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Viral Infections of CNSDr. Sunil Kumar SharmaSenior ResidentDept. of NeurologyGMC Kota
Viral Infections of CNSHundreds of viruses exhibit tropism for the central (CNS) and/or peripheral (PNS) nervous systems.
Viral infection of the nervous system can result in a variety of clinical presentations including acute or chronic meningitis, encephalitis, myelitis, ganglionitis, and polyradiculitis.
Viruses may also incite para- or postinfectious CNS inflammatory or autoimmune syndromes -(ADEM)
VIRUSES THAT CAUSE MENINGOENCEPHALITIS
Herpes simplex virus (HSV-1, HSV-2)
Other herpes viruses: varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpes virus 6 (HHV6)
Adenoviruses
Influenza A
Enteroviruses, poliovirus
VIRUSES THAT CAUSE MENINGOENCEPHALITIS
Measles, mumps and rubella viruses
Rabies
Arbovirusesfor example, Japanese B encephalitis, St Louis encephalitis virus, West Nile encephalitis virus, Eastern, Western, and Venezuelan equine encephalitis virus, tick borne encephalitis viruses, Chandipura virus, Dengue virus, chikungunya, KFD.
VIRUSES THAT CAUSE MENINGOENCEPHALITIS
Bunyavirusesfor example, La Crosse strain of California virus
Reovirusesfor example, Colorado tick fever virus
Arenavirusesfor example, lymphocytic choriomeningitis virus
Paramyxovirus Nipah virus, hendra virus
HERPES ENCEPHALITIS
Herpes simplex encephalitisMost common endemic encephalitis in the USA , causes 10-20% of all viral encephalitis.
In India exact incidence is not known.
Early diagnosis is important.
HSV1 causes 95% of HSE.
HSV2 causes 80-90% of neonatal encephalitis
Imaging Findings
Abnormal signal and enhancement of medial temporal and inferior frontal lobes
Limbic system: Temporal lobes, insula, subfrontal area and cingulate gyri typical
Typically bilateral disease, but asymmetric
Basal ganglia usually spared
Differential DiagnosesLimbic encephalitis
Infiltrating neoplasm
Ischemia
Status epileptius
limbic encephalitis
Rare paraneoplastic syndrome associated with a primary tumor, often lung and ovarian teratoma in female
Predilection for limbic system, often bilateral
Hemorrhage is not present
Imaging may be indistinguishable
Symptom onset usually weeks to months (vs acute in HSE)
Infiltrating neoplasm
Low grade gliomas often involve medial temporal lobe and cause epilepsy
Gliomatosis cerebri may involve the frontal and temporal lobes, may be bilateral
No enhancement in early stages
Onset usually indolent
Ischemia
Typical vascular distribution (MCA, ACA, PCA)
Acute onset
Status epileptius
Active seizures may disrupt BBB,cause signal abnormalities and enhancement
MRI Findings of Acute Viral MyelitisTlWI:Expanded cord, fills canalMay show central low signal simulating syrinx, but intensity higher than CSF
T2WI:Diffuse increase in signal intensity through involved segmentTl C+: Variable, non-focal enhancement of involved cord segment
DDx."Idiopathic" transverse myelitis
Multiple sclerosis (MS)
Acute disseminated encephalomyelitis (ADEM)
Neuromyelitis optica
Spinal arteriovenous malformation (AVM)
Arteritis
Acute cord infarct
Idiopathic" transverse myelitis
Identical clinical pictureNo etiology foundUp to 40% of cases preceded by upper respiratory tract infectionPresence of CSF lymphocytes and neutrophils indicative of some type of inflammation in most casesTypically long segment of cord involvement by swelling, edema, vague diffuse enhancement
Multiple sclerosis (MS)
Up to 33% may have isolated cord lesions Most lesions are focal (1-2 segments), may be multiple20% demonstrate mono segmental involvementAcute lesions exhibit focal enhancement with short segment edemaNo peripheral nervous system involvement90% of cases show oligo clonal bands
Acute disseminated encephalomyelitis(ADEM)
Mimic of multiple sclerosis
Related to vaccination or immune insult
Monophasic illness
HSV 2HSV2 along with TORCH agents are major causes of neonatal encephalitis.
Infections result from maternal birth canal or transplacental spread
Unlike HSV1, HSV2 infection in neonates is diffuse.
HSV 2Imaging findings are nonspecific.CT scans in early disease may be negative or show subtle areas of low density
Conventional MR and DWI show lesions better.
Lesions may be multifocal involving almost any area of brain or limited to temporal lobes brainstem and cerebellum.
Watershed infarcts may be seen
In-utero infections can result in microcephaly, encephalomalacia or calcification.
Axial T2WI MR shows areas of high signal in frontal lobes WM due to acute HSV-2Axial T1WI MR shows diffuse cystic encephalomalacia and prominent CSF-containing spacesCa++ in basal ganglia (BG), thalami, cortex,subcortical WM25
CONGENITAL CMVMicrocephaly
Cerebral parenchymal Calcification (40-70%)
Cerebellar hypoplasia
Cortical gyral abnormalities
Periventricular calcification
CONGENITAL CMVImaging recommendation-Cranial sonography for neonatal screening
NCCT when clinically suspected
MR brain to completely characterize abnormalities
CONGENITAL CMV
CT Findings Cerebral parenchymal Calcification (40-70%) Periventricular (subependymal)
Ventricular dilatation and WM volume loss
Cortical gyral abnormalities-Agyria
Cerebellar hypoplasia
CONGENITAL CMV
CONGENITAL CMV
LCM-Macrocephaly (43%) > microcephaly (13%)Toxo-Cerebral calcifications are randomPseudoTorch-Auto recessive Progressive cerebral and cerebellar demyelinationBasal ganglia Ca+++/- Periventricular Ca++
Japanese encephalitis (JE)
MC mosquito borne encephalitis In world.
JE is endemic to Indian subcontinent & is most common cause for epidemic encephalitis , particularly in the NE state of Assam and eastern UP.
Epidemics occur in the summer rainy season which favor breeding of mosquitoes.
Japanese encephalitis (JE)
Homogeneous T2 hyperintensities in BG and thalami,symmetric or asymmetric
Most characteristic finding in JE- Bilateral thalamic hyperintensities hemorrhage
JE is meningoencephalitis
HIV ENCEPHALITISBest diagnostic clue: Combination of atrophy and symmetric, periventricular or diffuse white matter (WM) disease suggests HIVE
Pathology/imaging varies with patient age, duration of the disease.
MTR allows differentiation of HIVE from PML
DDx- Progressive multifocal leukoencephalopathy-Chara.by Involvement of subcortical U fibre. CMV-associated CNS disease Herpes virus encephalitis Toxoplasmosis Primary CNS lymphoma-Solitary/multifocal lesions, deep> subcortical lesions Marked predilection for basal ganglia, cerebellar hemispheres, thalamus, brain stem, corpus callosum,and sub ependymal region
PMLAsymmetric T2 hyperintensity in periventricular, subcortical white matter
No or minimal enhancement -Characteristic
Often parieto-occipital region, may cross corpus callosum
Immunosuppressed patients, typically AIDS
Progressive multifocal leukoencephalopathy brain magnetic resonance imaging lesion patterns
A, Large, confluent, granular T2-weighted lesions(arrows). B, Deep gray matter involvement (arrow). C, Crescent-shaped cerebellar lesion
D, Gadolinium- enhancing lesions (arrow).
E, Tumefactive lesion (arrow).
F, Multiple sclerosis like appearance.
G, Transcallosal lesion (arrow).
HIV MyelopathyBest diagnostic clue: Spinal cord T2 hyperintensity,which may show patchy enhancement
Location: Thoracic> cervical; mid to low thoracic cord with rostral involvement as disease progresses
MR Findings
T1WIMay be normalCord atrophyT2WIMay be normalHyperintensity either diffusely or involving WM tracts laterally & symmetrically Cord atrophyT1 C+: Visible lesions may enhanceImaging Recommendations Best imaging tool: MRI C+
B12 deficiency May appear identical to HIV myelopathy Negative HIV testVaricella Zoster virus Intrinsic myelopathy PCR-positive for virus in CSF
CMV myelitis Cause of HIV-related polyradiculopathy MRI may show nerve root & conus leptomeningeal thickening, enhancement Characteristic intranuclear inclusionsTransverse myelitis Indistinguishable by imaging from HIV myelitis Inflammation across the width of enlarged spinal cord Uncertain etiology
Rabies encephalitis
Ill-defined mild hyperintensity in brainstem, hippocampi, thalami, WM, BG.
Paralytic rabies: Medulla and spinal cord hyperintensity
Rabies encephalitis
SSPE
MR FindingsTl WI: Areas of decreased signal in WM, corpus callosumT2WI:Diffuse increased signal in WM, corpus callosum, Involvement generally symmetricRare: Cystic temporal lobe lesionsLate: Diffuse atrophyInvolvement of basal ganglia/thalami is rare (especially adults)Tl C+: No enhancementImaging Recommendations Best imaging tool: MRI Protocol advice: Routine brain MRI with contrast
ADEMPost vaccination / postinfectious Autoimmune-mediated white matter (WM) demyelination of brain and/or spinal cord, usually with remyelination .
Post vaccination-Rabies , Influenza
Postinfectious-Measles,Rubella,VZV.
Drugs-Sulfonamides,PAS,Streptomycin.
Imaging Findings
Best diagnostic clue: Multifocal WM/basal ganglia lesions 10-14 days following infection/vaccination Location: May involve both brain and spinal cord predominantly WM but also gray matter (GM)Initial CT normal in 40%Multifocal punctate to large flocculent FLAIR hyperintensitiesDo not usually involve callososeptal interfacePunctate, ring, incomplete ring, peripheral EnhancementMay appear identical to MS repeat MR necessary to distinguish with certainty
Thank You
ReferencesDiagnostic Neuroradiology; Anne G. osborn(2007).
Diagnostic Imaging Brain, Osborn - 2004
Diagnostic Imaging Spine-Ross, Zawadzki, Moore,Crim, Chen, Katzman. 2004
Bradleys;Neurology In clinical practice,6th edition (2012).