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CEREBROVSCULAR DISEASES
By

Mohamed Saad
Professor of Neurology
Mansoura University

Cerebral arterial circulation :
 The carotid system.

 The vertebro-basilar system.

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The carotid system
Aortic arch

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Common carotid

Internal carotid

M.C.A.

A.C.A.

The vertebrobasilar system
Aortic arch

Subclavian

Subclavian

Vertebral

Vertebral

Basilar

P.C.A.

P.C.A.

A., M. & P. Cerebral arteries

Basal (central) branches

Superficial (cortical) branches

Circle of Willis
A.Com.A. A.C.A. M.C.A. I.C.A. P.Com.A. P.C.A. V.B. A. A.C.A. I.C.A. P.Com.A. P.C.A. M.C.A.

STROKE
 The commonest c.v. dis.  Called brain attack but not c.v.a.  The 3rd most common cause of death.  Incidence rate = 15-20 / 10,000.

Definition :Stroke is rapidly developing clinical

symptoms &/or signs of focal loss of brain function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

Types of stroke :

Ischemic stroke ( cerebral infarction ).

 Hemorrhagic stroke ( I.C. or S.A.H. ).

Ischemic stroke (Cerebral infarction)
70 – 80 % 0f all strokes

Pathogenesis of cerebral infarction
Sudden thrombotic or embolic occlusion of a cerebral artery

Causes of occlusion of a cerebral artery : Arterial diseases. (75%).  Cardioembolic causes(20%).  Hematologic disorders (5%).

Arterial diseases
 Large artery atheroembolism
Extracranial Intracranial

 Small artery disease
Microatheroma Lipohyalinosis

 Other arteriopathies
Dissiction Arteritis

Cardioemolic Causes
Atrial fibrillation Mitral stenosis Endocarditis Myocardial infarction Atrial myxoma Prothetic valve Mitral valve prolapse Cong. heart disease Cariomyopthy Cardiac surgery

Hematological disorders
Polycythemia Thrombocythemia Leukemia Sickle cell disease Hypercoagulable states

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Risk factors for cerebral infarction
Risk factors for a disease are characteristics of an individual or of a population, associated with an increased risk of that disease

Non-modifiable risk factors
 Increasing age  Male gender  African-American race  A prior stroke  +ve family history of stroke

Modifiable risk factors
(by medical treatment)
 Hypertension  Diabetes mellitus  Heart disease  TIAs  Raised hematocrite

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Modifiable risk factors
(by changing life style)
 Cigarette smoking  Hyperlipidemia  Physical inactivity  Obesity  Stressful life

Clinical features of ischemic stroke
 Focal loss of neurological function.  Negative in quality.  Rapidly developing.  Maximum at onset.

Focal neurological S. & S.
Caroid
Unilat. S. & S.
e.g. Hemiplegia, hemihyop esthesia, hemianopia, and aphasia ( lt. sided)

Vertebrobasilar
Unilat. Or bilat. S.& S.
+ Disturbance of cranial nerves and cerebellum e.g. crossed hemiplgia

Investigations of ischemic stroke

    

First line investigations. Brain CT scan. Duplex carotid ultrasound. Echocardiography. More specialized investigations.

First-line investigations
- Full blood count. - ESR. - Plasma glucose. - Plasma urea and electrolytes. - Plasma cholesterol. - Urine analysis. - ECG.

Brain CT scan

• • •

To exclude a non vascular cause of the suspected stroke. To distinguish intracranial hemorrhage from cerebral infarction. To ascertain the likely cause of the stroke.

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Duplex carotid ultrasound

Echocardiography

More specialized investigations
- MRI & MRA of the brain - Tests for collagen dis. - Transcranial doppler. - Angiography

Prognosis depends upon :
 Site of the infarction.  Size of the infarction.  Patient’s age.  Prior Co-morbidities.

With the best treatment
 30% die within the 1st one year of

stroke onset.
 30% remain disabled one year after

stroke onset.
 30% suffer a recurrent stroke within

the next 5 years of stroke onset

Cause of death
 Death within the first week after stroke:
- Direct effects of the brain damage. - Brain herniation.

 Death after one week of stroke onset:
- Bronchopneumonia. - Venous thrombosis. - Recurrent vascular events.

Treatment of ischemic stroke * Rapid diagnosis of stroke and
initiation of treatment are important.

* Patients with an acute stroke should
be admitted to hospital.

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Modern therapy for ischemic stroke
 Acute treatment.  Rehabilitation.  Prevention.

Acute treatment
 Emergency care.
- Care of respiration. - Care of circulation.

 Thrombolytic therapy.  Neuroprotective therapy.  Prevention of complications.

Care of respiration
To protect against airway obstruction, hypoventilation & aspiration.
- Pulse oximetry or arterial bl. Gases. - Supplemental oxygen. - Feeding tube. - Suction. - Mild hypothermia.

Care of circulation
To protect against myocardial ischemia, cardiac arrhythmias & sever hypertension.
- Cardiac monitoring (for 24-48 hours). - Blood pressure monitoring (frequently).

Control of blood pressure
 Systolic bl. p.

or

Diastolic bl. P. > 220 mm Hg

> 120 mm Hg IV Labetalol or Na Nitroprusside
 Systolic bl. p.

or

Diastolic bl. P. < 220 mm Hg

< 120 mm Hg Hypertensive before Cont. the same treat in the same dose Not hypertensive before Wait for 1 or 2 weeks If not corrected

Thrombolytic therapy
- To recanalize the occluded artery. - Carries the risk of major bleeding. - 0.9 mg / kg tissue plasminogen activator IV over 60 min.

Thrombolytic therapy is indicated in patients with :
- Acute ischemic stroke with clearly definable time of onset. - 3 Hours time window. - A base line CT excluding ICH & SAH. - Any age between 25 & 75 years.

Trombolytic therapy is contraindicated in patients with :
- His. of stroke or serious head injury (3 m.). - His. of GIT or UT hemorrhage (3 w.). - His. of major surgery (2 w.). - His. of anticoagulant intake (48 h.). - His. of ICH. - Syst. bL p >185 or diast. bl p >110 mm Hg. - Blood glucose > 400 or < 50 mg / dl. - Elevated PT or PTT or dec. Platelet count.

Neuroprotective therapy
To prevent or limit damage of brain tissue.
- Phenytoin (Epanutine). - Nimodipine (Nimotop). - Naloxone (Narcan). - Piracetam (Nootropil).

Prevention of complications
- Brain edema. - Pneumonia. - Seizures. - D.V.T. - Electrolyte disturbances. - Pressure sores. - Urosepsis. - Depression

Rehabilitation
Should start as soon as the diagnosis of stroke is established
 Physiotherapy.  Speech therapy.  Occupational therapy.

Prevention of stroke recurrence
 Antiplatelets.  Anticoagulants.  Carotid endarterectomy.  Control of risk factors.

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Antiplatelets
For thromboembolic strokes
- Aspirin 75-150 mg daily. - Clopidogrel 75 mg daily.

Anticoagulants
For cardioembolic ischemic strokes
- IV unfractionated heparin. - SC low molecular weight heparin. - Oral warfarine.

Carotid endarterectomy
- Sever carotid stenosis. - Non disabling symptoms.

Control of risk factors
- Avoid smoking. - Lipid lowering. - Control of diabetes. - Treatment of hypertension.

Transient Ischemic Attacks (TIAs)
Acute focal loss of brain function with symptoms lasting less than 24 hours and which is thought to be due to inadequate cerebral blood flow.

Pathogenesis of TIAs
 Sudden & temporary thrombotic or

embolic occlusion of a cerebral artery.

 Low flow distal to an already occluded

or highly stenosed artery.

Symptoms of carotid TIAs
 Ipsilateral transient visual loss.  Contralateral motor or sensory

dysfunction.
 Aphasia.  Convulsions.

Symptoms of vertebrobasilar TIAs
 Alternating hemiparesis or hemisensory

symptoms.
 Dysartheria, dysphagia, diplopia, vertigo,

impalance, vomiting, loss of consciousness or vital signs alterations.
 Drop attacks.  Homonymus hemianopia.

Investigations of TIAs
 Duplex carotid ultrasound.  Echocardiography.  Transcranial doppler.  Cerebral angiography.  CT or MRI of the brain.

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Treatment of TIAs
 Anticoagulants.  Antiplatelets.  Endarterectomy.  Control of risk factors.

Hemorrhagic stroke
(Cerebral hemorrhage)
Intracerebral hge
(ICH)

Subarachnoid hge
(SAH)

Intracerebral hemorrhage (ICH)
Hemorrhage into the brain

Causes of ICH
 Hypertension (1ry ICH).  Vascular malformations.  Bleeding disorders.  Hemorrhage into brain tumor.  Cerebral arterial amyloidosis.  Inf. of cerebral arteries.  Hemorrhagic infarction.  Trauma.

Primary (hypertensive) ICH
- The commonest type. - Due to chronic hypertension & degeneration

of cerebral arterites.
- The extravasated blood forms a mass that

disrupts and compresses the brain tissue.
- When the RAS & respiratory center are

compromised, coma and even death occurs.

Sites of 1ry ICH
 The putamin.  The cerebral lobes.  The thalamus.  The cerebellum.  The pons.

Clinical manifestations
 Manifestations of increased intracranial

pressure:

- Headache. - Vomiting. - Dep. level of consciousness. - Seizures.

 Manifestations related to the site of the

hematoma.

Putaminal hemorrhage
 The commonest type.  CP varies:

- From slight hemiparesis & dysarthria. - To sever coma and deceribrate rigidity.

Lobar hemorrhage
 Frontal hematomas

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hemiparesis more in u.l.
 Parietal hematomas

sensorimotor deficit + hemianopia.
 Dominant temporal hematomas

fluent aphasia.
 Occipital hematomas

homonymous hemianopia.

Thalamic hemorhage
 Produces hemiparesis with sever

sensory deficit.
 Dominant side lesions

fluent aphasia.
 Ext. into the subthalamus & high

mid brain ocular disturbances.
 Rupture into the 3rd ventricle

hydrocephalus.

Cerebellar hemorhage
 Sudden onset of vertigo,

headache, vomiting and inability to stand and walk.
 A triad of ipsilat. Ataxia,

gaze palsy and l.m. facial palsy is diagnostic.
 Abrupt deterioration to coma

and death may occur.

Pontine hemorhage
 The classic picture: Coma, quadriplegia, decerebrate rigidity, opthalmoplegia, pin point pupils, abnormalities of respiratory rhythm hyperthermia and death.  Rare less sever cases: Unilat. pontine cranial nerve affection + long tracts interruption.

Diagnosis of ICH
 Clinical features:
- Acute sever rise of bl. pr. In chronic hypertensive patient. - Vomiting at onset. - Sever headache. - Nuchal rigidity. - Seizures.

Diagnosis of ICH (Cont.)
 Brain CT scan: Superior to MRI.

 MRI of the brain: For brainstem hge.

D) Others: Pt, ptt, platelet count, etc.

Prognosis of ICH
 Immediate prognosis: Grave (1/3 of the patients die in 1 to 30 days).

 Late Prognosis: Better restoration of function than ischemic stroke.

Treatment of ICH

Emergency care:
To prevent airway obstruction, hypoventilation and aspiration.

Control of blood pressure:
Correction of bl. Pr. Is mandatory, but cautiously and slowly.

Control of intracranial pressure:
By hyperventilation, I.v. mannitol & dexamethasone

 

Prevention of complications:
As seizures, pneumonia, D.V.T., urosepsis, bed sores etc.

Surgical evacuation of the hematoma:

Subarachnoid hemorrhage (SAH(
Sudden flooding of the subarachnoid space with arterial blood

Etiology of SAH
A) Spontaneous:
due to a- Rupture of IC aneurysm. b- Rupture of IC AVM.

B) Traumatic:
due to Head trauma (rare cause).

Clinical picture of SAH
 Age & sex.  Premonitoring symptoms.  Onset.  Clinical manifestations.

Age and sex
- Both sexes are affected. - Aneurysmal group - Angiomatous group

4th & 5th decades. 2nd & 3rd decades.

Premonitoring symptoms
Usually absent or
- Periodic headache. - Recurrent ophthalmoplegia. - Seizures.

Onset
- Sudden. - During periods of activity. - May be ppted by:
* Physical strain. * Straining.

Clinical manifestations
A) Manifestations of rapidly increasing

intracranial pressure.
B) Manifestations of meningeal irritation. C) Focal manifestations.

Manifestations of rapidly increasing intracranial pressure
 Headache.  Vomiting.  Change of conscious.  Bradycardia & irrigular respiration.  Convulsions.  Papilloedema & retinal hemorrhage.

Manifestations of meningeal irritation
The patient is irritable and lies in an attitude of general flexion with:
 Neck rigidity.  +ve meningeal irritation signs.  Moderate pyrexia.  Pain in the back & lower limbs.

Focal manifestations
 Cranial nerve palsies:
Ocular nerves & visual pathways.

 Hemiplegia:
And may be aphasia.

Prognosis of SAH
 Half the cases recover from

the acute attack.
 Usually no residual disability.  1/3 of the survivors suffer from

recurrent fatal attacks.

Investigations of SAH
 Brain CT scan: Blood appears in the subarachnoid space.  CSF examination: The CSF is bloody with - Xanthochromic supernatant fluid. - Raised pressure. - Increased protein but normal sugar & cl. Slight lymphocytosis.  Four vessel angiography:

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Treatment of SAH
 Conservative: 1- Rest in bed. 2- Control of ICP. 3- Analgesics. 4Tranquilizers. Avoid straining. 6- Antifibrinolytics.  Surgical: Excision or clipping of the aneurysm or feeding vessel.  Embolization or radiotherapy.

5-

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