Pathology of Stroke (Cerebrovascular Disease)
Cerebral Infarction
focal brain necrosis due to complete and prolonged ischemia
Arteriovenous Malformation: Most Common Location
- most common location is MCA - involved blood vessels are located in the subarachnoid space and brain parenchyma or can be located in the brain only
Describe collateral blood flow in the brain and vulnerable areas.
- Circle of Willis is a significant source of collateral flow - thalamus, basal ganglia, deep white matter have no significant collateral supply (suffer severe ischemic damage in arterial occlusion)
Subdural Hematoma: Radiology
- L picture: large L subdural hematoma with L-to-R shift and ventricular narrowing which interdigitates with adjacent gyri and sulci but compresses the brain - R picture: bilateral subdural hematomas (R>L) with irregular bright areas within the subdurals (indicating hemorrhage is recent) and non-bright areas (indicating organization of the hematoma) - crescent shaped
Subdural Hematoma: Autopsy Findings
- Left picture: large subdural hematoma overlying L frontoparietal region - blood collects underneath the dura and can cross the region of the sutures
Cerebrovascular Disease: Diagnostic Testing
- Brain Imaging - Cardiovascular testing - Cerebral Angiography - Ultrasound
What parts of the brain are susceptible to global ischemia?
- CA1/Sommer sector (pyramidal layer of hippocampus) - Cerebellar Purkinje cells - Cortical pyramidal neurons in cerebral cortex
Epidural Hematoma: Clinical Presentation
- 10 to 15 minute LOC - 3 to 4 hours where patient is awake and reports no ill effects (LUCID interval) - a decline in mental status to unconsciousness - if not emergently evacuated, the expanding mass of blood leads to herniation and death
Saccular Aneurysms: Locations
- 90% are found near the major branch points of the arterial circulation
Most common sites of atherosclerosis leading to infarction?
- Carotid bifurcation - Origin of the MCA - Basilar artery
Cardiac mural thrombi: Etiology
- MI - valvular disease - atrial fibrillation
Cerebrovascular Disease: Cardiovascular testing
- MI or arrhythmia can result in embolic stroke - EKG to analyze rhythm - Echocardiography to look for lesions that may result in embolic stroke
Cerebrovascular Disease: Diagnostic Imaging
- Non-contrast CT in suggested stroke pt to determine etiology such as ischemic, intracerebral hemorrhage, SAH, tumor - CT important to differentiate hemorrhagic from ischemic - MRI for finding early ischemic infarcts
Histology of cerebellum
- Purkinje cells are particu ML=molecular layer GL=granular layer PL=layer of purkinje cells A=axons P=purkinje cells
Metastatic Tumors of the Brain
- account for 25 to 50% of intracranial tumors in hospitalized pts - may be the first sign of cancer
Saccular Aneurysms: Gross Morphology
- an unruptured saccular aneurysm is usually a thin-walled outpouching found at an arterial branch point in the circle of Willis - they are usually 2 to 3 mm in size - bright red shiny surface and thin translucent wall - neck may be wide or narrow; arterial wall adjacent to neck shows intimal thickening and attenuation of media - SM and intimal elastic lamina do not extend into neck, are absent from aneurysm sac itself which is made of thickened hyalinized intima and covering or adventitia - rupture occurs at the apex - rupture of an aneurysm leads to extravasation of blood Into the subarachnoid space ----------- A. view of base of brain showing circle of Willis with aneurysm of ACA B. Dissected circle of willis showing larg aneurysm C. section through saccular anerysm showing hyalinized fibrous vessel wall (H&E)
How can an embolus of the R side of circulation gain access to systemic circulation?
- anatomic defects that create openings between the left and right side of the heart, e.g. ASD or PFO - C shows blood clot lodged in PFO ---------------- ASD= Atrial Septal Defect LV=left ventricle RV = right ventricle RA = right atrium LA = left atrium PA = pulmonary artery PV= pulmonary vein PAVF = pulmonary arteriovenous vein fistula PFO= patent foramen ovale
Vascular Malformations: Types
- arteriovenous malformation - cavernous malformation - capillary telangiectasias - venous angioms
Focal Cerebral Ischemia: causes of thrombosis
- atherosclerosis - hypercoagulable states - dissecting aneurysms of extracranial arteries in the neck supplying the brain - drug abuse (cocaine, amphetamines, heroin)
(Multi-infarct) Vascular Dementia: Etiology
- atherosclerosis - thrombosis - embolization - arteriolar sclerosis secondary to chronic HTN
Forms of Thrombosis
- atherosclerosis - dissection, dysplasia - vasculitis - prothrombotic states
Subdural Hematoma: Pathogenesis
- bleeding usually occurs from bridging veins - bridging veins are particularly prone to tearing along their course through the dural layers and are the source of bleeding in most cases of subdural hematoma - can cross the suture line - brain is suspended in the CSF, but the venous sinuses are fixed relative to the dura, so the displacement of the brain that occurs in trauma can tear the veins at the point where they penetrate the dura
Global cerebral ischemia: border zone/watershed infarcts
- brain/SC regions with overlapping arterial zones (border zones) = areas that are at the most distal reaches of the arterial blood supply - anterior and middle cerebral artery border zone is particularly vulnerable - small border zones
Origins of Brain Embolus
- cardiac mural thrombi - arterial thromboemboli - paradoxical emboli - emboli associated with cardiac surgery - other emboli
Arterial thromboemboli: Etiology
- carotid artery: atheromatous plaques
Focal Cerebral Ischemia: Pathogenesis
- cerebral arterial occlusion → ischemia → infarction in the territory of the compromised vessel - size, shape, and location of lesion depends on the blood vessel involved and collateral circulation
Factors that affect probability of tissue survival
- collateral circulation - duration of ischemia - magnitude and rate of reduction in blood flow
Hypertensive Intracerebral Hemorrhage: Locations
- deep white matter - thalamus - brain stem - can extend into ventricular system
What does the degree of damage depend on in thrombosis or embolism?
- degree of damage is inversely proportional to collateral blood flow
(Multi-infarct) Vascular Dementia: symptoms
- dementia - gait abnormalities - pseudobulbar signs - focal neurologic deficits
Ischemia
- disruption of normal circulatory flow - obstruction and/or decreased perfusion pressure
Focal Cerebral Ischemia: atherosclerosis
- most common etiology - occlusion results from progressive narrowing of the lumen and thrombosis - fragmentation and embolization - associated with HTN and DM - sustained thrombosis or occlusion leads to infarction
(Multi-infarct) Vascular Dementia: Binswanger disease symptoms
- disruption of subcortical neural circuits that control executive cognitive functioning (short term memory, organization, mood, regulation of attention, ability to act or make decisions, and appropriate behavior) - psychomotor slowness (increase in length of time it takes for the fingers to turn the thought of a letter into the shape of a letter on a piece of paper)
Hypertensive Intracerebral Hemorrhage
- due to rupture of small intraparenchymal vessel - mid-adult life
What are paradoxical emboli?
- emboli that form in the venous system and cross over into the arterial system by way of anatomic defect of the heart
Subarachnoid Hemorrhage: Symptoms
- excruciating pain - thunderclap headache
Epidural Hematoma: Clinical Considerations
- expanding hematoma formation compressing brain (within suture lines) - dramatic elevation in intracranial pressure (requires prompt drainage) - progressive neuro deterioration - herniation - death
Focal cerebral ischemia: Clinical Features
- focal neurologic deficits (dependent on location) - neuro symptoms generally develop rapidly and continue to evolve in the following hours of the event - symptoms may improve with resolution of edema and salvage of the penumbra (at risk of progression but still reversible) - slow improvement may occur over period of months - TIA
Infarction: Clinical Presentation
- focal neurological deficit - abrupt onset in embolic infarcts - preceded by TIA, evolve over hours in arterothrombotic infarct
Brain Contusion: Clinical Signs
- frequently associated with edema, likely to cause increases in ICP - swelling is worst 4 to 6 days following the injury -
Subdural Hematoma: Clinical Presentation
- gradually increasing headache and confusion or focal signs (rare) - onset can be immediate, take minutes, or take days (venous blood)
Saccular Aneurysms: Risk Factors
- higher incidence in first degree relatives - more common in AD PKD, EDS, NF1, and Marfan - smoking - HTN
Mechanisms by which the brain can be deprived of oxygen?
- hypoxia - ischemia - infarction
Cerebral Venous Thrombosis: Diagnosis
- imaging studies - searching for thrombophilic state
Mechanisms of arterial occlusion
- in situ thrombosis - embolization - vasculitis
Who is more susceptible to subdural hematoma?
- increased rate of bleeding in elderly due to brain atrophy (veins are stretched) and more space for the brain to move - infants are also susceptible due to thin-walled bridging veins
Types of Hemorrhagic Stroke
- intracerebral - intraventricular - subarachnoid
Embolism
- intravascular solid, liquid, or gaseous mass that breaks free from its site of origin and migrates in the vasculature to a more distant site where it may occlude blood flow
Watershed infarct: Gross morphology
- involving watershed region between anterior and middle cerebral artery
Transient Ischemic Attack
- ischemia lasting less that 24 hours then resolves - caused by critical reduction of perfusion that impairs neuro function but is not severe enough to cause permanent tissue damage, or by emboli that break up soon after they occlude vessels
What are the 2 major categories of stroke/cerebrovascular disease?
- ischemic - hemorrhagic
Nonhemorrhagic infarct: Microscopic Morphology, 12 to 24 hours
- ischemic neuronal injury (red neurons) - eosinophils
Hypertensive Cerebrovascular Disease: 4 Types
- lacunar infarcts - slit hemorrhages - hypertensive encephalopathy - hypertensive intracerebral hemorrhage
Epidural Hematoma: Radiology
- lens shaped outline forms as the smooth dura becomes indented against the underlying cortex on the lateral aspect of the cerebrum - epidural hematoma is confined within an area bounded by the cranial sutures where the dura is firmly adherent to the skull - acute blood collection appears bright with CT scanning - mass effect with effacement of lateral ventricles and shift of midline to the left - biconvex lens
Hypoxia
- low partial pressure of O2 - impaired oxygen carrying capacity of the blood - impaired utilization of oxygen within the tissue
Metastatic Tumors of the Brain: Common Primary Sites
- lung - breast - skin (melanoma) - kidney - GI tract
Medullablastoma: Complications
- may grow to occlude the flow of CSF, leading to hydrocephalus - dissemination through CSF which can present as nodular masses along the SC called drop metastases
Subfalcine herniation: Structures at Risk
- may lead to compression of the anterior cerebral artery
Intracranial Hemorrhage: Etiology
- may occur as a secondary process within an infarction - epidural and subdural hemorrhages are usually due to trauma - intraparenchymal and SAH are usually due to underlying cerebrovascular disease but also seen with trauma
Infectious Vasculitis: Causes
- more common with immunosuppression and opportunistic infection - CMV, aspergillus - TB, syphilis
Arteriovenous Malformation
- most common type of clinically significant vascular malformation - mass of enlarged blood vessels and intervening gliotic tissue - arteriovenous shunting blood occurs with a high flow rate
Ruptured Saccular Aneurysms: Clinical Features
- most frequent in 5th decade - probability of rupture increases with size (10 mm aneurysm has 50% of bleeding per year)
Focal cerebral ischemia: Physical Examination
- neuro exam to localize the lesion - CV exam: preexisting HTN (greatest risk factor for stroke), cardiac arrhythmia, murmurs suggesting valvular lesions → emboli, carotid artery bruits (atherosclerosis→ emboli and thrombosis) - retina: signs of chronic HTN
Transient ischemic attack (TIA): Two Types
- nonhemorrhagic - hemorrhagic ---------- Based on macroscopic morphology and radiology
Shower embolization: Gross Morphology
- numerous hemorrhages in the white matter - above is shown a bone marrow embolization
Hypertensive Encephalopathy
- occurs in pts with malignant hypertension - sudden sustained rise in BP diastolic >130 mmHg
Cerebral Venous Thrombosis: Major Risk Factors
- prothrombotic conditions - oral contraceptives - pregnancy and puerperium - malignancy - infection - others
(Multi-infarct) Vascular Dementia: Progression
- pts generally report discrete episodes of sudden neuro deterioration - stepwise progression of disease is seen due to recurrent strokes
Lacunar Infarcts: Four syndromes
- pure motor hemiparesis (face and arm) - pure sensor stroke - ataxic hemiparesis - dysarthria and clumsy hand (dysarthria, facial weakness, dysphagia, and mild weakness and clumsiness of ipsilateral hand)
Epidural Hematoma
- rupture of a dural artery (most commonly middle meningeal artery) caused by a skull fracture (trauma) - arterial blood collects between the skull and the dura mater
Intracranial aneurysms: Types
- saccular (most common) - atherosclerotic (fusiform) - mostly basilar artery - mycotic - traumatic - dissection
Paradoxical emboli: Etiology
- secondary to cardiac anomalies
Hemorrhagic Infarct
- secondary to reperfusion of damaged vessels and tissue either by way of collaterals or after dissolution of intravascular occlusive material - usually associated with embolism - hemorrhage is thought to be related to reperfusion of damaged tissue - thrombolytic therapy contraindicated
Lacunar Infarcts: Gross Morphology
- single or multiple cavitary infarcts < 15 mm wide
Medullablastoma: Microscopic Morphology
- small tightly packed cells with hyperchromatic nuclei and scant cytoplasm
Why do lesions increase ICP?
- the brain and SC are protected by the skull and vertebral bodies - no room for generalized brain edema, increased CSF volume (hydrocephalus), expanding mass lesions
(Multi-infarct) Vascular Dementia
- the development of multiple, bilateral gray matter and white matter infarcts - long standing hypertension can produce multiple, small infarcts involving different parts of brain leading to dementia
Focal Cerebral Ischemia: Causes
- thrombosis - embolism
Causes of Ischemic Stroke
- thrombosis (focal) - embolism (focal) - hypoperfusion (global)
Infarction
- tissue death - end result of hypoxia and ischemia
Describe a shower embolization.
- tissue debris such as fat can be released after fracture of the bone - these particles gain access to the circulation and shower the brain with emboli causing widespread hemorrhagic lesions in the white matter - pts may experience general cerebral dysfunction with abnormalities of higher cortical function and consciousness and not necessarily have localized neuro deficits
Lacunar Infarcts: Microscopic Morphology
- tissue destruction - lipid-laden macrophages - surrounding gliosis
Subarachnoid Hemorrhage: Etiology
- trauma - rupture of aneurysm - rupture of hypertensive intracerebral hemorrhage into the ventricular system - vascular malformation - hematologic disturbances - tumors
What are the other forms of emboli?
- tumor - fat - air
Nonhemorrhagic (ischemic) infarct
- usually form acute vascular occlusion - usually associated with thrombosis - thrombolytic therapy may be useful
Arteriovenous Malformation: Clinical Presentation
- usually manifests between ages of 10 and 30 years with seizure disorder, intracerebral hemorrhage, and/or SAH
What are bridging veins?
- veins emptying from the cerebral hemispheres emptying into superior sagittal sinus - travel from convexities of the cerebral hemispheres through the subarachnoid space and the subdural space to empty into the superior sagittal sinus
Noncommunicating Hydrocephalus
-The obstruction of cerebrospinal fluid from a source within of the ventricular system e.g. mass in the third ventricle, so only the lateral ventricles are involved
Ruptured Saccular Aneurysms: Prognosis
25 to 50% die with their first rupture - those who survive often improve and recover consciousness within minutes - repeat bleeding is common in survivors - vasospasm may occur at the sight of the rupture causing ischemic infarction
Acute ischemic infarction: Microscopic Morphology, progression
A: At low magnification it is possible to see the demarcated areas of an acute infarction. In the underlying white matter, the areas of infarction are well shown by the myelin stain (borders identified by arrows). B: Acute ischemic injury causes diffuse eosinophilia of neurons, which are beginning to shrink. C: Infiltration of a cerebral infarct by neutrophils begins at the edges of the lesion where vascular supply has remained intact. D: After about 10 days, an area of infarction is characterized by the presence of macrophages and surrounding reactive gliosis. E, Remote small intracortical infarcts are seen as areas of tissue loss with residual gliosis.
(Multi-infarct) Vascular Dementia: Binswanger disease
AKE subcortical vascular dementia - term used when the injury preferentially involves large areas of subcortical white matter - widespread microscopic areas of damage to deep layers of white matter in the brain
Subdural Hematoma: Etiology
Acute (trauma, postop) or chronic (associated with cerebral atrophy)
Histology of hippocampus
CA1 area particularly vulnerable to hypoxia
Nonhemorrhagic infarct: Microscopic Morphology, 48 hours to 1 week
Phagocytic cells (monocytes and microglial cells) are seen and are the prominent cell type from day 2 to day 21
Subdural Hematoma
Collection of venous blood between inner surface of dura mater and external to the brain and arachnoid membrane - forms after a head trauma that severs the bridging veins from dura to brain
Epidural Hematoma: Gross Morphology
Hematoma formation in the cranial vault usually accompanied by a skull fracture with the hematoma also covering a portion of the dura
Lacunar Infarcts: Pathogenesis
Hypertension → cerebral vessels (deep penetrating arteries - basal ganglia, cortical white matter, brainstem) → arteriosclerosis → occlusion of artery → lacunar infarct (small cavity <15 mm lake like spaces)
Hemorrhagic infarct: Gross Morphology
Infarct stippled with petechiae or showing confluent larger hemorrhages
Arteriovenous Malformation: Microscopic Morphology
Jumble of abnormal vessels
Arteriovenous Malformation: In Newborns
Large AVM in newborn period can result in CHF
Lacunar Infarcts: Sites
Lenticular nucleus (putamen + globus pallidus) > thalamus > internal capsule > caudate nucleus > pons
Nonhemorrhagic infarct: Microscopic Morphology, 24 to 48 hours
Neutrophilic infiltration increases and peaks
Noninfectious Vasculitis Example
Polyarteritis Nodosa
Polyarteritis Nodosa Microscopic Morphology
extensive infiltrate of PMNs
Nonhemorrhagic infarct: Microscopic Morphology, after 1 week
Reactive astrocytosis (proliferation of astrocytes at the edge of the lesion as a result of liquefaction and phagocytosis)
Intracranial Hemorrhage
extravasation of blood within the skull
Saccular Aneurysms
Rupture of a saccular (berry) aneurysm - most frequent cause of SAH
Where do emboli tend to occlude?
The branch points of blood vessels or where a blood vessel is narrowed - most common sites of occlusion is that of the distribution of the middle cerebral artery
Describe the circle of Willis.
The circle of Willis gives rise to the other arteries that supply blood to the cerebral hemispheres and ensures continuity of the blood supply to the brain if any of the arteries are compromised.
Thromboembolus: Microscopic morphology
The source for this one was from a mural thrombus of the LA.
Cavernous Malformations: Etiology
familial inheritance
Cerebral Venous Thrombosis: Clinical Presentation
Variable - isolated intracranial HTN (headache with or without vomiting, papilledema, and vision problems) - focal syndrome (focal deficits and/or seizures) - encephalopathy (multifocal deficits, mental status changes, stupor, coma)
Ruptured Saccular Aneurysms: Symptoms
When blood under arterial pressure is driven into subarachnoid space: - sudden excruciating headache, then rapid LOC
Brain Contusion
a bruise of the brain associated with multiple microhemorrhages
Hydrocephalus
accumulation of excess CSF within the ventricular system
Infarction: affected areas
affects all tissue elements (neurons, glia, and vessels)
Capillary telangiectasia: Microscopic Morphology
aggregates of dilated thin-walled vessels separated by brain parenchyma
Nonhemorrhagic infarct: Microscopic Morphology, after months
astrocytic response decreases leaving a meshwork of glial fibers, new capillaries, and perivascular connective tissue. - residual cavity is formed
Metastatic Tumors of the Brain: Common Sites in Brain
at the junction of gray and white matter
Lacunar infarcts: prognosis
better short term prognosis than other types of infarcts
Cerebral Venous Thrombosis
blood clot that forms in the brain's venous sinuses
Subarachnoid Hemorrhage
blood in the subarachnoid space between the arachnoid mater and the pia mater
Nonhemorrhagic infarct: Gross Morphology after 2 to 10 days
brain is gelatinous and friable - border between normal and abnormal tissue becomes more distinct
Cavernous Malformations: Most common location
cerebellum, pons, subcortical areas
Acute Subdural Hematoma: Gross Morphology
collection of freshly clotted blood along the brain surface without extension into the depths of sulci - 1 week - clot lysis - 2 week - growth of fibroblast and granulation tissue from dural surface into hematoma - 1 to 3 months - hyalinized connective tissue ---------------- A, Large organizing subdural hematoma attached to the dura. B, Coronal section of the brain showing compression of the hemisphere underlying the subdural hematoma shown in A.
Cavernous Malformations: Microscopic Morphology
composed of large irregular vessels within thin collagenous walls - no intervening nervous tissue
Venous angiomas
consist of ectatic venous channels
Brain Contusion: Susceptible Areas
crest of gyri (most frequent sites of direct impact and to regions of the brain that overlie a rough and irregular inner skull surface such as the frontal lobes along the orbital ridges and the temporal lobes) - less freqeutn - over occipital lobe, brainstem, and cerebellum unless adjacent to a skull fracture in fracture ccontusions
Tonsillar herniation:Structures at Risk
crushes brainstem - crushes respiratory and cardiac centers in medulla oblongata (very life-threatening)
What is the presentation of increased ICP?
depending on the degree and rapidity of onset, subtle neuro deficits to death
Hydrocephalus ex vacuo
dilation of ventricular system with compensatory increase in CSF volume secondary to loss of brain parenchyma
Tonsillar herniation
displacement of cerebellar tonsils through foramen magnum
Subfalcine herniation
displacement of cingulate gyrus under the falx cerebri
Cerebrovascular disease due to hypoxia/ischemia/infarction develops secondary to:
due to impaired blood supply and oxygenation to the CNS
Hypertensive Encephalopathy: Gross Morphology
edema with or without transtentorial or tonsillar herniation
Global cerebral ischemia: gross morphology
general swelling/edema of the brain with widened gyri and narrowed sulci
Hypertensive Encephalopathy: symptoms
headaches, confusion, vomiting, convulsions, sometimes coma
Medullablastoma: Prognosis
highly malignant, but with total excision and irradiation, 5 year survival is 75%
Communicating Hydrocephalus
hydrocephalus caused by a problem with the normal uptake of CSF through the arachnoid granulations; whole CSF system would have increased pressure - enlargement of entire ventricular system
When is thrombolytic therapy indicated?
in a non-hemorrhagic (ischemic) stroke
Primary angiitis of the CNS
involves multiple small to medium sized parenchymal and subarachnoid vessels
Nonhemorrhagic infarct: Gross Morphology after 10 days to 3 weeks
lesion is a cystic cavity holding liquefied tissue - old MCA infarct in the picture
Herniations
occurs when brain expansion is too severe because the brain is contained within rigid dural folds
Medullablastoma: Gross Morphology
mass in the cerebellum - picture: sagittal section of brain showing medulloblastoma destroying the superior midline cerebellum
Hypertensive Encephalopathy: Microscopic Morphology
may show petechiae and fibrinoid necrosis of arterioles involving the gray and white matter - left is normal lined by endothelial cells (E) and a tunica media (M) which 2 to 3 layers of muscle - image on the right is an example of the effects of malignant HTN on blood vessels
Transtentorial (uncinate) herniation
medial temporal lobe compressed against the tentorium
Global cerebral (Diffuse ischemia / hypoxic encephalopathy): progression of mild ischemia
mild ischemia → transient post-ischemic confusion → complete recovery/no permanent tissue damage
Nonhemorrhagic infarct: Gross Morphology after 6 hours
minimal change
Chronic Subdural Hematoma
multiple episodes of bleeding (subdural membranes) (thin layer of reactive connective tissue) - caused by rebleeding from delicate vessels within granulation tissue
(Multi-infarct) Vascular Dementia: Radiology
multiple infarctions are seen on neuroimaging
Capillary telangiectasia: Most common location
pons
Cerebrovascular disease due to hemorrhage develops secondary to:
secondary to rupture of CNS vessels
Global cerebral (Diffuse ischemia / hypoxic encephalopathy): progression of severe ischemia
severe ischemia → widespread neuronal death → persistent vegetative state/brain death
Global cerebral ischemia: microscopic morphology
similar to focal (coming soon)
Hemorrhagic infarct: Microscopic Morphology
similar to ischemic infarction with the exception of blood extravasation and absorption
Lacunar infarcts
small ischemic infarcts involving the deep brain structures (basal ganglia and pons) and subcortical white matter (internal capsule, corona radiata). They are most often due to hypertensive aterioslclerosis of small, penetrating arterioles.
Epidural Hematoma: involved vessel
temperoparietal locus - usually middle meningeal artery - frontal locus = anterior ethmoidal artery - occipital locus = transverse or sigmoid sinuses - vertex locus = superior sagittal sinus
Transtentorial (uncinate) herniation: Structures at Risk
the 3rd CN may be crushed, resulting in pupillary dilation and impairments of ocular movements on the side of the herniation "down and out" eye
Lacunar Infarcts: Imaging
this diagram shows the deep penetrating arteries that are involved in small vessel strokes - thrombosis causes lacunar strokes
Thrombotic occlusion due to atherosclerosis: Gross Morphology
thrombus of blood vessel (R internal carotid artery in this picture) - base of brain
Nonhemorrhagic infarct: Gross Morphology after 48 hours
tissue is pale, soft, and swollen - indistinct corticomedullary junction - acute infarct in distribution of R MCA - swelling and early disintegration of infarcted area in picture
What is Rtpa alteplase?
tissue plasminogen activator is a protein involved in the breakdown of blood clots
Medullablastoma
tumor of the cerebellum that occurs predominantly in children
Capillary telangiectasia: Clinical Presentation
typically found incidentally on neuroimaging studies or at postmortem examinations - usually clinically silent
