Infections and inflammations Flashcards
What are the common causes of chronic meningitis?
TB, fungi
What are the routes of infection for meningitis?
Hematogenous spread - paranasal sinus/mastoid infection
Otitis media
Penetrating head injury
Prior surgery
What are the general imaging findings associated with meningitis?
Leptomeningeal enhancement and/or ependymal enhancement
High signal CSF on FLAIR - denotes protein (viral, bacterial) in CSF
What is the most common complication in child meningitis?
Hydrocephalus
What are the two common complications from adult meningitis?
Effusions and empyema
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?
2%
H influenza
Venous thrombosis, infarction, cerebritis, ventriculitis, abscesses
What is the patient population for pyogenic cerebral abscess?
10-30yo male with AIDS
What is the main cause of cerebral pyogenic abscess?
What are the routes of infection?
Bacteria
Hematogenous spread, paranasal sinusitis, otitis media, meningitis, penetrating head trauma
What are the stages of cerebritis?
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
What are the imaging features of a pyogenic cerebral abscess? Early vs late?
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
What is the main difference in the capsule between glioma/mets and cerebritis abscess?
Abscess rim is THIN and SMOOTH
What are the restricted diffusion characteristics of abscess? Which bugs have decreased relative restriction?
What does persistent restriction indicate?
Cavitary restricted diffusion
TB, toxoplasmosis, fungi may have less prominent restriction
Persistent restriction indicates treatment failure
What bug is most common in viral encephalitis?
Herpes type I
Where does HSV 1 reside prior to reactivation?
Where does it infect?
What is the CT/MRI appearance?
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
Which meningites has a propensity for hemorrhagic transformation?
Herpes 1
Who gets HSV2 encephalitis? Where?
Inoculation during vaginal delivery
Diffuse meningoencephalitis involving cerebellum
Who gets CMV encephalitis?
Where is the infection?
What are the CNS manifestations?
AIDS (
What are the associated findings with neonatal CMV?
Chorioretinits, microophthalmia
Periventricular calcifications in the setting of hydrocephalus and fever suggests what?
CMV meningitis
Basal ganglia calcification, atrophy, and microcephaly in a neonates suggests what?
HIV
What are the characteristic features of HIV encephalopathy?
What is the imaging appearance?
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
What is the main difference between HIV encephalopathy and PML?
HIV spares the subcortical U fibers and is symmetric
What is PML?, what is the virus?
Who is at risk? What drug associated with MS has a risk?
Progressive multifocal leukoencephalopathy
JC virus (papovavirus)
AIDS, transplant, hodgkin lymphoma, CLL, immunodeficiency, SLE, sarcoid, amyloidosis, scleroderma
Natalizumab
What is the pathology of PML?
What cell is affected?
What is the imaging appearance?
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)
What is the most common opportunistic infection in AIDS patients? What CD4 count?
Toxoplasmosis
What is the imaging appearance of toxoplasmosis? Where does it occur? What is the associated sign?
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
What is the main differential for basal ganglia toxoplasmosis? What are the key distinguishing features
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
What is the appearance of healed toxoplasmosis?
Focal malacia which can calcify
Ring enhancing lesion with marked surrounding edema and no restricted diffusion in the basal ganglia
Toxoplasmosis
What is the appearance of cryptococcus? What is the most common imaging finding?
What location is typical for involvement?
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
What are gelatinous pseudocyst
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
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
Cryptococcus Toxo PML HIV CMV
What are the CNS manifestations of TB?
Tuberculoma - localized TB granuloma, similar to pyogenic abscess, ring enhancing lesions
Meningitis - basilar cistern, leptomeningeal enhancement
Cerebritis -acutely
Where does TB occur in the CNS?
Gray white junctions at cerebrum, basal ganglia, cerebellum (kids)
Leptomeningeal enhancement in the basal cisterns
TB meningitis
What is the most common parasitic infection in immunocompetent patients?
Cysticercosis
What is the most common cause of acquired seizures worldwide?
Cysticercosis
Where does neurocystercicosis present with lesions?
Gray white junction > Intraventricular (4th vent, sylian aqueduct) > subarachnoid space
What are the stages of neurocystercicosis?
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
Cystic lesion in the ventricle with hyrdrocephalus
cystercicosis
What is meant by term racemose neurocystercicosis?
Variant without visible scolex
What are the symptoms with neurosarcoid?
CN palsies, aseptic meningitis, hydrocephalus, parenchymal lesions
Where does neurosarcoid typically infiltrate?
Pituitary, optic chiasm, hypothalamus
What is the appearance of neurosarcoid?
Nonspecific
Can present as cerebral lesions similar to MS
Can have dural involvement similar to meningioma
Usually enhancing lesions
What does enhancement indicate in MS?
Active lesions
What are the types of MS?
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
What is the pathophysiology of MS?
Lymphocytic attack on oligodendrocytes
What are dawsons fingers? What are black holes?
Periventricular ovioid lesions with T2 prolongation - involves the callosal septal interface
Black holes - dark on T1, associated with more severe demyelination and axonal loss
What is tumefactive MS?
mass like appearance with ring enhancement
NO MASS EFFECT, distinguishes vs mass
What is balo sclerosis?
Alternating concentric bands of normal and abnormal myelin
What is the marburg variant?
FULMINANT MS leading to death within months
What is devics disease?
Neuromyelitis optica - demyelination of spinal cord and optic nerves
Where does NMO occur? What is the confimatory blood test?
Periventricular (3rd and 4th) less commonly
Most commonly optic nerves, spinal cord
NMO-IgG - antibody to aquaporin 4
What is ADEM? Who gets it? What is the prognosis?
Acute Disseminated EncephaloMyelitis
Young kids 5-10yo following viral infection or vaccination
Usually resolve - minority will have permanent sequelae
What is the imaging in ADEM?
Very similar to MS
Bilateral, asymmetric, well defined hyperintensities
usually involves centrum semiovale
Deep gray matter involvement distinguishes between new onset MS
What is the Hurst variant?
Acute hemorrhagic leukoencephalitis
Rapidly fulminant form of ADEM that leads to death within days
Multifocal T2 FLAIR hyperintensities with associated WM hemorrhage
What are the clinical syndromes in CJD? What are the EEG findings
Rapid dementia, myoclonus, mutism
periodic high voltage sharp waves
What is the MRI finding in prion disease?
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
What is the pulvinar sign?
What is the hockey stick sign?
Bright DWI and FLAIR within the pulvinar nucleus of the thalamus
Bright DWI and FLAIR within the dorsomedial thalamus
Gyriform enhancement/DWI
What disease specifically spares the motor cortex?
Prion disease
What is rasmussen encephalitis?
What is the clinical syndrome? What age?
Chronic focal encephalitis that is progressive and unilateral
Progressive relentless seizures
8-10yo
What is the imaging in rasmussen encephalitis?
What are the KEY features?
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
What is the key feature distingushing ring enhancing MS from abscess/mass?
Lack of mass effect
What is Marchiafava bignami?
Fulminany demyelination of corpus callosum in male alcoholics
T2 signal and enhancement within mamillary bodies and medial thalamus?
Wernicke encephalopathy
