CNS (pathology CVA)

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  1. How much of the CO and O2 goes to brain?
  2. Which is more limiting in brain metabolism? O2 or substrate?
  3. Global cerebral ischemia (ischemic/hypoxic encephalopathy) occurs when ...........................................
    there is a generalized reduction of cerebral perfusion, as in cardiac arrest, shock, and severe hypotension
  4. Large and small vessel obstruction in the brain are the results of...............
    • large-vessel disease (such as embolic or thrombotic arterial occlusion, often in a setting of atherosclerosis)
    • small-vessel disease (such as vasculitis or occlusion secondary to arteriosclerotic lesions seen in hypertension).
  5. What is the pathophysiology of ischemic damage in neurons?
    • 1) The first result of energy depletion is failure of Na+ and K+ pumps, leading to depolarization of the neuronal membrane
    • 2) Synaptic function and conductivity cease at this point. Depolarization causes neurons to release glutamate into the synaptic cleft.
    • 3) Some glutamate receptors are non-selective cation-permeable ion channels. Initially, over-activation of these channels causes a passive influx of  Cl- (and Na+) into cells causing osmotic (cytotoxic) edema and rapid death.
    • 4) Additional structural damage develops hours or days later as a result of Ca++influx into neurons. The NMDA and AMPA receptors of glutamate are channels that are permeable to Ca++. Activation of these receptors by excess glutamate causes massive influx of Ca++ into neurons. 
    • 5) Ca++ activates catabolic enzymes(proteases, phospholipases, endonucleases). Ca++ also activates NO synthase, resulting in formation of the free radical NO. 
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  6. Cell death in area of infarct and penumbra are caused by.............and.............
    Necrosis and apoptosis
  7. What is penumbra?
    • In every infarct, there is a central core of total ischemia and necrosis which is irreversible. This area is surrounded by a zone of borderline ischemic tissue, the ischemic penumbra. Ischemia, in the penumbra, causes dysfunction due to ionic and metabolic dysfunction but is not severe enough to result in structural damage.
    • Critical period for saving penumbra is 3 hours
  8. Which cells are most sensitive to global ischemia?
  9. What is the clinical consequence of severe global ischemia?
    • Brain death due to BS death
    • PVS due to Diffuse cortical, thalamic, or combined neuronal loss (with intact brainstem) 
  10. Mild HIE, such as a brief cardiac arrest, may affect ...................... only
    CA1 pyramidal neurons of the hippocampus
  11. What are the most sensitive neurons to HIE?
    pyramidal cells of CA1 of the hippocampus, layers 3, 5, and 6 of the neocortex, Purkinje cells, and striatal neurons
  12. Bilateral CA1 damage causes...............
    • Korsakoff's amnesia. 
    • This is a memory disorder characterized by inability to retain new information (anterograde amnesia) and a less severe defect of recall of old memories (retrograde amnesia). Hippocampal amnesia (Korsakiff's amnesia) affects more severely episodic memory and less so semantic memory
    • SEMANTIC: Memory for facts (learning that), e.g., Kabul is the capital of Afghanistan. EPISODIC: Memory for personally experienced events, e.g., remembering where you parked your car this morning.
  13. PVS is defined by
    (loss of cognitive functions and emotion with preservation of sleep-wake cycles, autonomic function, and breathing).
  14. What are the characteristics of brain death?
    • Loss of cerebral and brainstem function.
    • The clinical criteria for brain death are complete unresponsiveness, absence of brain stem reflexes, electrical silence (flat EEG), and absence of cerebral perfusion. The latter is probably due to blockage of capillaries from endothelial swelling and cerebral edema.
  15. What is respirator brain?
    • When individuals with this pervasive form of injury are maintained on mechanical ventilation, the brain gradually undergoes an autolytic process—so-called “respirator brain.
    • No reactive gliosis or inflammation is present
  16. What are border zone infarcts?
    • Border zone (“watershed”) infarcts occur in the regions of the brain or spinal cord that lie at the most distal reaches of the arterial blood supply, the border zones between arterial territories.
    • In the cerebral hemispheres, the border zone between the anterior and the middle cerebral artery distributions is at greatest risk.
    • Damage to this region produces a sickle-shaped band of necrosis over the cerebral convexity a few centimeters lateral to the interhemispheric fissure.
  17. Border zone infarcts are usually seen ............................
    after hypotensive episodes.
  18. What is the first change in neurons following HIE ?
  19. What is the gross morphology of brain in HIE?
    • In the setting of global ischemia, the brain is swollen, the gyri are widened, and the sulci are narrowed.
    • The cut surface shows poor demarcation between gray and white matter.
  20. What are the changes encountered in the setting of HIE?
    • Early changes, occurring 12 to 24 hours after the insult, include acute neuronal changes (red neurons) characterized at first by microvacuolization, then eosinophilia of the neuronal cytoplasm, and later nuclear pyknosis and karyorrhexis. Similar acute changes occur somewhat later in astrocytes and oligodendroglia. After the acute injury, the reaction to tissue damage begins with infiltration by neutrophils
    • Subacute changes, occurring at 24 hours to 2 weeks, include necrosis of tissue, influx of macrophages, vascular proliferation, and reactive gliosis 
    • Repair, robust after approximately 2 weeks, is characterized by eventual removal of all necrotic tissue, loss of normally organized CNS structure, and gliosis. 
    • In the cerebral cortex the neuronal loss and gliosis produce an uneven destruction of the neocortex, with preservation of some layers and involvement of others, a pattern termed pseudolaminar necrosis
  21. Anoxic neurons pyknotic nuclei +shrunken eosinophilic cytoplasm
    Image Upload 2
  22. The size, location, and shape of the infarct and the extent of tissue damage that results are determined by modifying factors the most important being ..............................
    the adequacy of collateral flow.
  23. What is the major source of collateral flow in the brain?
    Willis circle
  24. Partial and inconstant reinforcement is available over the surface of the brain for the distal branches of the anterior, middle, and posterior cerebral arteries through ................................
    cortical-leptomeningeal anastomoses
  25. there is little if any collateral flow for the the brain
    deep penetrating vessels supplying structures such as the thalamus, basal ganglia, and deep white matter
  26. What is the clinical difference between ischemic embolic and thrombotic stroke?
    Thrombotic stroke usually evolves over minutes to hours and is often preceded by TIA in the same territory

    Embolic stroke produces symptoms that are maximal at onset, if it is preceded  by TIA, the symptoms vary between attacks
  27. What is the mcc of stroke?
  28. What is the mcc of thrombotic stroke?
  29. The most common sites of primary thrombosis causing cerebral infarction are ........................................................
    the carotid bifurcation, the origin of the middle cerebral artery, and either end of the basilar artery
  30. Occlusive cerebrovascular disease is frequently associated with...................
    DM and HTN
  31. What is the mcc of embolic stroke?
    Cardiac mural thrombi

     myocardial infarct, valvular disease, and atrial fibrillation are important predisposing factors
  32. What is the mc location for thrombombolic arterial stroke?
    atheromatous plaques within the carotid arteries
  33. What is the mc territory for embolic stroke?
  34. What are the symptoms of shower embolization?
    “Shower embolization,” as in fat embolism, may occur after fractures; affected individuals manifest generalized cerebral dysfunction with disturbances of higher cortical function and consciousness, often without localizing signs
  35. Widespread hemorrhagic lesions involving the white matter are characteristic of .........................................................
    • embolization of bone marrow after trauma
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  36. What is the mcc of infectious vasculitis in developed countries?
    immunosuppression and opportunistic infection (such as aspergillosis or CMV encephalitis)
  37. What are the features of primary CNS angiitis?
    • Involves multiple small- to medium-sized parenchymal and subarachnoid vessels and is characterized by chronic inflammation, multinucleated giant cells, Granuloma, and destruction of the vessel wall. 
    • Affected individuals manifest a diffuse encephalopathic or multifocal clinical picture, often with cognitive dysfunction; patients improve with steroid and immunosuppressive treatment.
  38. What are the types of brain infarct?
    • Hemorrhagic (red) infarction, characterized by multiple, sometimes confluent, petechial hemorrhages, is typically associated with embolic events (A ). The hemorrhage is presumed to be secondary to reperfusion of damaged vessels and tissue, either through collaterals or directly after dissolution of intravascular occlusive material.
    • In contrast, nonhemorrhagic (pale, bland, anemic) infarcts are usually associated with thrombosis (B ).
    • Thrombolytic therapy may be used in cases of thrombosis but is contraindicated in hemorrhagic infarcts
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  39. What are the macroscopic changes observed in nonhemorrhagic infarcts of the brain?
    • During the first 6 hours of irreversible injury, little can be observed.
    • By 48 hours the tissue becomes pale, soft, and swollen, and the corticomedullary junction becomes indistinct.
    • From 2 to 10 days, the brain becomes gelatinous and friable, and the previously ill-defined boundary between normal and abnormal tissue becomes more distinct as edema resolves in the adjacent tissue that has survived.
    • From 10 days to 3 weeks, the tissue liquefies, eventually leaving a fluid-filled cavity lined by dark gray tissue, which gradually expands as dead tissue is removed
  40. What are the microscopic appearance of  nonhemorrhagic infarct?
    • After the first 12 hours, ischemic neuronal change (red neurons) and both cytotoxic and vasogenic edema predominate. Endothelial and astrocytes, swell, and myelinated fibers begin to disintegrate. 
    • Up to 48 hours, neutrophilic emigration progressively increases and then falls off.
    • Phagocytic cells, derived from circulating monocytes and activated microglia, are evident at 48 hours and become the predominant celltype in the ensuing 2 to 3 weeks. 
    • The macrophages become stuffed with the products of myelin breakdown or blood and may persist in the lesion for months to years. Astrocytes at the edges of the lesion progressively enlarge, divide, and develop a prominent network of cytoplasmic extensions. Reactive astrocytes can be seen as early as 1 week after the insult.
    • After several months, the astrocytic response recedes, leaving behind a dense meshwork of glial fibers admixed with new capillaries and some perivascular connective tissue.
    • In the cerebral cortex, the cavity is separated from the meninges and subarachnoid space by a gliotic layer of tissue, derived from the molecular layer of the cortex. The pia and arachnoid are not affected and do not contribute to the healing process.
    • Infarcts undergo these reactive and reparative stages from the edges inward; thus, different areas of a lesion may look different, particularly during the early stages, revealing the natural progression of the response.
  41. What are the morphology of hemorrhagic infarcts?
    • The microscopic picture and evolution of hemorrhagic infarction parallel ischemic infarction, with the addition of blood extravasation and resorption.
    • In individuals receiving anticoagulant treatment, hemorrhagic infarcts may be associated with extensive intracerebral hematomas.
    • Venous infarcts are often hemorrhagic and may occur after thrombotic occlusion of the superior sagittal sinus or other sinuses or occlusion of the deep cerebral veins
  42. What are the pathophysiology of medial medullary syndrome?
    • Occlusion of vertebral artery or of branch of vertebral or lower basilar artery
    • On side of lesion: Paralysis with atrophy of one-half half the tongue: Ipsilateral twelfth nerve
    • On side opposite lesion: Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over one-half the body: Contralateral pyramidal tract and medial lemniscus
  43. What are the features of lateral medullary syndrome?
    • Occlusion of any of five vessels may be responsible—vertebral, posterior inferior cerebellar, superior, middle, or inferior lateral medullary arteries
    • On side of lesion: Pain, numbness, impaired sensation over one-half the face: Descending tract and nucleus fifth nerve, Ataxia of limbs, falling to side of lesion: Uncertain, Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting: Vestibular nucleus, Horner's syndrome (miosis, ptosis, decreased sweating): Descending sympathetic tract, Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag reflex: Issuing fibers ninth and tenth nerves, Loss of taste: Nucleus and tractus solitarius, Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei, Weakness of lower face: Genuflected upper motor neuron fibers to ipsilateral facial nucleus
    • On side opposite lesion: Impaired pain and thermal sense over half the body: Spinothalamic tract
  44. Medullary syndromes
    Image Upload 5
  45. What are the major symptoms and causes of Medial pontine syndromes?
    • Occlusion of paramedian branches of basilar artery
    • Diplopia on lateral gaze: Abducens nerve
    • On side opposite lesion: Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower pons, Impaired tactile and proprioceptive sense over one-half of the body: Medial lemniscus
    • Upper pons+MLF
    • Lower pons+ Paralysis of conjugate gaze to side of lesion (preservation of convergence): Center for conjugate lateral gaze
  46. What are the symptoms of lateral pontine syndrome?
    • Occlusion of AICA, SCA, or short circumferential
    • On side of lesion: Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopsia: Vestibular nerve or nucleus, Facial paralysis: Seventh nerve, Paralysis of conjugate gaze to side of lesion: Center for conjugate lateral gaze, Deafness, tinnitus: Auditory nerve or cochlear nucleus,  Ataxia: Middle cerebellar peduncle and cerebellar hemisphere, Impaired sensation over face: Descending tract and nucleus fifth nerve, Horner: descending hypothalamic tract
    • On side opposite lesion: Impaired pain and thermal sense over one-half the body (may include face): Spinothalamic tract
  47. What is the major difference in facial palsy in lateral and medial pontine syndrome?
    • Medial--> contralateral (corticobulbar)
    • Lateral --> ipsilateral (LMN)
  48. Pontine syndrome
    Image Upload 6
  49. What are the symptoms of midbrain stroke?
    • Medial midbrain syndrome: (paramedian branches of upper basilar and proximal posterior cerebral arteries)
    • On side of lesion: Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers
    • On side opposite lesion: Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus cerebri
  50. What are the symptoms of lateral midbrain stroke?
    • Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery)
    • On side of lesion: Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers and/or third nerve nucleus
    • On side opposite lesion: Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway
  51. midbrain
    Image Upload 7
  52. What are the symptoms of midbrain tegmentum involvement?
    • Ipsilateral CNIII
    • Contralateral Dentatothalamic fibersin SCP(contralateral hemiataxia and dysmetria)
  53. What are the causes of improvement in stroke symptoms ?
    reversal of injury in the ischemic penumbra followed by resolution of associated local edema
  54. Stroke in which territory is commonly associated with atherothrombotic rather than embolic disease?
    ICA (others emboli> atherothrombotic)
  55. What are the symptoms of ACA stroke?
    • Motor and/or sensory deficit (leg >> face, arm)
    • Grasp, sucking reflexes
    • Abulia, paratonic rigidity, gait apraxia
  56. What are the symptoms of MCA strokes?
    • Dominant hemisphere: aphasia, motor and sensory deficit (face, arm > leg > foot), may be complete hemiplegia if internal capsule involved, homonymous hemianopia
    • Non-dominant hemisphere: neglect, anosognosia, motor and sensory deficit (face, arm > leg > foot), homonymous hemianopia
  57. What are the symptoms of PCA stroke?
    • Homonymous hemianopia
    • alexia without agraphia (dominant hemisphere+ splenium of CC)
    • visual hallucinations, visual perseverations (calcarine cortex)
    • sensory loss, choreoathetosis, spontaneous pain (thalamus)
    • III nerve palsy, paresis of vertical eye movement, motor deficit (cerebral peduncle, midbrain)
  58. What are the symptoms of ICA stroke?
  59. What are the symptoms of lacunar stroke?
    • Pure motor hemiparesis (classic lacunar syndromes)
    • Pure sensory deficit
    • Pure sensory-motor deficit
    • Hemiparesis, homolateral ataxia
    • Dysarthria/clumsy hand
  60. What are the most important effects of HTN on the brain?
    • lacunar infarcts
    • slit hemorrhages
    • hypertensive encephalopathy
    • ICH
  61. What are the most common locations for lacunar infarcts?
    • lenticular nucleus> thalamus> internal capsule,
    • deep white matter, caudate nucleus, and pons,
  62. What is the pathophysiology of lacunar infarct?
    Hypertension affects the deep penetrating arteries and arterioles that supply the basal ganglia and hemispheric white matter as well as the brainstem. These cerebral vessels develop arteriolar sclerosis and may become occluded;
  63. What are the features of lacunar infarct?
    • Multiple, small, cavitary infarcts known as lacunae.
    • These are lake-like spaces, less than 15 mm wide, which occur in the lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons, in descending order of frequency.
    • On microscopic examination they consist of areas of tissue loss with scattered lipid-laden macrophages and surrounding gliosis.
    • Affected vessels may also be associated with widening of the perivascular spaces but without tissue infarction (état criblé).
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  64. What is the mc location for lacunar infarcts?
    Lenticular nucleus
  65. What are slit hemorrhages?
    • Hypertension also gives rise to rupture of the small-caliber penetrating vessels and the development of small hemorrhages.
    • In time these hemorrhages resorb, leaving behind a slitlike cavity (slit hemorrhage) surrounded by brownish discoloration
    • Focal tissue destruction, pigment-laden macrophages, and gliosis.
  66. What are the most dangerous time point for large infarcts?
    • day 3-4
    • Edema and high risk of herniation
  67. What are the clinical features of hypertensive encephalopathy?
    • individual with malignant hypertension
    • diffuse cerebral dysfunction, including headaches, confusion, vomiting, and convulsions, sometimes leading to coma
  68. What are the morphological features of brain in hypertensive encephalopathy?
    • edematous brain with or without transtentorial or tonsillar herniation.
    • Petechiae and fibrinoid necrosis of arterioles in the gray and white matter
  69. What are the features of multi-infarct dementia?
    • Individuals who, over the course of many months and years, suffer multiple, bilateral, gray matter (cortex, thalamus, basal ganglia) and white matter (centrum semiovale) infarcts may develop a distinctive clinical syndrome characterized by dementia, gait abnormalities, and pseudobulbar signs, often with superimposed focal neurologic deficits.
    • The syndrome, generally referred to as vascular (multi-infarct) dementia, is caused by multifocal vascular disease of several types, including (1) cerebral atherosclerosis, (2) vessel thrombosis or embolization from carotid vessels or from the heart, and (3) cerebral arteriolar sclerosis from chronic hypertension
  70. What are the features of Binswanger disease?
    When the pattern of injury in multiinfarct dementia preferentially involves large areas of the subcortical white matter with myelin and axon loss, the disorder is referred to as Binswanger disease
  71. What are the causes of secondary ICH?
    • Hemorrhage within infarcts in arterial border zones
    • in infarcts caused by only partial or transient vascular obstruction
  72. Most ICH are caused by rupture of .....................................
    a small intraparenchymal vessel.
  73. What are the two major etiologies of ICH?
    hypertension and cerebral amyloid angiopathy (CAA)
  74. What is the mcc of ICH?
  75. What vascular abnormality caused by HTN predispose to ICH?
    • 1) Accelerated atherosclerosis in larger arteries
    • 2) Hyaline arteriolosclerosis in smaller vessels
    • 3) In severe cases, proliferative changes and frank necrosis of arterioles.
    • 4) Arteriolar walls affected by hyaline change are presumably weaker than are normal vessels and are therefore more vulnerable to rupture.
    • 5) Chronic hypertension is associated with the development of minute aneurysms, termed Charcot-Bouchard microaneurysms, which may be the site of rupture. Charcot-Bouchard aneurysms, not to be confused with saccular aneurysms of larger intracranial vessels, occur in vessels that are less than 300 μm in diameter, most commonly within the basal ganglia.
  76. What are the mc site for charcot boucard aneurysm?
    Small vessels within BG
  77. Charcot-Bouchard microaneurysms is a result of.................
    chronic HTN
  78. The most common place for ICH is.............
  79. What are the common locations for ICH?
    putamen (50% to 60% of cases), thalamus, pons, cerebellar
  80. What are the morphological features of ICH?
    • Acute hemorrhages--> extravasation of blood with compression of the adjacent parenchyma.
    • Old hemorrhages --> cavitary destruction of brain with a rim of brownish discoloration.
    • On microscopic examination the early lesion consists of a central core of clotted blood surrounded by a rim of brain tissue showing anoxic neuronal and glial changes as well as edema.
    • Eventually the edema resolves, pigment- and lipid-laden macrophages appear, and proliferation of reactive astrocytes is seen at the periphery of the lesion.
  81. What are the features of CAA?
    • Amyloidogenic peptides, nearly always the same one found in Alzheimer disease (Aβ40), deposit in the walls of medium- and small-caliber meningeal and cortical vessels.
    • This deposition can result in weakening of the vessel wall and risk of hemorrhage.
    • There is an effect of the ApoE genotype (ε2 or ε4 allele-->higher risk of hemorrhage)
    • While some mutations in the precursor protein for the Aβ peptide (amyloid precursor protein, APP) cause familial Alzheimer disease, others result in autosomal dominant forms of CAA.
  82. What is the morphology of CAA?
    • 1)Restricted to the leptomeningeal and cerebral cortical arterioles and capillaries, although involvement of the molecular layer of the cerebellum can be observed as well.
    • 2) Involved vessels appear “stiff” on microscopic sections, remaining open with round lumens through tissue processing.
    • 3) Unlike with arteriolar sclerosis, there is no fibrosis; rather, dense and uniform deposits of amyloid are present
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  83. What are the features of Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)?
    • Mutations in the gene encoding the Notch3 receptor
    • Recurrent strokes (usually infarcts, less often hemorrhages) and dementia. Histopathologic study has shown abnormalities of white matter and leptomeningeal arteries (also involving non-CNS vessels) consisting of concentric thickening of the media and adventitia.
    • Basophilic, PAS-positive deposits, which appear as osmiophilic compact granular material by electron microscopy, have been consistently detected in the walls of affected vessels, as has loss of smooth muscle cells
  84. What is the mc location for berry aneurysms?
    • Junction of ACA and ACoA
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  85. What is the mcc of SAH?
    Rupture of berry aneurysm
  86. What are other causes of SAH?
    Subarachnoid hemorrhage may also result from extension of a traumatic hematoma, rupture of a hypertensive intracerebral hemorrhage into the ventricular system, vascular malformation, hematologic disturbances, and tumors.
  87. ................ is the most common type of intracranial aneurysm
    Saccular (Berry) aneurysm
  88. What are other types of cerebral arterial aneurysm besided berry aneurysm?
    • atherosclerotic (fusiform; mostly of the basilar artery), mycotic, traumatic, and dissecting.
    • These latter three, like saccular aneurysms, are most often found in the anterior circulation, but differ in that they more often cause cerebral infarction rather than subarachnoid hemorrhage
  89. What are the hereditary syndromes or conditions associated with berry aneurysm?
    AD polycystic kidney disease, Ehlers-Danlos syndrome type IV, NF1,  Marfan syndrome, FMD of extracranial arteries, and coarctation of the aorta
  90. True or false: berry aneurysm is present at birth
  91. Berry aneurysm develop in time due to underlying defect in ..............
  92. What are the most important predisposing factors for berry aneurysm?
    cigarette smoking and hypertension
  93. What are the morphological features of berry aneurysms?
    • bright red, shiny surface and a thin, translucent wall 
    • Atheromatous plaques, calcification, or thrombotic occlusion of the sac may be found in the wall or lumen of the aneurysm.
    • Brownish discoloration of the adjacent brain and meninges is evidence of prior hemorrhage.
    • Rupture usually occurs at the apex of the sac with extravasation of blood into the subarachnoid space, the substance of the brain, or both. 
    • The arterial wall adjacent to the neck of the aneurysm often shows some intimal thickening and gradual attenuation of the media as it approaches the neck.
    • At the neck of the aneurysm, the muscular wall and intimal elastic lamina stop short and are absent from the aneurysm sac itself.
    • The sac is made up of thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery.
  94. What layers are absent from aneurysmal sac?
    Internal elastic lamina and muscular wall
  95. Aneurysms greater than in diameter have a roughly 50% risk of bleeding per year
  96. What are the complications of SAH?
    • Rebleeding
    • Vasospasm (basal subarachnoid hemorrhage, in which vasospasm can involve major vessels of the circle of Willis)
    • Hydrocephalus
  97. What are the types of vascular malformations?
    arteriovenous malformations, cavernous malformations, capillary telangiectasias, and venous angiomas
  98. What are the mc vascular malformations of the brain?
  99. Which of the brain vascular malformations are associated with risk of hemorrhage and development of neurologic symptoms?
    AVM, cavernous malformations
  100. What are the mc locations for vascular malformations in the brain?
    • AVM-->MCA territory
    • Cavernous--> cerebellum
    • Capillary telangiectasias--> pons
  101. What are the morphological features of AVM?
    • Arteriovenous malformations (AVM) involve vessels in the subarachnoid space extending into brain parenchyma or may occur exclusively within the brain.
    • This tangled network of wormlike vascular channels has prominent, pulsatile arteriovenous shunting with high blood flow.
    • They are composed of greatly enlarged blood vessels separated by gliotic tissue, often with evidence of prior hemorrhage.
    • Some vessels can be recognized as arteries with duplication and fragmentation of the internal elastic lamina, while others show marked thickening or partial replacement of the media by hyalinized connective tissue.
  102. What are the histological features of Cavernous malformations?
    • Cavernous malformations consist of greatly distended, loosely organized vascular channels with thin, collagenized walls and are devoid of intervening nervous tissue (thus distinguishing them from capillary telangiectasias).
    • They occur most often in the cerebellum, pons, and subcortical regions, in decreasing order of frequency, and have a low flow without arteriovenous shunting.
  103. What are the features of Capillary telangiectasias?
    microscopic foci of dilated, thin-walled vascular channels separated by relatively normal brain parenchyma and occurring most frequently in the pons
  104. Venous angiomas (varices) consist of ..................................
    aggregates of ectatic venous channels
  105. Large arteriovenous malformations occurring in the newborn period can lead to ................
    CHF especially if involve vein of Galen
  106. What is unique in Cavernous malformations?
    • AD
    • Multiple
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CNS (pathology CVA)
CNS (pathology CVA)
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