Chemotherapy appears to be an effective primary postoperative treatment for many malignant brain tumors in young children. Disease control for one or two years in a large minority of patients permitted a delay in the delivery of radiation and, on the basis of preliminary results, a reduction in neurotoxicity. For patients who had undergone total surgical resection or who had a complete response to chemotherapy, the results are sufficiently encouraging to suggest that radiation therapy may not be needed in this subgroup of children after at least one year of chemotherapy.
ABSTRACT. Objective. To describe the epidemiologic, clinical, neuroimaging, and laboratory features; treatment; and outcome in a cohort of children with acute disseminated encephalomyelitis (ADEM).Methods. A 6-year retrospective chart review of children with the diagnosis of ADEM was conducted.Results. Eighteen cases were identified. Sixteen patients (88%) presented in either winter or spring. Thirteen children (72%) had a recent upper respiratory tract illness. Patients presented most often with motor deficits (77%) and secondly with altered consciousness (45%). Spinal fluid abnormalities occurred in 70%. Despite rigorous microbiologic testing, a definite microbiologic diagnosis was established only in 1 child with Epstein-Barr virus disease and probable or possible diagnoses in 3 children with Bartonella henselae, Mycoplasma pneumoniae, or rotavirus disease. Brain magnetic resonance imaging identified lesions in the cerebral cortex in 80%, in subcortical white matter in 93%, in periventricular white matter in 60%, in deep gray matter in 47%, and in brainstem in 47% of patients. Eleven patients (61%) were treated with corticosteroids, and 2 were treated with intravenous immunoglobulins. All patients survived. Three patients (17%) had long-term neurologic sequelae.Conclusions. Epidemiologic evidence from this study suggests an infectious cause for ADEM. The agent is most likely a difficult-to-diagnose winter/spring respiratory virus. Magnetic resonance imaging was the neuroimaging study of choice for establishing the diagnosis and for following the course of the disease. Prognosis for survival and outcome was excellent. Recurrent episodes of ADEM must be differentiated from multiple sclerosis. Pediatrics 2002;110:e0 -e0. URL: www.pediatrics.org/cgi/ doi/10.1542/peds.; acute disseminated encephalomyelitis, ADEM, encephalitis, postinfectious encephalitis, encephalomyelitis.ABBREVIATIONS. ADEM, acute disseminated encephalomyelitis; CNS, central nervous system; MRI, magnetic resonance imaging; FLAIR, fluid-attenuated inversion recovery; PCR, polymerase chain reaction; EBV, Epstein-Barr virus; Ig, immunoglobulin; TR, repetition time; TE, echo time; NSA, number of signal averages; FOV, field of view; CT, computerized tomography; WBC, white blood cell; CSF, cerebrospinal fluid; IVIG, intravenous gammaglobulin; MS, multiple sclerosis.A cute disseminated encephalomyelitis (ADEM) is considered a monophasic acute demyelinating disorder of the central nervous system (CNS) characterized by diffuse neurologic signs and symptoms coupled with evidence of multifocal lesions of demyelination on neuroimaging. The epidemiology of ADEM has changed since its original description by Lucas 1 in the early 18th century. At that time, ADEM commonly followed common childhood infections such as measles, smallpox, and chickenpox and was associated with significant mortality and morbidity. In a series of case reports in 1931 in The Lancet, McAlpine 2 described 3 sets of patients with ADEM: 1) postvaccination, 2) after infectious fevers such a...
Rabbit NHE2 and NHE3 are two epithelial isoform Na+/H+ exchangers (NHE), the messages for which are found predominantly and entirely, respectively, in renal, intestinal, and gastric mucosa. The current studies used Western analysis and immunohistochemistry to identify and characterize the apical vs. basolateral membrane distribution of NHE2 and NHE3 in intestinal epithelial cells. Based on Western analysis, NHE2 and NHE3 both are present in brush-border but not basolateral membranes of small intestine. Both NHE2 and NHE3 are 85-kDa proteins. Consistent with Western analysis, NHE2 and NHE3 are immunolocalired to the brush-border but not basolateral membranes of villus epithelial cells, but not goblet cells, in human jejunum and ileum and in surface epithelial cells in the ascending and descending colon and rectum. In addition, NHE2 and NHE3 are present in small amounts in the crypt cell brush border of human jejunum, ileum, ascending and descending colon, and rectum. In rabbit jejunum, ileum, and ascending colon, NHE2 and NHE3 are present in the brush border of epithelial and not goblet cells, again much more in the villus (small intestine)/ surface cells (colon) than the crypt. NHE2 but not NHE3 is present in the brush border of rabbit descending colon surface cells and in small amounts in crypt cells. NHE2 and NHE3 are both human and rabbit small intestinal and colonic epithelial cell brush-border Na+/H+ exchanger isoforms that colocalize in all intestinal segments except rabbit descending colon, which lacks NHE3.
ABSTRACT. We present a case in which human coronavirus was detected in the cerebrospinal fluid of a child presumed to have acute disseminated encephalomyelitis. In murine models, coronavirus has been found to cause a chronic demyelinating condition that resembles multiple sclerosis. Additionally, there is in vitro evidence of human coronavirus's ability to infect neural cells. This case report provides additional support for the hypothesis that coronavirus may be an important etiologic factor in the pathogenesis of demyelinating disease in humans. Pediatrics 2004;113:e73-e76. URL: http://www.pediatrics. org/cgi/content/full/113/1/e73; coronavirus, HCoV, acute disseminated encephalomyelitis, ADEM, postinfectious encephalitis, demyelination, child.ABBREVIATIONS. ADEM, acute disseminated encephalomyelitis; CNS, central nervous system; MRI, magnetic resonance imaging; CSF, cerebrospinal fluid; PCR, polymerase chain reaction; IgG, immunoglobulin G; RT, reverse transcription; HCoV, human coronavirus; MS, multiple sclerosis.A cute disseminated encephalomyelitis (ADEM) is a monophasic, demyelinating disease of the central nervous system (CNS) that primarily affects children and young adults. It is characterized by high-signal-intensity lesions in the white matter of the brain and spinal cord on T2-weighted magnetic resonance imaging (MRI). These lesions may be independent of the clinical findings. Children may present with diffuse encephalopathy, seizures, optic neuritis, hemiparesis, and/or symptoms suggestive of spinal cord transection.The epidemiology of the condition is unknown. A review of cases presenting to a children's hospital suggested a prevalence of ϳ4.5 cases per 10 000 pediatric hospital admissions, exclusive of newborns. 1 The etiology of the illness is cryptogenic, although the disorder is generally thought to be due to a paraor postinfectious process. Certainly, many case reports in the literature suggest an infectious process before the onset of CNS symptoms, and some have identified specific infectious agents in cases of ADEM. [2][3][4] However, in most cases, a specific etiologic infectious agent is not identified. For example, in a recent retrospective review of cases of ADEM, clinicians were able to identify an infectious agent in only 1 of 18 cases. 1 ADEM has also been described after immunizations. 5,6 Despite reports of the possible association between infection and ADEM, there is no clear understanding of the relationship between the infectious agent and the onset of demyelination. There is experimental evidence in mice for a relationship between coronavirus and CNS demyelination. [7][8][9] Little is known, however, about this virus's relationship to demyelinating disease in humans. Indeed, there have been no case reports of this virus in relation to ADEM. We report a case of demyelinating disease in a child in which cerebrospinal fluid (CSF) and nasopharyngeal specimens were positive for human coronavirus (HCoV) by polymerase chain reaction (PCR) and in whom a fourfold rise in antibody titer ...
The Pediatric Oncology Group (1986–1990) conducted a study in which 48 children <3 years of age with intracranial ependymomas were treated with prolonged postoperative chemotherapy (CT) and delayed RT. Thirty-one children, 0–23 months of age at diagnosis (Gp A) received 2 years of CT followed by RT; while 17 children, 24–36 months of age at diagnosis (Gp B) received CT for 1 year followed by radiation. One-year survivals were 87% (Gp A) and 94% (Gp B) and 2-year survivals were 67% (Gp A) and 82% (Gp B). In subsequent years a significant divergence in survivals according to age has been noted (p = 0.04). Five-year survivals were 25.7% (Gp A) vs. 63.3% (Gp B). The curves began to diverge 1 year following diagnosis. Other than age, the only significant prognostic factor was degree of surgical resection: 5-year survivals were 66% (total resection) vs. 25% (subtotal resection). Neither the presence of metastases, degree of anaplasia nor the degree of surgical resection varied significantly according to age at diagnosis. The most likely reason for the difference in survivals between the two age groups relates to the timing of radiation following CT, i.e., 1-year delay in children 24–36 months of age compared to a 2-year delay in children 0–23 months of age. An alternative but less likely hypothesis is that ependymomas in the younger children have a more aggressive biology. In contrast, survivals in the 24- to 36-month group are much better than previous reports in the literature suggesting that prolonged postoperative CT may allow both a delay in CRT as well as provide improved survivals. Based on these results, future treatment trials should emphasize maximal surgical resection and a delay in radiation of no more than 1 year.
Acellular dermis appears to be an effective method for preventing post-parotidectomy gustatory sweating, despite its higher complication rate.
Cranial irradiation and chemotherapy may have significant long-term deleterious effects on children with brain tumors. Intellectual deterioration, endocrinopathies, leukoencephalopathy, extraneural metastases, and oncogenesis may all complicate the treatment of central nervous system neoplasia. These long-term effects of therapy have important implications, as some are amenable to treatment and others may be prevented by the careful monitoring of drug and radiation administration. Until recently, the survivals of children with brain tumors were limited, so that concerns over long-term effects of therapy were unnecessary. As children with certain types of brain tumors now have a better prognosis, these long-term and possibly remediable effects have important implications. This article emphasizes radiation effects on intellect, endocrine function, and oncogenesis. Recommendations for baseline and longitudinal evaluations of children with brain tumors are suggested.Cancer 561841-1846, 1985.HE SURVIVAL of children with certain types of brain T tumors has increased over the last two decades.Recent data from the Surveillance Epidemiology End Results (SEER) registries suggested that 5-year survival rates of children with medulloblastomas, low-grade supratentorial astrocytomas, and cerebellar astrocytomas ranged from 40% to 90%. Eight hundred sixty-five children with brain tumors diagnosed from 1973 through 1981 from this registry had an overall 40% 5-year survival rate.' Pari pussu with these prolonged survivals has come the recognition of the potential long-term consequences of this therapy on the surviving children. Intellectual deterioration, endocrine deficiencies, leukoencephalopathy, and oncogenesis are areas of concern.The two most remarkable long-term sequelae of cranial irradiation with or without chemotherapy are the adverse effects on intelligence and endocrine function. Unfortunately, prospective evaluations of children with brain
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