Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Herpes simplex virus (HSV) is regarded as an agent that selectively affects temporal and frontal lobes with necrosis and hemorrhage, and no case of herpes simplex encephalitis (HSE) with white matter lesion in a diffuse fashion has previously been reported. A 2-year-old boy developed high fever, right hemi-convulsions and lethargy. Computed tomography (CT) showed wedge-shaped areas of high density in the left frontal region, whereas, cerebral angiography disclosed no vascular abnormality. T1-weighted magnetic resonance imaging (MRI) demonstrated cortical changes which were similar to those illustrated by CT. However, T2-weighted images depicted further spread high intensities of the lesion. The patient's symptoms spontaneously disappeared before an antiviral drug, acyclovir, was administered. After the significant increase of HSV antibody titers in serum and cerebro-spinal fluid (CSF) established a definite diagnosis, acyclovir was intravenously given at a daily dosage of 30 mg/kg for a period of 6 days in order to prevent the recurrence of HSE. Two months later, T2-weighted MRI visualized a diffuse lesion of increased signal intensities involving the white matter of both hemispheres, while both CSF protein and myelin basic protein were significantly elevated. Despite of these changes of the white matter, our patient developed a few symptoms such as mild speech disturbance, slight weakness of the right upper limb and sialorrhea. Although the mechanism of these changes in the white matter remains obscure, it is postulated that a direct invasion of HSV to the white matter, an immunological disorder following HSV infection and a side effect of acyclovir could have triggered a reversible process of demyelination of the cerebral white matter.
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PMID:[A case of herpes simplex encephalitis with cerebral white matter lesion after acyclovir administration]. 222 88

Six infants with disseminated HSV had no mucocutaneous lesions at any time during the course of the illness. These infants presented with lethargy, poor feeding, apnea, acidosis, and hepatomegaly. The diagnosis of HSV was made by culturing the infant's oropharynx and blood, and the maternal cervix. Eight infants with HSV encephalitis had no skin, eye, or mucous membrane lesions. These infants presented with lethargy and low-grade fever, followed within 24 hours by the onset of focal partial motor seizures. The seizures were refractory to anticonvulsant therapy. The mean CSF white cell count was 131 cells/mm3;the glucose and protein concentrations were in the normal range. Brain biopsy was required for the early diagnosis of HSV encephalitis. These 14 cases presented 70% (14/20) of all infants with neonatal HSV diagnosed during the study period. HSV infection should be considered in infants with no mucocutaneous lesions who have signs usually associated with bacterial sepsis or who develop focal seizures during the first three weeks of life.
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PMID:Neonatal herpes simplex infection in the absence of mucocutaneous lesions. 706 32

Neonatal herpes simplex virus infections can result in serious morbidity and mortality. Many of the infections result from asymptomatic cervical shedding of virus after a primary episode of genital HSV in the third trimester. Antibodies to HSV-2 have been detected in approximately 20 percent of pregnant women, but only 5 percent report a history of symptomatic infection. All primary episodes of HSV and secondary episodes near term or at the time of delivery should be treated with antiviral therapy. If active HSV infection is present at the time of delivery, cesarean section should be performed. Symptomatic and asymptomatic primary genital HSV infections are associated with preterm labor and low-birth-weight infants. The diagnosis of neonatal HSV can be difficult, but it should be suspected in any newborn with irritability, lethargy, fever or poor feeding at one week of age. Diagnosis is made by culturing the blood, cerebrospinal fluid, urine and fluid from eyes, nose and mucous membranes. All newborns suspected to have or who are diagnosed with HSV infection should be treated with parenteral acyclovir.
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PMID:Neonatal herpes simplex virus infections. 1192 91

Relapse of herpes simplex virus (HSV) encephalitis following acyclovir therapy has been reported infrequently in children beyond the neonatal period. The pathogenic mechanism of the recurrence is not fully understood. We report two new cases that support a mechanism of latent HSV infection with reactivation of the disease. Our patients were 2 years (#1) and 8 months (#2) old at initial infection. Both presented with fever, lethargy, focal seizures, and focal motor abnormalities. Serum HSV antibodies (Abs) were negative. The patients were treated with acyclovir for 14 and 21 days, respectively. They were readmitted at 1 month, and 4 days after discharge, respectively, with recurrent lethargy, seizures, and choreo-athetoid movements. Serum and CSF HSV Abs were significantly increased. CSF PCR was positive. In patient # 2 acyclovir-sensitive HSV was isolated from a brain biopsy. Both patients were re-treated with acyclovir, but progressed to a neurovegetative state. In our cases, latent HSV infection and reactivation is the most likely explanation for recurrent encephalitis. The immuno-pathogenic mechanisms of the infection recurrence are discussed. Based on the reported cases in the literature, patients younger than 2 years of age and with lower total dose of acyclovir treatments have a higher risk of recurrence.
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PMID:Relapse of herpes encephalitis after acyclovir therapy: report of two new cases and review of the literature. 1562 47

Here we report an infant who had herpes simplex virus (HSV) encephalitis and sustained severe bilateral damage to the posterior frontal lobes, postcentral gyri, and the thalami despite intravenous acyclovir treatment. At 7 months of age, the patient developed infantile spasms and was treated with corticotropin injections. After 10 days of corticotropin treatment, she developed lethargy, fever, and opisthotonic posturing. Her cerebrospinal fluid again was positive for HSV DNA, indicating recurrent HSV encephalitis, and repeat MRI revealed new lesions of the right frontal, parietal, temporal, and occipital lobes. Immunosuppression by corticotropin may have led to the reactivation of the HSV encephalitis. Corticotropin should be relatively contraindicated for use when a patient has a history of HSV infection, or intravenous acyclovir should be administered concurrently.
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PMID:Herpes simplex virus central nervous system relapse during treatment of infantile spasms with corticotropin. 1660 80