CEREBROVASCULAR DISEASE Stj. Dr. Berfin Gizem USLU

Introduction A neurologic symptom or symptom complex caused by cerebral ischemia or hemorrhage is commonly called a cerebrovascular disease, or stroke. Stroke includes all disorders in which an area of the brain is transiently or permanently affected by ischemia or bleeding. The cardinal clinical features are sudden or subacute onset and (except for subarachnoid hemorrhage) focal neurologic deficit.

Anterior Cerebral Circulation Anterior circulation; supplies cortex basal ganglia and internal capsule Internal carotid arteries Middle Cerebral Artery (MCA) Anterior Cerebral Artery (ACA) Anterior communicating artery Birden fazla slayt gerektirebilir

Posterior Cerebral Circulation Posterior circulation; supplies brain stem, cerebellum, talamus, occipital and temporal lobes Vertebral arteries Posterior inferior cerebellar artery (PICA) Basillar artery Superior cerebellar artery (SCA) Anterior inferior cerebellar artery (AICA) Pontine branches Posterior cerebral artery (PCA)

The Circle of Willis The circle of Willis connects arterial blood flow from the following arteries together: Anterior Cerebral Artery (ACA) Posterior Cerebral Arteries (PCA) Anterior communicating artery Posterior communicating artery

Stroke Stroke is a clinical syndrom that causes neurological signs and symptoms which is acute onset, vascular origin. It continues more than 24 hours and leads to death. Strokes can be classified into two major categories: Ischemic(%85) Hemorrhagic(%15) Intracerebral Hemorrhage Subarachnoid Hemorrhage

Risk Factors Controllable Risk Factors; Hypertension Smoking Atrial fibrillation MI Hyperlipidemia DM Transient Ischemic Attacks (TIA) Heavy alcohol consumption OCP use Hypercoagulopathy Uncontrollable Risk Factors; Age Gender Heredity and Race Prior stroke or heart Attack

Patophysiology of Brain Ischemia Cerebral blood flow is nearly 50-55 ml/100gr/min ; in gray matter 70- 80 ml/100gr/min , in white matter 30ml/100gr/min. Neurological symptoms occur under 30ml/100gr/min, EEG distrupts under 20 ml/100gr/min. Irreversible ischemia occur under 10 ml/100gr/min and there is penumbra around the ischemic zone. The aim of treatment is saving penumra in 4-6 hours. Result of the decrese cerebral flow causes irreversible neuron and glia damage and area called infaction zone. Great arteries infarction causes brain edema.

Transient Ischemic Attack Transient ischemic attack (TIA) – a temporary fall in the blood supply to one part of the brain, resulting in brief symptoms similar to stroke.  Transient ischemic attack causes a focal deficit such as a weak limb, aphasia or loss of vision lasting from a few seconds to 24 hours. There is complete recovery.The attack is usually sudden. TIA’s are usually the result of microemboli. Principal sources of emboli to the brain are cardiac thrombi and atheromatous plaques/thrombi within the great vessels and carotid and vertebral systems. Tx; Antikoagulan (heparin, warfarin) -Antiagregan (ASA, klopidogrel, dipiridamol), stent or surgery Treatment is very important ,1/3 of TIAs can repeat and cause infarction.

Intracerebral hemorrage ICH caused by small arterial dissection due to hypertension and hemorage into brain. %10-15 of all infarct. If hemorage forms hematoma and it stops but it last up to 24-36 hours in patient who taking anticoagulan treatment. Brain edema occursond causes KIBAS.Hematoma resorption stars after 48 hours and last 1-6 months. Usually, a basillaris and penetrating arteries leads to. Other etiologies: AVM Bleedin diathesis Anticoagulation Vasculit Bleeding in to tumor

CLINIC 60-80 years Headache, nausea, focal neurological signs Epileptic seizures (especially in frontal and temphoral hematoma) Coma (in great hematoma) LOCALIZATIONS: Lober Putaminal ,Talamik ,Pontin ,Serebellar ,Primer intraventriküler Tx; Airway must be open and blood pressure should decreased > 200/120 mmHg -- i.v. Nitroprussid or nitrogliserin 160-200 / 105-120 mmHg --- i.v. Labetolol, furasemid, oral kaptopril < 160 / 90 mmHg--- surgery If there is avm, tm, shift or obstructive hydrocephalia ,surgery should be considered

Subarachnoid Hemorrhage (SAH) Extravasation of blood into the subarachnoid space between the pia and arachnoid membranes. Most commonly caused by head trauma , aneurysm and AVMs. SAH due to rupture of cerebral aneurysm is %50 of all spontaneous traumatic intracranial hemorrhages. Incidence: 6-8/100 000 Overall mortality is 45% 10-15% of patients die before reaching medical care

Etiology Traumatic- most common Nontraumatic: Intracranial aneurysms (%75-80)-- most common in 20 to 60. Cerebral AVMs (%4-5) Vasculopathy Tumors Cerebral artery dissections Coagulation disorders Dural sinus thrombosis Spinal AVM Pituitary apoplexy No cause can be determined (%14-22)

Risk Factors Past history Aneurysm in other blood vessels High blood pressure Disorders associated with weakened blood vessels, including; Polycystic Kidney disease , Fibromuscular dysplasia or, Connective tissue disorders OCP use Smoking Alcohol Pregnancy Cocaine Family history of aneurysms

Symptoms Main symptom : severe headache ; that starts suddenly and is often worse near the back of the head. Patients often describe it as the "worst headache ever" and unlike any other type of headache pain. Other symptoms: Decreased consciousness and alertness Photophobia Mood and personality changes, including confusion and irritability Stiff neck, neck pain and shoulder pain Nausea and vomiting Numbness in part of the body Seizure, vision problem (double vision,blind spots,temporary vision loss in one eye)

Diagnosis Non-contrast high resolution CT; is the initial investigation, it will detect SAH in 95% of cases if scanned within 48 hours of SAH. LP : is not necessary if SAH is confirmed by CT, but should be performed if doubt remains. The CSF becomes yellow(xanthochromic) several hours after SAH. Visual inspection of the supernatant CSF is usually sufficiently reliable for diagnosis. In 5 - 10% of cases, the scan may be normal, especially if there has only been a small bleed. If the CT scan is normal, a lumbar puncture must be performed. CT angiography MR angiography; is usually performed in all potentially fit for surgery , Cerebral angiography

Grading SAH Hunt and Hess Grade 1: asymptomatic, or mild headache and slight nuchal rigiditity Grade 2: moderate to severe headache, nuchal regidity, cranial nerve palsy Grade 3: mild focal deficit, lethargy, or confusion Grade 4: stupor, moderate to severe hemiparesis, early decerebrate rigidity Grade 5: deep coma, decerebrate rigidity, moribound appearance Fisher Grade 1: no subarachnoid blood detected (5.8% mortality) Grade 2: diffuse or <1 mm blood (10.3% mortality) Grade 3: localized clot and/or >1 mm blood (32.8% mortality) Grade 4: intracerebral or intraventricular clot (45% mortality)

Grading SAH (Yasargil) Grade 0: a, unruptured aneurysm b, unruptured aneurysm, neurological deficit (+) Grade 1: a, asymptomatic b, focal neurological deficit (+) Grade 2: a, headache, nuchal rigidity Grade 3: a, lethargy, confusion, disorientation, agitation Grade 4: semi coma Grade 5: deep coma

Complications Rebleeding Hydrocephalus Acute (obstructive) hydrocephalus (20-27%) Chronic (communicating) hydrocephalus (14-23%) Delayed ischemic neurological deficit (DIND) attributed to vasospasm Hyponatremia with hypovolemia (10-34%) DVT and pulmonary embolism MI Seizures

Treatment Admit to ICU Bed rest with head of bed at 30º Low level of external stimulation IV fluids: 2ml/kg/h or 150ml/h (normal saline + 20 mEq KCl/L) Medications Prophylactic anticonvulsants Sedation, Analgesics, Dexamethasone Antiemetics Oxygenation Cardiac rhythm monitor Systolic blood pressure 120-130 mm Hg by cuff

CEREBRAL VASOSPASM Arterial vasospasm typically appears 3 to 4 days after rupture and reaches a peak in incidence and severity at 7- 10 days While 40% to 70% of patients have evidence of arterial narrowing ,only 20% to 30% develop the clinical syndrome. Symptomatic vasospasm typically begins 4-5 days after hemorrhage and is characterized by insidious onset of confusion and a decreasing level of consciousness Basillar artery vasospasm

Diagnosis & Treatment 4-20 days after pos-SAH Rule-out other causes of deterioration rebleeding hydrocephalus cerebral edema seizure metabolic disturbances (hyponatremia…) hypoxia sepsis Other tests transcranial doppler CBF studies SPECT cerebral angiography The main goal of current treatment plan is to prevent or limit the severity of arterial and symptomatic vasospasm. Only two treatments are generally accepted to be of substantial value in reducing the ischemic complications related to vasospasm: Nimodipine (cerebroselective ca canal blocker) Hypervolemic, hypertensive therapy is used to elevate the cerebral perfusion pressure

CEREBRAL ANEURYSM Brain aneurysms occur because of weakness in the wall of a a cerebral artery causes localized dilation or ballooning of blood vessels. An aneurysm by itself does not cause symptoms and may be found in up to %10 of the population , may be present from birth or it may develop later in life. Unrupture aneurysm: 0.5-1% Risk of bleeding 1-2%/per year Etiology: Congenital predisposition (defect in the muscular layer) Atherosclerotic or hypertensive Polycystic kidney disease Coarctation of aorta

Aneurysm Types Saccular; (most common also called ‘berry’) the aneurysm bulges from ane side of the artery and has a distinct neck at its base. Fusiform the aneurysm bulges in all directions and has no distinct neck Giant; may be saccular or fusiform and measures mor ethan 2.5 cm in diameter;The neck is often wide and may involve more than one artery. Traumatic ; caused by a closed head injury or penetrating trauma to the brain.

Distribution of Congenital Cerebral Aneurysm Anterior Circulation (85- 95%) ICA(%30) Oph A(%4) Posterior Com A (%22) Anterior choroidal(%4) ACA(%30) -Anterior Com A (%25) -Distal anterior cerebral artery (%5) MCA (%25) Posterior Circulation (5-15%) Vertebral Artery (%3) PCA(%2) Basilar Artery (%10) Basilar trunk

Signs and Symptoms If an aneurysm ruptures, it leaks blood into the space around the brain. This is called a “subarachnoid hemorrhage.” Depending on the amount of blood, it can produce: a sudden severe headache that can last from several hours to days( often described as ‘the worst headache of my life’) nausea and vomiting drowsiness and/or coma The ruptured aneurism may also damage the brain directly, usually from bleeding into the brain itself. This is called “hemorrhagic stroke.” weakness or paralysis of an arm or leg trouble speaking or understanding language vision problems Seizures Unruptured aneurysm: double vision, dilated pupils, Pain above and behind the eye

Diagnosis & Treatment Cerebral angiography or spiral CT scan angiography of the head to reveal the location and size of the aneurysm CT scan of the head MRI or MRI angiogram Tx; Repair an aneurysm: 1.Clipping: (most common) This is done during open brain surgery. 2. Endovascular repair (coiling) is a less invasive way to treat some aneurysms. Treatment may involve: Complete bedrest and activity restrictions Anti-epileptic drugs Control headaches and blood pressure

Types of Cerebrovascular Malformations Arteriovenous malformation ; abnormal tangle of blood vessels where arteries shunt directly into veins with no intervening capillary bed ; high pressure Cavernoma; abnormal cluster of enlarged capillaries with no significant feeding arteries or veins ,low pressure Venous malformation; abnormal cluster of enlarged veins resembling the spokes of a wheel with no feeding arteries,low pressure, rarely bleed and usually not treated Capillary telangiectasia; abnormal capillaries with enlarged areas (similar to cavernoma); very low pressure

ARTERIOVENOUS MALFORMATIONS An AVM is a tangled bundle of blood vessels where arteries connect directly to veins. This creates a system of multiple feeding arteries, the tangle and enlarged draining veins. Dilated arteries and veins with dysplastic vessels,without capillary bed. They have a higher rate of bleeding than normal vessels. They are very rare (% 0.14) Lifelong risk of bleeding of 2-4%/per year

Symptoms The symptoms of AVMs vary depending on their type and location. most AVMs do not show symptoms (asymptomatic) until a bleed occurs. Common signs of AVMs are: Hemorrhage (%50)--%10 mortal Sudden onset of a severe headache, vomiting, stiff neck (described as "worst headache of my life") Seizures,epilepsy Migraine-like headaches Bruit: an abnormal ringing sound in the ear caused by blood pulsing through the AVM

Diagnosis &Treatment -CT, MRI , Angiography Tx; Observation (anticonvulsant/ antihyperensive therapy) Stereotactic Radiosurgery Endovascular therapy Surgery During an endovascular procedure, a microcatheter is inserted into the arteries feeding the AVM. Materials, such as glue or coils, are inserted into the abnormal arteries to block the flow of blood into the AVM nidus.

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