CNS Infections and Neoplasms Flashcards

1
Q

How can infectious agents reach the CNS? Which route its the most common?

A
  • most common: hematogenous spread
  • other routes: direct implantation (due to trauma), local extension (from the skull or spine), and via the peripheral nerves (rabies and herpes zoster)
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2
Q

What is meningitis? What are the three major types? Which is a major medical emergency?

A
  • meningitis is the inflammation of the leptomeninges (pia mater and arachnoid mater) within the subarachnoid space; it also involves the ventricular system
  • major types: pyogenic/bacterial, aseptic/viral, and tuberculous (chronic)
  • pyogenic meningitis is a major medical emergency (fatal if left untreated); luckily, viral meningitis is much more common and less severe
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3
Q

What are the major agents involved in bacterial/pyogenic meningitis for different groups of patients?

A
  • neonates: Escherichia coli, group B streptococci (mainly Strep agalactiae), Listeria monocytogenes, HiB, Streptococci pneumoniae, Neisseria meningitidis
  • children: HiB (especially if unvaccinated), Neisseria meningitidis
  • young adults: N. meningitidis, Strep pneumoniae
  • older adults: Strep pneumoniae, L. monocytogenes
  • open head trauma/surgery: Staphylococcus aureus
  • (L. monocytogenes in age extremities, pregnancy, and immunocompromised; ingested from foods)
  • (note that in neonates, the E. coli and group B strep are from the vaginal canal)
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4
Q

What causes brain abscesses? What symptoms and signs result?

A
  • these are focal, discrete, walled-off lesions that are nearly always due to a bacterial agent (commonly, they occur secondary to bacterial endocarditis)
  • these are SOLs (space occupying lesions) leading to progressive focal deficits and general signs related to raised ICP (morning headaches, papilloedema)
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5
Q

What is encephalitis?

A
  • inflammation of the brain parenchyma; is usually viral
  • this nearly always occurs with a meningeal inflammation (rarely occurs on its own) = viral meningo-encephalitis
  • tends to be less severe and more self-limiting than bacterial meningitis
  • common agents: HSV-1, CMV (in fetuses and immunocompromised), rabies, HIV (affects microglial cells and can progress from there), JC virus (causes progressive multifocal leukoencephalopathy/PML)
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6
Q

What is Creutzfeldt-Jakob Disease (CJD)?

A
  • this is a rapidly progressive, deadly “infection” of the CNS with a prion
  • initial subtle changes in memory progress to coma and death in just 7 months
  • consider this in patients with rapidly developing and progressing dementia
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7
Q

Are primary or metastatic tumors more common in the CNS? Which primary malignant tumor is the most common? Most common benign?

A
  • in the CNS, primary tumors are more common! (prevalence of each is actually about 50%)
  • glioblastoma multiforme is most common malignant tumor in adults
  • meningioma is the most common benign tumor in adults
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8
Q

Where does the CNS receive most of its metastases from? Where do malignant CNS tumors metastasize to?

A
  • CNS gets metastatic disease from lungs, breasts, kidneys, skin, and GIT
  • even the most highly malignant CNS tumors rarely metastasize outside the brain, let alone the CNS
  • (however, medulloblastomas and ependymomas may seed into the CSF and enter the spinal cord/spine)
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9
Q

What are the key clinical features of pyogenic meningitis? What is the classic triad of symptoms for meningitis in general?

A
  • classic triad: nuchal rigidity/stiff neck, headache, and photophobia
  • also: rapid onset (12-24 hours), systemic signs of infection (fever, rash), altered mental state, seizures (20-40%) and increased ICP (raised ICP occurs in more than 90% of cases)
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10
Q

Major investigation for meningitis is lumbar puncture and CSF analysis - compare the CSF in bacterial and viral meningitis.

A
  • bacterial: yellow and cloudy, raised pressure, MANY neutrophils, LOTS of protein, LOW glucose (less than 50% plasma levels)
  • viral: clear, normal/raised pressure, raised lymphocytes, raised protein, normal glucose
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11
Q

What is the mortality rate of bacterial meningitis? How do we treat it? What are the most common residual deficits?

A
  • mortality rate of 10-20% (20% w/ S. pneumoniae; 15% w/ L. monocytogenes; 3-7% w/ HiB, N. meningitides, or group B strep)
  • immediately treat empirically (and then specifically if organism is found) with Vancomycin and Ceftriaxone w/ adjunctive Dexamethasone (to stabilize the BBB)
  • add doxycycline during tick season, and ampicillin if neonate, elderly, immunocompromised (for Listeria monocytogenes)
  • most common residual deficits are deafness, cognitive defects (retardation), and epilepsy
  • note that there are vaccines for HiB, Strep. pneumoniae, Mycobacterium tuberculosis, Neisseria meningitidis, Strep. agalactiae
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12
Q

Neisseria meningitidis

A
  • spread via saliva or aerosol droplets
  • this organism is responsible for meningitis epidemics
  • colonizes the nasopharynx and then spreads hematogenously to the CNS
  • meningitis is commonly preceded by a sore throat
  • associated with purpura fulminans (this severe rash is seen in any severe case of sepsis though) and with Waterhouse-Friderichsen syndrome (adrenal hemorrhage resulting in adrenal gland failure)
  • there is a vaccine
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13
Q

What is the major cause of aseptic/viral meningitis?

A
  • enterovirus (85-90%); specifically the coxsackievirus

- others: HIV, HSV, mumps

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14
Q

How common are noninfectious causes of meningitis? What are some major examples?

A
  • these are very rare
  • drugs (NSAID hypersensitivity)
  • autoimmune disorders (SLE)
  • neoplasm (metastatic carcinoma)
  • chemical agents (anesthetics)
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15
Q

Why do neonates have the highest risk of developing meningitis? What are some other high-risk groups?

A
  • neonates have poorly developed immune systems and relatively permeable BBBs
  • other high-risk groups: children and immunocompromised patients
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16
Q

Which organisms cause acute meningitis (fulminant, progresses in a few hours)? Which cause subacute/chronic meningitis (gradual onset of symptoms over days)?

A
  • acute: viruses; Strep pneumoniae (50%), Neisseria meningitidis (25%), group B Streptococci (mainly Strep agalactiae, 13%), Listeria monocytogenes (8%), Hib (7%)
  • subacute/chronic: Mycobacterium spp, spirochetes (such as Borrelia burgdorferi), Cryptococcus neoformans, Candida spp, Coccidiodes spp
17
Q

What are the major common and serious complications of pyogenic meningitis?

A
  • septic shock, coagulation disorders (especially involving the adrenal glands in Waterhouse-Friderichsen syndrome), endocarditis, pyogenic arthritis, fever
18
Q

What is the pediatric assessment triangle?

A
  • assessment of appearance, breathing, and circulation to skin
  • appearance: “TICLS” tone, interactivity (mental state), consolability, look/gaze, speech/cry strength
  • breathing: body position, pattern of breathing, abnormal sounds
  • circulation to skin: skin color (reflects cardiac output and vital organ perfusion)
19
Q

What is the most common suppurative CNS infection?

A
  • unfortunately, it is bacterial meningitis
20
Q

What is a major potential complication of brain tumors? How do we treat this complication?

A
  • brain herniation due to the raised ICP (because tumors are space occupying lesions)
  • treat herniation and raised ICP/edema with corticosteroids (dexamethasone and mannitol)
21
Q

What is the major chemotherapy drug used to treat malignant gliomas? What about primary cerebral lymphoma?

A
  • Temozolomide for gliomas

- Methotrexate for CNS lymphoma

22
Q

What symptoms and signs are associated with malignancy of the brain?

A
  • general: headache (usually worse upon waking up), cognitive defects, personality changes, gait disorders (usually due to raised ICP/hydrocephalus)
  • focal: hemiparesis, aphasia, visual field defects, seizures
23
Q

What investigations are indicated for patients with suspected CNS malignancy? How can you tell different lesions apart?

A
  • MRI w/ gadolinium contrast (and CT if MRI is contraindicated); the contrast will emphasize lesions that are highly malignant
  • low-grade glioma: no enhancement on contrast, hypointense on T1 and hyperintense on T2/FLAIR
  • meningioma: adjacent to bone, diffuse pattern of enhancement on contrast
  • high-grade glioma (GBM): irregular ring-like enhancement on contrast
  • metastases: multiple, well-circumscribed lesions in the white-grey matter junction, avid and clear enhancement on contrast
  • (follow up the MRI with a biopsy if a lesion is found)
24
Q

Management of Patient with Brain Tumor

A
  • steroids (dexamethasone) for edema and raised ICP and to prevent herniation and mass effect; the return to normal ICP will improve neurologic function
  • anticonvulsants in patients presenting with seizures (however, avoid carbamazepine and phenytoin if patient is on chemo agents)
  • anticoagulation prophylaxis to ALL patients (20-30% develop venous thromboembolism)
  • benign tumors are usually easily resectable, while malignant tumors benefit from radiation and chemo
25
Q

Compare the prevalence of symptoms/signs and the prognosis for high-grade gliomas, low-grade gliomas, meningiomas, and metastatic disease.

A
  • high-grade glioma: 12-15 mo; most prevalent symptoms are headache (50%), cognitive impairment (50%), and hemiparesis (40%); less common are seizures (20%) and aphasia (20%)
  • low-grade glioma: 7-12 yr; most prevalent are seizures (more than 70%) and headache (40%); less common are cognitive impairment (10%), hemiparesis (10%), and aphasia (less than 5%)
  • meningioma: 10-yr survival is 60%; most prevalent are headache (37%), hemiparesis (35%), and cognitive impairment (30%); less common are seizures (17%); aphasia is not seen
  • metastatic: 2-7 mo; most prevalent are cognitive impairment (60%), hemiparesis (60%), and headache (50%); less common are seizures (18%) and aphasia (18%); visual field loss is uncommon (7%), but relatively unique to metastatic disease
26
Q

Glioblastoma Multiforme (GBM)

A
  • a high-grade glioma originating from astrocytes (diffuse astrocytoma vs. pilocytic astrocytoma)
  • most common malignant primary CNS tumor in adults
  • arises in cerebral hemisphere, rapidly progressive, crosses to opposite hemisphere via the corpus callousm(“butterfly glioma”)
  • histo: dense area of necrosis surrounded by high density of highly pleomorphic cells; GFAP positive (because of astrocytic origin)
  • poor prognosis (12-15 months) as surgical resection is usually not possible and chemo/radiotherapy are more palliative than curative
27
Q

Meningioma

A
  • a benign tumor of arachnoid cells
  • most common benign primary CNS tumor in adults; females at greater risk (related to estrogen)
  • these compress underlying parenchyma rather than invading them
  • histo: classic whorled appearance w/ psammoma bodies (collections of calcium)
  • prognosis: 5-year survival is 70%, 10-year is 60%
28
Q

Schwannoma

A
  • a benign tumor or Schwann cells (involves cranial or spinal nerves); usually arising at the cerebellopontine angle
  • CN VIII is the most commonly affected; and in neurofibromatosis type II, bilateral Schwannomas of CN VIII occur
  • prognosis: 7-12 years (low-grade glioma)
29
Q

Oligodendroglioma

A
  • a malignant tumor of oligodendrocytes
  • this is a calcified tumor of the white matter, usually involves the frontal lobe
  • histo: classic “fried-egg” appearance (nucleus surrounded by a halo of clear cytoplasm) and chicken-wire fence capillary pattern
  • prognosis: 7-12 years (low-grade glioma); better prognosis than astrocytomas
30
Q

Pilocytic Astrocytoma

A
  • a benign tumor of astrocytes (pilocytic astrocytoma vs. diffuse astrocytoma)
  • most common CNS tumor in children, usually arising in the cerebellum
  • histo: Rosenthal fibers (thick eosinophilic corkscrew processes), GFAP positive (because astrocytic origin)
  • prognosis: 7-12 years (low-grade glioma)
31
Q

Medulloblastoma

A
  • a highly malignant tumor of cerebellar granular cells
  • usually occurs in children
  • histo: many small, round blue cells w/ Homer-Wright rosettes (blue cells surrounding pink neuritic processes)
  • poor prognosis because of rapid growth (but does respond well to radiotherapy), tendency to seed into the SAS/CSF, causing “drop metastases” in the spinal cord
  • granular cells are NOT glial cells - they are neurons; neurons rarely divide in adults, but DO divide in children
32
Q

Ependymoma

A
  • a malignant tumor of ependymal cells
  • usually seen in children, and usually of the 4th ventricle
  • histo: perivascular pseudorosettes (tumor cells line the blood vessels, giving off the “fake” rosette pattern)
  • poor prognosis
33
Q

Craniopharyngioma

A
  • a benign tumor of EPITHELIAL origin (from remnants of Rathke’s pouch, which give rise to the sella turcica)
  • these classically compress the optic chiasm, leading to bitemporal hemianopsia; classically occur in children
34
Q

Which primary CNS tumors are malignant? Which are benign?

A
  • malignant: glioblastoma multiforme, medulloblastoma, ependymoma, oligodendroglioma
  • benign: meningioma, pilocytic astrocytoma, Schwannoma, craniopharyngioma
35
Q

Poliomyelits damages what part of the CNS? If these symptoms are present at birth, what disorder may the patient have?

A
  • poliovirus targets the anterior horns of the spinal cord, resulting in LMN lesions
  • if this occurs at birth, the child most likely has Werdnig-Hoffman disease (an inherited degeneration disorder of the anterior horns); the neonate is a “floppy baby” and death usually arises within a few years