1. CEREBROVASCULAR DISEASE
Stj. Dr. Berfin Gizem USLU

2. 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.

4. 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

6. 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)

8. 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

10. 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

11. 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

12. Patophysiology of Brain Ischemia
Cerebral blood flow is nearly ml/100gr/min ; in gray matter 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.

13. 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.

14. 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 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

15. 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
/ mmHg --- i.v. Labetolol, furasemid, oral kaptopril
< 160 / 90 mmHg--- surgery
If there is avm, tm, shift or obstructive hydrocephalia ,surgery should be considered

16. 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/
Overall mortality is 45%
10-15% of patients die before reaching medical care

17. 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)

18. 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

19. 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)

20. 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 % 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

21. 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)

22. 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

23. 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

24. 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 mm Hg by cuff

25. CEREBRAL VASOSPASM
Arterial vasospasm typically appears 3 to 4 days after rupture and reaches a peak in incidence and severity at 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

26. 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

27. 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

28. 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.

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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.

36. References
Good, David C. "Cerebrovascular Disease." Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd Edition. U.S. National Library of Medicine, 01 Jan Web. 05 May <
Kalaria, Raj N. "Cerebrovascular Disease and Mechanisms of Cognitive Impairment."Stroke. American Heart Association, Inc., 01 Sept Web. 05 May <
"Cerebrovascular Diseases - Department of Neurology - Mayo Clinic Research." Mayo Clinic. N.p., n.d. Web. 05 May < divisions/department-neurology/cerebrovascular-diseases>.
Spine, Mayfield Brain &. "Aneurysm Surgery: Clipping." Aneurysm Clipping | Mayfield Brain & Spine. N.p., n.d. Web. 05 May <
Arteriovenous Malformation (AVM). N.p., n.d. Web. 05 May <