LETTER TO THE EDITOR
|Year : 2016 | Volume
| Issue : 2 | Page : 164-165
Status epilepticus in a child with influenza A H1N1 infection: An expansion of neurological abnormalities
Rohan R Mahale, Anish Mehta, Srinivasa Rangasetty
Department of Neurology, MS Ramaiah Medical College and Hospital, Bengaluru, Karnataka, India
|Date of Web Publication||3-Aug-2016|
Rohan R Mahale
Department of Neurology, MS Ramaiah Medical College and Hospital, Bengaluru - 560 054, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mahale RR, Mehta A, Rangasetty S. Status epilepticus in a child with influenza A H1N1 infection: An expansion of neurological abnormalities. J Pediatr Neurosci 2016;11:164-5
The first case of a novel H1N1 influenza A virus was detected in Mexico in 2009. A global pandemic was declared by June of 2009. Pandemic A/H1N1 virus affected 60 million people worldwide and accounted for over 12,000 deaths.  Neurological manifestations associated with pandemic A/H1N1 virus include encephalopathy, encephalitis, meningitis, and seizures. We report a 5-year-old child who presented with febrile status epilepticus (SE) and was found to have reverse transcription polymerase chain reaction (RT-PCR) positivity in the nasopharyngeal swab for A/H1N1 virus infection.
A 5-year-old girl was brought with the history of fever of 2 days with dry cough. She had one episode of generalized tonic-clonic seizure (GTCS) with prolonged postictal state in home. After admission, she had two more episodes of GTCS with no recovery of sensorium in between episodes suggesting SE. There was no vomiting, loose stools, or weakness of limbs. Her motor and language milestones were normal. On examination, she was febrile (100.2°C); pulse rate was 130/min, blood pressure of 102/78 mm Hg, and respiratory rate of 24 cycles/min. There was throat congestion. Neurologically, she was obtunded with eye opening to mild painful stimulus. She was moving all limbs to mild painful stimulus. There was no neck stiffness. Fundus examination was normal. Deep tendon reflexes were present with mute plantar response. Complete hemogram showed leukocytosis with normal platelet count. Renal and hepatic functions including serum electrolytes were normal. Arterial blood gas analysis did not show abnormality. Brain magnetic resonance imaging with contrast was normal. Electroencephalogram showed epileptiform discharges in the form of spikes from the both hemispheres [Figure 1]. Cerebrospinal fluid (CSF) examination was normal including negative deoxynucleic acid PCR for herpes simplex virus. Dengue serology was negative. Nasopharyngeal swab RT-PCR for A/H1N1 virus infection was positive. She was started on oseltamivir, phenytoin with the addition of sodium valproate subsequently as seizure recurred with phenytoin. She regained sensorium within 48 h of admission. She was discharged after 1 week and was afebrile with no recurrence of seizures.
|Figure 1: Electroencephalogram (bipolar longitudinal montage, sensitivity 7.5 mV/mm, low-frequency filter 1 Hz, high-frequency filter 70 Hz, notch 50 Hz, speed 30 mm/s) shows spikes discharge from the both hemispheres|
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A/(H1N1) affected individuals mainly <24 years of age, including young children. Nearly 13% of affected individuals were between the ages of 0 and 4 years and 60% were between 5 and 24 years.  The neurological manifestations of influenza A (H1N1) are well-documented and consist of seizures and/or encephalopathy in approximately 7% of H1N1 cases.  SE is a rare complication of H1N1 infection in both pediatric and adult population. H1N1 infection usually presents initially as a febrile respiratory illness with subsequent progression to involve multiple systems. The pathogenesis of neurological complications of H1N1 infection is not fully understood. H1N1 virus or its RNA detection in the CSF of few reported patients may suggest direct viral penetration into the central nervous system (CNS). However, CSF of H1N1 infected patients having neurological complications shows lack of pleocytosis and viral PCR has been negative on many occasions. This suggests rather indirect virus-induced inflammatory process than direct CNS invasion. It has been demonstrated that the neurotoxic effects are due to massive cytokine release from the virus-stimulated glial cells.  Children with preexisting neurological conditions are 6.5 times more likely to have CNS complications.
There are few reports on the occurrence of SE in children with seizures complicating H1N1 infection worldwide. Yildizdas et al. reported eight children with neurological complications, four of them had SE and all had full recovery.  Glaser et al., reported 44 cases of seizures related to severe H1N1 virus infection from California, but the occurrence of SE in these patients were not commented.  Okumura et al. reported twenty children with H1N1 encephalopathy from Japan, of them four had SE. 
H1N1 infection can present as SE on initial presentation. H1N1 infection should be considered as one of the infective etiologies for SE regardless of the patient's age. This report expands the neurological abnormalities in A/H1N1 virus infection. SE due to H1N1 infection in pediatric age group has not been reported so far from the Indian subcontinent.
We would like to thank Dr. ATK Rau, Professor of Paediatrics, MS Ramaiah Medical College and Hospital, Bengaluru, India.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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