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Neuro > CNS pathology > Flashcards

CNS pathology Flashcards

1
Q

Stains for CNS cells

A
  • H&E
  • Luxol blue: stains myelin blue (white matter dark blue, gray matter very light blue)
  • Silver stain: stains neurofilaments black
  • Immunoperoxidase stains to stain for synaptic protein (synaptophysin), localized neurofilaments or NTs
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2
Q

Ischemic cell change (red neuron)

A
  • Red is dead, occurs in response to deprivation of O2
  • Btwn 8-24hrs after insult, neuron shrinks and cytoplasm becomes eosinophilic (pink/red on H&E)
  • Nucleus is darkly stained, then lost
  • Changes are irreversible
  • Insult requires deprivation of O2 to tissue for several minutes for irreversible damage, but then 8-24hrs is required for these changes to be observed
  • Cellular changes: depletion of ATP, acidosis, impaired reuptake of GLU by glial cells and resulting excitotoxicity, accumulation of intracellular Ca, ROS generation
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3
Q

Wallerian degeneration

A
  • Occurs when an axon is transected by trauma
  • Axon and myelin distal to transection degenerate, leading to impaired axonal transport
  • Disappearance of neurofibrils and breaking of axon into short fragments (parts are phargocytosed)
  • This occurs over weeks in PNS and months in CNS
  • Sprouting of new axons from cell body possible in PNS, but not CNS
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4
Q

Central chromatolysis

A
  • Occurs after transection injury to neuron’s axon, usually seen in large motor neurons
  • Consists of swelling of cell body, dissolution of nissl substance, and migration of nucleus to the periphery of the body
  • Reversible
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5
Q

Distal axonopathy

A
  • Degeneration of the axon and myelin first develops in the most distal part of the axon
  • The axon “dies back”
  • Usually a result of toxins (pesticides, acrylamide, ect) or metabolic problems (diabetes, renal failure, alcoholism)
  • When the metabolic needs of the cell are not met, the most distal part of the axon dies first
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6
Q

Inclusion bodies

A
  • Abnormal deposits in neurons
  • Stains w/ silver stain: cytoplasmic neurofibrilary tangles (AD) and Pick bodies (Pick disease)
  • Stains w/ H&E: cytoplasmic lewy bodies (PD) and negri bodies (rabies)
  • Stains w/ H&E: nuclear cowdry type A (herpes and CMV)
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6
Q

Oligodendrocytes

A
  • All glia are neuroectodermal in origin (except for microglia, which are mesodermal- bone marrow- derived)
  • Reside mostly in white matter (also some in grey) and myelin ate the axons
  • Have small, round nuclei and no apparent cytoplasm
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7
Q

Myelin loss (pathologic oligodendrocytes)

A
  • Demonstrated by luxol stain, turing myelin blue
  • Demyelinating disease such as MS (autoimmune) leave large plaques of absent blue color (axons left intact)
  • MS plaques are usually periventricular, larger, and more confluent that PML
  • Progressive multifocal leukoencephalopathy (PML) forms small plaques of demyelination (most severe at grey-white matter junctions) when oligodendrocytes die and myelin degenerates
  • Oligodendrocytes can die from viruses, like the papova virus (causes PML). This virus results in a homogenous, glassy nuclear inclusion in the oligos
  • Leukodystrophies are due to genetic mutations. Myelin is abnormally formed and is unstable so it breaks down
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9
Q

Astrocytes 1

A
  • Astrocytes present in gray and white matter, have large oval nuclei (larger than oligo’s) with more euchromatin than oligo’s
  • Processes can only be seen when stained w/ glial fibrillary acidic protein (GFAP)
  • These processes surround the small arteries of the brain and play a role in maintaining the BBB and ionic environment
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9
Q

Astrogliosis (gliosis)

A
  • Astrocytes respond to almost any brain injury by gliosis, which includes proliferation and hypertrophy
  • Cytoplasm becomes very apparent and eosinophilic due to GFAP (referred to as gemistocytes)
  • This process does not result in fibrosis
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10
Q

Astrocytes 2

A
  • Astrocytes present in gray and white matter, have large oval nuclei (larger than oligo’s) with more euchromatin than oligo’s
  • Processes can only be seen when stained w/ glial fibrillary acidic protein (GFAP)
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11
Q

Microglia

A
  • Derived from bone marrow (mesoderm), infiltrate developing brain along w/ blood vessels
  • Slow turnover during life
  • Appear as small elongated, dark-staining nuclei
  • Can respond to injury by differentiating and acting as macrophages
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12
Q

Reactive microglial cell

A
  • Activated microglia (due to brain injury or local immune response) look rod-shaped
  • May up regulate expression of MHC and inflammatory cytokines
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13
Q

Macrophage response

A
  • Microglia may differentiate into macrophages, especially during brain necrosis
  • The macrophages phagocytose the tissue debris (lipid-laden macrophages, or glitter cells)
  • Monocytes may enter brain after injury, and differentiate into macrophages as they do so
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14
Q

Microglial nodule

A
  • Microglia may respond to single damaged neurons in encephalitis, by encircling the neuron and phagocytosing it (neurophagia)
  • This results in the formation of a microglial nodule
  • Microglial nodules may also be present in white mater, especially in HIV encephalitis
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15
Q

Multinucleated giant cell reaction

A
  • Formed either from fusion or failure to divide
  • In HIV encephalitis groups of microglial cells may accumulate in the white matter
  • Some will fuse to form the multinucleate giant cell
  • Can often be seen in AIDS dementia pts
16
Q

Vasogenic edema

A
  • Loss of integrity of BBB (broken tight junctions) may result in entrance of excess water and solutes into extracellular space of brain
  • The fluid collect predominantly in white matter
  • Results in increased brain volume and intracranial pressure, leads to mass effect
18
Q

Vasogenic edema

A
  • Loss of integrity of BBB (broken tight junctions) may result in entrance of excess water and solutes into extracellular space of brain
  • The fluid collect predominantly in white matter
  • Results in increased brain volume and intracranial pressure (new water entering brain)
18
Q

Hypoxia vs ischemia

A
  • When the brain is deprived of O2 (hypoxia) it is usually due to the brain being deprived of blood (ischemia)
  • Pure hypoxia causes mostly reversible (to an extent) failure of electrical activity and synaptic transmission, and doesn’t cause necrosis
  • Ischemia results in decreased O2, glc, and a build up of toxic metabolites and thus is much more damaging
19
Q

Cytotoxic edema

A
  • Toxic or metabolic events that affect normal neuronal and glial membranes may result in intracellular accumulation of fluid, or lysing of cells
  • More likely to affect cells in gray matter and usually do not lead to mass effect (not introducing any new water- just releasing the water from cytoplasm)
20
Q

Selective neuronal necrosis (global hypoxia-ischemia)

A
  • Cells in the CNS have differing sensitivity to hypoxia-ischemia (during intermediate severity of ischemia)
  • Neurons (especially cortical neurons) are more vulnerable to ischemia than glial cells and endothelial cells (most vulnerable layers in cortex: layers 3 and 5)
  • Neurons in brainstem and spinal cord are more resistant to hypoxia-ischemia than neurons in the cortex
  • Water-shed areas are first to be affected because they lack sufficient collateral circulation (i.e. hippocampus), usually btwn ACA, MCA, and PCA
  • Histologic changes seen only after 12-24 hrs of insult
  • Results in eosinophilic ischemic necrosis: neurons shrink, cyto becomes eosinophilic, nucleus becomes blurry. Eventually the neuron disappears
21
Q

Selective neuronal necrosis (global hypoxia-ischemia)

A
  • Cells in the CNS have differing sensitivity to hypoxia-ischemia (during intermediate severity of ischemia)
  • Neurons (especially cortical neurons) are more vulnerable to ischemia than glial cells and endothelial cells (most vulnerable layers in cortex: layers 3 and 5)
  • Neurons in hippocampus most susceptible to hypoxia than another part of brain (lose recent memory)
  • Neurons in brainstem and spinal cord are more resistant to hypoxia-ischemia than neurons in the cortex
  • Water-shed areas are first to be affected because they lack sufficient collateral circulation (i.e. hippocampus), usually btwn ACA, MCA, and PCA
  • Histologic changes seen only after 12-24 hrs of insult
  • Results in eosinophilic ischemic necrosis: neurons shrink, cyto becomes eosinophilic, nucleus becomes blurry. Eventually the neuron disappears
22
Q

Focal ischemia and infarction

A
  • Leads to deprivation of a specific area of blood, causing excitotoxicity (increased extracellular GLU and ASP), increased lactic acid and tissue acidosis
  • The center of the infarct (core) is unsalvageable
  • But btwn the core and the healthy tissue is the penumbra, an area of constrained blood but partially preserved metabolism
  • The penumbra is at risk of infarction, yet potentially salvageable
  • Requires 12-24hrs after insult for histologic changes to be seen
23
Q

Causes of CNS infarcts

A
  • Atherosclerosis predominantly affects larger vessels (common carotid, especially at bifurcation, MCA, and basilar a)
  • Atheroscelrotic plaques can lead to thrombotic occlusions, which do not move unless they embolize (form at site of infarction)
  • Most large infarcts are caused by thromboembolisms of the MCA
  • Hemorrhages are most often seen in infarcts of embolic origin
24
Q

Microscopic features of infarcts

A
  • Earliest changes: pallor and vacuolization (falls apart) of neuropil, endothelial swelling and eosinophilic ischemic necrosis (EIN)
  • Next there are some PMNs infiltrating, followed by macrophages
  • Finally there is cavitation w/ surrounding gliosis
  • During gliosis and PMN/mac infiltration the brain appears hypercellular
25
Q

Embolic vs thrombotic infarction

A
  • Embolic infarctions are more common, and the heart is frequently the source (arrhythmias such as a fib and vulvar disease)
  • Other sources: bits of thrombus, atherosclerotic plaque, talc protein, others
  • The MCA is most often affected by embolic infarcts
  • Embolisms are more likely to cause multiple infarcts than thrombotic
  • Embolic infarcts are more likely to be complicated by hemorrhage into infarcted tissue (blood is restored to dead tissue and the capillaries hemorrhage)
  • Always check for hemorrhage (indicates embolic) and multiple infarcts (indicates embolic)
26
Q

Vasculitis infarct

A
  • Vasculitis (inflammation of blood vessels) can cause infarction
  • May be part of systemic vasculitis or isolated to CNS
  • May be multiple and hemorrhagic, and has many causes (such as infection)
  • Often suspected but rarely Dx
  • Vessel walls infiltrated by inflammatory cells, damage to vessel wall can result in thrombosis
27
Q

Lacunar infarcts

A
  • Type of ischemic small vessel disease (HTN high risk factor for this and intracerebral hemorrhage)
  • Small infarcts (often multiple) due to small vessel atherosclerosis w/ chronic HTN and diabetes being major risk factors
  • Often found in pons and basal ganglia
  • May be asymptomatic, or isolated neurological deficits (or dementia if multiple)
28
Q

Intracerebral hemorrhage

A
  • Associated with HTN and often occur in basal ganglia, thalamus, brainstem, or cerebellum
  • Will cause a mass effect
  • The ipsilateral ventricle will be small, while the contralateral one will be large due to obstruction of CSF flow
  • The obstruction to CSF flow and the mass affect both raise intracranial pressure
29
Q

Fibrinoid change

A
  • Deposition of proteins in vessel walls, causes damage to the walls
  • Due to chronic HTN (less severe, more chronic than fibrinoid necrosis)
  • If extreme HTN, the vessels may undergo fibrinoid necrosis
30
Q

Amyloid angiopathy

A
  • Amyloid stains w/ congo red, gives a green birefringence under polarized light
  • Deposition of amyloid in cerebral vessels is another way of developing intracerebral hemorrhage (sometimes multiple)
  • These hemorrhages are usually located superficially in the cerebral hemispheres, with a predilection for the occipital lobe
  • Common in AD
31
Q

Cerebral aneurysm

A
  • Can cause excruciating headaches, loss of consciousness, stiff neck, subarachnoid hemorrhage
  • Blood in subarachnoid space causes: blockage to CSF flow, vasospasms (other vessels may hemorrhage)
  • Often arise at bifurcations, circle of willis and communicating arteries, basilar artery
  • Often are multiple and rebleed, often fatal
  • Can result in intraventricular and intracerebral hemorrhage
31
Q

Vascular malformations

A
  • Congenital problems that cause abnormal flow, hemorrhage, seizures, and focal deficits
  • Usually superficial, typically over cerebral convexity
  • Can easily be seen on angiogram, where its a large bundle of unorganized vessels
32
Q

Cavernous hemangioma

A
  • Back-back thin walled vessels
  • Located more deeply in the brain usually than AVMs
  • Most common symptom is seizure by also may bleed
  • Typically has less brain parenchyma btwn vessels than AVMs
  • Can often be asymptomatic
33
Q

Arteriovenous malformations (AVM)

A
  • Congenital problems that cause abnormal flow, hemorrhage, seizures, and focal deficits
  • May be asymptomatic, but are more dangerous than cavernous hemangiomas
  • Usually superficial, typically over cerebral convexity
  • Can easily be seen on angiogram, where its a large bundle of unorganized vessels
  • Often will have arteries connecting to veins without going through a capillary bed (microscopically seen as many vessels of various sizes )
  • Tend to bleed b/c arteriole blood under high pressure directly enters veinules that can’t handle the pressure
  • The vessel walls and size of vessels vary btwn one another (can be fibrotic)
34
Q

Uncal herniation

A
  • A complication of any space-occupying intracerebral lesion (mass affect), including hemorrhage and infarction
  • Uncus herniates thru the incisura of the tentorium and compresses the brainstem
  • Can lead to hemorrhages in the midline brainstem (duret hemorrhages- from shearing of other arteries)
  • PCA can be affected by duret hemorrhages
35
Q

Cavernous hemangioma

A
  • Back-back thin walled vessels
  • Located more deeply in the brain usually than AVMs
  • Most common symptom is seizure by also may bleed
  • Typically has less brain parenchyma btwn vessels than AVMs, vessels tend to be thinner (fibrosis in the walls of vessels)
  • Can often be asymptomatic
36
Q

Types of hematomas

A
  • Epidural: lesion in the middle meningeal artery, bleeds above the dura and causes mass effect
  • Subdural: lesion in the bridging vein, leads to slowly enlarging hematoma that causes mass effect
  • Subarachnoid: lesion in the cerebral arteries, causes blood to enter CSF (worst headache ever, drowsiness, confusion), no mass effect
  • Intracranial hemorrhage: lesion of a vessel within the brain tissue, causes mass effect

Neuro (62 decks)

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