Abdominal manifestations of neurologic disorders.

A variety of disorders-including infectious, inflammatory, hereditary, and metabolic diseases-may affect both the brain and abdominal cavity, and the findings in one region may help establish the diagnosis or limit the differential diagnosis. Establishing an accurate early diagnosis enables clinicians to adequately manage these unusual diseases and potentially avert life-threatening complications. For example, an early diagnosis of Gardner syndrome enables annual sigmoid- or colonoscopy and ultrasonography. In many conditions, abdominal manifestations precede neurologic manifestations and may have prognostic significance. Patients with celiac disease more often present with abdominal manifestations such as duodenitis, slow transit time, reversal of the jejunal-ileal fold pattern, and transient small bowel intussusception than with intracranial manifestations. In other conditions, the neurologic manifestations may be the same as the presenting symptoms. For example, patients with Gardner syndrome may initially present with multiple mandibular or sinonasal osteomas. In addition, sarcoidosis may manifest with multifocal enhancing dural masses. Abdominal and neurologic manifestations may even occur simultaneously, as in several of the phakomatoses such as neurofibromatosis type 1, tuberous sclerosis complex, and von Hippel-Lindau syndrome. Ultimately, familiarity with the appearances of these conditions allows radiologists to pinpoint a diagnosis, even when imaging findings in either location are nonspecific.

Genetic susceptibility to respiratory syncytial virus infection in inbred mice.

Differences in the severity of respiratory syncytial virus (RSV)-induced lower respiratory disease in infants have been attributed to multiple environmental and genetic factors. To identify the genetic factor(s) influencing RSV susceptibility, we examined RSV infection in eight inbred mouse strains. Lung RSV titers differed significantly between mouse strains: the RSV titers were 15-fold higher in AKR/J (permissive) mice compared with C57BL/6J (resistant) mice at 4 days after inoculation. This strain-specific difference in RSV titers suggested that susceptibility to RSV infection was attributable to genetic differences between strains. To examine the mode of inheritance of RSV susceptibility, F1 and backcross (F1 x AKR/J) progeny were infected and RSV titers determined. RSV titers in the F1 progeny were similar to those found in the resistant (C57BL/6J) parent, suggesting resistance was inherited as a dominant trait. The distribution of RSV titers in backcross progeny were discordant with that predicted for a single gene effect, suggesting susceptibility was influenced by more than one gene. These data suggest that RSV susceptibility is a multigenic trait that should be amenable to resolution by genomic analysis.