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Pathophysiology - Neurology > Pathology of Brain Tumors and Infections > Flashcards

Pathology of Brain Tumors and Infections Flashcards

1
Q

Where do most brain tumors in children arise and what are the most common examples?

A

Posterior fossa / infratentorial

Pilocytic astrocytoma
Ependymoma
Medullablastoma

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2
Q

What are the most common brain tumors of adults and where do they arise?

A

More commonly in the supratentorial region

Metastases (carcinomas, not seen in children)
Astrocytomas
Meningiomas

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3
Q

What are the clinical symptoms of most brain tumors?

A

Increased ICP -> headache, papilledema, due to mass effect

Local damage to structures -> focal neural deficits

Damage to cerebral cortex -> seizures

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4
Q

What does benign vs malignant mean for primary brain tumors and what is their prognosis generally based on?

A

Distinction is difficult and useless as CNS tumors rarely metastasize outside of CNS -> better to judge based on histological criteria (low grade vs high grade)

Ultimately, prognosis depends on location and resectability rather than histologic type. The same tumor can have widely different outcomes depending on where it forms

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5
Q

What does WHO grades for primary brain tumors mean?

A

Grades 1-2 = Low grade, relatively good long-term prognosis

Grades 3-4 = High grade, relatively poor long-term prognosis

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6
Q

What is the largest family / most common type of primary brain tumor?

A

Diffuse gliomas

-> usually derived from astrocytes or oligodendrocytes

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7
Q

What is meant by a solid vs infiltrative growth pattern and which is harder to treat?

A

Solid - well-circumscribed, easily resectable mass

Infiltrative - tumor infiltrates between normal tissue. Generally not amenable to resection because surgery would take normal brain with it

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8
Q

What is a grade IV astrocytoma called? What is its growth pattern?

A

Glioblastoma multiforme

Growth pattern is pseudopalisading
- tumor cells border areas of necrosis and hemorrhage

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9
Q

What is the most common brain tumor of adults, and what is it called when it crosses the corpus callosum?

A

Glioblastoma multiforme

Called a “butterfly glioma”

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10
Q

What is a normal Ki-67 value for brain tissue?

A

0% -> nothing should be dividing unless there was damage causing gliosis

Thus, even small values of Ki-67 can indicate a tumor

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11
Q

What molecular abnormalities characterize oligodendroglioma and what is its clinical presentation? What area of the brain is usually involved?

A

Codeletion of 1q and 19p chromosomes, and isocitrate DH

Clinical presentation - slow-growing tumor in young adults which may contain calcifications. Most often in frontal lobe, causing seizures

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12
Q

What is characteristic of the histology of oligodendroglioma?

A

Fried egg cells - round nuclei with clear cytoplasm
-often calcified

Represents oligodendrocytes

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13
Q

What is the most common CNS tumor in children and where does it tend to arise in adults and children? Include the disease association.

A

Pilocytic astrocytoma - low-grade astrocytoma which does not progress like diffuse gliomas

Children - cerebellum
Adults - cerebral cortex, spinal cord, or associated with optic nerve (optic glioma of NF-1)

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14
Q

How does pilocytic astrocytoma appear grossly and microscopically?

A

Grossly - cystic lesion with nodular mass which grows adjacently on its wall.

Microscopically - Rosenthal fibers -> thick, eosinophilic aggregates of alpha-B-crystalline which accomulates in processes of astrocytes

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15
Q

What tumor is characterized by perivascular pseudorosettes? Why does it form this pattern, and who tends to get it?

A

Ependymoma - tumor of ependymal cells which form rosettes around vasculature -> similar to choroid-plexus type function

Tends to be in children, but can also appear in adults in the spinal cord or ventricles

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16
Q

Where do ependymomas tend to grow, and what is their clinical presentation?

A

Typically children with hydrocephalus - grows out from a stalk into the 4th ventricle, obstructing CSF flow -> symptoms of increased ICP

Has poor prognosis

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17
Q

Who tends to get choroid plexus tumors and what is the major presenting symptom?

A

Tends to occur in children, even infants -> symptom is often congenital hydrocephalus (if in infants) -> overproduction of CSF, or blockade of outflow

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18
Q

What is the most common type of embryonal tumor and who does it tend to occur in? What is the pattern of growth and metastasis?

A

Medulloblastoma - occurs in children

Grows in cerebellum, compressing 4th ventricle and causing noncommunicating hydrocephalus

Disseminates into subarachnoid space and even outside CNS

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19
Q

What is “drop metastasis”?

A

Metastasis to cauda equina -> lower spinal cord

-> spread of medulloblastoma thru CSF

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20
Q

What is the microscopic appearance of medulloblastoma?

A

Homer-Wright Rosettes - small round blue cells wrapping radially around pink neuritic processes (neuropil).

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21
Q

What is the most common benign CNS tumor in adults and who tends to get it? What is the cell of origin?

A

Meningiomas - more commonly seen in women because it expresses the estrogen receptor

Cell of origin - arachnoid cells (neural crest derived)

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22
Q

What chromosome is frequently associated with meningiomas?

A

Chromosome 22 deletions

-> reason why NF-2 is associated with meningiomas

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23
Q

What is the microscopic morphology of meningioma?

A

Spindle cells concentrically arranged in a whorled pattern

-> forms calcified “psammoma bodies”

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24
Q

What are the symptoms of meningioma? Where are the tumors?

A

They are “extra-axial” tumors which typically lie in the superior sagittal sinus

Seizures or focal neurologic signs
-> due to compression of underlying brain and increased ICP

25
Q

How do tumors of Schwann cells affect neural function?

A

By mass effect -> interference of nerve conduction of cranial nerves or peripheral neurons

26
Q

How is a Schwannoma different from a neurofibroma, and what genetic disease is associated with each?

A

Schwannoma - generally grow as solid masses - often associated with NF-2 (bilateral acoustic Schwannoma)

Neurofibromas - infiltrative growth pattern in nerve - associated with NF-1 - unable to resect without nerve damage

27
Q

What is considered the AIDS-defining brain tumor and what co-infection is it associated with?

A

Primary CNS lymphoma - associated with EBV infection

This is a high-grade B cell lymphoma

28
Q

Who gets primary CNS lymphoma and what is it growth pattern?

A

Elderly or immunosuppressed individuals (especially HIV)

May be solid or infiltrative in its growth pattern

29
Q

Where do primary CNS germ cell tumors tend to arise?

A

Pineal gland (pinealoma) and hypothalamus

30
Q

What are common sources of metastatic cancer to the brain?

A

Lung carcinoma, breast carcinoma, malignant melanoma

Others: Kidney, GI tract, systemic symphomas

31
Q

What is Leptomeningeal carcinomatosis? What does it mimic?

A

Spread of tumor cells into subarachnoid space and through CSF
-> mimics acute or chronic leptomeningitis due to high CSF protein, hydrocephalus, and involvement of multiple cranial and spinal nerve roots

32
Q

What is cerebritis vs encephalitis?

A

Cerebritis - focal abscess of brain parenchyma

Encephalitis - disseminated infection of brain parenchyma

33
Q

What is meningoencephalitis vs myelitis vs encephalomyelitis?

A

Meningoencephalitis - diffuse meningeal (layers of mater) and parenchymal process

Myelitis - inflammation localized to spinal cord, often immune-mediated

Encephalomyelitis - involving gray or white matter throughout the nervous system

34
Q

What are the routes of CNS infection?

A
  1. Hematogenous - most common
  2. Direct implantation - traumatic or iatrogenic
  3. Local extension - from skull or sinuses
  4. Axonal transport - i.e. herpesviruses (retrograde)
  5. CSF pathways - to disseminate
35
Q

What are Brudzinski’s and Kernig’s signs and what are they indicative of?

A

Indicative of acute meningeal irritation

Brudzinski - “B”ringing the neck forward in flexion -> observe for any flexing of hips and knees

Kernig sign - Starting from flexed hip / knee - extension of knee is resisted

36
Q

What are the CSF findings of acute purulent (usually pyogenic bacterial, but maybe fungi in immunosuppressed or even protozoans) leptomeningitis?

A 
Elevated pressure (>200mmHg)
Elevated protein (>50 mg/dL)
Decreased glucose (<40 mg/dL) -> use by organisms / immune system
Leukocytosis - mainly PMNs
Organism detectable by gram stain
37
Q

What is Waterhouse-Friderichsen syndrome?

A

Syndrome associated with Neisseria meningitidis (meningococci)
-> adrenal insufficiency, fever, DIC, septic shock

38
Q

What is acute lymphocytic meningitis generally caused by and what agents can cause a similar syndrome?

A

Viral agents - usually enteroviruses “aseptic meningitis”

Similar syndromes caused by carcinomatous meningitis (cancer), chemicals / drugs

39
Q

How does the clinical syndrome of aseptic meningitis differ from acute purulent meningitis?

A

Systemic signs of fever / headache are still there, but it is generally milder and does not cause significant alteration in levels of consciousness. Mild and self-limiting.

-> acute purulent often causes focal CNS signs, seizures, and alteration of consciousness

40
Q

What does protein, glucose, WBC count, and % PMNs show for aseptic meningitis?

A

Protein - mild elevation
Glucose - unchanged / normal**
WBC - very mild leukocytosis
%PMNs - elevated early. If done later -> mostly lymphocytes

41
Q

What is chronic meningitis and what is it caused by?

A

Chronic inflammatory process of leptomeninges

  • > relatively persistent or indolent agents
  • > TB, sarcoidosis, meningovascular syphilis, etc
42
Q

How is chronic meningitis diagnosed? CSF characteristics?

A

Non-specific findings of slowly evolving headache, low-grade fevers, rarely seizures / cognitive dysfunction. Difficult to diagnose.

CSF - increased pressure due to blockage of CSF flow
Increased protein
Decreased glucose, but not as much as acute
Leukocytosis - predominantly lymphocytes and monocytes (forming granulomas)

43
Q

What is the brain pathology seen in chronic meningitis?

A

Basal meningitis - mononuclear inflammation and fibrosis seen most prominently in the base of the brain

Granulomas may be present depending on agent

44
Q

What are the two main locations which empyemas / abscesses fall in?

A
  1. Subdural / epidural empyema

2. Brain parenchymal abscess - “cerebritis”

45
Q

What are the clinical consequences of chronic meningitis longterm?

A

Progressive fibrosis:

  1. Non-obstructive or obstructive hydrocephalus
  2. Damage to blood vessels with sclerosis - obliterative endarteritis
  3. Vascular insufficiency due to blood vessel damage
46
Q

What defines a true abscess and what are some possible clinical outcomes?

A

Formation of fibrous capsule around abscess

Possible: mass effect increases ICP, leakage into subarachnoid space by rupture -> septicemia and acute meningitis, focal neurological deficits

-needs drainage and surgical removal

47
Q

What part of the brain does acute viral encephalitis affect? Is it lytic?

A

Affects whatever part of the brain that particular virus infections via its cell tropism

Can be lytic or non-lytic

Symptoms vary depending on which cells are affected

48
Q

What type of encephalitis does HSV1 cause?

A

Necrotizing encephalitis of medial temporal lobes

-> due to retrograde axonal transport via olfactory nerve into temporal lobes

49
Q

Where do CMV and polio affect?

A

Polio - Lower motor neuron paralysis via anterior horn cell destruction

CMV - periventricular tissues, especially in congenital infection

50
Q

What cells does Rabies affect?

A

Pyramidal cells of the hippocampus (think of pyramid in boat with seahorse) + Purkinje cells of cerebellum (think of bungee cords from tree (folia of cerebellum)

Cytoplasmic inclusions = Negri bodies

51
Q

What are the Arboviruses which cause encephalitis?

A

Transmitted by arthropod vectors

Flaviviruses - I.e. West Nile

Togaviruses - i.e. Eastern equine encephalitis

52
Q

How does virus usually spread to the brain, and how is encephalitis diagnosed?

A

Sometimes by axonal transport, but usually hematogenous spread

  • > Diagnosed via index of suspicion especially following aseptic CSF findings
  • > can do PCR assay for virus (HSV1 most common)
53
Q

What are a few examples of agents causing chronic “slow” viral hepatitis?

A

HIV - AIDS dementia

JC virus - PML

Measles - SSPE

HTLV-1 - tropical spastic paraparesis

54
Q

How are PML and AIDS dementia related?

A

PML is much more likely in patients with HIV -> reactivation of latent JC virus

55
Q

What are the features of PML? How is it treated?

A

Infection and destruction of oligodendrocytes -> progressive demyelination (nonenhancing lesions on CT)

Can treat by improving immune status if due to immunosuppression

56
Q

What is the pathogenesis of meningitis in HIV?

A

Acute - can cause acute aseptic meningitis during primary infection

Chronic HIV encephalitis - progressive dementia and infected monocytes / T cells cross BBB and infect microglia / damage white matter -> progressive demyelination like PML

57
Q

What are common opportunistic CNS infections assocatied with HIV?

A

Toxoplasma cerebritis - multiple ring-enhancing abscesses on CT

Cryptococcus meningitis + encephalitis (soap bubble lesions)

PML

CMV encephalitis

58
Q

What are the only true epithelial tumors of the CNS which can be classified as benign vs malignant?

A

Choroid plexus tumors (epithelial cells)

Benign - Choroid plexus papilloma

Malignant - Choroid plexus carcinoma

Pathophysiology - Neurology (21 decks)

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