Journal of Neuroinfectious Diseases
Open Access

Influenza, commonly known as the flu, is a viral respiratory infection that affects millions of people worldwide each year. While most cases are self-limiting, influenza can occasionally lead to severe complications, one of the most serious being influenza-associated encephalopathy (IAE). IAE is a rare neurological complication characterized by acute brain dysfunction following influenza infection. It primarily affects children, especially those under five years of age, but can also occur in adults. The condition carries significant morbidity and mortality if not recognized and managed promptly. Understanding its clinical features, risk factors, and management strategies is essential for improving outcomes [1,2].

Discussion

Influenza-associated encephalopathy typically develops within 1–4 days after the onset of influenza symptoms. Patients may present with sudden fever, vomiting, altered consciousness, seizures, and in severe cases, coma. The pathophysiology of IAE is not fully understood, but it is thought to involve an excessive immune response rather than direct viral invasion of the central nervous system. Cytokine dysregulation, particularly elevated levels of interleukins and tumor necrosis factor, is believed to contribute to brain edema and neuronal damage. Genetic susceptibility, such as mutations in the RANBP2 gene, has been identified in certain populations, increasing the risk of severe IAE [3-6].

Epidemiologically, IAE has been reported worldwide, with higher incidence in East Asian countries like Japan, where annual surveillance highlights the condition as a significant pediatric concern. Mortality rates vary from 10% to 30%, and long-term neurological sequelae, including cognitive impairment, motor deficits, and epilepsy, are observed in a substantial proportion of survivors. Early recognition is crucial, as rapid deterioration can occur, and delayed intervention is associated with worse outcomes [7,8].

Diagnosis of IAE relies on clinical suspicion, especially during influenza outbreaks. Laboratory tests typically show normal cerebrospinal fluid or mild protein elevation, while imaging such as MRI may reveal brain edema or lesions in the thalamus, brainstem, or cerebellum. Electroencephalography can show diffuse slowing indicative of encephalopathy. Differential diagnosis includes other causes of acute encephalopathy, such as bacterial meningitis, viral encephalitis, metabolic disorders, and post-infectious syndromes [9,10].

Management of IAE is primarily supportive. Patients may require intensive care, including mechanical ventilation, seizure control, and management of increased intracranial pressure. Antiviral therapy, such as oseltamivir, is recommended early in the course of influenza to reduce viral replication, although its direct effect on neurological outcomes is unclear.

Conclusion

Influenza-associated encephalopathy, though rare, is a severe complication of influenza infection with high potential for mortality and long-term neurological impairment. Prompt recognition, supportive management, and early antiviral therapy are essential to improve outcomes. Public health measures, including vaccination, remain vital in preventing influenza and its associated complications. Increased awareness among clinicians, caregivers, and public health authorities is crucial, particularly during seasonal influenza outbreaks, to reduce the burden of this potentially devastating condition.

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