neurologykota

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).