Stroke by Abdulkadir risk factors and mangement

Neurology
Notes
Reference book: Davidsons 23rd Edition+Amboss+First
Aid (Step1)
By: Abdulkadir Sayid

Time poor Time rich
1- https://youtu.be/PW5MZtX5scw
https://youtu.be/7lpqxDEfszY
2- https://youtu.be/abxcrAvw-O0
3- https://youtu.be/4NKx7lE3INw
4- https://youtu.be/t47ZbHh3Ytg
5- https://youtu.be/1F1dZmJpvwc
6-https://youtu.be/vZhNwdKRzcQ
Stroke
is the most common clinical manifestation of cerebrovascular disease and results in episodes of brain
dysfunction due to focal ischaemia or haemorrhage.

Presenting Problems
Weakness
-Unilateral weakness is the classical presentation of stroke
-The weakness is sudden, progresses rapidly and follows a hemiplegic pattern - 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.
Speech disturbance
Dysphasia indicates damage to the dominant frontal or parietal lobe
dysarthria is a non-localising feature that reflects weakness or incoordination of the face, pharynx,
lips, tongue or palate.
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.
Ischaemia of the occipital cortex or post-chiasmic nerve tracts results in a contralateral hemianopia
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.

Ataxia damage to the
cerebellum
associated brainstem features such as diplopia and vertigo. The
differential diagnosis includes vestibular disorders
Headache
Sudden severe headache is the cardinal symptom of SAH
Seizure
Seizure is unusual in acute stroke but may be generalised or focal (especially in cerebral venous
disease).
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

Pathophysiology
-Cerebral infarction is mostly caused by thromboembolic disease secondary to atherosclerosis in the
major extracranial arteries (carotid artery and aortic arch).
- About 20% of infarctions are due to embolism from the heart, and a further 20% are due to
thrombosis in situ caused by intrinsic disease of small perforating vessels (lenticulostriate arteries),
producing so-called lacunar infarctions.
-Cerebral infarction takes some hours to complete, even though the patient’s deficit may be maximal
shortly after the vascular occlusion.
-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. -Similarly, reduction in
perfusion pressure leads to compensatory homeostatic changes to maintain tissue oxygenation
-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
transient ischaemic attack (TIA). -Hypoxia leads to an inadequate
supply of adenosine triphosphate (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
astrocytes causes death of all cell types in the area of maximum
ischaemia.
-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.
-Radiologically, a cerebral infarct can be seen as a lesion that comprises a mixture of dead brain
tissue that is already undergoing autolysis, and tissue that is ischaemic and swollen but recoverable
(the ‘ischaemic penumbra’).
- The infarct swells with time and is at its maximal size a couple of days after stroke onset. - At this
stage, it may be big enough to exert mass effect both clinically and radiologically; sometimes,
decompressive craniectomy is required .
-After a few weeks, the oedema subsides and the infarcted area is replaced by a sharply defined
fluidfilled cavity.

it usually results from rupture of a blood vessel within the brain parenchyma but may also occur in a
patient with SAH if the artery ruptures into the brain substance as well as the subarachnoid space.
-the haemorrhage itself may expand over the first
minutes or hours, or it may be associated with a rim
of cerebral oedema, which, along with the
haematoma, acts like a mass lesion to cause
progression of the neurological deficit.
-If big enough, this can cause shift of the intracranial
contents, producing transtentorial coning and
sometimes rapid death .
- If the patient survives, the haematoma is gradually
absorbed, leaving a haemosiderin-lined slit in the
brain parenchyma.
Intracerebral haemorrhage

‫بشكل‬ ‫للفهم‬ ‫خارجي‬
‫افضل‬

the lesion
aze preference toward the side of
G
eglect (nondominant)
N
phasia (dominant)
A
emiparesis
H
loss in the face and arm
ontralateral paresis and sensory
C
es—
CHANG
MCA stroke can cause

cerebellum.
-The combination of severe headache and vomiting at the onset of the focal deficit is suggestive of
intracerebral haemorrhage.
-Transient ischaemic attack (TIA) describes a stroke in which symptoms resolve within 24 hours
indicating that underlying cerebral haemorrhage or extensive cerebral infarction is extremely unlikely.
-TIA traditionally also includes patients with amaurosis fugax, usually due to a vascular occlusion in
the retina.
- Stroke describes those events in which symptoms last more than 24 hours.
-The term ‘minor stroke’ is sometimes used to refer to symptoms lasting over 24 hours but not
causing significant disability.
-Progressing stroke (or stroke in evolution) describes a stroke in which the focal neurological deficit
worsens after the patient first presents. Such worsening may be due to increasing volume of
infarction, haemorrhagic transformation or increasing cerebral oedema.
-Completed stroke describes a stroke in which the focal deficit persists and is not progressing.
brainstem or
Ataxia, diplopia, vertigo and/or bilateral weakness usually indicate a lesion in the
-
cerebral hemisphere.
eld defect usually places the lesion in the
fi
or a visual
cit such as aphasia or neglect,
fi
cit, a higher cerebral function de
fi
The presence of a unilateral motor de
-

-Brain imaging with either CT or MRI should be performed in all patients with acute stroke.
Exceptions are where results would not influence management, such as in the advanced stage of a
terminal illness.
-CT remains the most practical and widely available method of imaging the brain.
- It will usually exclude non-stroke lesions, including subdural haematomas and brain tumours, and
will demonstrate intracerebral haemorrhage within minutes of stroke onset .
Investigations
Neuroimaging
Risk factor analysis

-However, especially within the first few hours after symptom onset, CT changes in cerebral infarction
may be completely absent or only very subtle.
-MRI diffusion weighted imaging (DWI) can detect ischaemia earlier than CT.
-MRI is more sensitive than CT in detecting strokes affecting the brainstem and cerebellum, and,
unlike CT, can reliably distinguish haemorrhagic from ischaemic stroke even several weeks after the
onset

Vascular imaging
Extracranial arterial disease can be non-invasively identified with duplex ultrasound, MRA or CTA , or
occasionally by intra-arterial contrast radiography
Cardiac investigations
-Approximately 20% of ischaemic strokes are due to embolism from the heart.
-The most common causes are atrial fibrillation, prosthetic heart valves, other valvular abnormalities
and recent myocardial infarction.
-These may be identified by clinical examination and ECG,
-but a transthoracic or transoesophageal echocardiogram is also required to confirm the presence of
a clinically apparent cardiac source or to identify an unsuspected source such as endocarditis, atrial
myxoma, intracardiac thrombus or patent foramen ovale.
-Such findings may lead on to specific cardiac treatment.

patients.
pressure should be considered in appropriate
to reduce intracranial
Surgical decompression
-
.
cial ventilation
fi
arti
or
mannitol
such as
anti-oedema agents,
t from
fi
hemispheres may bene
infarction with massive oedema in the cerebral
Some patients with large haematomas or
-
of a ventricular drain and/or decompressive surgery
insertion
t from
fi
hydrocephalus and some will bene
may develop obstructive
with mass effect
haematomas or infarcts
Patients with cerebellar
-
Management

Reperfusion (thrombolysis and thrombectomy)
-Rapid reperfusion in ischaemic stroke can reduce the extent of brain damage.
-Intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) increases the risk of
haemorrhagic transformation of the cerebral infarct with potentially fatal results.
-The main contraindications are bleeding risk (recent haemorrhage, anticoagulant therapy) and delay
to treatment; the earlier treatment is given, the greater the benefit.
-However, if given within 4.5 hours of symptom onset to carefully selected patients, the haemorrhagic
risk is offset by an improved overall outcome.
- Recently mechanical clot retrieval (thrombectomy) in patients with a large-vessel occlusion can
greatly improve the chances of avoiding disability
Aspirin
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.
-Aspirin reduces the risk of early recurrence and has a small but clinically worthwhile effect on
longterm outcome ; it may be given by rectal suppository or by nasogastric tube in dysphagic patients.
Heparin
- routine use of heparin does not result in better long-term outcomes, and therefore it should not be
used in the routine management of acute stroke.
-Intracranial haemorrhage must be excluded on brain imaging before considering anticoagulation.
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.
-There is no evidence that clotting factors are useful in the absence of a clotting defect.
Unusual causes
-A minority of strokes are caused by arterial dissection of the carotid (carotid dissection) or vertebral
artery (vertebral artery dissection).
-The presenting history often includes minor injury and face or neck pain.
-After confirmation on angiography (MRA or CTA), treatment is with either antiplatelet drugs or
anticoagulation.
- Reversible vasoconstriction syndromes require good physiological control (particularly blood
pressure).

Subarachnoid Hemorrhage
-Women are affected more commonly than men and the condition usually presents before the age of
65.
-The immediate mortality of aneurysmal SAH is about 30%; survivors have a recurrence (or rebleed)
rate of about 40% in the first 4 weeks and 3% annually thereafter.
-Some 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%), posterior
communicating artery (25%) or middle cerebral artery (20%).
-There is an increased risk in first-degree relatives of those with saccular aneurysms, and in patients
with polycystic kidney disease and congenital connective tissue defects such as Ehlers–Danlos
syndrome .
-In about 10% of cases, SAHs are non-aneurysmal haemorrhages (so-called peri-mesencephalic
haemorrhages), which have a very characteristic appearance on CT and a benign outcome in terms of
mortality and recurrence.
- Around 5% of SAHs are due to arteriovenous malformations and vertebral artery dissection.

optic nerve.
represents blood tracking along the subarachnoid space around the
, which
subhyaloid haemorrhage
may reveal a
Fundoscopy
5-
, but this is rare.
posterior communicating artery
aneurysm of the
may be present due to local pressure from an
third nerve palsy
A
4-
if there is an associated intracerebral haematoma.
hemiparesis or aphasia
Focal hemisphere signs, such as
3-
may take some hours to develop.
due to subarachnoid blood but this
neck stiffness
There may be
2-
.
photophobia
, with
distressed and irritable
the patient is usually
1-
On examination
considered if a patient is found comatose.
, so SAH should be
loss of consciousness at the onset
There may be
-
.
excitement
physical exertion, straining and sexual
It commonly occurs on
-
.
pressure and neck stiffness or pain
omiting, raised blood
for hours or even days, often accompanied by v
(often occipital), which lasts
‘thunderclap’ headache
sudden, severe,
-
Clinical features

Investigations
If either of these tests is positive, cerebral angiography is required to determine the optimal approach
to prevent recurrent bleeding.
Management
1-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.
2-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.

3-Arteriovenous malformations can be managed either by surgical removal, by ligation of the blood
vessels that feed or drain the lesion, or by injection of material to occlude the fistula or draining veins.
4-Treatment may also be needed for complications of SAH,
A- which include obstructive hydrocephalus (that may require drainage via a shunt),
B- delayed cerebral ischaemia due to vasospasm (which may be treated with vasodilators),
C-hyponatraemia (best managed by fluid restriction)
D- systemic complications associated with immobility, such as chest infection and venous thrombosis.

Cerebral venous disease
-MR venography demonstrates a filling defect in the affected vessel.
-Anticoagulation, initially with heparin followed by warfarin, is beneficial, even in the presence of
venous haemorrhage.
-In selected patients, endovascular thrombolysis has been advocated.
- Management of underlying causes and complications, 1-such as
persistently raised intracranial pressure.
About 10% of cerebral venous sinus thrombosis, particularly cavernous sinus thrombosis, is
associated with infection (most commonly Staphylococcus aureus), needing antibiotic treatment.
Investigations and management

Mnemonic
Mnemonic
Mnemonic
Mnemonic

Stroke by Abdulkadir risk factors and mangement

Stroke by Abdulkadir risk factors and mangement

More Related Content

Similar to Stroke by Abdulkadir risk factors and mangement

Recently uploaded

Stroke by Abdulkadir risk factors and mangement