Cerebral Vascular Diseases. Nabila Hamdi MD, PhD

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1 Cerebral Vascular Diseases Nabila Hamdi MD, PhD

2 Outline I. Stroke statistics II. Cerebral circulation III. Clinical symptoms of stroke IV. Pathogenesis of cerebral infarcts (Stroke) 1. Ischemic - Thrombotic - Embolic - Lacunar/small vessel disease 2. Hemorrhagic - Primary brain parenchymal hemorrhage - Subarachnoid hemorrhage & saccular aneurysm V. Traumatic brain vascular injury - Epidural hematoma - Subdural hematoma 2

3 ILOs 1. To distinguish ischemic stroke from hemorrhagic stroke in terms of etiology and pathology 2. To know the most common causes of ischemic infarcts 3. Explain small vessel disease, mention 2 conditions that cause it and know its effects on the brain 4. Know 4 different causes of intracerebral hemorrhage 5. Understand the role of hypertension in the pathogenesis of hemorrhagic strokes 6. Explain the subarachnoid hemorrhage resulting from the rupture of saccular aneurysms 7. Distinguish intracerebral hemorrhage from traumatic brain hemorrhages 8. Differentiate between epidural and subdural hematoma 3

4 Stroke Statistics About 795,000 Americans each year suffer a new or recurrent stroke. That means, on average, a stroke occurs every 40 seconds. No. 3 cause of death after cardiovascular diseases and cancer About 1 of every 18 deaths. On average, every 4 minutes someone dies of stroke. Of all strokes, 87% are ischemic, 10% are intracerebral hemorrhages, and 3% are subarachnoid hemorrhages The estimated direct and indirect cost of stroke for 2009 is $68.9 billion (inpatient care, rehabilitation and follow-up care necessary for lasting deficits) 4

5 Cerebral Circulation Neuro4Students, Cerebrovascular attack 5

6 Cerebral Circulation Circle of Willis: source of collateral flow major little if any collateral flow for the deep penetrating vessels (thalamus, basal ganglia, and deep white matter) 6

7 Stroke Ischemic (Clots) 87% Hemorrhagic (Bleeds) 13% Stroke Ischemic injury/infarction of specific regions of the brain, depending on the vessel involved. Hemorrhage leads to direct tissue damage as well as secondary ischemic injury 3% subarachnoid hemorrhage 10% intracerebral hemorrhage 7

8 Stroke Focal neurological deficit Longer than 24 hours Less than 24 hours (minutes) Permanent tissue damage No permanent tissue damage Stroke Transient ischemic attacks (TIAs) 1/3 of patients with TIA develop clinically significant infarcts within 5 years 8

9 Signs & Symptoms of Stroke 9

10 Signs & Symptoms of Stroke Hemiplegia: Sudden paralysis of a leg, arm or one side of the face Hemiparesis: Sudden numbness or weakness of arm, leg or face Consciousness: +/- loss of consciousness Aphasia: loss/impairment of the power to use or comprehend words. Dysarthria: affects the mechanics of speech. Amaurosis fugas sudden loss of vision in one or both eyes: gray or black shade coming down over their eye Hemianopsia: loss of half of the visual field. Ataxia: Sudden trouble walking, dizziness, loss of balance or coordination, leading to difficulty in walking normally Vertigo (spinning form of feeling dizzy) Sudden severe headache with no known cause Memory, emotions, orientation, Incontinence 10

Is the person unable to speak or hard to understand? Ask the person to repeat a simple sentence. Is the sentence repeated correctly?

11 Warning Symptoms of Stroke Does one side of the face droop or is it numb? Ask the person to smile. Is the person's smile uneven? Is one arm weak or numb? Ask the person to raise both arms. Does one arm drift downward? Is speech slurred? Is the person unable to speak or hard to understand? Ask the person to repeat a simple sentence. Is the sentence repeated correctly? even if the symptoms go away, call emergency and get the person to the hospital immediately. Check the time so you'll know when the first symptoms appeared 11

12 Ischemic Stroke Definition: Ischemic stroke or cerebral infarct is a focal brain necrosis due to complete and prolonged ischemia that affects all tissue elements, neurons, glia and vessels. Risk factors: Modifiable Hypertension Age >55 Diabetes Atrial fibrillation Smoking Hyperlipidemia Carotid stenosis Male gender Black race Non modifiable Family history of stroke Personal history of stroke Sickle Cell Disease Lack of physical activity Major Causes: 1. Atherosclerosis 2. Embolisms 3. Small vessel disease 4. Vascular spasm (following hemorrhagic stroke) Other: Vasculitis, hypercoagulability, dissection of a vessel wall, sickel cell disease

13 Ischemic Stroke 1. Atherosclerosis (most common cause) Kindly refer to CVS lecture Neuro4Students Cerebrovascular attack 13

14 Left MCA Right ACA Left PCA Neuroradiology Unit, S P Institute of Neurosciences,Solapur,Maharashtra, INDIA Radiology department of the Rijnland Hospital in Leiderdorp, the Netherlands Lacunar infarct 14

15 1. Atherosclerosis Risk factors! Ischemic Stroke Atheromatous plaques can cause narrowing or occlusion of the vascular lumen by themselves or after rupture and thrombosis Bifurcation points of large arteries & major cervical and intracranial arteries (blood flow!) Atherothrombotic infarcts evolve within hours or days The most severe atherosclerotic lesions are typically encountered within large vessels However, Some patients have an asymptomatic occlusion of a cervical internal carotid artery?! Cerebrovascular anatomy and common sites of atherosclerosis 15

2. Embolism Ischemic Stroke Most emboli are fragments of blood clot that originate in the heart or major vessels MI, atrial fibrillation and other arythmias, endocarditis Rarer causes are fat, air

16 2. Embolism Ischemic Stroke Most emboli are fragments of blood clot that originate in the heart or major vessels MI, atrial fibrillation and other arythmias, endocarditis Rarer causes are fat, air and tumor emboli Embolic infarcts have an abrupt onset Assumed if: - source of embolism is present - multiple infarcts in the brain - infarcts in other organs - absence of atherosclerosis - absence of other vascular disease 16 UCSF Department of Surgery, The University of California, San Francisco

3. Lacunar Infarcts Ischemic Stroke Occlusion of deep penetrating branches of major cerebral arteries Deeper parts of the brain (basal ganglia, thalamus, deep white matter) and brain stem.

17 3. Lacunar Infarcts Ischemic Stroke Occlusion of deep penetrating branches of major cerebral arteries Deeper parts of the brain (basal ganglia, thalamus, deep white matter) and brain stem. The infarcts are generally from 2-20 mm in diameter Typically, no impairments in cognition, memory, speech, or level of consciousness (cortex not affected) Atherosclerosis of small arteries Small vessel disease; hyaline arteriosclerosis in hypertension and diabetes, but occurs in old age w/o these predisposing conditions. Lacunar stroke 17

18 Intracranial Hemorrhages Subarachnoid Hemorrhage (Saccular Aneurysms) Non- Traumatic Primary Brain Parenchymal Hemorrhage Epidural Hematoma Subdural Hematoma Traumatic 18

Primary Brain Parenchymal Hemorrhage Spontaneous, nontraumatic intraparenchymal hemorrhages Rupture of small penetrating arteries (basal ganglia & thalamus) Accounts for 15% of deaths among patients

19 Primary Brain Parenchymal Hemorrhage Spontaneous, nontraumatic intraparenchymal hemorrhages Rupture of small penetrating arteries (basal ganglia & thalamus) Accounts for 15% of deaths among patients with chronic hypertension Hypertension is the most underlying cause Small vessel disease: arteriolar walls affected by hyaline change are weaker than normal vessels and are therefore more vulnerable to rupture. Other causes: aging, smoking, oral contraceptives, drug abuse, excessive alcohol intake 19

Primary Brain Parenchymal Hemorrhage Brain is asymmetrically distorted effect + associated edema) (mass Hematoma may dissect into the ventricles Onset is always abrupt with evidence of increased

20 Primary Brain Parenchymal Hemorrhage Brain is asymmetrically distorted effect + associated edema) (mass Hematoma may dissect into the ventricles Onset is always abrupt with evidence of increased intracranial pressure: severe headache, vomiting, seizures, rapid loss of consciousness, papilledema (swelling of optic disc) Risk of herniation of cerebellum and brain stem compression deep coma, irregular respirations, dilated nonresponsive pupils and spasticity Massive hypertensive hemorrhage rupturing into a lateral ventricle 20

21 Normal cerebellar tonsils Cerebellar tonsils are pushed through the foramen magnum into the spinal canal Cerebellar Herniation 21 Mayfield Clinic, University of Cincinnati Department of Neurosurgery

22 Subarachnoid Hemorrhage 22

23 Subarachnoid Hemorrhage Rupture of saccular aneurysms is the most common cause of nontraumatic SAH Saccular (berry) aneurysms are present in 1% of the general population Arise most commonly at arterial bifurcations in the territories of ICA To a less extent in posterior (vertebrobasilar) circulation Enlarge with time and are at greatest risk for rupture once they reach 6-10 mm in diameter Relative frequency of common sites of saccular (berry) aneurysms in the circle of Willis 23

24 Subarachnoid Hemorrhage SAH resulting from rupture of saccular aneurysm is less common than primary cerebral hemorrhage, with women being more affected than males with most cases before age of 50 Abrupt onset with severe headache, often described as the "worst headache of my life, vomiting and loss of consciousness (increased ICP) Meningeal signs are usually present (neck rigidity and pain, back pain, and bilateral leg pain). Seizures during the acute phase of SAH occur in 10-25% of patients. They result from the sudden rise in ICP or direct cortical irritation by blood. Blood in CSF(lumbar punction) 50% dye within several days of onset of symptoms Might be acutely complicated by cerebral infarcts (arterial spasm), acute hydrocephalus (increased accumulation of CSF in ventricles) and herniation. 24

25 Traumatic Vascular Injury 25

26 Traumatic Vascular Injury C. Large organizing subdural hematoma attached to the dura B. Epidural hematoma covering a portion of the dura 26

$Epidural Hematoma Neurosurgical emergency Rupture of a meningeal artery Middle meningeal artery, fracture of temporal bone Compression of subjacent dura Risks: herniation, brain stem compression and$

27 Epidural Hematoma Neurosurgical emergency Rupture of a meningeal artery Middle meningeal artery, fracture of temporal bone Compression of subjacent dura Risks: herniation, brain stem compression and death Lucid interval is typical: time in which the conditions of the patients improve after a head trauma before deteriorating (loss of consciousness) Neurosurgical emergency requiring prompt drainage Rescuers say that he maintained consciousness when they first reached him, but his health quickly deteriorated 27

Subdural Hematoma Tearing of bridging veins that extend from brain surface to dural sinuses Rapid change in head velocity: head blows, violent shaking in infants In elderly, even after minor

28 Subdural Hematoma Tearing of bridging veins that extend from brain surface to dural sinuses Rapid change in head velocity: head blows, violent shaking in infants In elderly, even after minor trauma: brain atrophy, veins are stretched out (more space for movement) Size vary from small to massive hemorrhage with mass effect Sudden and progressive worsening of symptoms No lucid interval!! 28

29 References ROBBINS Basic Pathology 8 th Edition Cerebrovascular diseases, Clinical aspects. Dr. Michael P. Merchut FERNE: Foundation for Education and Research in Neurological Emergencies, Stroke Pathophysiology, Sid Shah, MD 29

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Overview of Stroke: Etiologies, Demographics, Syndromes, and Outcomes. Alex Abou-Chebl, MD, FSVIN Medical Director, Stroke Baptist Health Louisville

Overview of Stroke: Etiologies, Demographics, Syndromes, and Outcomes Alex Abou-Chebl, MD, FSVIN Medical Director, Stroke Baptist Health Louisville Disclosure Statement of Financial Interest Within the