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Brain and Behavior Part 2 > CNS Histology and Infections > Flashcards

CNS Histology and Infections Flashcards

She packed a lot of info into this lecture. Most of the details are here... but as they can only ask a small number of questions per lecture on the test, broader concepts are emphasized. Hopefully.

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1
Q

What are Virchow-Robin spaces?

A

Subarachnoid and subpial spaces that surround blood vessels in the brain.

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2
Q

What are arachnoid villi?

A

Same thing as arachnoid granulations - penetrations into the dural sinuses that conduct CSF into the circulation.

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3
Q

Is the arachnoid normally clear or opaque?

A

Normal is clear. The arachnoid becomes opaque with age, but opacity can also be caused by pathological process.

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4
Q

Review: What are Nissl bodies?

A

Rough ER, basophilic, present in neurons (unless they’re dying)

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5
Q

How can you tell a neuron’s axon from its dendrite histologically?

A

The axon hillock lacks Nissl substance.

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6
Q

What stain can you use to identify astrocytes histologically?

A

GFAP (immunostain)

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7
Q

How do the nuclei of oligodendrocytes contrast from those of astrocytes?

A

Those of oligos are smaller, rounder, stain darker, and usually lack nucleoli.

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8
Q

What are two types of specialized glial cells that resemble epithelial? What makes them not real epithelia?

A

Ependyma and choroid plexus. They lack a basement membrane.

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9
Q

Where are the ependyma located?

A

They line the ventricles.

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10
Q

Where is there choroid plexus?

A

Lateral ventricles and 4th ventricle.

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11
Q

What are the six layers of the neocortex?

A 
I: Molecular
II: External granular
III: External pyramidal
IV: Internal granular
V: Internal pyramidal
VI: Plexiform
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12
Q

What cortex might not have 6 layers? Two specific examples of such structures?

A

Archi/palleocortex has fewer than 6 layers. Hippocampus and cerebellum.

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13
Q

Review: How many layers does the cerebellar cortex have, and what are they?

A

3: Molecular, Perkinje, and Granular. (molecular is outermost)

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14
Q

What are 3 patterns of neuron injury in the CNS?

A

Acute ischemic injury, chronic injury (cell loss), neuronal inclusions

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15
Q

What’s the term for how glial cells respond to injury?

A

Reactive gliosis

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16
Q

2 modes of inflammatory cell response to CNS injury?

A

Microglia-based

Inflammatory infiltrates

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17
Q

Describe the changes that happen to neurons in acute ischemic injury? (3 things)

A

“Red” neuron:
Shrunken cell body, intense cytoplasmic eosinophilia with complete loss of Nissl basophilia, dark nucleus without a nucleolus.

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18
Q

What region of the cerebellum is most sensitive to ischemic injury?

A

The Perkinje cells.

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19
Q

What are 2 types of normal (non-pathological) neuronal cytoplasmic inclusions?

A

Lipofuschin (normal in aging neurons, esp. large motorneurons)
Neuromelanin - seen in catecholaminergic neurons (substantia nigrata, locus ceruleus, dorsal motor nucleus)

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20
Q

What are 3 pathological neuronal inclusions?

A

Cytoplasmic flame-shape neurofibrillary tangles of AD.
Cytoplasmic round Lewy bodies of PD etc.
Intranuclear / cytoplasmic viral inclusions of CMV etc.

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21
Q

3 changes that happen to astrocytes during gliosis?

A

Hypertrophy, hyperplasia, and increased connections

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22
Q

What are 4 ways that infectious organisms access the CNS? Which is most common?

A 
Hematogenous spread (most common)
Local extensions (from paranasal sinuses, middle ear)
Retrograde transport from PNS (eg. HSV, rabies)
Direct implantation (trauma, surgery, intrathecal injection)
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23
Q

4 predisposing factors for CNS infection.

A

Immunosuppression
Mechanical devices / surgical intervention (e.g. shunts)
Anatomical congenital malformations.
Hyposplenism and asplenia (poorer clearance of encapsulated bacteria)

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24
Q

What’s pachymeningitis?

A

Spread of infection into layers of dura mater.

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25
Q

What’s meningitis/leptomeningitis? (What does “lepto-“ mean?)

A

Inflammation of pia and arachnoid. (“Lepto-“ = thin)

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26
Q

What’s encephalitis? (what kind of inflammation / etiological agent)

A

Inflammation of brain parenchyma with mononuclear cells- “chronic inflammation.” Usually caused by viruses.

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27
Q

What’s cerebritis? what kind of inflammation / etiological agent)

A

Inflammation of brain parenchyma with neutrophils - “acute inflammation.” Usually caused by bacteria.

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28
Q

What’s myelitis?

A

Inflammation of spinal cord.

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29
Q

What’s poliomyelitis?

A

Inflammation of spinal gray matter.

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30
Q

What’s ganglionitis?

A

Inflammation of dorsal root ganglia.

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31
Q

What’s radiculitis?

A

Inflammation of intradural spinal nerve roots.

32
Q

Which categories of organisms induce granulomatous inflammation in the CNS? (name 4)

A

Mycobacteria, spirochetes, fungi, parasites

33
Q

With what type of inflammation are microglial nodules associated?

A

Viral encelphalitis.

34
Q

4 CNS compartments for bacterial infection? Processes associated with those compartments?

A

Epidural space - epidural abscess
Subdural spaces - subdural abscess or empyema (pus)
Subarachnoid space - leptomeningitis/meningitis
Parenchyma - abcess, diffuse cerebritis

35
Q

What’s the most common location / process associated with bacterial CNS infection?

A

Leptomeningitis/meningitis in the subarachnoid space.

36
Q

3 most common bacterial species that cause meningitis?

A

S. pneumoniae, N. meningiditis, and H. influenzae

37
Q

3 most common bacterial species that cause meningitis in neonates (0 - 6mo)?

A

Group B Strep
E. coli
L. monocytogenes

38
Q

3 most common bacterial species that cause meningitis is children / adults 6mo - 60 years?

A

S. pneumoniae, N. meningiditis, H. influenzae

39
Q

2 most common bacterial species that cause meningitis in adults > 60 years and immunosuppressed pts?

A

S. pneumoniae, L. monocytogenes

40
Q

2 broad sources of infections that cause brain abscesses?

A

Local (sinusitis-otitis, mastoiditis), hemotogenous

41
Q

2 origins of hematogenous seeding of brain abscesses? Which is most common?

A

Most common: septic emboli, esp. from bacterial endocarditis
Cyanotic congenital cardiac disease (i.e. right to left shunts, ostensibly because venous bacteria are getting pumped straight to the brain)

42
Q

Most common organisms that cause brain abscesses? (name 2+)

A

S. aureus, Streptococci, but often polymicrobial.

43
Q

3 features of the gross pathology of brain abscesses?

A

Discrete, round lesions with central liquefactive necrosis / purulent stuff.
Surroundin fibrotic capsule.
Mass effect, possibly causing herniation.

44
Q

How do brain abscesses appear on imaging?

A

“Ring-enhancing lesions”

45
Q

Describe early vs. late microscopic findings of brain abscesses. About how long does it take for the “late” processes to appear?

A

Early: lots of PMNs
Late: PMNs and debris surrounded by fibroblasitc collagenous capsule.
Capsule starts appearing at about 10 days.

46
Q

What’s the most common form of mycobacterial CNS infection?

A

Tuberculous meningitis.

47
Q

4 pathological features of tuberculous meningitis?

A

Necrotizing granulomas, lymphocytes, multinucleated giant cells, and fibrosis. (Pretty standard stuff for a TB granuloma)

48
Q

3 forms of neurosyphilis?

A 
Meningovascular neurosyphilis
Paretic neurosyphilis (damage to cerebral cortex)
Tabes dorsalis
49
Q

4 features of neuroborreliosis?

A

Aseptic lymphocytic meningitis
Facial nerve palsy
Neuropathies / polyradiculitis
Encephalopathy

50
Q

4 manifestations of CNS viral infections? What tissue is affected in each?

A

“Aseptic” meningitis: Inflammation restricted to meninges.
Polioencephalitis (encephalitis) / poliomyelitis: Hits gray matter.
Panencephalitis/panmyelitis: Hits both gray and white matter.
Leukoencephalitis: Hits white matter.

51
Q

What viruses are most commonly associated with “aseptic” meningitis?

A

Enterovirus (>80%)

52
Q

What viruses are most commonly associated with (polio)encephalitis/poliomyelitis?

A

poliovirus, arboviruses, coxsackieviruses, echoviruses, tick-born, rabies, etc. etc.

53
Q

What viruses are most commonly associated with panencephalitis/panmyelitis?

A

HSV (necrotizing herpresviruses), and many non-necrotizing viruses such as HIV.

54
Q

What viruses are most commonly associated with leukoencephalitis?

A

JC virus, HIV

55
Q

What do you see in an LP of “aseptic” meningitis?

A

Increased lymphocytes and mononuclear cells, absence of bacteria or fungi

56
Q

What type of acute viral encephalitis shows seasonality?

A

That caused by arboviruses (e.g. West Nile Virus)

57
Q

4 pathological features of acute viral encephalitis?

A

Perivascular inflammatory infiltrate
Microglial nodules
Neuronophagia
Intranuclear viral inclusions

58
Q

What pattern of necrosis is classical for HSV-1 encephalitis?

A

Bilateral, assymetric hemorrhagic necrosis of the temporal lobes.

59
Q

What are the only 2 ways you’ll see CMV encephalitis?

A

Intrauterine infection. Immunosuppression.

60
Q

Micro review: Characteristic pathological finding of rabies encephalitis?

A

Negri bodies

61
Q

6 manifestations of CNS fungal infections?

A

Diffuse encephalitis
Leptomeningitis
Fungal mycetoma of the meninges
Space-occupying lesions (granulomas, abscesses)
Septic infarct from vascular invasion/thrombosis
Hemorrhage from mycotic aneurysm formation / rupture

62
Q

Micro review: Microscopic difference between Aspergillus and mucor?

A

Mucor hyphae are wider, non-septate, (and branch at angles closer to 90 degrees)

63
Q

2 classical clinical scenarios associated with mucor?

A

Diabetic ketoacidosis, rhinocerebral disease

64
Q

What’s the one organism we should know about that causes amebic encephalitis?

A

Naegleria fowleri

65
Q

Where do N. fowleri live when causing amebic encephalitis? What do they look like?

A

Live in subarachnoid space. They look somewhat like macrophages. Vesicular nucleus with prominent nucleolus.

66
Q

What’s the most common helminthic CNS disease? How do people get it?

A

Cysticercosis. Eating undercooked pork.

67
Q

Grossly, what does cysticercosis look like?

A

Cysts errywhere. (Parenchyma, meninges, ventricles, and rarely the spinal cord).

68
Q

What are 4 notable CNS infections that hit immunocompromised hosts?

A

Cryptococcal meningitis, toxoplasmosis, HIV encephalopathy, progressive multifocal encephalopathy.

69
Q

Pathology seen in cryptococcal meningitis: Where? What inflammatory cells?

A

Gelatinous, pseudocystic dilations of Virchow-Robin spaces (“bubbles”)
Minimal inflammatory reaction - with lymphos, plasma cells, eosinophils, and multi-nucleated giant cells.

70
Q

Micro review: Classic diagnostic tool for cryptococcus?

A

India ink stain of CNS. But culture or cryptococcal antigen assays usually work fine.

71
Q

Pathological feature of toxoplasmosis?

A

Multiple ring-enhancing lesions - abscesses.

72
Q

What unusual cells are seen in HIV encephalitis?

A

Multinucleated giant cells.

73
Q

What parts of the brain does HIV encephalitis hit?

A

Subcortical white matter, basal ganglia, brainstem.

74
Q

Pathological features of HIV encephalitis? 3-4 things.

A

Widespread low-grade inflammation.
Perivascular and parenchymal lymphos and microglial nodules.
Multinucleated giant cells.
Patchy demyelination and variable gliosis in the white matter (leukoencephalopathy).

75
Q

What virus causes progressive multifocal leukoencephalopathy (PML)?

A

JC Virus

76
Q

For what cells is JC virus tropic?

A

Oligodendrocytes

77
Q

4 pathological features of progressive multifocal leukoencephalopathy?

A

Ill-defined demyelinating lesions
Lipid-laden macrophages
Intranuclear viral inclusions (“Glassy nuclei”)
Bizarre astrocytes with atypia.

Brain and Behavior Part 2 (58 decks)

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