Neuro -- Infection

Front 1

1. What determines the severity of findings in congenital CMV?
2. What are the imaging findings in congenital CMV?
3. What is the pattern of congenital toxoplasmosis?

Back 1

1. The SEVERITY of the findings is directly related to the GESTATIONAL AGE of the fetus at the time of infection.
Earlier infection = severe migrational and developmental anomalies.
Early second trimester infection = complete lissencephaly.
Later second trimester infection = Polymicrogyria.
Third trimester infection = Normal gyral pattern or focal areas of polymicrogyria.
2.
- VENTRICULAR ENLARGEMENT due to hydrocephalus or brain atrophy.
- PERIVENTRICULAR pattern of CALCIFICATIONS
- LENTICULOSTRIATE calcifications
- Paraventricular subependymal cysts
- DISTURBED neuronal MIGRATION (lissencephaly, cortical dysplasia)
- Cerebellar hypoplasia/dysplasia.
3. Toxoplasmosis:
- No migrational abnormalities
- Scattered pattern of calcifications.

Front 2

1. What are the imaging findings in congenital toxoplasmosis?
2. How do you differentiate Toxo from CMV infection?
3. What happens to the calcifications after treatment?

Back 2

1.
- Ventricular dilation (not cerebral atrophy as there is normal sulci)
- Scattered calcifications
- Areas of encephalomalacia
- Bilateral chorioretinitis
2.
- Like CMV the earlier the infection with Toxo, the more severe the findings.
- Calcifications in Toxo are scattered, whereas in CMV they are periventricular.
- CMV is associated with cortical dysplasia whereas Toxo is not.
- Toxo has areas of encephalomalacia; CMV does not.
3. After treatment, intracranial calcifications may regress or even resolve over time. This correlates with intensity of antimicrobial therapy and is accompanied by neurological improvement.

Front 3

1. How does primary HSV-2 infection in neonates differ from reactivated latent HSV-1 or HSV-2 infection in older children and adults
2. How is HSV-2 acquired?
3. When do infants present with HSV-2 encephalitis?
4. What are the extra-cranial manifestations of systemic infection?
5. What are the early findings in HSV-2 encephalitis?
6. What are the late findings in HSV-2 encephalitis?

Back 3

1. Primary HSV-2 infection in neonates causes a diffuse brain infection; whereas, HSV-1 predominantly affects the inferior frontal and temporal lobes.
2.
- Contact with active herpetic lesion in the vagina during delivery: Most common.
- Hematogenous transplacental infection: rare.
3. Infants usually present in the first 2-4 weeks of life with fever, irritability, and lethargy.
4. DIC and hepatic failure may be seen.
5.
- Hypodensity in the periventricular white matter and cortex due to brain edema. NOTE: edema may be difficult to detect in unmyelinated brain; a clue to cortical edema is isointensity of cortex to white matter.
- Leptomeningeal enhancement.
6.
- High density in the cortex due to petechial hemorrhage and calcifications.
- Brain atrophy
- Multicystic encephalomalacia resulting in a "Swiss Cheese" appearance.

Front 4

1. What is the most common CNS infection in children?
2. What is the etiology of meningitis in infants?
3. What are the imaging findings of uncomplicated meningitis?
4. What are the findings of complicated meningitis?

Back 4

1. Meningitis
2. GBBS which is acquired during the passge through an infected birth canal or caused by an ascending infection in the setting of PROM.
3. Manifestations of uncomplicated meningitis:
- Normal study
- Communicating hydrocephalus
- Leptomeningeal and/or ependymal enhancement.
4. Manifestation of complicated meningitis:
- Arterial infarction 2/2 infectious vasculopathy.
- Venous thrombosis 2/2 sepsis or dehydration
- Brain abscess
- Subdural or epidural empyema

Front 5

1. What are the common organisms to cause meningitis in older neonates and children?
2. What is more common: viral or bacterial meningitis?
3. What is the DDX of sudural fluid collection?
4. What is the etiology of subdural effusion in the setting of meningitis?
5. What findings favor subdural empyema over subdural effusion?

Back 5

1. H. influenza, pneumococcus, and meningococcus.
2. Viral meningitis is more common than bacterial meningitis.
3.
- Benign enlargement of the subarachnoid space.
- Prior trauma
- Subdural effusion
- Subdural empyema
4. Irritation of the meninges with transudative fluid.
5.
- Hyperintensity on FLAIR
- Marked dural/pial enhancement
- Empyema are usually unilateral; effusions are usually bilateral.

Front 6

1. What percentage of infants born to HIV+ mothers get infected with HIV?
2. What are the imaging findings in congenital HIV infection?
3. What are the complications of CNS HIV/AIDS?

Back 6

- Congenital HIV infection occurs in ~30% of infants born to HIV infected women
- Risk of infection varies with maternal plasma titers of the HIV virus.
2.
- Cerebral atrophy (prominence fo ventricles and sulci).
- Calcifications in the basal ganglia and subcortical white matter of the frontal lobes
3.
- Lymphoma
- Toxoplasmosis
- PML
- HIV associated vasculopathy resulting in intracranial hemorrhage and infarction.

Front 7

1. What is the DDX of diffuse cerebellar inflammation (cerebellitis)?
2. What are the imaging findings of cerebellitis?

Back 7

1.
- Infectious (viral) or more often parainfectious
- Demyelinating processes (ADEM)
- Vasculitis
- Toxic exposures
- Paraneoplastic syndrome (associated with lung or breast cancer).
2.
- Diffuse low attenuation throughout the cerebellar hemispheres
- Effacement of the 4th ventricle and prepontine cisterns.
- Hydrocephalus.
- Variable enhancement
- Late scans demonstrate volume loss/encephalomalacia.

Front 8

1. What are the major routes that result in cerebral abscess formation?
2. What are the complications of brain abscess?
3. What are the causes of abscess in post-transplant pts?
4. What are the causes of abscess in HIV pt?

Back 8

1.
- Hematogenous spread from extracranial stie of infection.
- Right to left shunt from congenital cardiac malformations or pulmonary arteriovenous fistulas
- Direct extension from infected paranasal sinuses or mastoid air cells.
- Direct implantation of organisms in the setting of surgery or trauma.
2.
- Ventriculitis (enhancement of the ependymal surface).
- Rupture into the subarachnoid space
- Choroid plexitis (enlarged intensely enhancing plexus)
- Formation of daughter abscesses
3. Aspergillus, Nocardia, Candida.
4. Toxoplasmosis, TB

Front 9

1. What part of the neuroaxis is affected by neurocysticercosis?
2. What are the 4 stages seen in the brain parenchyma?
3. What is the appearance of neurocysticercosis in the subarachnoid space?
4. What is the appearance of neurocysticercosis in the ventricles?

Back 9

1. Neurocysticercosis may affect the brain parenchyma, subarachnoid spaces, ventricles, and spinal cord.
2.
VESICULAR STAGE:
- viable organism exists as a thin walled vesicle (<2 cm in size) containing CSF like fluid
- mural nodule representing the scolex is usually seen.
- inflammatory response is minimal or absent.
COLLOID STAGE:
- viable cyst dies
- cyst fluid becomes a turbid colloid suspension with antigenic material leaking across the cyst wall.
- Inflammatory reaction leads to breakdown of BBB with lesion demonstrating surrounding edema and peripheral enhancement.
NODULAR GRANULAR STAGE:
- lesion undergoes involution and begins to calcify.
- Solid nodule or thick ring of enhancement.
CALCIFIED STAGE:
- lesion is shrunken and completely mineralized.
3.
- Multiple vesicles which are often large and lack a scolex (known as racesoe form--grapelike).
- Progression to the colloid stage leads to exudative inflammation of the meninges (meningeal enhancement).
- Inflammation leads to arteritis leading to parenchymal infarction.
- Calcifications are not seen in the subarachnoid space.
4. One or severeal cysts may be seen within the ventricle. Obstrution may occur at the level of foramen of monro or cerebral aqueduct.


NOTE: Same pt may harbor lesions at different stages.

Front 10

1. How can TB affect the brain?
2. What does the LP reveal?
3. How does a tuberculoma differ from tuberculous abscess?
4. What are the stages of tuberculoma?

Back 10

1. From a pulmonary source, the bacilli disseminate hematogenously to the cerebrum resulting in
- Meningitis
- Tuberculous granulomas (intracranial or spinal).
- Tuberculous abscess (rare; more commonly seen in pts with HIV).
- Osteomyelitis of skull or spine.
2. Low glucose levels
3. Tuberculomas occur in immunocompetent pts; tuberculous abscess occurs in HIV pts.
4.
- Cerebritis stage: nonspecific edema, ill-defined enhancement.
- Solid granulomatous stage: enhancing nodules with surrounding edema.
- Central caseation stage: central HYPOINTENSITY on T2WI.
- Involution stage: multiple calcified nodules.

Front 11

1. What is the most common cause of CNS mass lesion in a pt with HIV?
2. What are the imaging findings in CNS toxoplasmosis?
3. What findings distinguish lymphoma from CNS toxo?

Back 11

1. CNS toxoplasmosis.
2.
- Multifocal lesions with surrounding edema; solitary in 30%.
- Can affect any area but the basal ganglia is a favored site.
- Small lesions enhance in a nodular fashion.
- Larger lesions enhance peripherally with a rim of variable thickness.
- ECCENTRIC TARGET SIGN refers to eccentric enhancing nodule adjacent to the peripherally enhancing rim of the lesion.
- After therapy, lesions may completely regress or may calcify.
3. Lymphoma demonstrates ependymal or subarachnoid spread of disease. Lymphoma may also be dense on NECT.

Front 12

1. What are the imaging findings of lyme disease?
2. What is the DDX?

Back 12

1.
- Patchy white matter lesions with variable enhancement.
- Leptomeningeal enhancement
- Cranial nerve enhancement.
2.
- MS: frequent involvement of the CC, enhancement of cranial nerves does not occur except CNII.
- ADEM
- Vasculitis
- Sarcoidosis

Front 13

1. What patient population is at risk for developing aspergillus infection?
2. What is the pattern of involvement in the CNS?
3. What is characteristic of fungal and TB abscesses on MRI?
4. What are some important points about aspergillosis?

Back 13

1.
- Organ transplant recipients
- pts with hematologic malignancies
- Diabetics
- Pts on corticosteroids
- Pts on chemotherapy
- AIDS
2.
- Abscesses with hemorrhagic necrosis.
- Angioinvasion resulting in large-vessel thrombosis (stroke) and/or mycotic aneurysm formation (subarachnoid hemorrhage).
- Meningitis with leptomeningeal inflammation.
3. Fungal and TB abscess are T2 hypointense centrally.
4.
- Suspect Aspergillosis in an immunocompromised host who develops paranasal sinusitis, proptosis, mastoiditis, unexplained infarction, and/or cerebral abscess.
- Pts who are immunocompromised or on steroids may manifest little or no enhancement of parenchymal abscesses.
- In a patient with paranasal sinus aspergillus infection, dural enhancement indicates intracranial extension.

Front 14

1. What is the ddx of confluent white matter disease?
2. What are the imaging findings in HIV encephalopathy?

Back 14

1.
- HIV encephalopathy
- PML
- Vasculitis
- Leukoencephalopathies (toxic, radiation, metabolic)
2.
- Cerebral atrophy
- SYMMETRIC areas of high T2 SI with a predilection for the frontal white matter and genu of corpus callosum.
- Subcortical U fibers are spared.
- No mass effect or enhancement.
- MR SPECT demonstrates reduction in N-aceyl aspartate.

Front 15

1. What is the cause of PML?
2. What are the imaging findings in PML?

Back 15

1. PML is a progressive demyelinating disease from infection with the JC virus in immunocompromised pts.
2.
- Cerebral atrophy
- ASYMMETRIC, multifocal areas low T1 and high T2 SI in the white matter involving the parieto-occipital lobes.
- Involves the subcortical U fibers.
- May involve any portion of the brain including the posterior fossa (cerebellum).
- Mass effect, hemorrhage, and enhancement are usually absent or are mild if present.

Front 16

1. What are the patterns of CNS involvement by cryptococcus?
2. What are the imaging findings of gelatinous pseudocysts?
3. What do cryptococcal pseudocyst mimic on imaging?
4. What are the imaging findings of cryptococcomas?

Back 16

1. Meningitis, Gelatinous pseudocyst, Cryptococcomas.
2.
- Expansion of perivascular spaces in the basal ganglia, thalamus, and midbrain that occurs due to accumulation of mucinous material, inflammatory cells, and organisms. May demonstrate peripheral enhancement.
3. Cryptococcal pseudocysts mimic prominent perivascular spaces and lacunar infarcts.
4. Scattered focal enhancing lesions with vasogenic edema. Looks similar to tuberculoma, oother fungal granuloma, or lymphoma.

Front 17

1. What are the imaging findings of CMV ventrinculoencephalitis?
2. What processes CMV ventriculitis?

Back 17

- Focal or diffuse hyperintensities in the white matter (mimics HIV encephalopathy and PML).
- Ependymal periventricular T2 hyperintensity and enhancement; Ependymal enhancement is never normal; On T2/FLAIR, look for thick irregular, or asymmetric high signal (thin, regular rim of high SI is normal).
2.
- Bacterial ventriculitis: may be a complication of ruptured abscess or placement of ventricular shunt.
- CNS lyphoma may occasionally demonstrate thin, regular periventricular enhancement; however, typically, the enhancement is more nodular and irregular.

Front 18

1. What are the complications of sinusitis?

Back 18

1.
- Subdural/epidural empyema
- Thrombosis of cortical veins or dural sinuses with secondary venous infarction.
- Cerebritis/abscess formation.

Front 19

What are common CNS infections seen in pts with AIDS?

Back 19

1. HIV (results in HIV encephalopathy)
2. Toxoplasmosis
3. Cryptococcus
4. TB

Front 20

1. What are the imaging findings of herpes encephalitis?
2. Herpes encephalitis spares what region of the brain?
3. What is the DDX of increased T2 SI in the temporal lobe?
4. What is the etiology of herpes encephalitis in children and adults?
5. What is the etiology of herpes encephalitis in children and neonates?

Back 20

1. Low T1 and high T2 SI in the mesotemporal lobe is an early sign. Later, the insula, inferior frontal lobes, and cingulate gyrus demonstrate a bilateral, asymmetric, abnormally high T2SI. Enhancement is present in areas of cortical involvement.
2. Herpes encephalitis spares the putamen and basal ganglia.
3. Infarct, low grade glioma
4. HSV-1. It is thought that it penetrates the oral mucosa and infiltrates the gasserian ganglion. When it reactivates, it spreads towards the limbic strucures in the frontal and temporal lobes through branches of the trigeminal nerves.
5. Neonatal herpes encephalitis is caused by HSV-2.
6. Ddx: limbic encephalitis, infiltrating glioma, status epilepticus, ischemia.

Front 21

1. What is the etiology of progressive multifocal leukoencephalopathy (PML)?
2. What is the patient population that is prone to developing PML?
3. What are the imaging findings of PML?

Back 21

1. PML is secondary to infection by JC virus. Viral infection of oligodendrocytes leads to myelin destruction and lymphocytic infiltration.
2. PML is seen in pts with leukemia, immunosuppression, transplant, HIV.
3.
- Multiple subcortical areas of increased signal on T2 and decreased Sl on T1WI within the white matter with sparing of the cortex.
- Lesions do not enhance and show no evidence of mass effect distinguishing them from metastatic disease.