1. Herpes Encephalitis
Neurology & Neuroradiology Conference
Oct 28, 2016
Tanat Tabtieang MD
Department of Radiology
Faculty of Medicine, Chulalongkorn University
King Chulalongkorn Memorial Hospital
24. CECT findings (Sep 16, 2016)
ā¢ Well-defined non enhancing hypodense lesion at gray and
white matter of left inferior frontal lobe, inferior aspect of
left basal ganglia, left insular cortex, and left medial
temporal lobe
ā¢ Mass effect of the lesion causing effacement of left sylvian
fissure
ā¢ A well-defined lobulated thick rim enhancing hypodense
lesion with perilesional edema at gray-white matter junction
of right parasagittal area
41. MRI findings (Sep 20, 2016)
ā¢ Bilateral non-enhancing T2/FLAIR lesion with mild
restricted diffusion and gyral swelling at bilateral
hippocampi, parahippocampal gyri, amygdala nuclei, cortex
of anterior and lateral temporal lobes, insular cortices,
inferior and parasagittal frontal lobes, and cingulate gyri
ā¢ Two small thick irregular rim enhancing lesion with
hemosiderin deposit at parasagittal area of right frontal lobe
and left precentral gyrus
43. Herpes Encephalitis
ā¢ Best imaging clue
ā¢ T2/FLAIR hyperintensity of limbic
system (medial temporal and inferior
frontal cortex) with DWI restriction
ā¢ Typically bilateral disease, but
asymmetric
ā¢ Deep gray nuclei usually spared
ā¢ CT often normal early
ā¢ MR with DWI most sensitive for
early diagnosis
ā¢ T2/FLAIR: Cortical, subcortical
hyperintensity with relative white
matter sparing
NECT
T2
44. Herpes Encephalitis
ā¢ GRE: If hemorrhagic,
hypointensity "blooms" within
edematous brain
ā¢ DWI: Restricted diffusion in
limbic system
ā¢ T1WI C+: May see mild, patchy
enhancement early
ā¢ Image Interpretation Pearls
ā¢ CT often normal early, MR with
FLAIR/DWI most sensitive for
early diagnosis
ā¢ Presence of hemorrhage is
suggestive of herpes encephalitis
FLAIR
DWI
45. Paraneoplastic limbic encephalitis
ā¢ Paraneoplastic syndrome often associated with CA lung
ā¢ Predilection for limbic system, often bilateral
ā¢ Non-hemorrhagic
ā¢ Symptom onset weeks to months (vs. acute in HSE)
ā¢ Location
ā¢ Mesial temporal lobes and limbic systems
ā¢ Basal ganglia frequently involved
ā¢ Less common lateral temporal lobe and insula
46. Paraneoplastic limbic encephalitis
ā¢ CT often normal early
ā¢ Cortical thickening and increased
T2/FLAIR signal intensity
ā¢ Commonly bilateral involvement
ā¢ Patchy areas of enhancement can
be seen
ā¢ True diffusion restriction (i.e.
low ADC values) and
haemorrhage are not common.
NECT
FLAIR
47. Status epilepticus
ā¢ Active seizures may disrupt blood-brain barrier, cause signal
abnormalities and enhancement
ā¢ Temporal lobe epilepsy hyperperfusion may mimic HSE
ā¢ Best diagnostic clue
ā¢ T2 hyperintensity in gray matter and/or subcortical white matter with
mild mass effect
ā¢ May focally involve hippocampus, corpus callosum, thalamus
ā¢ No hemorrhage in status epilepticus
ā¢ Location
ā¢ Supratentorial, related to epileptogenic focus
ā¢ Typically cortex &/or subcortical WM
ā¢ May involve focal structures: Hippocampus (febrile or partial complex
seizures), Splenium of corpus callosum, Pulvinar of thalamus
ā¢ Occasionally cerebellar involvement
48. Status epilepticus
CT findings
ā¢ NECT
ā¢ Hypodensity in cortex &/or subcortical WM
ā¢ Blurring of corticomedullary junction
ā¢ Hippocampus, splenium of corpus callosum, thalamus (particularly
pulvinar nucleus) may be involved
ā¢ No hemorrhage
ā¢ CECT
ā¢ Variable enhancement: None to marked
49. Status epilepticus
MR Findings
ā¢ T1WI
ā¢ Hypointensity in cortex and/or
subcortical WM
ā¢ Swelling and increased volume of
involved cortical gyri
ā¢ Blurring of corticomedullary junction
ā¢ Mild mass effect
ā¢ Hippocampus, splenium of corpus
callosum, thalamus (particularly pulvinar
nucleus) may be involved
ā¢ Rarely cerebellar involvement
ā¢ T2WI
ā¢ Hyperintensity in cortex and/or
subcortical WM
ā¢ Swelling and increased volume of
involved cortical gyri
ā¢ Mild edema and mass effect
ā¢ No hemorrhage
T1
FLAIR
50. Status epilepticus
ā¢ FLAIR
ā¢ Hyperintensity in cortex and/or
subcortical WM
ā¢ Mild edema and mass effect
ā¢ DWI
ā¢ Restricted diffusion with decrease in
ADC map acutely
ā¢ ADC maps normal interictally, elevated
in chronic seizures
ā¢ T1WI C+
ā¢ Variable enhancement: None to marked
ā¢ May see gyriform or leptomeningeal
enhancement
DWI
T1 +C
51. Herpes Encephalitis
ā¢ Brain parenchyma infection caused by herpes simplex virus
type 1 (HSV1)
ā¢ Age
ā¢ May occur at any age
ā¢ Highest incidence in adolescents and young adults
ā¢ ~ 1/3 of all patients < 20 years old
ā¢ Gender: M = F
52. Herpes Encephalitis
ā¢ Most common signs/symptoms
ā¢ Fever, headache, seizures, Ā± viral prodrome
ā¢ Children often present with nonspecific symptoms
ā¢ Behavioral changes, fever, headaches, seizures
ā¢ Patients typically immunocompetent
ā¢ HSV1 uncommon in AIDS patients
ā¢ Other signs/symptoms
ā¢ Altered mental status
ā¢ Focal or diffuse neurologic deficit (< 30%)
53. Herpes Encephalitis
ā¢ Brain parenchyma infection caused by herpes simplex virus type 1
ā¢ Acute onset, often with fever
ā¢ Best diagnostic clue
ā¢ Abnormal signal in medial temporal and inferior frontal cortex with
DWI restriction
ā¢ Involvement of cingulate gyrus and contralateral temporal lobe highly
suggestive
ā¢ Typically blood products
ā¢ Location
ā¢ Limbic system: Temporal lobes, insula, subfrontal area, cingulate gyri
typical
ā¢ Cerebral convexity, posterior occipital cortex may become involved
ā¢ Typically asymmetrical bilateral disease
ā¢ Basal ganglia usually spared
54. Herpes Encephalitis
CT findings
ā¢ NECT
ā¢ CT often normal early
ā¢ Low attenuation, mild mass
effect in medial temporal lobes,
insula
ā¢ Hemorrhage typically late feature
ā¢ Predilection for limbic system;
basal ganglia spared
ā¢ Earliest CT findings at 3 days
after symptom onset
ā¢ CECT
ā¢ Patchy or gyriform enhancement
of temporal lobes (late
acute/subacute feature)
NECT
NECT
55. Herpes Encephalitis
MR findings
ā¢ T1WI
ā¢ Cortical swelling with loss of gray-white junction,
mass effect
ā¢ May see subacute hemorrhage as increased signal
within edematous brain
ā¢ Atrophy, encephalomalacia in late
subacute/chronic cases
ā¢ T2WI/FLAIR
ā¢ Cortical and subcortical hyperintensity with
relative white matter sparing
ā¢ May see subacute hemorrhage as increased signal
within edematous brain
ā¢ GRE T2*
ā¢ If hemorrhagic, hypointensity "blooms" within
edematous brain
T1 +C
SWI
56. Herpes Encephalitis
ā¢ DWI
ā¢ Restricted diffusion in limbic system
ā¢ Most sensitive for early diagnosis
ā¢ T1WI C+
ā¢ May see mild, patchy enhancement in early
ā¢ Gyriform enhancement usually seen 1 week after initial symptoms
ā¢ Meningeal enhancement occasionally seen
ā¢ Enhancement seen in temporal lobes, insular cortex, subfrontal area,
cingulate gyrus
ā¢ Presence of hemorrhage is suggestive of herpes encephalitis
DWI