cerebrovascular disease 1- ischemic stroke 2- intracerebral haemorrhage 3- SAH

1. Cerebrovascular Disease
Dr Mohamed Rizk Khodair
Lecturer of neurology
October 6 Universirty

2. Definition:
Stroke is a sudden onset focal
and or generalized neurological
deficit, lasting more than 24
hours. Strokes occur due to
either ischemia (about 85%) or
hemorrhage (15%).
Transient ischemic attack (TIA)
is defined as sudden onset
focal neurological deficit lasting
less than 24 hours.

3. Types:
A) Ischemic Stroke :
Most ischemic strokes
are due to thrombosis
or embolism
B) Hemorrhagic
stroke: Intracerebral
hemorrhage and
Subarachnoid
hemorrhage

4. Etiology of ischemic stroke
Thrombosis: The commonest cause is atherosclerosis
Predisposing (Risk) Factors
A stroke may happen to anybody at any age. However, if you have specific risk factors, your chances of having a stroke increase. Some stroke
risk factors are modifiable, while others are not.
Non-Modifiable Factors:
 Older age. Incidence doubles each decade past 55 years.
 Race. African American race has twofold increased risk than whites. This is partly because the African American population has a greater
incidence of high blood pressure.
 Gender. Strokes are more common in men. (1.25 times that of females).
 History of prior stroke. There is a higher risk for having a second stroke after you have already had a stroke.
 Heredity or genetics. People with a positive family history of stroke are more likely to have a stroke.
Modifiable Factors:
 Hypertension: 3-4 folds increase of stroke.
 Dyslipidemia: high total cholesterol and low-density lipoprotein (LDL) are related to atherosclerosis and increase risk.
 Diabetes mellitus (DM): 2-4, folds increase of stroke, pathogenetic factor in cerebral small vessel disease. DM produces rheological
abnormalities and aggravates atherosclerosis. DM increases morbidity and mortality after
 stroke.
 Heart diseases
 Smoking (2-3 times greater than non-smokers), heavy alcohol consumption.

5. Embolism: Embolism (from the heart is also a common cause) include valvular disease, artificial heart valves, recent myocardial
infarction, endocarditis and cardiac tumors. Also, paradoxical embolism as in a patient with an atrial septal defect or patent
foramen oval.
Other causes include:
1. Arterial (e.g., carotid or vertebral) dissection
2. Vasculitis
3. Hematological disorders: polycythemia, thrombocythemia, sickle cell disease, leukemia and antiphospholipid syndrome
4. Genetic disorders: as Cerebral autosomal dominant arteriopathy with subcortical infarcts and Leukoencephalopathy
(CADASIL) and Mitochondrial encephalomyopathy, lactic acidosis, and Stroke-like episodes (MELAS).
5. Recreational drug use: cocaine, amphetamine
6. Hypoperfusion of the brain leading to so-called watershed or border zone infarcts as in shock, excessive blood loss, excessive
hypotensive drugs, low cardiac output (as in myocardia infarction or arrhythmia),hemoconcentration( as in dehydration) .
7. Venous disease as due to cerebral venous sinus thrombosis.

7. Clinical Picture: Symptoms and signs depend upon the occluded blood vessel.

8. The carotid system
(Anterior circulation).
Blood Supply of the brain
The vertebral system
(Posterior circulation).
.

9. The carotid system (Anterior circulation):
Each internal carotid artery enters the cranial
cavity through the carotid foramen and canal to
the cavernous sinus where it lies lateral to optic
chiasma.
The artery in the sinus gives off three small
branches:
- The ophthalmic artery.
- The anterior choroidal artery.
- The posterior communicating artery.
The internal carotid artery then divides into its
two terminal branches → the middle and
anterior cerebral arteries.

10. A. The middle cerebral artery gives 2 branches:
Capsular branch: supplying dorsal half of
internal capsule (Lenticulostriate branch of middle
cerebral artery).
Cortical branches:
Frontal branch supplying the lower part of the motor
area (face, U.L. and trunk), and the motor speech areas.
Parietal branch supplying the lower part of the sensory
area, the angular and supramarginal and the upper fibers
of the optic radiation.
lower fibers of the optic
Temporal branches supplying the auditory
areas and the lower fibers of the optic radiation.

11. B. The anterior cerebral artery supplies:
The anterior cerebral artery runs medially on the medial surface of the cerebral
hemisphere, then around the corpus callosum as far as the parieto-occipital sulcus. This
artery supplies the medial aspect of the anterior 3/5 of the cerebral hemisphere and the
upper edge of the lateral surface.
It gives the following branches:
• Capsular branch (Heubner's artery) supplying the ventral half of the anterior limb of
the internal capsule.
• Cortical branches:
a) Frontal branch supplying the pre-frontal area (area of mentality and inhibition of primitive reflexes).
b) Paracentral branch supplying the motor and sensory areas of the L.L., and the paracentral lobule (cortical
bladder center).
c) Callosal branch supplying the corpus callosum.

12. The vertebral system (Posterior circulation):
Vertebral Arteries
Course and branches:
The left and right vertebral arteries originate from their
respective subclavian arteries, on the posterosuperior aspect.
The vertebral arteries then proceed to enter
the transverse foramina of the spine at level C6 and
continue superiorly.
After passing through the transverse foramen of C1, the arteries
traverse the foramen magnum.
The vertebral arteries give off the following branches once within the
cranial vault:
 Posterior inferior cerebellar artery (PICA) – this is the largest
branch of the vertebral artery and is one of three main arteries
supplying the cerebellum
 Anterior and posterior meningeal arteries – supply the dura mater
 Anterior and posterior spinal arteries – supply the spinal cord
along its entire length
The vertebral arteries then converge to form one midline single artery,
basilar artery, at the base of the pons, inside the cranium.

13. Basilar Arteries
Course and branches:
The basilar artery runs superiorly within the central
groove of the pons, giving off several branches
including the pontine arteries, which supply
the pons.
The basilar artery anastomoses with the circle of
Willis via the posterior cerebral arteries and
posterior communicating arteries.
Branches of posterior cerebral artery :
Cortical branches: supply occpital lobe and
posterior communicating artery to circle of willis
Capsular branche: thalamogeniculate artery (
ventral aspect of genu and posterior limb of internal
capsule)

15. Circle of Willis
The terminal branches of
the anterior and posterior circulation form
an anastomosis to create a ring-like vascular
structure known as the circle of Willis, located
within the base of the cranium.
The left and right internal carotid arteries continue
as the middle cerebral arteries (MCA), after each
giving off a branch to supply
the anterior cerebral arteries (ACA).
The anterior communicating artery links the two
anterior cerebral arteries together.
The internal carotid arteries also give off
the posterior communicating arteries (PCoA),
linking the middle cerebral arteries (MCA) with
the posterior cerebral arteries (PCA).

16. The Internal capsule
It is a broad band of white fibers lying in the depth of the cerebral hemisphere.
It is formed of:
1. The anterior limb which is placed between the caudate nucleus medially and the lentiform
nucleus laterally.
2. The genu.
3. The posterior limb which is placed between the thalamus medially and the lentiform nucleus
laterally.
Fibers passing through the internal capsule:
a) Pyramidal fibers descend in the genu, adjacent part of anterior limb and anterior 1/2 of
posterior limb. The fibers supplying the arm are followed by those supplying the head, trunk,
and lastly the lower limb.
b)Sensory fibers from the thalamus ascend in the PL.
c) Auditory and optic radiations pass in the posterior part of PL.
d)Associative fibers pass in the anterior part of AL.

17. Blood supply of the internal capsule
• Upper part: MCA (lenticulostriate artery).
• Lower part:
Anterior limb; ACA (recurrent artery of Heubner).
Posterior limb: PCA (thalamogeniculate artery).

19. (1) Anterior circulation (carotid system) infarction
A) Middle cerebral artery occlusion:
Contralateral hemiparesis (face and arm > leg)
Contralateral hemisensory loss (face and arm > leg)
Homonymous hemianopia
Contralateral gaze palsy
Neglect
Aphasia (if dominant hemisphere is affected)

21. B) Anterior cerebral artery occlusion:
• Contralateral hemiparesis (leg > arm)
• Contralateral hemisensory loss (leg > arm)
• Mental changes
• Sphincteric disturbances in massive infarction

24. (2) Posterior circulation (vertebrobasilar territory) infarct
A) Posterior cerebral artery occlusion:
• Contralateral homonymous hemianopia
(which may be macular sparing, as this may
be supplied by the middle cerebral artery).
• Thalamic pain (spontaneous intractable and
persistent pain).
• Transient hemiparesis.
• Visual agnosia.

25. B) Posterior inferior cerebellar artery (Lateral medullary syndrome; Wallenberg syndrome) crossed
hemianesthesia
• Contralateral impairment of
pain/temperature sensation in the limb with
ipsilateral impairment of pain/temperature in
the face
• Ipsilateral Horner‘s syndrome
• Ipsilateral cerebellar signs (ataxia),
• Ipsilateral dysarthria, vertigo, vomiting,
dysphagia

26. C) Other brainstem stroke syndromes
• Apart from the lateral medullary syndrome, other brainstem stroke syndromes are rare, e.g., the medial
medullary syndrome which causes ipsilateral tongue weakness and contralateral hemiparesis in the arm
and leg. (crossed hemiplegia)
D) Lacunar strokes:
These infarcts are usually less than 1 cm in diameter and are caused by the occlusion of small penetrating
arteries supplying deep structures in the brain as basal ganglia, thalamus, pons. It include:
• Pure motor strokes (face, arm, and leg) in the posterior limb of internal capsule.
• Pure sensory stroke (thalamus).
• Ataxic hemiparesis (weakness and ataxia affecting the same side) due to a pontine lesion.
• Clumsy hand/dysarthria due to a lesion in the pons or internal capsule.

27. Investigations
A) Imaging studies: Should be performed within 24 hours to exclude haemorrhagic stroke and other causes,
e.g., tumors.
1- CT: It is the first diagnostic tool to exclude hemorrhage , Ct is free in 1st 48 hours of onset of ischemic stroke.
2- MRI: Diffusion-weighted images (DWIs) show changes within minutes (most diagnostic tools). Useful to
distinguish acute from chronic changes.
3- Imaging of extracranial vessels should be performed in all patients with TIA or stroke for diagnosis of
partial or complete obstruction of the extracranial vessels as: Carotid and vertebral ultrasonography; MR or CT
angiography (MRA/CTA).
4- Imaging of intracranial vessels should be performed in all patients for diagnosis of partial or complete
obstruction of the intracranial vessels as: Trascranial color coded duplex; MR or CT angiography (MRA/CTA).
5- ECG and Echocardiography :for diagnosis of cardiac diseases as a cause for stroke.

28. Normal vs ischemic vs hemorrhagic

29. Treatment of acute ischemic stroke:
A) Specific treatment
1- Thrombolysis
Thrombolysis with IV rt-PA was used for the treatment of acute ischemic stroke
within 4,5 hours of onset to achieve early recanalization of a thrombosed artery.
2- Antiplatelet Therapy:
• Aspirin
All patients should be initially treated with aspirin; 150-325 mg/day; following
acute ischemic stroke unless they are being treated with thrombolytic therapy.
Beyond the initial treatment period following ischemic stroke, most patients should
be maintained on antiplatelet therapy to reduce the long-term risk of recurrent
stroke.
• Clopidogrel, Ticlopidine and combined aspirin and dipyridamole (
persantine) are acceptable alternative to aspirin.

30. 3- Anticoagulant therapy :
The goal of anticoagulation in acute ischemic stroke is to prevent early recurrent
cerebral embolism as cardioembolic stroke due to atrial fibrillation or prevention of DVT due to recumbency.
4- Treatment of risk factors: as antihypertensive, control of diabetes, antiarrhythmic.
5- Dehydrating measures: especially in massive infarction. Mannitol 1-2 mg/kg/day used for 48 hours.
6- Nootropic drugs: as Piracetam (Nootropil). These drugs enhance the brain metabolism and brain
oxygenation.
B) General treatment: in comatose patients
1-Care of skin by changing the position of patient.
2- Care of respiration by maintaining patent airways, frequent suctions of secretions
3- Care of nutrition and fluids 4- Care of urinary bladder 5- physiotherapy

31. ΙΙ- Hemorrhagic :
It may be in the brain ‫״‬intracerebral hemorrhage or within the subarachnoid space ―subarachnoid
hemorrhage.

32. Spontaneous Intracerebral hemorrhage (ICH)
ICH is the second most common form of
stroke (about 15–30% of all strokes).
Risk factors:
Risk factors for ICH are like those with
ischemic stroke:
• Age;
• Male gender
• Hypertension
• Smoking
• Diabetes
• Excess alcohol use.

33. Causes of ICH:
1. Chronic hypertension.
2. Excess anticoagulant use, antiplatelet use,
Thrombolytic therapy.
3. Rupture of intracranial aneurysms, arteriovenous
malformations and cavernomas.
4. Hemorrhagic blood diseases as in purpura, leukemia
5. Moya Moya syndrome
6. Trauma to the head.
Common sites for ICH:
Basal ganglia., Thalamus, Pons, Cerebellum, Cerebrum
(lobar hemorrhage) and Brainstem.

34. Clinical picture:
1- Prodromal symptoms are related to hypertension as severe headache, vomiting, and alterations in
level of consciousness as confusion may be more common.
2- The focal symptoms ad signs depend upon the site of hemorrhage.
3- Onset is usually very sudden.
4- Convulsions are common and may point to the onset of hemorrhagic stroke.

35. Investigations:
A) Imaging studies:
1. CT scan: Non contrast brain CT scan is the
usual initial imaging procedure of choice.
2. CT angiography (CTA): CTA is very
sensitive and specific in detecting vascular
lesions (e.g., AVM or aneurysm).
3. MRI with appropriate scanning
sequences.

36. Treatment:
A) Nonsurgical management:
1. Airway, breathing and circulation should be the initial focus.
2. Hypertension (HTN) should be controlled.
3. Intubate if GSC ≤ 8 as patient can‘t maintain his or her airways.
4. Monitoring of intracranial pressure and treatment of elevated ICP with dehydrating measures (as mannitol),
and hyperventilation.
5. Fluid management.
6. Anticonvulsants drugs.
7. Maintain body temperature.
B) Surgical treatment:
1. Evacuation of large, surfacing and manifesting ICH with imminent transtentorial herniation..
2. Endoventricular drainage for intraventricular hemorrhage.
3. large cerebellar hemorrhage >3cm.
3. Definitive treatment of the underlying cause as AVM or aneurysm

37. Subarachnoid hemorrhage
Dr mohamed rizk khodair
Lecturer of neurology
Mohamedrizk.med@o6u.edu.eg

38. Definition
Extravasation of blood into the subarachnoid space

39. Etiology of SAH:
Ruptured saccular aneurysm (75%):
- M=F, 5th or 6th decade, with elevated BP.
- Usually, congenital berry aneurysms in circle of Willis.
-Sites:
40% Anterior Communicating artery
30% posterior communicating
20% MCA
10% posterior circulation
- 2-3% mycotic aneurysm (especially infective endocarditis).
Arteriovenous Malformation (AVM) (10%):
- M >F, 2nd to 4th decades, or other vascular malformations
Other less common causes:
Hemostatic failure
Cerebral vasculitis
Brain tumors
Trauma
Drug abuse

40. Risk Factors:
a) Hypertension.
b) Smoking, alcohol.
c) Family history.
d) Polycystic kidneys, Ehlers-Danlos Type IV, pseudoxanthoma elasticum, fibromuscular dysplasia.

41. Clinical Features:
Thunderclap Headache:
Acute, paroxysmal, and sudden in onset, "worst headache in my life".
Develop in seconds; achieve maximal intensity in minutes, and last hours to days (6 - 72).
■ 10 - 43% of patients have a warning leak (sentinel headaches an mild to moderate in intensity,
usually occur within 2 weeks of overt SAH, and are not accompanied by other neurological
symptoms).
Loss of consciousness: in about 50% of cases
Partial or generalized seizures

42. Focal symptoms & signs if:
Associated ICH
Local pressure of aneurysm (Ex, Post com art aneurysm compress 3rd nerve).
Cerebral ischemia
Meningismus:
Nuchal stiffness, especially in flexion, may be absent in deep coma.
Kernig's sign (flex thigh to 90" with knee bent, then straighten knee, positive sign if this causes pain
in the hamstrings)
Brudzinski's sign (flex patient's neck, involuntary hip flexion is a positive sign).
Raising leg sign (Lasègue’s sign).
Ocular Hemorrhage: Between retina & vitreous.
Subhyaloid Hemorrhage: blood seen near the optic disc obscuring the retinal vessels
Irritability or photophobia
Sudden death

43. Physical Findings:
Nuchal stiffness. Papilledema
Diminished consciousness Third nerve palsy.
Bilateral weakness in legs. Sixth nerve palsy
Aphasia, hemiparesis Nystagmus or ataxia.
Visual neglect Retinal & subhyaloid
hemorrhage.

44. Diagnostic approach
A. Non contrast CT scan:
1. The clinical diagnosis of SAH is best confirmed
with brain CT. Sensitivity: 95 -98% sensitivity of
CT scanning within 12 hours.
2. CT confirms the presence of SAH and
hydrocephalus, intraparenchymal hematoma,
intraventricular hemorrhage, or subdural
hemorrhage.

45. B. Lumbar Puncture:
Indication :
Classic history of SAH and negative noncontract CT.
Should never be done prior to CT scanning.
Finding :
 Three tube test: should see a  in traumatic tap versus steady level of RBCs in true SAH
  Opening pressure (>20 cm H20) seen in 60% of cases.
 Xanthochromia:
□ Represents lysis of RBCs with degradation of heme products into bilirubin
□ Present as early as 4-6 hours after SAH and persist for 2-3 weeks.
□ Detected by centrifugation or spectrophotometry which is more sensitive.
Contraindication :
1) Infection at the site.
2) Coagulopathy, drug induced or otherwise.
3) Raised ICP particularly with posterior fossa pathology.
Risk : rebleeding , herintation

46. C. Magnetic Resonance Imaging (MRI) brain:
1. The most sensitive sequences were FLAIR and
T2* (gradient echo).
2. The sensitivity of T2* was 94% under 4 days from
the ictus and 100% between 4 &14 days.
D. Angiography:
Indication
1) Positive CT or lumbar puncture.
2) Screening in selected circumstances:
a. Positive family History.
b. Inherited condition associated with incidence of
intracranial aneurysms.

47. Complications
Neurological complications
Neurological complications
1) Rebleeding:
Risk factors of rebleeding
Uncontrolled blood pressure
Fibrinolysis of clot around the ruptured aneurysm

48. 2) Vasospasm:
Def Clinical or symptomatic vasospasm: Delayed ischemic neurological deficit (DIND)
Radiographic vasospasm: On cerebral angio  arterial narrowing with slowing of filling
Timing Occurs 4 to 14 days after hemorrhage.
Spontaneously resolve over the next 7days.
Risk factors 1) Poor initial clinical state
2) Large SAH or IVH
3) Increased age
4) Angiographic dye
5) Hypertension
6) Hypotension
Mech Unknown but may be:
Direct effect of blood on the adventitia of the artery
Release of VC sub (serotonine, PGs) from vessel wall or blood clot
C/P Causes infarction in 30% of patients (Spasm of major arteries  stroke syndromes).
Diagnosis 1) Angiography: arterial narrowing with slowing of filling.
2) Transcranial Doppler: narrowing of arterial lumen & blood flow velocity.

49. 3) Seizure:
4) Hydrocephalus:
a. Immediate:
Within 3 days, due to intraventricular blood.
Ttt by ventriculostomy
b. Delayed (subacute):
 Develops over a few days or weeks progressive drowsiness or slowed mentation (abulia) with
incontinence,
Due to pia-arachnoid adhesions or permanent impairment of the arachnoid granulations.
5) Others:
- Brain edema.
- Intracerebral hematoma.
- Cognitive & personality changes.

50. Systemic complications
a. Neurogenic pulmonary edema.
b. Cardiac ECG changes:
• Prolonged QT, ST segment or T wave changes.
• Arrhythmias especially ventricular tachycardias.
c. Hypertension: due to pain, ↑catecholamines.
d. GIT hemorrhage.
e. Hyponatremia: due to Syndrome of Inappropriate ADH Secretion (SIADH) , Cerebral salt-wasting syndrome

51. Differential diagnosis:
Differential diagnosis of sudden unexpected headache
Sudden severe headache with neck rigidity Sudden severe headache without neck rigidity
1) SAH:
Abrupt & reach maximum within seconds
Diffuse & poorly localized spread to back of head, neck & back
(as blood track down the spinal arachnoid space)
1) Migraine:
Preceeded by aura
Unilateral, throbbing
Associated with photophobia
2) Meningitis/ encephalitis:
Less abrupt over 1-2days
Associated with high fever, tachycardia, seizures
2) Post-traumatic headache: due to
Soft tissue damage after injury
Dilatation of intracranial vessels pulsating headache worsen
with head movement, sneezing or exertion
3) Stroke:
Cerebellar stroke: sudden severe headache + nausea, vomiting +
vertigo, ataxia
Intraventricular hemorrhage: may mimic SAH
3)Thunderclap headache
4) Acute obstructive hydrocephalus

52. Treatment
1. Hospitalization:
ICU monitoring
Bed rest in dark quiet room
2. General Management:
as stroke

53. 3. Medical management:
1`-Analgesics Codeine 30-60mg/2-3hr
Morphine 2-3mg IV/2-3hr
Acetylsalicylic acid is CI
2-Sedation As phenobarbital 30-60mg IV/6hr prophylaxis against seizures & bl pressure
Over sedation is CI
3-Anti-emetics Avoid Phenothiazine which lower seizures threshold.
4-H2 blokers  risk of stress uler
5-Constipation
6-Nimodipine 60mg/4hr

54. 4. Surgical management
Ruptured saccular
aneurysm
Neurosurgial clipping Endovasular coiling
Aim Exclude the aneurysm from
circulation
Promote thrombosis of the
aneurysm
Tecq Open craniotomy with
placement of 1 or more clips
on aneurysmal neck
Placement of 1 or more platinum
coils via intrarterial catheter
Advant The definitive ttt
High efficacy
Diagnostic & therapeutic
Craniotomy not needed
Disadv Requires craniotomy
Clip may damage neural or
vascular structures
High short-term mortality
(31%) & morbidity
Risk of vessel perforation
 24% mortality.

55. C. Specific Management:
1) Vasospasm:
a) Nimodipine (60 mg orally q 4 h) improves outcome (SE; hypotension).
b) "Triple-H" therapy (hypertension, hemodilution, and hypervolemia).
c) Plasma volume expansion / dopamine --> raise arterial pressure -> increase cerebral perfusion; requires monitoring of BP and CVP.
d) MgS04; inhibit vasospasm.
e) Endovascular: - Percutaneous transluminal angioplasty (balloon dilatation)
2) Rebleeding: prophylactic;
a. Avoid ↑ BP, cough, straining.
b. Mild sedation.
c. Short term antifibrinolytic.
d. Early surgical treatment.
3) hydrocephalus:
a. Acute hydrocephalus; may clear spontaneously or require ventricular drainage
b. Chronic hydrocephalus; ventricular shunting.
4) Increased ICP:
a. Emergent ventriculostomy
b. Medical therapies: mild hyperventilation, mannitol, and sedation.

56. Monitoring patient by:
1) Clinical examination.
2) Continuous ECG.
3) Follow up; BP, electrolytes, fluid balance.
4) TC

57. Thank you
Mohamedrizk.med@o6u.edu.eg