursofonsetoffocalneurologic
symptomsthathavebeenpresentforatleast30minuteswithout
significantimprovement.

49. Inclusion criteria
 Diagnosis of ischemic stroke causing measurable neurological deficit
 Onset of symptoms <3 hours before beginning treatment
 Aged ≥18 years
Exclusion criteria
 Significant head trauma or prior stroke in previous 3 months
 Symptoms suggest subarachnoid hemorrhage
 Arterial puncture at noncompressible site in previous 7 days
 History of previous intracranial hemorrhage
 Intracranial neoplasm, arteriovenous malformation, or aneurysm
 Recent intracranial or intraspinal surgery
 Elevated blood pressure (systolic >185 mm Hg or diastolic >110 mm Hg)
 Active internal bleeding
 Acute bleeding diathesis, including but not limited to
 Platelet count <100 000/mm3
 Heparin received within 48 hours, resulting in abnormally elevated aPTT
greater than the upper limit of normal
 Current use of anticoagulant with INR >1.7 or PT >15 seconds
 Current use of direct thrombin inhibitors or direct factor Xa inhibitors with
elevated sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT; TT;
or appropriate factor Xa activity assays)
 Blood glucose concentration <50 mg/dL (2.7 mmol/L)
 CT demonstrates multilobar infarction (hypodensity >1/3 cerebral
hemisphere)
Relative exclusion criteria
 Only minor or rapidly improving stroke symptoms (clearing
spontaneously)
 Pregnancy
 Seizure at onset with postictal residual neurological impairments
 Major surgery or serious trauma within previous 14 days
 Recent gastrointestinal or urinary tract hemorrhage (within previous 21
days)
 Recent acute myocardial infarction (within previous 3 months)

50.  Intra-arterial thrombolysis requires specialized
facilities and experienced neuroradiologists, limiting its
widespread applicability. Moreover, the need to
establish arterial access increases the delay to
treatment compared with the intravenous route .
 There are therefore studies in progress investigating
the benefits of arterial thrombolysis following an initial
intravenous dose of alteplase, to determine if this
combination results in superior outcomes in patients
who do not initially benefit from an intravenous agent.
Intra-arterial thrombolysis may also have a particular
role in patients with basilar artery thrombosis, possibly
up to 12 hours after onset, particularly if infarction in
the posterior circulation has not yet developed (Furlan
et al., 2015).
Fibrinolytic Therapy

51. Mechanical recanalization
 A number of devices are being developed to
extract or break up thrombus occluding the larger
intracranial blood vessels following acute
ischaemic stroke, using microcatheters

52. Antiplatelet therapy with aspirin/ acetylsalicylic acid
All acute stroke patients not already on an antiplatelet agent should be given at
least160mgofaspirinimmediatelyasaonetimeloadingdose(evidencelevelA).
In patients treated with rtPA, aspirin should be delayed until after the 24hour
postthrombolysisscanhasexcludedintracranialhemorrhage(evidencelevelB).
Inpatientsalreadyonaspirinpriortoischemicstrokeortransientischemicattack,
clopidigrelmaybeconsideredasanalternative(evidencelevelB).
If patients have a recent (within the past 24 hours) TIA or minor ischemic stroke,
clopidogrelmaybeaddedtoaspirinforthefirst21–90days(evidencelevelB)

53. Anticoagulationtherapy
The data do not support the routine use of any of
the currently available anticoagulants in acute
ischemicstroketopreventearlyrecurrentstroke.

54.  Early mobilization and adequate hydration should
be encouraged for all acute stroke patients
(evidence level C).
 Patients at high risk of venous thromboembolism
should be started on venous thromboembolism
prophylaxis immediately (evidence level A).
 LMWH should be considered for patients with
acute ischemic stroke at high risk of venous
thromboembolism; or UFH for patients with renal
failure (evidence level B).
Sub-acute care.

55. Neuroprotection
 Currently, data are inadequate to justify the
routine use of heparin or other anticoagulants in
the acute management of ischemic stroke.[126]
Patients with embolic stroke who have another
indication for anticoagulation (eg, atrial
fibrillation) may be placed on anticoagulation
therapy nonemergently, with the goal of
preventing further embolic disease; however, the
potential benefits of that intervention must be
weighed against the risk of hemorrhagic
transformation.[1] For more information

56. Stroke Prevention
 Carotid revascularization
 CEA should be performed by a surgeon with a
known perioperative morbidity and mortality of
less than 6% (evidence level A).

57. Secondary prevention guidelines
 All patients with ischemic stroke or TIA should be
prescribed antiplatelet therapy immediately for
secondary (evidence level A).
 Aspirin, combined aspirin (25 mg) and ER
dipyridamole (200 mg), or clopidogrel (75 mg)
are all appropriate options (evidence level A).
 Longterm concurrent use of aspirin and
clopidogrel is not recommended for secondary
stroke prevention unless there is a compelling
indication (evidence level B).

58. preventionofrecurrentischemicstrokeofcardiacorigin
 Patients with TIA and AF should begin oral anticoagulation (warfarin,
dabigatran, rivaroxaban, or apixaban) immediately after brain imaging has
excludedintracranialhemorrhageorlargeinfarct(evidencelevelB).
 For patients presenting with acute ischemic stroke and AF, the immediate use
ofheparin/heparinoidanticoagulationisnotrecommended(evidencelevelA).
 The optimal timing of oral anticoagulation following acute stroke for patients
in AF is unclear; it is common practice to wait 2–14 days and repeat brain
imaging(CTorMRI)toruleoutasymptomaticintracranialhemorrhagebefore
startingwarfarin(evidencelevelC).