The document discusses various viral infections that can cause meningoencephalitis and myelitis. It provides details on imaging findings and differential diagnoses for different viruses. Key points include that herpes simplex virus is a common cause of viral encephalitis in the US. Japanese encephalitis virus typically causes bilateral thalamic hyperintensities on MRI. Congenital cytomegalovirus can cause microcephaly, cerebral calcifications, and cerebellar hypoplasia. HIV encephalitis is suggested by atrophy and symmetric periventricular or diffuse white matter disease on MRI.

1. Dr. Sunil Kumar Sharma
Senior Resident
Dept. of Neurology
GMC Kota

2. Viral Infections of CNS
 Hundreds 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)

3. 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

4. VIRUSES THAT CAUSE
MENINGOENCEPHALITIS…
 Measles, mumps and rubella viruses
 Rabies
 Arboviruses—for 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.

5. VIRUSES THAT CAUSE
MENINGOENCEPHALITIS…
 Bunyaviruses—for example, La Crosse strain of
California virus
 Reoviruses—for example, Colorado tick fever
virus
 Arenaviruses—for example, lymphocytic
choriomeningitis virus
 Paramyxovirus – Nipah virus, hendra virus

6. HERPES ENCEPHALITIS

7. Herpes simplex encephalitis
 Most 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

8. 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

12. Differential Diagnoses
 Limbic encephalitis
 Infiltrating neoplasm
 Ischemia
 Status epileptius

13. 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)

14. 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

15. Ischemia
• Typical vascular
distribution
(MCA, ACA, PCA)
• Acute onset

16. Status epileptius
•Active seizures may
disrupt BBB,cause
signal abnormalities
and enhancement

17. MRI Findings of Acute Viral Myelitis
TlWI:
 Expanded cord, fills canal
 May show central low signal simulating syrinx, but
intensity higher than CSF
T2WI:
 Diffuse increase in signal intensity through
involved segment
 Tl C+: Variable, non-focal enhancement of involved
cord segment

19. DDx.
 "Idiopathic" transverse myelitis
 Multiple sclerosis (MS)
 Acute disseminated encephalomyelitis (ADEM)
 Neuromyelitis optica
 Spinal arteriovenous malformation (AVM)
 Arteritis
 Acute cord infarct

20. Idiopathic" transverse myelitis
 Identical clinical picture
 No etiology found
 Up to 40% of cases preceded by
upper respiratory tract infection
 Presence of CSF lymphocytes and
neutrophils indicative of some type
of inflammation in most cases
 Typically long segment of cord
involvement by swelling, edema,
vague diffuse enhancement

21. Multiple sclerosis (MS)
 Up to 33% may have isolated cord
lesions
 Most lesions are focal (1-2
segments), may be multiple
 20% demonstrate mono
segmental involvement
 Acute lesions exhibit focal
enhancement with short segment edema
 No peripheral nervous system
involvement
 90% of cases show oligo clonal bands

22. Acute disseminated encephalomyelitis
(ADEM)
 Mimic of multiple sclerosis
 Related to vaccination or
immune insult
 Monophasic illness

23. HSV 2
 HSV2 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.

24. HSV 2
Imaging 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.

25. Axial T2WI MR shows areas
of high signal in frontal lobes
WM due to acute HSV-2
•Axial T1WI MR shows
diffuse cystic
encephalomalacia and
prominent CSF-
containing spaces
•Ca++ in basal ganglia
(BG), thalami, cortex,
subcortical WM
25

26. CONGENITAL CMV
 Microcephaly
 Cerebral parenchymal Calcification (40-70%)
 Cerebellar hypoplasia
 Cortical gyral abnormalities
 Periventricular calcification

27. CONGENITAL CMV
Imaging recommendation-
 Cranial sonography for neonatal screening
 NCCT when clinically suspected
 MR brain to completely characterize abnormalities

28. CONGENITAL CMV
CT Findings
• Cerebral parenchymal Calcification
(40-70%) Periventricular
(subependymal)
• Ventricular dilatation and WM
volume loss
• Cortical gyral abnormalities-Agyria
• Cerebellar hypoplasia

29. CONGENITAL CMV

30. CONGENITAL CMV

32. LCM-Macrocephaly (43%) > microcephaly
(13%)
Toxo-Cerebral calcifications are random PseudoTorch-
Auto recessive
Progressive cerebral and cerebellar
demyelination
Basal ganglia Ca++
+/- Periventricular Ca++

33. 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.

34. 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

36. HIV ENCEPHALITIS
 Best 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

38. 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

39. PML
 Asymmetric T2 hyperintensity in periventricular,
subcortical white matter
 No or minimal enhancement -Characteristic
 Often parieto-occipital region, may cross
corpus callosum
 Immunosuppressed patients, typically AIDS

41. 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

42. • D, Gadolinium-
enhancing lesions
(arrow).
• E, Tumefactive lesion
(arrow).
• F, Multiple sclerosis–
like appearance.
•G, Transcallosal lesion
(arrow).

43. HIV Myelopathy
 Best 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

44. MR Findings
T1WI
 May be normal
 Cord atrophy
T2WI
 May be normal
 Hyperintensity either diffusely or involving WM
tracts laterally & symmetrically Cord atrophy
 T1 C+: Visible lesions may enhance
Imaging Recommendations
 • Best imaging tool: MRI C+

46. B12 deficiency
• May appear
identical to HIV
myelopathy
• Negative HIV test
Varicella Zoster
virus
• Intrinsic
myelopathy
• PCR-positive
for virus in CSF

47. CMV myelitis
• Cause of HIV-related
polyradiculopathy
• MRI may show nerve
root & conus
leptomeningeal
thickening,
enhancement
• Characteristic
intranuclear inclusions
Transverse myelitis
• Indistinguishable by
imaging from HIV
myelitis
• Inflammation across
the width of enlarged spinal cord
• Uncertain etiology

48. Rabies encephalitis
 Ill-defined mild hyperintensity in brainstem,
hippocampi, thalami, WM, BG.
 Paralytic rabies: Medulla and spinal cord
hyperintensity

49. Rabies encephalitis

50. SSPE

51. MR Findings
Tl WI: Areas of decreased signal in WM, corpus callosum
T2WI:
 Diffuse increased signal in WM, corpus callosum,
 Involvement generally symmetric
 Rare: Cystic temporal lobe lesions
 Late: Diffuse atrophy
 Involvement of basal ganglia/thalami is rare (especially
adults)
 Tl C+: No enhancement
 Imaging Recommendations
 • Best imaging tool: MRI
 • Protocol advice: Routine brain MRI with contrast

53. ADEM
 Post 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.

54. 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
hyperintensities
 Do not usually involve callososeptal interface
 Punctate, ring, incomplete ring, peripheral Enhancement
 May appear identical to MS repeat MR necessary to
distinguish with certainty

56. Thank You

57. References
 Diagnostic 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,6’th edition
(2012).