Journal of Acute Care
Volume 1 | Issue 2 | Year 2022

Acute Viral Encephalitis in Adults

Sarath Kumar1, Shiv Kumar2, Darshan U Siddappa3

1,3Department of Critical Care Medicine, Manipal Hospitals, Bengaluru, Karnataka, India

2Department of Critical Care Medicine, Narayana, Bengaluru, Karnataka, India

Corresponding Author: Sarath Kumar, Department of Critical Care Medicine, Manipal Hospitals, Bengaluru, Karnataka, India, Phone: +91 9148535357, e-mail:

Received on: 13 September 2022; Accepted on: 26 September 2022; Published on: 31 December 2022


Encephalitis is a syndrome characterized by altered mental status along with acute fever, seizures, and neurological deficits. The syndrome has many causes, the most commonly identified causes are neurotropic viruses. Herpes simplex virus (HSV) encephalitis is a potentially life-threatening condition which can be diagnosed with a combination of history, examination, magnetic resonance imaging (MRI) brain, and lumbar puncture. We report a case of a young immunocompetent adult presented with fever, altered mentation, and seizure. We are reporting classical findings of HSV encephalitis in an MRI brain study. We also described a few common viral encephalitis encountered in clinical practice.

How to cite this article: Kumar S, Kumar S, Siddappa DU. Acute Viral Encephalitis in Adults. J Acute Care 2022;1(2):112-117.

Source of support: Nil

Conflict of interest: None

Keywords: Encephalitis, Herpes simplex virus, Magnetic resonance imaging.


Encephalitis is a syndrome characterized by altered mental status along with acute fever, seizures, and neurological deficits.1 The syndrome has many causes, the most commonly identified causes are neurotropic viruses. HSV 1 and 2 account for 10–20% of all viral encephalitis cases.2 Cerebrospinal fluid (CSF) analysis with HSV polymerase chain reaction (PCR) is the gold standard for diagnosis, however, false-negative PCR assay can be seen in patients with low viral load in the initial phases of illness.3 MRI can be used as an adjunct in diagnosis in cases with negative PCR assay and high clinical suspicion or in patients whose lumbar puncture could not be performed. We described a young patient who presented with fever and altered sensorium and was diagnosed with HSV encephalitis and characteristic MRI findings and subsequent discussion on common encephalitis syndromes in the form of a tutorial.


We report a case of a 24-year-old male patient who was in good health 3 days prior to admission to our hospital when he developed acute onset fever and headache followed by an episode of seizure with subsequent loss of consciousness and altered sensorium. The past medical history was insignificant.

On admission, the patient was febrile and in the postictal phase with the Glasgow Coma Scale (GCS) of E3V4M5 with no focal neurological deficits. Initial laboratory evaluation for the metabolic cause of altered sensorium was not contributory. He was started on empirical antimicrobials with suspicion of meningoencephalitis, and other supportive measures after sending appropriate cultures.

Magnetic resonance imaging brain with contrast was done which revealed some tell-tale features. Bilateral asymmetric medial temporal lobe fluid-attenuated inversion recovery (FLAIR) hyperintensities (right > left) involving hippocampus and amygdala (Figs 1 to 3) and FLAIR hyperintensities in the insular cortex, perisylvian cortex bilateral, basifrontal lobes, and inferolateral external capsule along with edema of these areas (Fig. 4). Diffusion-weighted sequences showed diffusion restriction in the cortex of the above-mentioned regions (Figs 5) and apparent diffusion coefficient (ADC) showed T2 shine through (Fig. 6). There is evidence of intracerebral hemorrhage (Fig. 7). There was no involvement of basal ganglia and cingulate gyri.

Fig. 1: Coronal T2: hyperintensity in the medial temporal lobe—hippocampus, amygdala, and adjacent insular cortex

Fig. 2: Axial T2 FLAIR-basifrontal lobe adjacent to median temporal lobe hyperintense lesions

Fig. 3: Axial T2 FLAIR-bilateral (right > left) medial temporal lobe, hippocampus, parahippocampus, and amygdala

Fig. 4: Axial FLAIR-insular cortex hyperintense lesion

Figs 5A to D: (A) Axial FLAIR-insular cortex hyperintense lesion; (B) Diffusion-weighted image (DWI)—axial-restriction in cortex-right medial temporal lobe; (C) DWI—axial-restriction in cortex-right medial temporal lobe; (D) DWI—axial-restriction in cortex-right medial temporal lobe

Fig. 6: Axial ADC-T2 shine through (to differentiate vasogenic edema—from cytotoxic edema-infarct)

Fig. 7: Susceptibility weighted images (SWI)—axial—no hemorrhage

Lumbar puncture revealed a lymphocytic predominant picture with elevated protein levels. The CSF PCR encephalitis panel was reported to be positive for HSV 1.

The antiviral acyclovir 15 mg/kg every 8 hours that was initiated was continued along with other supportive measures. Gradually there was an improvement in his neurological status with no neurological deficits, there were no further episodes of seizures, and he was discharged home after 5 days.

Early and accurate diagnosis by MRI and CSF findings and prompt treatment with acyclovir helped in early and complete recovery.

Table 1: Features of meningitis, encephalitis, and meningoencephalitis
Meningitis Encephalitis Meningoencephalitis
Causes Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis Herpes simplex virus (HSV), varicella-zoster virus (VZV), enterovirus HSV, VZV, listeria
Systemic signs and symptoms (fever, endocytosis) Present Present Present
Meningeal signs Present Not seen Present
Mental status changes Sometimes Hallmark feature Incidence more than in meningitis
Seizures Uncommon Often
Focal neurological deficits 50% of patients—usually late in the course Hallmark feature More often than meningitis
Table 2: Clinical features of viral encephalitis1
Altered level of consciousness Dysphasia
Agitation Seizures
Inattentiveness Cranial neuropathies
Drowsiness Focal deficits in limbs
Comatose Movement disorders
Impaired cognition Meningism
Confusion Photophobia
Disorientation Neck stiffness
Amnesia Headache
Behavioral change
Table 3: MRI findings in common encephalitis in India
Type Site MRI findings
Herpes simplex virus 14 Frontal and temporal lobes. Rarely extratemporal T2 hyperintensity, diffusion restriction, sometimes hemorrhage
Herpes simplex virus 24 Diffuse brain involvement T2 hyperintensity, diffusion restriction, sometimes hemorrhage
Japanese encephalitis5,6 Thalami is commonly involved. Basal ganglia, pons, midbrain, cerebellum are involved T2 hyperintensity, restricted diffusion, sometimes hemorrhage (Fig. 11)
Dengue encephalitis7,8 Bilateral thalami, pons, medulla Hyperintensity on T2 images with areas of restricted diffusion, sometimes petechial hemorrhages and diffuse cerebral edema are seen (Fig. 10)
COVID-19 encephalitis3,9,10 Mesial temporal lobe, white matter lesions Unilateral FLAIR and/or diffusion hyperintensities in the mesial temporal lobe (Fig. 9) followed by non-confluent, multifocal white matter hyperintensities, variable white matter microhemorrhages (Fig. 8)
HIV encephalitis11,12 Periventricular and deep white matter Diffuse cerebral atrophy, T2 hyperintensities in periventricular, deep white matter

Figs 8A and B: (A) Diffusion-weighted image (DWI) of the brain showed high signal intensity at the site of splenium of corpus callosum; (B) ADC map extracted from DWI demonstrated a slight decrease in ADC value on the same lesion

Figs 9A to D: Axial FLAIR in four different COVID-19 patients (A) FLAIR hyperintensities located in the left medial temporal lobe; (B) FLAIR ovoid hyperintense lesion located in the central part of splenium of corpus collosum; (C) Extensive and confluent supratentorial white matter FLAIR hyperintensities; (D) Hyperintense lesions involving both middle cerebellar peduncles

Figs 10A to F: Axial FLAIR images show bilateral symmetrical hyperintensities in thalami, pons, bilateral temporal lobe and cerebellum (A and B). GRE image show loss of signal in bilateral thalamus (C). DWI and ADC images shows restriction on diffusion in bilateral thalamus (D and E). Post contrast image show peripheral enhancement in bilateral thalami (F)

Figs 11A and B: (A) MRI, T2 FLAIR (fluid-attenuated inversion recovery) depicting symmetrical hyperintense signals in bilateral thalamus and basal ganglia; (B) T2 FLAIR image demonstrated hyperintense signal changes in midbrain

A CT scan or MRI of the head is frequently ordered by clinicians prior to performing a lumbar puncture to rule out an intracranial abnormality which can cause a herniation.

Infectious Diseases Society of America16 recommends imaging before lumbar puncture in the following conditions:

Despite guidelines, many clinicians tend to perform imaging before lumbar puncture which leads to delays in diagnosis and institution of treatment. Swedish guidelines modified earlier recommendations and removed altered mental status from the list of indications to perform imaging before lumbar puncture, this practice has led to earlier treatment and better outcomes.17


Magnetic resonance imaging is an important step in the approach to patients with suspected viral encephalitis and MRI patterns specific for a few diseases. Knowledge about various patterns helps in early appropriate diagnosis and management.


Sarath Kumar


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