Psychiatric manifestations in a case of viral limbic encephalitis

Limbic encephalitis (LE), first described by Brierley et al. in 1960,[1] usually involving the medial temporal lobe, cingulate cortex, or hippocampus.[2] The clinical picture includes subacute recent onset of short-term memory loss, cognitive deficits,[3] confusion, seizures, autonomic disturbances, and sleep disturbances.[4] It is a rare cause of encephalitis and may or may not be associated with paraneoplastic cancers. The prognosis of the patient is better if the diagnosis is clinched early and prompt treatment is instituted.[1] Psychiatrists should keep the diagnosis of LE in mind when the patient presents with psychiatric manifestations along with seizures.

A 60-year-old male, a known case of diabetes mellitus, hypertension, cerebrovascular accident, seizure disorder with poor drug compliance, and irregular follow-up presented with a history of multiple episodes of generalized tonic-clonic seizures within a span of 3 h. The patient had also developed vesicular lesions over the face on the right side, 3 days before onset of seizures. He was treated with injection levetiracetam 1000 mg for episodes of seizures in Emergency when the call was placed to the psychiatrist to rule out alcohol withdrawal. History revealed that the patient was a moderate drinker for the last 25 years and the last drink consumed was 3 days ago. The patient was asymptomatic till the onset of seizures. Mental status examination revealed an ill-kempt, agitated, restless, confused individual with cognitive deficit. The Glasgow Coma Score (GCS) of the patient deteriorated to5 (E2V1M2) and SPO2 levels fell to 80%. In view of low GCS, not maintaining oxygen saturation levels, the patient was intubated. Hematological investigations, biochemical parameters, serum electrolytes, liver function tests were unremarkable. Cerebrospinal fluid (CSF) analysis revealed lymphocytosis, raised protein, and globulin levels which was suggestive of viral etiology. Noncontrast enhanced computed tomography head showed cerebral edema and ill-defined hypodense lesions in the temporal region. Magnetic resonance imaging (MRI) [Figure 1] T2-weighted and fluid-attenuated inversion recovery revealed hyperintense lesions in medial temporal lobes and cingulate gyrus which were compatible with LE. Based on the suspected facial lesions, investigations suggesting viral etiology, and suboptimal response to treatment, the patient was started on injection acyclovir 600 mg intravenously thrice a day along with antiepileptic medications. The patient was taken off ventilator and sedation was stopped on 4^th day. On reassessment, he was found to be aggressive and restless. Mental status examination revealed an ill-kempt, uncooperative individual with increased motor activity with agitation and aggressive behavior. Speech was incoherent, most of the time struggling at high pitch. The patient had fluctuating levels of consciousness and had memory loss. The clinical cognitive evaluation revealed attention to be arousable; however, concentration was ill-sustained. Following antiviral and antiepileptic medications, the patient's mental status improved over the next 2 weeks. However, he had less improvement in cognitive deficits. Over the following 2 weeks, overall gradual improvement was observed and the patient's behavior became less disorganized and became ambulatory.

Figure 1.

Magnetic resonance imaging showing hyperintense lesions in both medial temporal lobes compatible with limbic gyrus

LE shows many symptoms ranging from delusions, confusion, hallucinations, aggression, irritability, memory impairment, and seizure disorders. The medial temporal lobe is the usual site of origin of seizures. It later develops into secondary generalized seizures which are resistive to most of the anti-epileptic drugs.[5] The triggering factors may be paraneoplastic tumors, viral infections, or immune checkpoint inhibitors There are multiple antibodies which are responsible for diverse symptoms present in the patients. Imaging and CSF analysis is required to rule out tumors and viral encephalitis respectively.[6] LE generally presents in individuals over the age of 45 years and gender depends on the type of antibody present.[6] Antibodies associated with LE are initiated by a peripheral immune response.[7] The diagnostic criteria for LE include various neuropsychiatric manifestations, findings of CSF suggestive of ongoing inflammation, and typical abnormality in radio-imaging. Diagnosis is often missed and probably underreported. MRI plays a pivotal role in establishing a diagnosis, where it shows hyper-intensive lesions, usually in the medial part of the temporal lobes. Prompt treatment should be initiated to prevent long-term sequela and to allow a speedy recovery.

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The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

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