Infantile nonconvulsive status epilepticus caused by herpes encephalitis

Infantile nonconvulsive status epilepticus caused by herpes encephalitis

Classic herpes simplex virus encephalitis (HSVE) is an acute viral infection that usually follows a monophasic disease course; however some patients, mainly children, experience a relapse within weeks or months after the initial event. We aimed to characterize this poorly understood population, investigating epidemiological factors potentially related to disease etiology, particularly season of onset. Louis encephalitis. The following day (2 days ago), she refused to eat. An infectious encephalitis occurred in 30%, infection-associated encephalopathy in 8%, immune-mediated/autoantibody-associated encephalitis in 34%, and unknown encephalitis in 28%. The authors report data on six children who had at least one relapse of HSE. Brain computed tomography (CT) revealed a low-density lesion in the right frontal lobe.

While the boy further clinically deteriorated and cMRI revealed diffuse hyperintensity in the right hemisphere, a repeat analysis of HSV PCR in CSF was initiated and gave a positive result. Even with early administration of therapy after the onset of disease, nearly two thirds of survivors will have significant residual neurologic deficits. An electroencephalogram (EEG) pointed out diffuse slow-wave activity without focal changes. Case report. An etiology was found in 76%: 37% infectious, 16% postinfectious, and 23% noninfectious. Lesions were extended bilaterally to frontotemporal lobes on MRI in the second week of hospitalization []. CSF examination yielded increased herpes simplex virus (HSV) Ig M (4.7 RU/ ml, N: 01 RU/ml) and Ig G (33.7 RU/ml, N: 0–20 RU/ml) antibodies.

Infantile nonconvulsive status epilepticus caused by herpes encephalitis
Acyclovir therapy was administered for 3 weeks. In Southeast Asian countries like Cambodia and Vietnam, Japanese encephalitis virus (JEV) has been the leading reported cause of acute encephalitis in children, accounting for 31% to 45% of cases [4], [5]. Focal seizures were under control on the fifth day of therapy. The CSF PCR for HSV is no longer positive, the MRI does not show new necrotic lesions, and symptoms do not respond to antiviral therapy. MRI readings were classified as normal, atrophied, or otherwise abnormal. Typically, arbovirus encephalitides begin with the acute onset of fever, headache, and vomiting; progress to signs of meningeal involvement (stiff neck and back); and go on to show evidence of neuronal damage (drowsiness, coma, paralysis, convulsions, ataxia, organic psychoses). Past Medical History: She was born via normal spontaneous vaginal delivery.

CSF examination revealed 300/mm3 erythrocytes, and CSF protein and glucose levels were 40 mg/dl and 60 mg/dl, respectively. EEG pointed out a persistent epileptic activity []. Acyclovir readjusted for recurrent HSE over 21 days. Midasolam infusions and valproat were used in order to control the epileptic activity. There was no alteration on the MRI findings. CSF examination for HSV polymerase chain reaction (PCR) and the HSV IgM antibody was negative; besides, the HSV IgG antibody level was increased up to 92.7 RU/ml (N: 0-0.20 RU/ml). She had a Glasgow coma score of 14.

In brief, clinicians submitted specimens and clinical history of suspected encephalitis cases from >220 facilities in California. Progressive mental and behavioral deterioration following herpes encephalitis has been reported.[2] Most of these patients developed intractable seizures, slowly progressive hemiparesis, and cognitive decline in a few years after contracting the disease, and neuropathological studies of these patients showed chronic active encephalitis.[2] We could not perform brain biopsy to our patient, and it is difficult to make a decision about the exact cause of the clinical picture. The prognosis of relapsing HSE cases is poor. The outcome of the majority of patients is either death, or moderate-to-severe neurological impairment. Primer and probe sequences are listed in and were all adapted from previous publications except for those targeted at Me Tri/Semliki Forest virus which were newly designed [10]. Some clinical improvement has been obtained in our patient, but not a complete recovery. Alternatively, the HSV-induced intense inflammatory response in limbic structures, usually accompanied by necrosis, could release and appropriately present abundantly expressed local NMDAR epitopes to the immunological system, breaking tolerance and initiating an autoimmune response.

Most initial EEGs were abnormal, and the majority of patients ultimately had a seizure during their disease course (N = 17 and 19 for NT-NMDARe, N = 3 and 5 for T-NMDARe for initial EEG abnormality and seizure prevalence, respectively). Louis encephalitis are uncommon. She appears to have a facial droop on the right.

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