You are on page 1of 102

www.mansfans.

com
www.mansfans.com

CEREBROVSCULAR
DISEASES

By

Mohamed Saad
Professor of Neurology
Mansoura University
Cerebral arterial circulation :

 The carotid system.

 The vertebro-basilar system.


www.mansfans.com
www.mansfans.com
The carotid system

Aortic arch

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) Superficial (cortical)


branches branches
Circle of Willis
A.Com.A.

A.C.A. A.C.A.

M.C.A. I.C.A. I.C.A. M.C.A.

P.Com.A. P.Com.A.

P.C.A. P.C.A.

V.B. 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
www.mansfans.com
Hematological disorders

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
www.mansfans.com
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 Vertebrobasilar
Unilat. S. & S. Unilat. Or bilat. S.& S.
e.g. +
Hemiplegia, hemihyop Disturbance of cranial
esthesia, hemianopia, nerves and cerebellum
and aphasia ( lt. sided) 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.
www.mansfans.com
www.mansfans.com
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.
www.mansfans.com

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 Not hypertensive before


Cont. the same treat Wait for 1 or 2 weeks
in the same dose 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.


www.mansfans.com

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.


www.mansfans.com

Treatment of TIAs

 Anticoagulants.

 Antiplatelets.

 Endarterectomy.

 Control of risk factors.


Hemorrhagic stroke
(Cerebral hemorrhage)

Intracerebral hge Subarachnoid hge


(ICH) (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.
www.mansfans.com
Lobar hemorrhage
 Frontal hematomas
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 4th & 5th decades.


- Angiomatous group 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:
www.mansfans.com
www.mansfans.com
Treatment of SAH
 Conservative:
1- Rest in bed. 2- Control of ICP.
3- Analgesics. 4-
Tranquilizers. 5-
Avoid straining. 6- Antifibrinolytics.

 Surgical:
Excision or clipping of the aneurysm
or feeding vessel.
 Embolization or radiotherapy.
www.mansfans.com

THANK YOU

You might also like