This document provides an overview of stroke, including: - Stroke is defined as rapid neurological deficit caused by focal brain infarction or hemorrhage. - Risk factors include hypertension, atrial fibrillation, diabetes, hyperlipidemia, and smoking. - Strokes are either ischemic (85%) due to thrombosis or embolism, or hemorrhagic (15%) due to bleeding. - Clinical features depend on the location of brain injury but may include weakness, speech problems, visual issues, and headache. - Investigations include brain imaging (CT or MRI), blood tests, and cardiac workup to determine the cause. - Treatment involves supportive care, thrombolysis

1. CBU-KTH SITE
STROKE
PRESENTER:MBEWE STEWARD

2. CONTENTS
• INTRODUCTION
• EPIDEMIOLOGY
• ANATOMY
• RISK FACTORS
• STROKE MECHANISMS
• CLINICAL FEATURES
• INVESTIGATIONS
• MANAGEMENT
• COMPLICATIONS

3. INTRODUCTION
• Stroke is defined as a syndrome of rapid onset neurological deficit
caused by focal cerebral, spinal or retinal infarction or haemorrhage.
• To the public, stroke means weakness, usually permanent on one
side, often with loss of speech (apahasia).
• Also known as cerebrovascular accident (CVA)
• Transient ischaemic attack (TIA) means a brief episode of
neurological dysfunction due to temporary focal cerebral or retinal
ischaemia without infarction.
• Time limit of 24hrs no longer used.

4. EPIDEMIOLOGY
• Stroke is the third most common cause of death in high-income
countries.
• Leading cause of adult disability worldwide.
• Approximately two-thirds of the global burden of stroke is in middle-
and low-income countries.
• Stroke rates are higher in Asian and black African populations than in
Caucasians.
• Stroke risk increases with age but one-quarter of all strokes occur
before the age of 65.
• The death rate following stroke is 20–25%

5. REVIEW OF BLOOD SUPPLY TO BRAIN

6. BASIC FUNCTIONAL ANATOMY

7. • In health, regulatory mechanisms maintain a constant cerebral
blood flow across a wide range of arterial blood pressures to
meet the high resting metabolic activity of brain tissue.
• Cerebral blood vessels dilate when systemic blood pressure is lowered
and constrict when it is raised. This autoregulatory mechanism
can be disrupted after stroke.

8. RISK FACTORS OF STROKE

9. STROKE MECHANISMS
The underlying pathology responsible for stroke is either infarction
or haemorrhage.
1. ISCHAEMIC STROKE/INFARCTION (85%)
• Thrombotic →Thrombosis at the site of ruptured mural plaque.
• Large-artery Stenosis → acts as an embolic source rather than by occluding
the vessel
• Small-vessel Disease → occlusive vasculopathy – lipohyalinosis – that is a
consequence of hypertension

10. • Cardio-embolic→ The heart is a common source of embolic material.
Atrial fibrillation (and other arrhythmias) is the most common cause.
Cardiac valve disease, including congenital valve disorders, infective
vegetations, and rheumatic and degenerative calcific changes, may
cause embolization.
A patent foramen ovale (PFO), may allow passage of fragments of
thrombus (e.g. from a lower limb DVT) from the right atrium to the left
during Valsalva. Pulmonary AV fistulas may also act as a conduit for
paradoxical embolization.
Rarer causes include fat emboli after long bone fracture, atrial myxomas
and iatrogenic causes, such as cardiac bypass and air embolism.
• Hypoperfusion → Severe hypotension, such as in cardiac
arrest.

12. PATHOPHYSIOLOGY OF ISCHEMIC STROKE
• After the occlusion of a cerebral artery, infarction may be
forestalled by the opening of anastomotic channels from other
arterial territories that restore perfusion to its territory.
• Reduction in perfusion pressure leads to compensatory
homeostatic changes to maintain tissue oxygenation.
• These compensatory changes can sometimes prevent
occlusion of even a carotid artery from having any clinically
apparent effect.

14. • However, if and when these homeostatic mechanisms fail,
the process of ischaemia starts, and ultimately leads to
infarction unless the vascular supply is restored.
• As the cerebral blood flow declines, different neuronal
functions fail at various thresholds. Once blood flow falls
below the threshold for the maintenance of electrical
activity, neurological deficit develops.
• At this level of blood flow, neurons are still viable; if blood
flow increases again, function returns and the patient will
have had a (TIA).

15. • However, if blood flow falls further, a level is reached at
which irreversible cell death starts.
• Hypoxia leads to an inadequate supply of (ATP), which leads
to failure of membrane pumps.
• Thereby allowing influx of sodium and water into cells
(cytotoxic oedema) and release of the excitatory
neurotransmitter glutamate into the extracellular fluid
• Glutamate opens membrane channels, allowing influx of
calcium and more sodium into the neurons. Calcium
activates intracellular enzymes that complete the destructive
process.
• The release of inflammatory mediators by microglia and
astrocyte causes death of all cell types in the area of
maximum ischaemia.

16. •The infarction process is worsened by anaerobic
production of lactic acid and consequent fall in
tissue pH.
•Subsequent restoration of blood flow may cause
haemorrhage into the infarcted area
(‘haemorrhagic
transformation’). This is particularly likely in
patients given antithrombotic or thrombolytic
drugs, and in patients with larger infarcts.

18. CLINICAL FEATURES
1. Weakness→ Unilateral weakness is the classical presentation of
stroke and, much more rarely, of CVT. The weakness is sudden,
progresses rapidly and follows a hemiplegic pattern. Reflexes are
initially reduced but then become increased with a spastic pattern
of increased tone. Upper motor neuron weakness of the face (7th
cranial nerve) is often present.
2. Speech disturbance→ Dysphasia and dysarthria are the most
common presentations of disturbed speech in stroke.
3. Visual deficit→ Visual loss can be due to unilateral optic ischaemia
(called amaurosis fugax if transient), caused by disturbance of blood
flow in the internal carotid artery and ophthalmic artery, leading to
monocular blindness

19. 4. Visuo-spatial dysfunction→ Damage to the non-dominant cortex
often results in contralateral visuo-spatial dysfunction, e.g. sensory
or visual neglect and apraxia (inability to perform complex tasks
despite normal motor, sensory and cerebellar function), sometimes
misdiagnosed as delirium.

20. 5. Ataxia→ Stroke causing damage to the cerebellum and its
connections can present as an acute ataxia
6. Headache→ Sudden severe headache is the cardinal symptom of
SAH but also occurs in intracerebral haemorrhage. Although
headache is common in acute ischaemic stroke, it is rarely a
dominant feature.
7. Seizure→ Seizure is unusual in acute stroke.
8. Coma→ Coma is uncommon, though it may occur with a brainstem
event. If present in the first 24 hours, it usually indicates a
subarachnoid
or intracerebral haemorrhage.

21. STROKE INVESTIGATIONS
A. Immediate urgent investigations
Ideally within 1 hour of presentation
• CT brain scan
• Blood count and glucose (and clotting studies if anticoagulated)
B. Further investigations
(Within 24 h)
• Routine blood tests – blood count, erythrocyte sedimentation
rate, glucose, clotting studies, lipids.
• Electrocardiography (ECG) and later 24-h ECG for atrial fibrillation
• Carotid Doppler studies (in patients with anterior circulation
stroke fit for surgery)

22. C. In addition
In selected patients, e.g. young stroke or no cause identified
• CT or MR angiography
• MRI brain scan with dissection protocol
• Echocardiogram (consider transoesophageal echocardiography)
• Prolonged cardiac monitoring for paroxysmal atrial fibrillation in
cryptogenic stroke, e.g. implantable loop recorder
• Vasculitis screen
• Antiphospholipid antibodies
• Thrombophilia screen
• Other: genetics for CADASIL and mitochondrial disorders;
alphagalactosidase for Fabry’s disease; drugs of abuse screen, e.g.
cocaine

23. Ischemic stroke CT

24. Localising a Lesion

25. Acute stroke: Immediate care
• Stroke is a medical emergency.
• Encouraged to make the diagnosis of stroke on a simple
history and examination – FAST:
Face – sudden weakness of the face
Arm – sudden weakness of one or both arms
Speech – difficulty speaking, slurred speech
Time – the sooner treatment can be started, the better.

26. MANAGEMENT
Aimed at:
• Identifying the cause,
• Minimising the volume of brain that is irreversibly damaged
• Preventing complications and
• Reducing the patient’s disability and handicap through rehabilitation

27. Approach to Stroke Management

28. Supportive Care

29. Specific Management of Ischemic Stroke
1. Thrombolysis
Thrombolysis significantly increases the chances of having no or
minimal disability after stroke, by reducing infarct size.
Two categories:
1. Fibrin-Specific agents- Alteplase (r-tPA), Tenectaplase,
Reteplase—Produce limited plasminogen conversion in
absence of fibrin.
2. Non-Fibrin specific agents- Streptokinase, Urokinase–
catalyse systemic fibrinolysis.

30. Intravenous thrombolysis with recombinant tissue
plasminogen activator (rt-PA) increases the risk of
haemorrhagic transformation of the cerebral infarct with
potentially fatal results.
Earlier treatment within the 4.5-hour time window
significantly improves outcome, so every minute counts.
*NOT ALL PATIENTS ARE ELIGIBLE FOR THROMBOLYSIS

31. Dose of i.v. alteplase (t-PA)
• Total dose 0.9 mg/kg (max. 90 mg)
• 10% of total dose by initial i.v. bolus over 1 min
• Remainder infused intravenously over 60 min

32. 2. Aspirin (Antiplatelet Therapy)
In the absence of contraindications, aspirin (300 mg daily) should be started
immediately after an ischaemic stroke unless rt-PA has been given, in which case it
should be withheld for at least 24 hours.
3. Heparin (Anticoagulation Therapy)
Anticoagulants are started for atrial fibrillation-associated cardio-embolic stroke
usually after 2 weeks to reduce the risk of acute haemorrhagic transformation of
infarcts
4. Coagulation abnormalities
In those with intracerebral haemorrhage, coagulation abnormalities should be
reversed as quickly as possible to reduce the likelihood of the haematoma
enlarging. This most commonly arises in those on warfarin therapy.

33. Thrombolysis Criteria in Ischemic Stroke

35. Secondary Prevention
Antihypertensive therapy
• Recognition and good control of high blood pressure are the major factors in
primary and secondary stroke prevention. Transient hypertension, often seen
following stroke, usually does not require treatment, provided diastolic pressure
does not rise above 100mmHg. Sustained severe hypertension needs treatment
after 72 hours blood pressure should be lowered slowly to avoid any sudden fall
in perfusion.
Lipid-lowering therapy
• Statins, typically atorvastatin 40mg, should be offered to all patients
unless there is a contraindication, aiming for a target total cholesterol below
4mmol/L (low-density lipoprotein <2mmol/L).

36. Lifestyle modification and education
• Education of patient and family is an essential aspect of secondary
prevention. Smoking cessation and advice about diet, exercise,
weight reduction and alcohol consumption should be started on the
stroke unit and continued after discharge.
Rehabilitation: multidisciplinary approach
• Physiotherapy has particular value in the first few weeks after stroke
to relieve spasticity, prevent contractures and teach patients to use
walking aids.
• Speech and language therapists have a vital understanding of
aphasic patients’ problems and frustration

37. 2. HAEMORRHAGIC STROKE (10%)
Due to Intracranial Haemorrhage
Comprises; Intracerebral and Subarachnoid hemorrhage
Intracerebral Haemorrhage
• It is associated with a higher mortality than ischaemic stroke (up to
50%).
• A large haematoma may act as a space-occupying lesion, causing
raised intracranial pressure with brain displacement and herniation.

38. Aetiology
a) Hypertension →Rupture of microaneurysms (Charcot–Bouchard
aneurysms and degeneration of small, deep, penetrating arteries are
the principal pathologies.
b) Cerebral amyloid angiopathy (CAA)→ Deposition of amyloid-β in the
walls of small and medium-sized arteries in normotensive patients,
particularly over 60years, causes lobar intracerebral haemorrhage
(especially posterior, i.e. occipital/parietal lobes), which is often
recurrent.
c) Secondary→ Arteriovenous malformations, cavernomas, aneurysms
and dural venous thrombosis cause around 20% of intracerebral
haemorrhages. Coagulopathies, anticoagulants and thrombolysis may
cause haemorrhage. Haemorrhagic transformation of a large
ischaemic infarct may sometimes present as a haemorrhage.

39. Clinical Features
• At the bedside, there is no entirely reliable way of
distinguishing between haemorrhage and ischaemic infarcts.
• Intracerebral haemorrhage is more often associated with
severe headache or coma.
• Patients on oral anticoagulants should be assumed to have had
a haemorrhage unless it is proved otherwise.
• Brain haemorrhage is seen on CT imaging immediately as
intraparenchymal, intraventricular or subarachnoid blood.

40. Investigations
• Brain haemorrhage is seen on CT imaging immediately (compare
infarction) as intraparenchymal, intraventricular or subarachnoid
blood.
• Routine MRI may not identify an acute small haemorrhage reliably in
the first few hours. MRI and MR angiography are necessary to identify
underlying vascular malformations such as AVMs or aneurysms.
• Catheter angiography may be required in selected patients with no
obvious risk factors or no underlying cause identified on imaging.

41. Intracerebral Hemorrhage on CT

42. MANAGEMENT
A. Medical
• Treatment should be on a stroke unit or a neurological intensive care
unit
• Monitoring of GCS and neurological signs
• Antiplatelet drugs are, of course, contraindicated
• Anticoagulation should be rapidly reversed where possible (for
patients on warfarin give intravenous vitamin K and clotting factor
concentrates).
• Control of hypertension is vital with intravenous drugs in an intensive
care unit setting for systolic blood pressure higher than 180mmHg
• Measures to reduce intracranial pressure may be required, including
mechanical ventilation and mannitol

43. B. Surgical
• Cerebellar haematomas may cause obstructive hydrocephalus or
coma due to brainstem compression.
• Urgent neurosurgical clot evacuation is lifesaving (and is required
where the haematoma is >3cm or the patient is drowsy or
deteriorating).
• Placement of an external ventricular drain is needed if obstructive
hydrocephalus develops

44. SUBARACHNOID HAEMORRHAGE
• Subarachnoid haemorrhage (SAH) is less common than ischaemic
stroke or intracerebral haemorrhage
• Women are affected more commonly than men and the condition
usually presents before the age of 65.
• 85% of cases of SAH are caused by saccular or ‘berry’ aneurysms
arising from the bifurcation of cerebral arteries, particularly in the
region of the circle of Willis. The most common sites are in the
anterior communicating artery (30%).

45. CLINICAL FEATURES
• SAH typically presents with a sudden, severe, ‘thunderclap’ headache (often
occipital), which lasts for hours or even days, often accompanied by vomiting,
raised blood pressure and neck stiffness or pain.
• It commonly occurs on physical exertion, straining and sexual excitement.
There may be loss of consciousness at the onset, so SAH should be considered
if a patient is found comatose.
• About 1 patient in 8 with a sudden severe headache has SAH and, in view of
this, all who present in this way require investigation to exclude it

46. • The patient is usually distressed and irritable, with
photophobia.
• There may be neck stiffness and a positive Kernig’s sign due to
subarachnoid blood.
• Fundoscopy may reveal a subhyaloid haemorrhage, which
represents blood tracking along the subarachnoid space
around the optic nerve.

47. INVESTIGATIONS
• CT imaging is the immediate investigation. Subarachnoid and/or
intraventricular blood is usually seen (sensitivity of CT
to detect subarachnoid blood is 95% within 24hours of onset but
much lower over subsequent days.
• Lumbar puncture → not necessary if SAH is confirmed by CT, but
should be performed if doubt remains. CSF becomes yellow
(xanthochromic) within 12hours of SAH and remains detectable for
2weeks.
• CT angiography or catheter angiography to identify the aneurysm or
other source of bleeding is performed in patients potentially fit for
surgery.

48. Hyperdense CT appearance

49. MANAGEMENT
A. Medical
• Immediate treatment of SAH involves bed rest and supportive measures.
• Hypertension should be controlled.
• Nimodipine ((30–60 mg IV for 5–14 days, followed by 360 mg orally for a further 7
days) is usually given to prevent delayed ischaemia in the acute phase), a calcium
channel blocker given for 3weeks, reduces mortality.
• All SAH cases should be discussed urgently with a neurosurgical
centre. Nearly half of SAH cases are either dead or moribund before
reaching hospital.

50. B. SURGICAL
• Insertion of platinum coils into an aneurysm (via an endovascular
procedure) or surgical clipping of the aneurysm
neck reduces the risk of both early and late recurrence.
• Arteriovenous malformations can be managed either by surgical
removal, by ligation of the blood vessels that feed or drain the lesion.

51. 3. Others (5%)
• arterial dissection
• venous sinus thrombosis
• vasculitis

52. COMPLICATIONS OF ACUTE STROKE

53. THANK YOU FOR
YOUR ATTENTION