Pathoma - Cerebrovascular Disease, Trauma, Demyelinating Disorders - Fundamentals Of Pathology

Front 1

What is cerebrovascular disease?

Back 1

Neurologic deficit that arises due to cerebrovascular compromise.

Front 2

Cerebrovascular disease is due to what?

Back 2

(1) Ischemia (85%)
(2) Hemorrhage into the brain (15%)

Front 3

Ischemia as a cause of cerebrovascular disease can be divided. How?

Back 3

It can be focal or global

Front 4

Causes of global cerebral ischemia?

Back 4

(1) Atherosclerosis - Low perfusion
(2) Shock - Acute decrease in blood flow
(3) Anemia - Chronic hypoxia
(4) Insulinoma - Repeated episodes of hypoglycemia
- Has the same effect as global cerebral hypoxia.

Front 5

Clinical features of global cerebral ischemia?

Back 5

Depends on severity.

(1) Mild global ischemia
- Transient confusion with complete recovery, e.g. insulinoma
(2) Severe global ischemia
- Diffuse necrosis of brain. Patient probably wouldn't survive. If they do, they enter a vegetative state.
(3) Moderate global ischemia
- Infarcts in watershed areas.
- Infarcts in highly vulnerable regions (pyramidal neurons in layers 3, 5 and 6, pyramidal neurons of the hippocampus, purkinje cells in cerebellum)

Front 6

What is a watershed area?

Back 6

A region that is fed by the very end of a circulation.

Front 7

What is corticolaminar necrosis?

Back 7

Moderate global ischemia that causes damage/necrosis of pyramidal neurons in layers 3, 5 and 6.

Front 8

Ischemic causes of global cerebral ischemia can be focal or global. If it is focal, and the neurologic deficits lasts less than 24 hours, what do we call that? Greater?

Back 8

Transient ischemic attack. Greater, then we call it a stroke.

Front 9

There are three ways by which you can develop an ischemic stroke. What are they?

Back 9

(1) Thrombotic
(2) Embolic
(3) Lacunar

Front 10

Thrombotic stroke arises due to ________________. It usually develops at ____________. What does it result in?

Back 10

rupture of an atherosclerotic plaque; branch points

It results in a pale infarct at the periphery of the cortex.

Front 11

Embolic stroke usually arises from __________.

Back 11

left side of the heart (think a-fib)

Front 12

Embolic strokes usually involves the _______________ artery.

Back 12

middle cerebral

Front 13

What is the result of an embolic stroke in the cortex?

Back 13

Hemorrhagic infarct (clot lyses) at the periphery of the cortex.

Front 14

Why doesn't the body lyse the clot in thrombotic stroke and cause a hemorrhagic stroke?

Back 14

It becomes quickly reformed

Front 15

What is a lacunar stroke? What artery is most commonly involved?

Back 15

Stroke that involves small blood vessels of the brain that undergo hyaline arteriolosclerosis (think benign HTN or diabetes). The small vessel feeds a tiny region creating a tiny infarct which gets resorbed producing a cystic region. They call it lacunar because of the circular area that is formed.

Front 16

Early finding of liquefactive necrosis? How long does it take before they develop?

Back 16

Red neurons

About 12 hours

Front 17

After red neurons die completely, what happens?

Back 17

Inflammation with neutrophils and microglial cells ("macrophages"), and granulation tissue ensue. After about a month you will have a fluid-filled cystic space surrounded by gliosis.

Front 18

Hemorrhage into the brain as a cause of cerebrovascular disease can be divided. How?

Back 18

(1) Intracerebral
(2) Subarachnoid

Front 19

Intracerebral hemorrhage is classically due ______________ which is a complication of ___________.

Back 19

Rupture of Charcot-Bouchard aneurysms; HTN

Front 20

Most common site of intracerebral hemorrhage?

Back 20

Basal ganglia

Front 21

How does intracerebral hemorrhage present?

Back 21

(1) Headache
(2) Nausea
(3) Vomiting
(4) Eventual coma

Front 22

In subarachnoid hemorrhage, a LP would show what?

Back 22

Xanthochromia (yellowish)

Front 23

What is this?

Back 23

Subarachnoid hemorrhage

Front 24

MCC of subarachnoid hemorrhage is what?

Back 24

Rupture of berry aneurysm

Front 25

Berry aneurysms are most frequently located where? Why?

Back 25

Most frequently located in anterior circle of Willis (branch points of anterior communicating artery)

Front 26

Why do we see berry aneurysms at branch points?

Back 26

Media fail to form at branch points ("turns"). That means it will be a weak wall.

Front 27

Berry aneurysms are associated with __________ and _________.

Back 27

Marfan's; ADPKD

Front 28

Where does blood collect in an epidural hematoma?

Back 28

Blood collects between the dura and skull ("lens-shaped")

Front 29

Epidural hematoma is usually due to?

Back 29

Due to fracture of temporal bone with rupture of middle meningeal artery.

Front 30

What is classically called a "talk-and-die syndrome"?

Back 30

Epidural hematoma. The lens-shaped hematoma may at some point expand, causing herniation.

Patient can be for example asymptomatic for a few hours then all of a sudden cause a lethal herniation.

Front 31

Subdural hematoma is a collection of blood ______________.

Back 31

beneath the dura

Front 32

Subdural hematoma is due to what?

Back 32

Due to tearing of bridging veins between dura and arachnoid.

Front 33

Subdural hematoma usually arises with ___________.

Back 33

trauma

Front 34

What is this?

Back 34

Subdural hematoma

Front 35

Elderly are particularly susceptible to this type of hematoma, why?

Back 35

Subdural. Because of possible atrophy of the brain with stretching of bridging veins.

Front 36

Subdural hematoma doesn't have a lucid interval before any neurologic symptoms (as in epidural). How does it present?

Back 36

Progressive neurologic signs. Herniation is a lethal complication.

Front 37

Herniation is _______________.

Back 37

displacement (forskyvning) of brain tissue

Front 38

Herniation is due to _________ or _____________.

Back 38

mass effect; increased intracranial pressure

Front 39

Complication of subfalcine herniation?

Back 39

Compression of anterior cerebral artery

Front 40

Complications of uncal herniation?

Back 40

Compression of three structures:

(1) CN III --> Eyes move down and out, mydriasis
(2) Posterior cerebral artery
(3) Paramedian artery

Front 41

In a demyelinating disorder you get demyelination of _____ or ______.

Back 41

myelin; oligodendrocytes

Front 42

What happens after demyelination?

Back 42

Axons are preserved, but conduction of impulse is impaired.

Front 43

What is a leukodystrophy?

Back 43

Means "problem with white matter"

Inherited mutations in enzymes necessary for production or maintenance of myelin.

Front 44

What enzyme is deficient in metachromatic leukodystrophy?

Back 44

Aryl sulfatase.

Front 45

This is the MC leukodystrophy. What happens?

Back 45

Metachromatic leukodystrophy

Myelin cannot be degraded; accumulates within lysosomes.

Front 46

What is Krabbe disease?

Back 46

Deficiency of galactocerebroside beta-galactosidase. Accumulation of galactocerebroside within macrophages.

Front 47

What is adrenoleukodystrophy?

Back 47

Problem with adrenal glands and white matter. Due to impaired addition of coenzyme A to long-chain fatty acids. FAs accumulate, damaging the gland and white matter.

Front 48

What is MS?

Back 48

Autoimmune destruction of CNS myelin and oligodendrocytes.

Front 49

What is the most common chronic CNS disease of young adults?

Back 49

MS

Front 50

MS is associated with _______.

Back 50

HLA-DR2

Front 51

Where do we usually see MS occur in higher frequencies?

Back 51

More commonly seen in regions away from the equator

Front 52

Clinical features of MS?

Back 52

Depends on region involved.

(1) Blurry vision on one eye (optic)
(2) Vertigo and scanning speech (brainstem)
(3) Internuclear ophthalmoplegia (MLF)
(4) Hemiparesis or unilateral loss of sensation (cerebral white matter)
(5) Lower extremity loss of sensation or weakness (spinal cord)
(6) Bowel, bladder, sexual dysfunction (ANS)

Front 53

What is scanning speech?

Back 53

Speech resembles the speech of someone who is drunk.

Front 54

What is internuclear ophthalmoplegia?

Back 54

Cranial nerve VI is blocked from coordinating eye movement via MLF.

Front 55

Diagnosis of MS is made by what? What does it show?

Back 55

MRI reveals plaques. Lumbar puncture can be done and it would show increased lymphocytes, increased Ig with oligoclonal IgG bands and myelin basic protein.

Front 56

What could this be?

Back 56

The brain is grey in areas where it should be white. could be MS.

Front 57

Treatment of MS?

Back 57

(1) Acute attacks - high dose steroids
(2) Interferon gamma has been shown to slow progression of the disease.

Front 58

What is subacute sclerosing panencephalitis?

Back 58

Progressive, debilitating encephalitis leading to death (pan = both gray and white matter). Due to slowly progressing, persistent infection of the brain by measles virus.

Front 59

When does infection occur leading to subacute sclerosing panencephalitis?

Back 59

During infancy; neurologic signs arise years later.

Front 60

Subacute sclerosing panencephalitis is characterized by what (microscopically)?

Back 60

Viral inclusions within neurons (gray matter) and oligodendrocytes (white matter)

Front 61

What is progressive multifocal leukoencephalopathy?

Back 61

JC virus infection of oligodendrocytes. Immunosuppression leads to reactivation of the virus.

Front 62

How does progressive multifocal leukoencephalopathy present?

Back 62

Rapidly progressive neurological signs leading to death (e.g., patient with leukemia or AIDS)

Front 63

What is central pontine myelinolysis?

Back 63

Focal demyelination of pons. Due to rapid IV correction of hyponatremia.

Front 64

Central pontine myelinolysis occurs in what patients?

Back 64

Severely malnourished patients (e.g., alcoholic)

Front 65

Central pontine myelinolysis presents as?

Back 65

Classically presents as acute paralysis ('locked in' syndrome). Voluntary movements are completely paralysed from head to toe. They can only move the eyes.