Cerebrovascular diseases
Vascular occlusive diseases (ischemic stroke) Intracerebral hemorrhage (hemorrhagic stroke)
Incidence of stroke new cases per population per year 2-3rd leading cause of death 1st leading cause disability
Ischemic stroke Atherosclerosis of great cerebral vessels20-40% –Stenosis of vessels –Atherothromboembolism Cardiac embolism15-30% Nonatherosclerotic vasculopaties and hematological abnormalities10-20% Unknown10-30%
Common sites of atherosclerotic disease.
Normal blood flow 55 ml/100g per min - average – ml/100g per min for gray mater –25-30 ml/100g per min for white matter <20 ml/100g - ischemic stroke
Acute ischemia Transient Ischemic attack – neurological deficit that resolves during 24 hours Reversible neurological deficit (minor stroke) – deficit that resolves completely during more then 24 hours Ischemic stroke – persistent neurological deficit
Clinical presentations of ischemic stroke Subacute begining (acute in cases of embosilsm) Consciousness is clear or short term lost of consiousness. Not often unconsciousness Focal neurological deficit – main in clinical picture Headaches, meningeal signs are not often History of TIAs, no history of hypertention
Treatment of acute ischemia 1. Acute resuscitation 2. Reperfusion of the ischemic brain 3. Decreasing cerebral metabolic demands 4. Inhibition of the degradative ischemic cascade
1. Acute resuscitation Respiration –Intubation with ventilation for patients in coma –Supplementary oxygen for other patient Arterial pressure –Maintaining mild hypertension (if there is no evidence of hemorrhage) or at least normal blood pressure Maintaining of adequate intravessel volume Controling heart output and arrhythmias Controlling of glucose level
2. Reperfusion of the ischemic brain Thrombolytic therapy – recombinant activator for tissue plasminogen –In first 4-6 hours after onset –If intracerebral hemorrhage is excluded with CT Hypervolemic Hemodilution Therapy Anticoagulation ???
3. Decreasing cerebral metabolic demands Hypothermia ??? Barbiturates
Surgical treatment for acute ischemia Possible only in cases of stenosis of great brain vessels (common carotid, internal carotid, middle cerebral arteries) – endarterectomia in first 2-3 hours.
Primary stroke prevention – controlling of risk factors Hypertension (increases risk of stroke in4-5 times) Smoking (1,5) Diabetes. (2,5-4) Lipids. Cardiac Disease. –Atrial fibrillation, (5) –valvular heart disease, (4) –myocardial infarction (5)
Secondary Stroke Prevention (After Transient Ischemic Attack or Ischemic Stroke) Aspirin mg per day Or Ticlopidine Treatment or heart diseases Surgical
Surgical prevention of ischemia EXTRACRANIAL-TO-INTRACRANIAL CAROTID ARTERY BYPASS CAROTID ENDARTERECTOMY
Indications –Patients with TIAs with high grade stenosis of CCA or ICA confirmed with ultrasound-dopler and angiography –Patients after stroke (strokes) that do not cause severe diability
angiograms of cervical carotid artery showing varied appearance of critical stenosis of the internal carotid artery. A Smoothly tapered segmental narrowing. B Sharply demarcated stenosis.
endarterectomy
Causes of nontraumatic intracranial hemorrhage Intracerebral hemorrhage –Arterial hypertention (hemorrhagic stroke) –Bleeding from Arterio-venous malformation (AVM) –Rupture of aneurysm of cerebral vessel –Coagulopathies –vasculitis Subarachnoid hemorrhage –Rupture of aneurysm of cerebral vessel –Bleeding from Arterio-venous malformation (AVM)
Clinical signs of hemorrhagic stroke due to hypertension Sudden and fast onset (seconds – minutes) Unconsciousness (semicoma-coma) Severe neurological deficit Vegetative symptoms: high arterial pressure; bradycardia, red face and cyanotic limbs, sweating. Severe headache in contact patients
Diagnostic procedures Computed tomography (CT) Angiography EchoEG
Medial (thalamic) hematoma
Lobar hematoma
Brainstem (pontine) hemorrhage
Treatment Conservative only – – for patients in clear consciousness or severe coma (GCS 3-5) –Medial hemorrhage (into basal ganglia) –Hemorrhage into brainstem Surgical + conservative - for other patients
Conservative treatment Respiration control –Intubation for comatose patients –Supplementary oxygen Arterial pressure control –Severe hypertention must be treated gently – decrease pressure to mild hypertention during several hours. Coagulative status control and correction
Surgical treatment Removal of intracerebral hematoma Ventricular draining in case of occlusive hydrocephalus
Clinical presentation of SAH Sudden onset Severe headache Meningeal signs Minimal focal neurological deficit More rarely depressed level of consciousness and major neurological deficit
Diagnostic procedures for SAH CT Lumbar puncture with CSF examination –Blood in the CSF –High pressure of CSF –SAH and possible intracerebral hemorrhage Angiography – the main to reveal the cause of SAH – aneurisms and arterio-venous malformations
Aneurisms of cerebral arteries Localization –Anterior cerebral a. and anterior communicans. - 45% –Internal carotid a. – 32% –Middle cerebral a. – 20% –Vertebrobasilar circulation – 4%
Aneurisms of cerebral arteries Saccular Others (traumatic, atherosclerotic, mycotic, neoplastic, inflamatory) Saccular aneurisms – ovoid-shaped outpouching of vessel wall, cased by congenital insufficiency of elastic component of vessel wall
SAH due to ruptured aneurism First rupture of aneurism – SAH only Repeated rupture in 20-50% of cases, most of them during 3-20 days after first 50-85% mortality after repeated rupture, Intracerebral hemorrhage are often at repeated rupture Often complicated with vasospasm and consequent ischemical changes
Surgical treatment of aneurism Any aneurism should be excluded from circulation as early as possible –Putting clips on the neck of aneurism –Endovascular embolisation of aneurism With coils With balloons
Angiography 1 – in first day 2 – 3 rd day – angiospasm of middle cerebral atery 3 – 4 th day (after treatment)
Internal carotid bifurcation aneurysm.
Aneurysm Clipping
Clipping of the aneurysm
Coiling of an aneurysm
Arteriovenous malformations heterogeneous group of vascular developmental anomalies of the brain composed of a mass of abnormal arteries and veins of different sizes. Functionally, they represent direct artery-to-vein shunting with no intervening capillaries, angiographically are seen as early filling of veins.
Schematic drawing of AVM
Clinical presentations of AVMs Intracranial hemorrhage –Intraparenchymal –Subarachnoid Seizures headache, progressive neurological deficit, cardiac failure.
Diagnosis Angiography MRI
Angiography
MRI – AVM in occipital lobe
Treatment of AVMs Observation Surgical excision Endovascular embolization Radiosurgery –Hamma-knife –Linear proton accelerator
Hamma-knife