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
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
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
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
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
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
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
35.
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
37.
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
40.
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
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+
45.
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
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
52.
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