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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).