Cerebrovascular DX pathology Flashcards
Central sulcus form and functions
Primary motor cortex (Precentral gyrus)- anterior to the central sulcus (part of the frontal lobe, from temporal lobe is the face–> hand–> Arm–> trunk– in the longitudinal fissure leg–> foot)
Primary somatosensory cortex (Post central cortex)- posterior to the central cortex, Corresponds to the primary motor cortex but its what feels
Brocas area sits at the sylvian fissure in the fronal lobe LEFT- Speech production
Wernickes area- in the temporal lobe, in the LEFT- Speech comprehension
Circle of willis anatomy
The posterior inferior cerebellar artery (PICA)s join the vertebral arteries ( which receive the anterior spinal artery) at the crotch
The Vertebral arteries join with the Anterior infereior cerebellar artery to form the basilar artery
Out of the basilar artery are the pontine arteries
2 arms on each side jut out of the basilar artery the bottom one is the Superior Cerebellar artery, and the the posterior cerebral artery
The Posterior communicating artery joins the internal carotid arteries
opthalmic artery comes off the internal carotid arteries
Off the internal carotid artery is the anterior chordial artery and continues to the sides as medial cerebral artery
They contiinue as the anterior cerebral artery ( and attach to each other via the communicating artery
And continue forward as the ACA
ACA (anterior cerebral artery) divisions
The collosal marginal aretey comesout and forward on top of the cingulate gyrus
And right on the corpus collosum is the pericallosal artery
What does the cortes receieve
Aca is the highway in the middle
MCA is the sides ( (tempoal and lots of the frontal lobe)
PCA- back highway and the base of the brain
MCA divisions
The lenticulostriate arteries coming of the main MCA supply the basal ganglia (caudate, putamen and globus palludus) The mca in th the sylvian fissure also divides in a Superior and inferior division
The lenticulostriate arteries are very susceptibel to HTN
Watershed teritories
Kind of betweeen two areas of main blood supply
ACA- MCA watershed area
MCA and PCA watershed area in the frontal lobe and temppral obe
Cerbrovascular disease general concepts and definition
Hypoxia
Hypoxia (deprivation of O2) - in brain occurs by several mechanisms:
Low level of O2 in blood (respiratory arrest, near drowining, severe anemia, CO2 poisoning)
Low blood glow to tissue ischemia ( cardiac arrest, vessel obstruction, increased intracranial pressure)
Oxygen utilization by tissue is impaired ( cyanide poisoind)
Many cases of hypoxia also decrease cardiac output resulting in combined hepoxia and ischemic brain inury
Cerbrovascular disease general concepts and definition
Ischemia
Ischemia is low blood flow
Ischemia casuses MORE damage than hypoxia
Global ischemia- systoloic pressure <50 mmHg, generalized reduction in cerebral perfusion, usually due to cardiac arrest, shock, or severe hypotension- clinical outcome dependent upon severity and duration of ischemia
Brain damage is most severe in watershed/borderzone territories
If ischemia is severe, widespread neuronal death may result–> persistent vegetative state, brain death
Focal ischemia- infarction from obstruction of local blood supply stroke, results most often from arterial stenosis and or thrombosis, atheroemboli or thromboemboli
Cerbrovascular disease general concepts and definition
Selective vulnerability
Certain brain cells and regions are more susceptible to hypoxia and ischemia than others
Most vulnerable cells (in decreasing order)– Neurons, oligodendrocytes, astrocytes
Most vulnerable regions (adults)- in decreasing order- hippocampus (Ca1 secotr- sommer sector), Lamina 3 and 5 of cerebran cortex (laminar necrosis), purkinje cells in cerebellum
What determinesthe selective vulnerability- varible oxygen/energy requirements of different neurons and neuronal populations, glutamate receptor densities, glutamate is neurotoxic when in excess as occurs in hypoxic and ischemicbrain damage
histology of hypoxic and ischemic neurons
red is dead
pyknotic - irreversible chromatin condenstation, cell with a shrunken and dark nucleus, no nucleolus visible
red cytoplasm no nissl substance is visible
hippocamus looks like jelly
lamina 3 and 5 looks granular
severe global ischemia
severe ischemia causes widespread neuronal death, irrespecting of regional vulnerability
Clinical S/S: persistent vegetative state- unconscious but with retention of sleep-wake cycle, primitive orienting responses, brainstem and diencephalon reflexes
Brain death- diffuse irreversible cortical injury with brainstem injury (absent reflexes and respiratory drive)
Severe global ischemia gross morphology
corresponds to brain death, non perfused brain, gross (swollen brain slit like ventricles, often some herniation)
Pallor, vacuolation of parenchyma, sparse eosinophilic neurons
Focal ischemia infarcts, and strokes causes- thrombosis
Thrombosis- atherosclerosis, most common sites (carotid bifurcation, origin of middle cerebral artery, origin or end of basilar artery
Will result in cytotoxic edema due to no na atpase activity
Focal ischemia infarcts, and strokes causes- emboli
emboli - infarcts are more likely than hemorrhagic
Cardiac source- mural thrombus (left atrium or left ventricle)- Pre disposing factors (myocardial infarct, valve disease, atrial fibrillation paradoxical embolism, endocarditis- bacterial or marantic
Non cardiac source- atheroma (from plaques in carotid arteris) fat neoplasm and air, middle cerebral artery is most frequent affected by emboli
lacunar infarcts /slit hemorrhages
hyaline arteriolosclerosis caused by hypertension and diabetes mellitus, causes lacunes (small strokes) in subcortical brain structures - usually basal ganglia, internal capsule, thalamus, white matter, pons
May be hemorrhagic
morphology of infarct
gross- acute (<48 hrs, soft, swollen, gray white distinction blurred), subacute (up to 2-3 weeks, liquefactive necrosis), chronic (several months- cavitated all dead tissue is removed)
Microscopic examination: acute (8-12 hours red neurons, pallow, up to 48 hrs PMNs)
Subacute- 48 hrs to 3 weeks, macrphages, necrotic tissue, reacitve astrocytes vascular proliferation
Chronic - several months cavity with glial scar
Acutely there wont be really anything on CT/MRI, diffusion imaging will start showing stuff
Subacutely- cytotoxic edema
Chronic- it will me a hole with meninges with lots of scar
Cerebral venous thrombosis
Causes hemorrhagic infarcts, usually superior sagittal sinus or later sinuses
Results in parasagittal hemorrhagic infarcts
Causes- infection, injury, neoplasm surgery
Pregnancy, oral contraceptives, hematologic abnormalities, dehydration and malignancy dehydration
intracerebral hemorrhage (ICH) causes
Hypertension- most common cause of primary ICH, peak occurence in 60s, abrupt onset of severe neurologic dysfunction when hematoma is large, putamen thalamus pons and celebellum, hyaline arteriorscleorsis
Vascular malformations, amyloid angiopathy
Vascular malformations
2 most common
- arteriovenous malformation- most common vascular malformation, M>F, presentation between 10-30 yrs, most often in distribution of MCA (just look like a huge mesh of veins), lower the bp, the veins recieve arterial bp and burst into bloody pool, usually deep
- Cavernous angioma- cerebellum, pons, white matter, no intervening brain tissue, evidence of prior bleeding
lobar hemorrhage
Neoplasms, drugs, vasculitis, hemorrhagic diathesis, amyloid angiopathy
Amyloid angiopathy (beta amyloid stains congo red, and deposits on the blood vessels and weakens them
on the cortex
subarachnoid hemorrhage
trauma, aneutrysms
Saccular (berry) the worst headache the persons ever had, increased risk with HTN, smoking, AVM
Increasing risk of rupture as size increases, not present at birth, but defect in media is congenital and the aneurysm develops over time
Occur typically at branch points, 90% in the anterior circulation
Mycotic (fungus), fusiform, atherosclerotic)
most at the ACA and communicating
Treated with titanium coils
what is a stroke
A sudden failure of brain function due to diminished blood flow to a part of the brain, or due to bleeding inside the brain
how does a stroke happen
Thrombotic- something is wrong with the vessel right there and it breaks and messes up and creates a clot (usually a lacunar)
Embolism- somewhere else and travels
Pump
cardioembolism- 20-30% of strokes, atrial fibrillation, valvular defects
Strokes are in large vessels or at the end branches- (grey white border), MCA is the most common site
especially the left sided
Hypoperfusion- no flow- cortical laminar necrosis, low flow (water shed injury)
Pipes
large vessel disease, carotid plaque, vertebral artery stenosis, intracranial stenosis
Plaque rupture- leadas to artery to artery embolism
Anatomically appear as embolic (end vessels and bifurcation) but the lesions are restricted to the territory of the vessel involved- its better to give aspirin with a primary stroke, with a secondary stroke you cant stent
Small vessel disease- lipohyalinosis, intravscular plaque, insitu thrombosis, lacunar strokes, vessel rupture (intracerebral hemorrhage
passengers
clotting can be caused by blood disorder- rare
venous or arterial
large vessel more than small
Hypercoagulable state- genetic - prothrombingene mutation, factor v leiden, sickle cell disease
Acquired- lupus anticoagulant, polycythemia, DIC, TTP
