LETTER TO EDITOR
|Year : 2009 | Volume
| Issue : 2 | Page : 141-143
Acute encephalopathy associated rotavirus gastroenteritis
Faruk Incecik, M Ozlem Herguner, Sakir Altunbasak, Huseyin Solgun
Division of Pediatric Neurology, Department of Pediatrics, Çukurova University Faculty of Medicine, Adana, Turkey
|Date of Web Publication||29-Oct-2009|
Toros Mah. 40. sok. Ömer Bayram Havuz apt. Kat: 11, No: 11, Adana, Türkiye
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Incecik F, Herguner M O, Altunbasak S, Solgun H. Acute encephalopathy associated rotavirus gastroenteritis. J Pediatr Neurosci 2009;4:141-3
Rotavirus infection is usually characterised by diarrhea, vomiting and dehydration.  Recently central nervous system (CNS) involvement has also been reported in patients with rotavirus gastroenteritis. ,
A previously healthy 13-month-old girl infant was admitted to our clinic with the complaints of a 3-4 days history of watery, non-bloody diarrhea, vomiting, mild fever and loss of conciousness. She had also manifested generalised tonic-clonic (GTC) convulsions within last twelve hours. She was born at term after an uneventful pregnancy. There were no convulsive disorders in her family history. Her developmental milestones were normal. She was lethargic on admission and her physical examination was consistent with mild dehydratation.
Laboratory examination revealed the following laboratory values: C-reactive protein 6.8 mg/dl, aspartate aminotransferase 66 IU/L, alanine aminotransferase 51 IU/L, blood urea nitrogen 31 mg/dl, creatinine 0.5 mg/dl. Hemogram, serum sodium, potassium, glucose, albumin, calcium, and magnesium levels were also normal. Cerebrospinal fluid (CSF) sample showed normal cell counts, glucose and protein levels. Rotavirus antigen was detected in stools by latex agglutination. Cultures of blood, CSF, urine, throat, and stool samples were negative. The serum and urine aminoacids and organic acid analysis in urine were no abnormality. Magnetic resonance imaging (MRI) of the brain and inter-ictal electroencephalogram (EEG) were normal. The diagnosis of mild dehydration, acute encephalopathy and seizure due to rotavirus infection was made, and the patient was treated with intravenous hydration and short lasting phenobarbitale.
Rotavirus is the primary cause of severe gastroenteritis in children in the winter and spring. Infection is localized in the intestine, and only rare reports suggest any morbidity resulting from extraintestinal involvement. Recently, however a number of investigators have reported CNS complications in association with rotavirus gastroenteritis. ,
There are many reports indicating the incidence of CNS involvement at rotavirus gastroenteritis as 2-5.3%. Concomination of CNS involvement to rotavirus infection can represent by different clinical findings. Menengitis, encephalitis, encephalopathy, febrile and afebrile convulsions, hemorrhagic shock, Guillian Barre syndrome and Reye syndrome are the reported neurological antites untill now.  Our patient showed a neurological involvement of encephalopathy and seizures during gastroenteritis. Encephalopathic findings started after the diarrhea, addiationaly as CSF and serum electrolyties and cranial imagining findings were normal; diagnose of encephalopathy was corrected.
Until now, although some hypothesis about the mechanism of rotavirus CNS involvement, it is unclear. Ushijima et al. established rotavirus both at intestinal and CSF observation; so by this knowledge rotavirus seem to make CNS invasion after a primer intestinal enfection.
McCormak.  reported concominance of rashes at a rate of 5% with rotavirus gastroenteritis. This concominance may indicate CNS involvement by viremia. But viremia is thought to be at least three days later. Our patient showed encephalopathy signs after the 3-4 days of diarrhea, but no rashes. Minami et al. measured elevation at serum IL-6 and TNF- a, CSF IL-6 and IL-8 levels so relationaly reported the cause of encephalopaty as systemic immune response to cytotoxicity. Rotavirus may cause damage directly at neuronal cells by replication or indirectly to neurological complications by enterotoxine spreading to CNS. Ball et al. reported that virus and its' particules can spread to CSF by destruction of the blood-brain barier. An other hypothesis is establishment of rotavirus at CSF and gaita; can represent that rotavirus has an affinity to neuronal cells and it is neurotropic. 
Concominance of febril and afebrile convulsions to rotavirus gastroenteritis reported as 1.2-6.4 % at studies. Chen et al. at Taiwan reported the incidences of convulsions as 6.4%, Lynch et al. at US as 4%, Wong  at Hong Kong as 3.5%, Abe et al. at Japan as 2.6%, and Swanson et al. as 1.2% at US.
Electrolyte imbalances, destructýon of bood-brain barier by fever or encephalopaty and encephalitis are the causes for occurence of convulsions. Usually recürrence convulsions and encephalopathy at rotavirus enfection show a benýng course. In our patient recurrrence convulsions occured at the 3-4.th day of gastroenteritis and didn't repeated at the following 3 month of controls and the EEG and neurological signs seem to be normal.
Convulsions due to rotavirus are reported to be tonic clonic and GTC.  In our patient GTC convulsions were observed. As previously our patients' had a normal mental motor development, the observed convulsions were GTC; serum electrolyties, CSF, EEG and neuroimaging were normal, prognosis was well and at gaita examination ratovirus was determýned the clinic findings thought to be due to rotavirus related encephalopathy.
In conclusion; rotavirus gastroenteritis seem frequently in our country and can show different clinical courses. If diarrhea is concominated with encaphalopathy and convulsions at child; rotavirus must to be thought at etiologic.
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