Infections and inflammations Flashcards

1
Q

What are the common causes of chronic meningitis?

A

TB, fungi

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2
Q

What are the routes of infection for meningitis?

A

Hematogenous spread - paranasal sinus/mastoid infection
Otitis media
Penetrating head injury
Prior surgery

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3
Q

What are the general imaging findings associated with meningitis?

A

Leptomeningeal enhancement and/or ependymal enhancement

High signal CSF on FLAIR - denotes protein (viral, bacterial) in CSF

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4
Q

What is the most common complication in child meningitis?

A

Hydrocephalus

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5
Q

What are the two common complications from adult meningitis?

A

Effusions and empyema

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6
Q

What percentage of meningeal effusions turn into empyema?

What is the most common cause of sterile effusion?

What are the complications associated with subdural empyema?

A

2%

H influenza

Venous thrombosis, infarction, cerebritis, ventriculitis, abscesses

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7
Q

What is the patient population for pyogenic cerebral abscess?

A

10-30yo male with AIDS

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8
Q

What is the main cause of cerebral pyogenic abscess?

What are the routes of infection?

A

Bacteria

Hematogenous spread, paranasal sinusitis, otitis media, meningitis, penetrating head trauma

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9
Q

What are the stages of cerebritis?

A
Early cerebritis (5 days)
Late cerebritis (4-11 days) - central necrosis
Early abscess (10-18 days) - early capsule formation
Late abscess (14-19 days) - rim enhancing lesion, may last up to 8 months
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10
Q

What are the imaging features of a pyogenic cerebral abscess? Early vs late?

A

Early - nonspecific T2 prolongation with heterogenous enhancement

Late - capsule with low T2/FLAIR high T1 signal, SMOOTH THIN capsule (vs glioma or mets), vasogenic edema, rim is thicker on side of grey matter

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11
Q

What is the main difference in the capsule between glioma/mets and cerebritis abscess?

A

Abscess rim is THIN and SMOOTH

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12
Q

What are the restricted diffusion characteristics of abscess? Which bugs have decreased relative restriction?

What does persistent restriction indicate?

A

Cavitary restricted diffusion

TB, toxoplasmosis, fungi may have less prominent restriction

Persistent restriction indicates treatment failure

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13
Q

What bug is most common in viral encephalitis?

A

Herpes type I

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14
Q

Where does HSV 1 reside prior to reactivation?

Where does it infect?

What is the CT/MRI appearance?

A

trigeminal ganglia

Mesial temporal lobe, insula and orbital surface of frontal lobes

CT: often normal, can show ill defined hypoattenuation in the affected regions

MR: bilateral T2 signal in medial temporal lobe, insular cortex, cingulate gyrus, and inferior frontal lobe, restricts diffusion

Gyral enhancement later

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15
Q

Which meningites has a propensity for hemorrhagic transformation?

A

Herpes 1

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16
Q

Who gets HSV2 encephalitis? Where?

A

Inoculation during vaginal delivery

Diffuse meningoencephalitis involving cerebellum

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17
Q

Who gets CMV encephalitis?

Where is the infection?

What are the CNS manifestations?

A

AIDS (

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18
Q

What are the associated findings with neonatal CMV?

A

Chorioretinits, microophthalmia

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19
Q

Periventricular calcifications in the setting of hydrocephalus and fever suggests what?

A

CMV meningitis

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20
Q

Basal ganglia calcification, atrophy, and microcephaly in a neonates suggests what?

A

HIV

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21
Q

What are the characteristic features of HIV encephalopathy?

What is the imaging appearance?

A

Demyelination, gliosis, multinucleated giant cells

MR: Confluent, ill defined T2/FLAIR signal in white matter of FRONTAL and PARIETAL lobes WITHOUT enhancement, diffuse atrophy

Diffuse cerebral atrophy with T2/FLAIR prolongation in periventricular and deep white matter

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22
Q

What is the main difference between HIV encephalopathy and PML?

A

HIV spares the subcortical U fibers and is symmetric

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23
Q

What is PML?, what is the virus?

Who is at risk? What drug associated with MS has a risk?

A

Progressive multifocal leukoencephalopathy

JC virus (papovavirus)

AIDS, transplant, hodgkin lymphoma, CLL, immunodeficiency, SLE, sarcoid, amyloidosis, scleroderma

Natalizumab

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24
Q

What is the pathology of PML?

What cell is affected?

What is the imaging appearance?

A

Demyelination of oligodendrocytes

ASYMMETRIC multifocal white matter lesions with little or no mass effect and NO enhancement

Usually occipitoparietal

INVOLVES subcortical U fibers (unlike HIV)

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25
Q

What is the most common opportunistic infection in AIDS patients? What CD4 count?

A

Toxoplasmosis

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26
Q

What is the imaging appearance of toxoplasmosis? Where does it occur? What is the associated sign?

A

Single or multiple ring enhancing lesions in the BASAL GANGLIA and grey white junctions

Ring enhancing lesions with MARKED surrounding edema

Asymmetric target sign - eccentric nodule of enhancement along the enhancing wall of the toxoplasmosis lesion

DOESNT restrict diffusion

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27
Q

What is the main differential for basal ganglia toxoplasmosis? What are the key distinguishing features

A

Lymphoma - will restrict diffusion, has increased CBV, avid on thallium scan and PET

Tox will respond to treatment in 2-4 weeks, if not consider lymphoma

28
Q

What is the appearance of healed toxoplasmosis?

A

Focal malacia which can calcify

29
Q

Ring enhancing lesion with marked surrounding edema and no restricted diffusion in the basal ganglia

A

Toxoplasmosis

30
Q

What is the appearance of cryptococcus? What is the most common imaging finding?

What location is typical for involvement?

A

Meningitis with mucoid exudate - WIDENING of subarachnoid and perivascular spaces

Most commonly has a NORMAL study, but usually has nonspecific hydrocephalus

Basal ganglia with gelatinous pseudocysts

Spreads to choroid pleus at VENTRICULAR ATRIUMS with intraventricular ring enhancing lesions

31
Q

What are gelatinous pseudocyst

A

Seen in Cryptococcus

Results from spread along basal ganglia prevascular spaces which leaves behing cystic basal ganglia lesions - round water intensity signal lesions on T1/T2

32
Q

What are the bugs associated with the following classic findings?

Cystic basal ganglia lesions
Ring enhancing lesion in basal ganglia
Asymmetric WM lesions involving subcortical U fibers
Symmetric FLAIR without u fiber involvement
Periventricular calcification

A
Cryptococcus
Toxo
PML
HIV
CMV
33
Q

What are the CNS manifestations of TB?

A

Tuberculoma - localized TB granuloma, similar to pyogenic abscess, ring enhancing lesions

Meningitis - basilar cistern, leptomeningeal enhancement

Cerebritis -acutely

34
Q

Where does TB occur in the CNS?

A

Gray white junctions at cerebrum, basal ganglia, cerebellum (kids)

35
Q

Leptomeningeal enhancement in the basal cisterns

A

TB meningitis

36
Q

What is the most common parasitic infection in immunocompetent patients?

A

Cysticercosis

37
Q

What is the most common cause of acquired seizures worldwide?

A

Cysticercosis

38
Q

Where does neurocystercicosis present with lesions?

A

Gray white junction > Intraventricular (4th vent, sylian aqueduct) > subarachnoid space

39
Q

What are the stages of neurocystercicosis?

A

Vesciular: cyst like lesion with mural nodule (scolex), no enhancement

Colloidal: ring enhancing lesion, representing death of cyst with inflammatory reaction (increased diffusion, no restricted)

Granular: cyst wall thickens and edema decreases with involution

Nodular: small parenchymal calcifications with small susceptibilty artifacts

40
Q

Cystic lesion in the ventricle with hyrdrocephalus

A

cystercicosis

41
Q

What is meant by term racemose neurocystercicosis?

A

Variant without visible scolex

42
Q

What are the symptoms with neurosarcoid?

A

CN palsies, aseptic meningitis, hydrocephalus, parenchymal lesions

43
Q

Where does neurosarcoid typically infiltrate?

A

Pituitary, optic chiasm, hypothalamus

44
Q

What is the appearance of neurosarcoid?

A

Nonspecific

Can present as cerebral lesions similar to MS

Can have dural involvement similar to meningioma

Usually enhancing lesions

45
Q

What does enhancement indicate in MS?

A

Active lesions

46
Q

What are the types of MS?

A

Relapsing remitting: partial or complete resolution between attacks

Primary progressive: slow onset without discrete exacerbation

Secondary progressive: Less complete resolution between attacks compared to relapsing remitting

47
Q

What is the pathophysiology of MS?

A

Lymphocytic attack on oligodendrocytes

48
Q

What are dawsons fingers? What are black holes?

A

Periventricular ovioid lesions with T2 prolongation - involves the callosal septal interface

Black holes - dark on T1, associated with more severe demyelination and axonal loss

49
Q

What is tumefactive MS?

A

mass like appearance with ring enhancement

NO MASS EFFECT, distinguishes vs mass

50
Q

What is balo sclerosis?

A

Alternating concentric bands of normal and abnormal myelin

51
Q

What is the marburg variant?

A

FULMINANT MS leading to death within months

52
Q

What is devics disease?

A

Neuromyelitis optica - demyelination of spinal cord and optic nerves

53
Q

Where does NMO occur? What is the confimatory blood test?

A

Periventricular (3rd and 4th) less commonly

Most commonly optic nerves, spinal cord

NMO-IgG - antibody to aquaporin 4

54
Q

What is ADEM? Who gets it? What is the prognosis?

A

Acute Disseminated EncephaloMyelitis

Young kids 5-10yo following viral infection or vaccination

Usually resolve - minority will have permanent sequelae

55
Q

What is the imaging in ADEM?

A

Very similar to MS

Bilateral, asymmetric, well defined hyperintensities

usually involves centrum semiovale

Deep gray matter involvement distinguishes between new onset MS

56
Q

What is the Hurst variant?

A

Acute hemorrhagic leukoencephalitis

Rapidly fulminant form of ADEM that leads to death within days

Multifocal T2 FLAIR hyperintensities with associated WM hemorrhage

57
Q

What are the clinical syndromes in CJD? What are the EEG findings

A

Rapid dementia, myoclonus, mutism

periodic high voltage sharp waves

58
Q

What is the MRI finding in prion disease?

A

Cortical ribboning - ribbonlike FLAIR hyperintensity and restricted diffusion of the cerebral cortex, basal ganglia, and thalamus

Spares motor cortex

Symmetrical high signal in basal ganglia best seen in FLAIR and DWI

Bilateral symmetric involvement of thalamic pulvinar

CT usually shows only atrophy

59
Q

What is the pulvinar sign?

What is the hockey stick sign?

A

Bright DWI and FLAIR within the pulvinar nucleus of the thalamus

Bright DWI and FLAIR within the dorsomedial thalamus

Gyriform enhancement/DWI

60
Q

What disease specifically spares the motor cortex?

A

Prion disease

61
Q

What is rasmussen encephalitis?

What is the clinical syndrome? What age?

A

Chronic focal encephalitis that is progressive and unilateral

Progressive relentless seizures

8-10yo

62
Q

What is the imaging in rasmussen encephalitis?

What are the KEY features?

A

MR: Swelling and T2/FLAIR signal in the cortex and progressive unilateral volume loss; cortical enhancement is rare

PET shows unilateral decreased metabolism

UNILATERAL, lack of enhancement

63
Q

What is the key feature distingushing ring enhancing MS from abscess/mass?

A

Lack of mass effect

64
Q

What is Marchiafava bignami?

A

Fulminany demyelination of corpus callosum in male alcoholics

65
Q

T2 signal and enhancement within mamillary bodies and medial thalamus?

A

Wernicke encephalopathy