Cerebrovascular DX pathology

Question 1

Central sulcus form and functions

Answer 1

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

Question 2

Circle of willis anatomy

Answer 2

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

Question 3

ACA (anterior cerebral artery) divisions

Answer 3

The collosal marginal aretey comesout and forward on top of the cingulate gyrus
And right on the corpus collosum is the pericallosal artery

Question 4

What does the cortes receieve

Answer 4

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

Question 5

MCA divisions

Answer 5

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

Question 6

Watershed teritories

Answer 6

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

Question 7

Cerbrovascular disease general concepts and definition

Hypoxia

Answer 7

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

Question 8

Cerbrovascular disease general concepts and definition

Ischemia

Answer 8

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

Question 9

Cerbrovascular disease general concepts and definition

Selective vulnerability

Answer 9

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

Question 10

histology of hypoxic and ischemic neurons

Answer 10

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

Question 11

severe global ischemia

Answer 11

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)

Question 12

Severe global ischemia gross morphology

Answer 12

corresponds to brain death, non perfused brain, gross (swollen brain slit like ventricles, often some herniation)
Pallor, vacuolation of parenchyma, sparse eosinophilic neurons

Question 13

Focal ischemia infarcts, and strokes causes- thrombosis

Answer 13

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

Question 14

Focal ischemia infarcts, and strokes causes- emboli

Answer 14

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

Question 15

lacunar infarcts /slit hemorrhages

Answer 15

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

Question 16

morphology of infarct

Answer 16

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

Question 17

Cerebral venous thrombosis

Answer 17

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

Question 18

intracerebral hemorrhage (ICH) causes

Answer 18

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

Question 19

Vascular malformations

Answer 19

2 most common

1. 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
2. Cavernous angioma- cerebellum, pons, white matter, no intervening brain tissue, evidence of prior bleeding

Question 20

lobar hemorrhage

Answer 20

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

Question 21

subarachnoid hemorrhage

Answer 21

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

Question 22

what is a stroke

Answer 22

A sudden failure of brain function due to diminished blood flow to a part of the brain, or due to bleeding inside the brain

Question 23

how does a stroke happen

Answer 23

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

Question 24

Pump

Answer 24

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)

Question 25

Pipes

Answer 25

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

Question 26

passengers

Answer 26

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