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Professor of Neurology
Cerebral arterial circulation :
The carotid system.
The vertebro-basilar system.
The carotid system
The vertebrobasilar system
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.
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%).
Large artery atheroembolism
Small artery disease
Atrial fibrillation Mitral stenosis Endocarditis Myocardial infarction Atrial myxoma Prothetic valve Mitral valve prolapse Cong. heart disease Cariomyopthy Cardiac surgery
Polycythemia Thrombocythemia Leukemia Sickle cell disease Hypercoagulable states
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
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.
Unilat. S. & S.
e.g. Hemiplegia, hemihyop esthesia, hemianopia, and aphasia ( lt. sided)
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.
- 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.
Duplex carotid ultrasound
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
30% remain disabled one year after
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.
Modern therapy for ischemic stroke
Acute treatment. Rehabilitation. Prevention.
- 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.
Diastolic bl. P. > 220 mm Hg
> 120 mm Hg IV Labetalol or Na Nitroprusside
Systolic bl. p.
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
- 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.
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
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.
For thromboembolic strokes
- Aspirin 75-150 mg daily. - Clopidogrel 75 mg daily.
For cardioembolic ischemic strokes
- IV unfractionated heparin. - SC low molecular weight heparin. - Oral warfarine.
- 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
Symptoms of vertebrobasilar TIAs
Alternating hemiparesis or hemisensory
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.
Treatment of TIAs
Anticoagulants. Antiplatelets. Endarterectomy. Control of risk factors.
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.
Manifestations of increased intracranial
- Headache. - Vomiting. - Dep. level of consciousness. - Seizures.
Manifestations related to the site of the
The commonest type. CP varies:
- From slight hemiparesis & dysarthria. - To sever coma and deceribrate rigidity.
hemiparesis more in u.l.
sensorimotor deficit + hemianopia.
Dominant temporal hematomas
Produces hemiparesis with sever
Dominant side lesions
Ext. into the subthalamus & high
mid brain ocular disturbances.
Rupture into the 3rd ventricle
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.
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
- 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
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
due to a- Rupture of IC aneurysm. b- Rupture of IC AVM.
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.
Usually absent or
- Periodic headache. - Recurrent ophthalmoplegia. - Seizures.
- Sudden. - During periods of activity. - May be ppted by:
* Physical strain. * Straining.
A) Manifestations of rapidly increasing
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.
Cranial nerve palsies:
Ocular nerves & visual pathways.
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:
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.