CEREBROVASCULAR DISEASES By: Shifaa AlQa qa
Cerebrovascular diseases Brain disorders caused by pathologic processes involving blood vessels 3 pathogenic mechanisms (1) thrombotic occlusion, (2) embolic occlusion, (3) vascular rupture/hemorrhage First two result in blocking the BV while last one result with rupture and bleeding
Stroke: it is a medical condition in which poor blood flow to the brain results in brain death. Hemorrhage, ischemia, infarction all these leads to stroke. is the clinical term for acute-onset neurologic deficits resulting from hemorrhagic or obstructive vascular lesions. Symptoms Symptoms depend on which part has been occluded, but mainly: Paralysis on one part (hemiparalysis) Difficulty in speak and swallowing Decrease level of consciousness Loss of vision on one side (hemilateral) transient ischemic attack (TIA)????
Good perfusion with low oxygen concentration Decrease blood supply End result of sustained ischemia. (Necrosis) Hypoxia, Ischemia, and Infarction The brain may be deprived of oxygen by two general mechanisms: Functional hypoxia: - low partial pressure of oxygen (e.g., high altitude), - impaired oxygen-carrying capacity (e.g., severe anemia, carbon monoxide poisoning), - inhibition of oxygen use by tissue (e.g., cyanide poisoning) Ischemia is divided according the cause into: Global ischemia ( due to systemic hypertension) Focal ischemia ( due to vascular obstruction) It can be transient like in TIA or permanent and leads to stroke Ischemia: - Hypoperfusion ----- hypotension, vascular obstruction - transient or permanent
Global Cerebral Ischemia occur in the setting of severe systemic hypotension, usually when systolic pressures fall below 50 mm Hg, as in cardiac arrest, shock, and severe hypotension. Neurons are more susceptible to hypoxic injury than are glial cells The most susceptible neurons (vulnerable areas) are: - The pyramidal cells of the hippocampus and neocortex - Purkinje cells of the cerebellum Areas that are affected even with mild ischemia: - In severe global cerebral ischemia, widespread neuronal death occurs irrespective of regional vulnerability
MORPHOLOGY: the brain is swollen, wide gyri, narrowed sulci. The cut surface shows poor demarcation between gray and white matter
Irreversible ischemic injury---- infarction Early changes (12 to 24 hours): - acute neuronal cell change - the reaction to tissue damage begins with infiltration by neutrophils Subacute changes (24 hours to 2 weeks) - necrosis of tissue - influx of macrophages - vascular proliferation, - reactive gliosis Repair (after 2 weeks) - removal of all necrotic tissue - Loss of organized CNS structure - gliosis Normally there is no neutrophils in the brain but in case of infarction they re seen And the give a clue that there s infarction and it is has been since 12-24h This is seen in global ischemia due to pseudolaminar necrosis, which means that the areas that is necrotic is uneven with the gliaiotic areas resulting in layering of gliaosis and necrosis
The distribution of neuronal loss and gliosis in the neocortex typically is uneven with preservation of some layers and devastation of others a pattern termed pseudolaminar necrosis.
This is an infarction at the end of arterial supply btw the ant. And middle cerebral artery and they are also vulnerable for infarction and they become with wedge-shaped Border zone ( watershed ) infarcts: - wedge shaped - regions of the brain and spinal cord that lie at the most distal portions of arterial territories. - In the cerebral hemispheres, the border zone between the anterior and the middle cerebral artery distributions is at greatest risk.
Veget ativ e s t at e المريض بكون زي النبات فقط بصحى و بنام و يأكل و يتنفس But he is unaware and bedridden Here the main injury is in the cerebrum while the cerebellum and brain stem are normal thus the respiratory and cvs functions are tho. -No need for mechanical ventilation The clinical outcome varies with the severity and duration of the insult: Mild insult---- only a transient postischemic confusional state, with eventual complete recovery If the ischemia was sever - - - leads to brain damage in the form of vegetative state or brain death Severe insult ---- vegetative state, brain death--- mechanical ventilation---- brain autolysis brain death Here the patient will lose motor reflexes and respiratory functions and the EEG of brain is flat showing no activity of the brain -Needs mechanical ventilation which lead to brain autolysis
Focal Cerebral Ischemia Cerebral arterial occlusion ----- focal ischemia ------ infarction in the distribution of the compromised vessel. Accessory blood vessel between two arteries, once the artery is occluded it opens to compensate and they re more effective with age thus old patient with MI is less severe than young one. modified by collateral blood flow -------- the circle of Willis or cortical-leptomeningeal anastomoses These are the most common places for collateral BVs in the brain And collaterals are not found in deep parts of the brain thus the deep part are more susceptible for ischemia
By contrast, there is little if any collateral flow to structures such as the thalamus, basal ganglia, and deep white matter, which are supplied by deep penetrating vessels.
Causes: - Emboli ---------- more common - Thrombosis Occurs with atherosclerosis patient when a plaque starts to form and develops into clot It is dislodge of an embolus or clot that moves toward different parts of the body -Origin of it outside the brain
Emboli: - Cardiac mural thrombi (myocardial dysfunction, valvular disease, and atrial fibrillation) It is a thrombosis in the heart dislodges and goes to the brain via the arterial blood supply - Arterial thromboemboli (atheromatous plaques within the carotid arteries or aortic arch) A thrombi that has been lodged and caused thromboemboli - Venous emboli/paradoxical embolism (thromboemboli from deep leg veins and fat emboli) In normal people venous thrombi goes to the lungs but we can have a venous thrombi going to the brain if a person has a shunt btween the Rt. and Lt. sides of the heart which is abnormal The name of this emboli is : parodoxial embolism
The territory of the middle cerebral artery, a direct extension of the internal carotid artery, is most frequently affected by embolic infarction. Emboli tend to lodge where vessels branch or in areas of stenosis, usually caused by atherosclerosis.
Thrombosis: - Thrombotic occlusions usually are superimposed on atherosclerotic plaques - common sites are: The carotid bifurcation, The origin of the middle cerebral artery, At either end of the basilar artery.
Infarcts can be divided into two broad groups: Nonhemorrhagic infarcts--- Occurs due to reperfusion injury either due to the patient has been given a treatment or the emboli has been automatically dislodged Hemorrhagic infarcts--- result from reperfusion of ischemic tissue, either through collaterals or after dissolution of emboli ----- multiple, petechial hemorrhages In the hemorrhage infarction the brain comes in the form of : petechial hemorrhage ( very small in size 1mm and multiple ) Thrombolytic therapies????
MORPHOLOGY: Macroscopic appearance of a nonhemorrhagic infarct: first 6 hours---no change 48 hours--- tissue is pale, soft, and swollen days 2 to 10--- the brain turns gelatinous and friable, and the boundary between normal and abnormal tissue becomes more distinct as edema resolves in the adjacent viable tissue. day 10 to week 3--- the tissue liquefies, eventually leaving a fluid-filled cavity lined by dark gray tissue, which gradually expands as dead tissue is resorbed The boundaries of necrosis is unclear unless the edema resolves The tissue of the brain become liquid and from here we came up with liquefactive necrosis The liquid will make a cavity filled with a fluid ( cyst ) with a dark gray color
Microscopically: After the first 12 hours: - ischemic neuronal change (red neurons) - cytotoxic and vasogenic edema. Endothelial and glial cells, mainly astrocytes, swell - myelinated fibers begin to disintegrate. Up to 48 hours: neutrophilic emigration 2 to 3 weeks: - Macrophages - astrocytes at the edges of the lesion progressively enlarge, divide, and develop a prominent network of cytoplasmic extensions After several months: - the striking astrocytic nuclear and cytoplasmic enlargement regresses - dense feltwork of glial fibers admixed with new capillaries lining the cavity wall
Hemorrhagic infarction: + blood extravasation
Intracranial Hemorrhage intracerebral hemorrhage (intraventricular, intraparenchymal) subarachnoid hemorrhage epidural hemorrhage subdural hemorrhage
Primary Brain Parenchymal Hemorrhage Spontaneous ----- nontraumatic peak incidence at about 60 years of age rupture of a small intraparenchymal vessels
Hypertension is the leading underlying cause Hypertensive intraparenchymal hemorrhages typically occur in the basal ganglia, thalamus, pons, cerebellum
it can affect small regions and be clinically silent can be clinically devastating when it affects large portions of the brain or extends into the ventricular system
MORPHOLOGY: extravasated blood cavity with a brown, discolored rim Anoxic neuronal and glial changes Edema pigment- and lipid-laden macrophages reactive astrocytes
Cerebral Amyloid Angiopathy It is one of the causes that leads to primary intraparynchemal hemorrhage Bet Amyloid will deposit on the BVs walls in the brain making the walls thin and weakens results in ruptured and hemorrhage is a disease in which amyloidogenic peptides (beta amyloid), typically the same ones found in Alzheimer disease, deposit in the walls of medium- and small-caliber meningeal and cortical vessels. Amyloid deposition weakens vessel walls and increases the risk of hemorrhages
CAA-associated hemorrhages often occur in the lobes of the cerebral cortex (lobar hemorrhages) ----- Primary intraparenchymal hemorrhages
Hypertensive Cerebrovascular Disease Features or changes of the arteries when there s hypertension: hyaline arteriole sclerosis which makes the artery weak and susceptible to be ruptured Hypertension --- hyaline arteriolar sclerosis --- -weakened wall---- vulnerable to rupture arteries and arterioles that supply: the basal ganglia, the hemispheric white matter, and the brain stem
In some instances, minute aneurysms (Charcot-Bouchard microaneurysms) form in vessels less than 300 μm in diameter. This is an important lesion Now aneurysm is a dilation in the BV making the wall thin and weakens -in hypertensive this aneurysm is micro less than 300 micrometer -it gives an indication that the patient has had hypertension
Pathologic brain processes are related to hypertension: - Intracerebral hemorrhage - Lacunar infarcts - slit hemorrhage - Acute hypertensive encephalopathy
Lacunar infarcts: - are small cavitary infarcts - found most commonly in: deep gray matter (basal ganglia and thalamus), the deep white matter, the pons - caused by occlusion of a single penetrating branch of a large cerebral artery
Slit hemorrhage: - Rupture of the small-caliber penetrating vessels - hemorrhages resorb, leaving behind a slitlike cavity
Acute hypertensive encephalopathy: - sudden sustained rises in diastolic blood pressure to greater than 130 mm Hg - increased intracranial pressure - global cerebral dysfunction headaches, confusion, vomiting, convulsions, coma - brain edema, - transtentorial or tonsillar herniation - Petechiae and fibrinoid necrosis of arterioles in the gray and white matter may be seen microscopically
Vasculitis cause cerebral infarction Infectious Can be primary - - - vasculitis that mainly affecting brain BVs like in autoimmune Secondary - - - associated with systemic diseases like SLE or polyarteritis nodosa OR secondary to infection like in TB, fungi or opportunistic infection. systemic forms of vasculitis Primary angiitis of the CNS