imaging of viral encephalitis

Imaging of viral encephalitis

Osama A. RagabAssist,Lec of Neurology

introduction The word “virus” is derived from the Latin word for

poison.

Viruses are infectious, obligate intracellular parasites

whose genomes consist of either DNA or RNA.

A minimal virus consists of a genome plus a

proteinaceous coat, known as a capsid.

Enveloped viruses, are enclosed by a host cell-

derived lipid bilayer studded with virus-specified

glycoproteins.

Virus structure

Nucleic Acid

Spike

Projections

Protein

Capsid

Lipid Envelope

Virion

Associated

Polymerase

Virus taxonomy

Within the ICTV( the International Committee for

Taxonomy of Viruses) system ,the two major

taxonomic divisions are the viruses with RNA

genomes and those with DNA genomes.

Subsequent taxonomic levels are based on the size

and structure of the capsid and then the nature of

the genome (single-stranded or double-stranded,

linear or circular, segmented or non-segmented).

HERPESVIRIDAE

HEPADNAVIRIDAE

ENVELOPED

PAPILLOMAVIRIDAE

POLYOMAVIRIDAE(formerly grouped together as the

PAPOVAVIRIDAE)

CIRCULAR

ADENOVIRIDAE

LINEAR

NON-ENVELOPED

DOUBLE STRANDED

PARVOVIRIDAE

SINGLE STRANDED

NON-ENVELOPED

POXVIRIDAE

COMPLEX

ENVELOPED

DNA VIRUSES

Virus taxonomy

FLAVIVIRIDAETOGAVIRIDAE

RETROVIRIDAE

ICOSAHEDRAL

CORONAVIRIDAE

HELICAL

ENVELOPED

ICOSAHEDRAL

PICORNAVIRIDAECALICIVIRIDAE

ASTROVIRIDAE

NONENVELOPED

SINGLE STRANDEDpositive sense

BUNYAVIRIDAEARENAVIRIDAE

ORTHOMYXOVIRIDAEPARAMYXOVIRIDAE

RHABDOVIRIDAEFILOVIRIDAE

SINGLE STRANDEDnegative sense

REOVIRIDAE

DOUBLE STRANDED

RNA VIRUSES

ENVELOPED

HELICAL ICOSAHEDRAL

NONENVELOPED

Virus taxonomy

Geographic distribution of selected viruses causing central nervous system infection.

Neurotopic virus

HERPESVIRUSES

HERPESVIRUSES

Family Herpesviridae includes over 80 viruses

distributed among three subfamilies: Alpha, Beta and

Gamma.

Human viruses are members of the Alpha

herpesvirinae: HSV-1 and HSV-2 and varicella-

voster virus .

Human Beta herpesvirinae include human

cytomegalovirus human herpesviruses 6A and 6B

and human herpesviruses 7.

Human Gamma herpesvirinae are hosts to Epstein–

Barr virus and human herpesvirus 8 .

These viruses are neurotropic and establish latent

infections in ganglionic neurons during primary

infection, subsequently reactivating to cause

recurrent disease or subclinical virus shedding,

promoting spread to new hosts.

Associated diseases include peripheral neuropathies

such as postherpetic neuralgia, Bell’s palsy, and

potentially life-threatening encephalitis .

HERPESVIRUSES

Pathologically, HSV-1 results in a necrotizing

infection involving the :

inferomedial aspect of the temporal lobes.

the inferior frontal cortex .

the cingulate cortex .

the subfrontal and insular regions.

Further progression of disease may result in

petechial hemorrhages and eventual cavitation

Herpes simplex virus 1 (HSV-1)

CT is often normal, although non-specifichypoattenuating lesions in the temporal and/orfrontal lobes with or without enhancement andsuperimposed hemorrhage may be demonstrated insevere illness .

MRI can be normal in up to 10% of patients.

The most characteristic pattern finding is unilateralhigh T2 signal involving the insula, medial temporaland inferior frontal lobes with or withoutinvolvement of the adjacent limbic structures.

Enhancement and hemorrhage become moreprominent with disease progression


51-year-old diabetic woman with fever and confusion. (a) Unenhanced axialCT scan shows no significant changes in the left temporal lobe. (b) 2 dayslater unenhanced axial CT scan is still unremarkable. (c) 14 days later,unenhanced axial CT scan shows marked hypodensity in the left temporallobe


Axial fluid attenuated inversion recovery image(A) demonstrates a region of increased signalintensity in the right temporal lobe .


Herpes simplex virus 1 (HSV-1)Axial T1 Image demonstrate curvilinear regions of high T1 signal intensitywithin the right temporal lobe (arrow,), compatible with petechialhemorrhage in this patient with herpes encephalitis.

DWI demonstrates regions of patchy

restricted diffusion and may be more sensitive

than T2-weighted or FLAIR imaging in

depicting regions of encephalitis


DWI classic herpes encephalites note abnormalhyperintense signal abnormallity in bilateal mesialtemporal corex .


classic herpes encephalites noteabnormal hyperintense signalabnormallity in bilateal mesial temporalcorex & cingulate gyri on T2 & FLAIRimages with reduced diffusivity.


T1 with contrast

HSV-2 may result in severe neonatal encephalitis,

with transmission most commonly occurring through

an infected birth canal .

Pathologic examination demonstrates diffuse

parenchymal and leptomeningeal inflammation

which can progress to hemorrhage and necrosis.

MR demonstrating loss of gray–white differentiation

and high T2 signal within the periventricular and

subcortical white matter, with relative sparing of the

central gray matter (basal ganglia, thalami) and

posterior fossa.


With disease progression, decreased T2 signal

intensity within the cortex may develop

corresponding to the presence of focal hemorrhagic

necrosis and parenchymal calcifications .

Severe cerebral sequelae such as cystic

encephalomalacia or hydranencephaly may

eventually be seen with more advanced disease


Cortical blurring and gyral/leptomeningeal enhancement in neonatal HSV-2encephalitis in different patients.

A Axial T2-weighted image demonstrates reduced cortical gray white matterdifferentiation (arrowheads) in the right temporal lobe.

B Gyral/leptomeningeal contrast enhancement (arrows) in the right temporalregion on the coronal image after gadolinium administration in the samepatient .

a Axial FLAIR image is normal in this 13-dayold patient presenting with signs of sepsis andculture negative meningitis 2 days prior to thisexamination. No abnormality was seen on anyof the conventional MR images .


Axial DW image demonstrates a focus of

restricted diffusion (arrow) in the uncal

region of the medial anterior left temporal

lobe,

Axial DW image demonstrates

restricted diffusion in the left caudate

nucleus head (arrowhead) and the right

lentiform nucleus (arrow) in addition to

the left occipitotemporoparietal and

right parietal regions


Axial CT image of the same patient as in a

obtained 3 years later demonstrates cystic

encephalomalacia in the left occipito-

temporo-parietal region (asterisk).

There is also hypoattenuation in the left

caudate nucleus head (arrowhead) and the

right lentiform nucleus (arrow), indicative

of old necrosis.

Axial DW image in another patientdemonstrates restricted diffusionin the pons (arrow) and deepcerebellar hemispheres(arrowheads).


End-stage neonatal HSV-2 encephalitis

This axial noncontrast CT image

demonstrates severe necrotic changes

and encephalomalacia involving the

frontal and parietal lobes bilaterally. The

relative prominence of the basal ganglia

(arrowheads) and thalami (arrows)

Meningoencephalitis with MRI demonstrating diffuse,

multifocal areas of high T2 signal intensity within the

cerebral cortex.

Diffuse encephalitis results in non-specific regions of

high T2 signal within the white matter.

VZV involvement of large vessels at the base of the

brain may result in a variety of pathologic findings,

ranging from necrotizing arteritis to remote vascular

occlusion within the small blood vessels of the brain

resembling atherosclerotic disease.

Varizella-zoster virus (VZV)

The spread of VZV from blood vessels to the

ependymal cells lining the ventricles may result in

ventriculitis, resulting in abnormal ependymal

enhancement and high T2/FLAIR signal intensity.

spread of VZV to oligodendrocytes can result in a

multifocal leukoencephalopathy which manifests as

subcortical high T2 signal plaques which may

demonstrate enhancement after gadolinium contrast

administration

Varizella-zoster virus (VZV)

Varicella-zoster virus encephalitis with multifocal vasculopathy. Axial fluid

attenuated inversion recovery (FLAIR) (A) and T2-weighted image (B)

demonstrate high FLAIR signal in the left caudate nucleus and in the posterior

limb of the internal capsule as well as hyperintense T2 signal along the right

paramedian frontal lobe. Magnetic resonane angiogram (C) demonstrates

irregular narrowing in the left proximal middle cerebral and right anterior cerebral

artery.

Magnetic resonance image of a 6-month-old boy. (a, b) AxialT2 gradient echo sequence: blood in the ventricles andhydrocephaly. (c) Axial TI sequence after gadolinium infusion:no abnormal enhancement. (d) FLAIR sequence: noparenchymal abnormality.

Magnetic resonance image of a 35-year-old man. (a-c) Cranial magnetic resonance image, FLAIRsequence showing punctiform hyperintensities subcortical (right frontal and left temporal) and in thepons. (d) Sagittal dorsal spinal cord, T2 sequence: hypersignal at the T7-T8 level.

Magnetic resonanceimage of a 20-year-oldman. Narrowing of the Mlsegment of the middlecerebral artery.

Epstein-Barr virus (EBV)

EBV infection of the nervous system is uncommon

but may result in meninigitis, encephalitis, myelitis,

and/or cranial nerve palsies .

CT findings are often normal .

MRI may demonstrate non-specific high signal

intensity within the cerbral cortex, at the gray–white

junction, and/or within the deep nuclei (basal

ganglia, thalamus) on T2-weighted images which

may resolve on subsequent imaging.

case reports of progression to hemorrhagic

encephalitis have been published and should be a

consideration with worsening neurologic deficits.

EBV infection has a high association with primary

CNS lymphoma in the setting of acquired immune

deficiency syndrome (AIDS) .

Epstein-Barr virus (EBV)

Epstein–Barr virus. Axial T2-weighted image (A) imaging demonstrates

abnormal increased signal in the right temporal lobe. Axial T2-weighted image

(B) performed 3 days later demonstrates progression of abnormal signal in the

right temporal lobe.

Anon-contrast CT scan (C) performed the same daydemonstrates partial hemorrhagic conversion of thelesion with adjacent swelling and right-to-left midlineshift.

Initial MR imaging of the patient. T1-weighted image does not reveal anyabnormality (A). T2-weighted image depicts high signal intensity in the SCC(B). Turbo spin-echo FLAIR sequence shows additional high signals in bothposterior hemispheres (C). All lesions had clearly elevated diffusioncoefficients with high signal intensity on DWI (D), whereas ADC maps in thesplenium were decreased (E). The T1-weighted image with gadoliniumshows no contrast enhancement.

Brain MRI scan findings in a 12-year-old boy with Epstein–Barr virusencephalitis. The scans were performed 1 day before the patient died. (A,B)These axial diffusion-weighted images show focal lesions of increasedsignal intensity— indicative of cytotoxic edema in the cerebellum, brainstem,basal ganglia and hippocampus—scattered throughout the subcortical whitematter and cerebral cortex. Ventricles are not significantly narrowed. (C)Sagittal T1-weighted image that shows generalized cerebral edema withherniation of the brainstem and cerebellar tonsils into the foramen magnum.

CMV infection of the nervous system is most often seen

with immunocompromised patients .

CMV is the leading cause of congenital CNS infection,

with an incidence of approximately 1–2% of live births.

The resultant imaging findings reflect the distribution of

disease: meningitis, encephalitis,

ventriculoencephalitis, myelitis, and retinitis .

CT imaging is less sensitive than MRI and may

demonstrate non-specific cortical atrophy and/or

decreased attenuation within the white matter .

With contrast-enhanced imaging, periventricular

enhancment may be present, indicative of underlying

ventriculoencephalitis .

Cytomegalovirus (CMV)

MRI demonstrates non-specific increased T2 and

decreased T1 signal abnormalities in the white

matter which may have a patchy or confluent

distribution .

Nodular increased T2 signal abnormalities may also

be noted within the brainstem, basal ganglia,

cerebellum, and hippocampus, some of which may

undergo hemorrhagic transformation.

Occasionally, CMV infection may present as a ring-

enhancing cerebral mass with marked edema

mimicking an intracranial neoplasm.


CT imaging in infants with congenital CMV infection

classically shows intracranial calcifications in a

periventricular distribution, hydrocephalus, cortical

atrophy, subdural hematomas, or effusion and non-

specific white-matter hypodensities

CMV infection early in utero results in abnormal fetal

brain development, migrational, cortical gyral

abnormalities, delayed myelination, cerebellar

hypoplasia and porencephalic cysts.


In uterocytomegalovirus (CMV) infection. Coronal true inversion recovery image

demonstrates thickened and disordered cortex in the right frontal and temporal

lobes (arrows) compatible with pachygyria in this infant within uteroCMV infection.

In utero cytomegalovirus (CMV) infection. Axial non-contrast computed

tomography scan of the head demonstrates massive hydrocephalus as well as

bilateral periventricu-lar calcifications in this infant with in utero CMV infection.

In uterocytomegalovirus (CMV) infection. Coronal T2-weighted image

demonstrates thickened and disordered cortex in the right frontal and temporal

lobes (arrows) compat-ible with pachygyria in this infant with in utero CMV

infection.

Axial (a) T1 and (b) T2 weighted MRI show mild ventricular dilatation and multiple tiny nodular T2 high-signal intensity lesions in basal ganglia and right frontal subcorticalwhite matter without definite periventricular signal change. (c) Axial fluid attenuated inversion recovery image shows thin curvilinear high-signal intensities along the walls ofboth lateral ventricles and multifocal faint high-signal intensities at right frontal and basal ganglia regions. (d) Axial contrast enhanced T1 weighted image shows subtlesubependymal enhancement (arrow). (e,f) Diffusion weighted image shows striking curvilinear high-signal intensities along the ventricular wall with a subtle low apparentdiffusion coefficient value (arrow).

Reactivation of latent HHV-6 infection in

immunocompromised patients, may result in an

encephalitis, leptomeningitis, or neuritis .

The most common findings include symmetric or

asymmetric high T2 signal within the uncus,

amgydala, and hippocampal body with extension to

the rhinal cortex .

DWI may show the earliest signs of the underlying

inflammatory changes with patchy regions of

restricted diffusion in the involved neural tissue



Human herpesvirus-6 (HHV) infection. Axial fluid attenuated inversion recovery

image of the brain demonstrates symmetric high signal abnormalitywithin the

limbic system in this patient who developed HHV-6 infection after a bone mar-

row transplant for treatment of lymphoma.

Flaviviruses

Humans typically acquire infection through the bite ofan infected mosquito or tick .

The major human pathogens among the Flavivirus genusare yellow fever virus, Dengue virus, Japaneseencephalitis virus (JEV), St. Louis encephalitis virus(SLEV), tick-borne encephalitis virus (TBEV), and WNV

( West Nile virus ).

Flaviviruses

JEV primarily affects developing neurons in thalamus,hippocampus, and midbrain, while anterior horn cells ofthe spinal cord and brainstem are the primary targets ofTBEV.

The disease spectrum of JEV ranges from non-specificfebrile illness to aseptic meningitis, meningoencephalitis,flaccid paralysis, and encephalitis .

Parkinsonian movement disorder and seizures have alsobeen reported. Clinical syndromes associated with WNVinclude meningitis, encephalitis, and acute flaccidparalysis

Flaviviruses

St. Louis encephalitis (SLE)

SLE is transmitted through a mosquito-borne virus

and has resulted in several epidemics in the eastern

and central United States .

perivascular inflammatory changes with neuronal

degeneration and microglial proliferation, most

prominent within the substantia nigra , pons ,insular

cortex and thalami

St. Louis encephalitis. Axial T2-weighted images demonstrate symmetricincreased signal intensity involving the insular cortex and thalami as wellas the substantia nigra, midbrain, and pons

St. Louis encephalitis (SLE)

West Nile encephalitis

West Nile encephalitis is an emerging infection with

a rapid increase in incidence and geographic range.

Transmission is most often through a mosquito-

infected vector, although transmission through

breastfeeding, transplacental has been reported .

Imaging findings in cases of West Nile encephalitis

are non-specific, with a case series reporting

increased T2 signal abnormality most often within

the mesial temporal lobe and midbrain .

Meningeal, cerebellar, cortical, and white-matter

imaging abnormalities are less commonly found .

West Nile encephalitis. Axial fluid attenuated inversion recoveryimages (A, B) demonstrate increased signal in the thalami andcorpus striatum. Increased signal intensity is also noted in themedial temporal lobes and cerebellum (curved arrow,B). Axial T1postcontrast image (C) demonstrates enhancement in the thalami.

West Nile encephalitis

Japanese encephalitis

Japanese encephalitis (JE) is the most frequent

global cause of mosquito-borne encephalitis and is

associated with significant morbidity and mortality.

Pathology studies have demonstrated diffuse

inflammatory changes involving the basal ganglia,

thalamus, cerebral cortex, brainstem, and

cerebellum.

The most consistent finding on MRI is bilateral

increased T2 signal abnormality in the thalami with

or without hemorrhage.

Japanese encephalitis

Japanese encephalitis. Axial fluid attenuated inversion recovery images in

two different patients with Japanese encephalitis demonstrate bilateral

symmetric increased signal intensity (A) and asymmetric right thalamus

signal abnormality B) respectively.

Bunyaviridae

Between the period of October 2003 and April 2005

an epidemic of RVF encephalitis appeared in the

region of Khafer Al-Sheikh Governorate.

Humans can get RVF as a result of bits from

mosquitoes and possibly other blood sucking insects

that serve as vectors. Humans can also get the

disease if they are exposed to either the blood or

other body fluids of infected animals.

MRI of the brain demonstrated the following: patchy

areas of edema targeting the cortical and subcortical

deep white matter and diffusely involving both

cerebral hemispheres. These were evident in the

temporal, frontal, perisylvian and occipitoparietal

regions. Patchy involvement of the mesencephalon,

basal ganglia and posterior nuclei of both thalami .

the affected tissues are emitting subtle decrease in

signal intensity on T1-Weighted images and bright

signal intensity on T2-weighted and FLAIR pulse

sequences

. No associated enhancement or leptomeningeal

reaction.

C.T brain scan demonstrate gray matter affection with

diffuse white matter affection & mainly in the region of

basal ganglia

MRI of the brain T2 weighted images demonstrate evidence ofgray

matter affection with diffuse white matter edema

Arenaviruses

Arenaviruses

Lymphocytic choriomeningitis virus can cause

aseptic meningitis (rarely fatal), hydrocephalus, and

more severe CNS disease.

Transmission to human via contact with rodents .

Encephalitis develops in 5–34% of patients.

lymphocytic choriomeningitis virus (LCMV)

prenatal disease may result in devastatingneuroteratogenic effects.

the most common abnormalities included microcephalyand periventricular calcification. Other additionalabnormalities included prominent gyral malformation,ventriculomegaly, hydrocephalus, porencephalic andperiventricular cysts, encephalomalacia, and isolatedcerebellar hypoplasia

2 children with congenital LCMV infection (B, C). (B) The most common abnormalitiesin congenital LCMV infection include periventricular calcifications (arrows) andventriculo-megaly (V), often due either to noncommunicating hydrocephalus or tocerebral atrophy. (C) Some patients with congenital LCMV infection have regions ofencephalomalacia (*), reflecting focal tissue destruction. In addition to massiveencephalomalacia, this patient has periventricular calcifications (arrow). LCMV,lymphocytic choriomeningitis virus.

(B) In congenital LCMV infection, the virus can impair

cerebellar growth and lead to cerebellar hypoplasia

(arrow).

Retroviruses

Retroviruses

The major human retroviruses include human T

lymphotropic viruses 1 and 2 and HIV-1 and -2.

Both HTLV-1 and HTLV-2 have been associated with

HTLV-associated myelopathy/ tropical spastic

paraparesis, a chronic progressive demyelinating

disease that affects the spinal cord and white matter

of the CNS.

Retroviruses

HIV-associated neurologic disorders include

neurocognitive disorders and peripheral

neuropathies as well as vacuolar myelopathy

Other primary neurologic syndromes associated with

HIV include aseptic meningitis, multiple sclerosis-like

disorders, ischemic and hemorrhagic strokes,

primary HIV-induced headache and psychiatric

disorders.

Early changes of HIV encephalitis manifest as

multifocal subcentimeter white-matter lesions

appearing bright on T2-weighted images. These are

generally symmetric and spare the subcortical U-

fibers.

The chronic stage of HIV infection manifests as

progressive white-matter signal abnormality in

conjunction with brain atrophy.

With progression of disease, however, these become

confluent and may extend to involve the basal

ganglia, cortex, cerebellum, brainstem, and spinal

cord

Human immunodeficiency virus

Another chronic feature of HIV infection is

progressive cerebral atrophy, which is most

prominent centrally, resulting in ex vacuo ventricular

dilatation out of proportion to sulcal prominence.

Human immunodeficiency virus

Polyomaviruses

The first human members of family Polyomaviridae, JCvirus (JCV) and BK virus (BKV) (both of genusOrthopolyomavirus).

Reactivation of latent JCV in immune-compromisedindividuals may cause PML.

Polyomaviruses

Progressive multifocal leukoencephalopathy

PML is most commonly seen in the setting of

underlying HIV-1 infection, it may also be seen in the

context of hematologic malignancies and treatment

with immunosuppressive medications.

Lesions appear hyperintense on T2-weighted

images and hypointense on T1-weighted images.

Lesions are most commonly found in the subcortical

and periventricular white matter of the frontal and

parieto-occipital lobes; they are also seen in the

white matter of the cerebellar peduncles or

hemispheres, and in the brainstem

Early on, the lesions may be small but then progress

to form larger areas of involvement, often with a

scalloped border.

The lesions are classically bilateral, asymmetric,

multifocal, and lacking in mass effect. Only 9% of

cases demonstrate enhancement, which is typically

faint and peripheral .

Spinal cord involvement is rare.


This is an MRI of the brain of a PML survivor (PML-S).On the left is a fluid attenuated inverse recovery (FLAIR)image, which shows a large hyperintense lesion in theleft cerebral hemisphere, sparing the cortex. On the rightis the corresponding T1 with gadolinium (contrast) image,which shows no enhancement within the hypointensePML lesion.

This is an MRI of the brain of a PML- survivor. On the left, FLAIR imageshows a large hyperintense lesion in the white matter of the left hemisphere.There is also a shift of the midline (arrow) and disappearance of the sulci(arrowheads), signifying mass effect, as seen in excessive inflammation. Onthe right is the corresponding T1+Gad image; the arrows show enhancementwithin the PML lesion.


Paramyxoviruses

Paramyxoviruses

Measles virus infections can lead to three neurologic

diseases.

Acute disseminated encephalomyelitis that occurs

about a week after the rash phase .

inclusion body encephalitis in immune-suppressed

individuals .

subacute sclerosing panencephalitis .

Aseptic meningitis is the most common neurologic

manifestation of mumps virus infection.

Subacute sclerosing panencephalitis (SSPE)

SSPE is a chronic and progressive encephalitis

caused by a persistent infection of the brain by

measles virus.

Early changes include bilateral, multifocal,

asymmetric T2 hyperintense lesions of the

periventricular and subcortical white matter .

There is a predilection for involvement of the parietal

and occipital lobes .

With time, these lesions may become larger, more

numerous, and more confluent, and appear more

symmetric. Late changes of SSPE include abnormal

signal in the basal ganglia (typically the putamen),

subacute sclerosing panencephalitis (SSPE). Axial T2-weighted image

demonstrates symmetric regions of increased signal intensity in the

subcortical white matter, predominantly in the posterior cerebrum. Serology

titers and electroencephalogram findings were compatible with SSPE.

Rhabdoviruses

Rhabdoviruses

Rabies virus transmitted through skin by animal bites

the virus is transmitted directly to peripheral neurons

and then to the brain, or neuronal transmission

occurs after amplification in skeletal muscles.

Disseminated infection, including transmission from

the brain to salivary glands, occurs late in disease.

Rabies encephalitis

MR features of rabies encephalitis describe ill-

defined mild areas of T2 hyperintensity in the

brainstem, hippocampi, hypothalami, deep and

subcortical white matter, and deep and cortical gray

matter .

Picornaviruses

that include viruses of humans are Enterovirus,Hepatovirus, and Parechovirus. The human enterovirusesinclude poliovirus types 1–3, coxsackieviruses,echoviruses, and rhinoviruses.

Neurologic diseases include the flaccid paralysis of polio,aseptic meningitis, and encephalitis

Picornaviruses

Enteroviral encephalitis

EV71 characteristic MR findings are hyperintensity in

the posterior portions of the medulla and pons,

Severe cases demonstrated involvement of the

ventral horns of the spinal cord, basal ganglia, and

thalami.

The MR finding most characteristic of poliomyelitis is

hyperintensity involving the region of the anterior

horn cells on T2-weighted images .

Enteroviral encephalitis. Axial T2-weighted image demonstrates

symmetric regions of increased signal intensity involving the posterior

pons

Orthomyxoviruse

s

Orthomyxoviruses

Influenza viruses A, B, and C are well known as the

causes of influenza.

Neurologic manifestations of influenza virus include

Reye’s syndrome, febrile seizures, encephalitis,

myelitis, and acute necrotizing encephalopathy

(ANE).

ANE is characterized by bilaterally symmetric

necrotic brain lesions in the thalami, cerebral white

matter, brainstem, and cerebellum .

Influenza A. Axial fluid attenuated inversion recovery (A)andT1postcontrastimage(B)demonstrate bilateral asymmetric non-enhancing regions of high signal intensityinvolving the thalami. A peripheralrim of restricted diffusion is demonstrated on thediffusion-weighted images (arrow,C). The imaging findings are consistent with acutenecrotizing encephalopathy in this patient with serologic titers positive for underlyinginfluenza A infection.

Influenza

imaging of viral encephalitis

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