Respiratory syncytial virus infection and neurologic abnormalities: retrospective cohort study

Respiratory syncytial virus is a common cause of acute respiratory infection in children. Previous reports have associated respiratory syncytial virus infection and acute neurologic symptoms, including apnea and seizures. This study examined the prevalence of acute neurologic symptoms associated with respiratory syncytial virus and non-respiratory syncytial virus respiratory infections in children requiring admission to a pediatric intensive care unit. We screened all admissions over a 4-year period at a single center, identifying children between birth and 2 years of age with bronchiolitis or acute upper respiratory infection. Children with a history of prematurity, preexisting medical conditions, or prior neurologic problems were excluded. Retrospective chart review of 236 admissions was conducted, identifying the etiology of respiratory infection and the presence or absence of acute neurologic signs or symptoms. This study demonstrated a prevalence of acute neurologic signs or symptoms in 36.4% of respiratory syncytial virus-negative patients (n = 115) and 39.1% in the respiratory syncytial virus-positive group (n = 121). Apnea, the most common symptom, was observed in 19.8% of respiratory syncytial virus-positive cases and 16.5% of negative patients. Seizures were reported in 6.6% of the positive cases and in 12.2% of the negative cohort. These differences showed no statistical significance. Although neurologic signs and symptoms are common in this population of children with acute respiratory infection, there was no significant difference in the prevalence of neurologic problems between respiratory syncytial virus-positive and -negative patients.     

Patient versus informant perspectives of Quality of Life in Mild Cognitive Impairment and Alzheimer's disease

BACKGROUND: Prior studies on Quality of Life (QOL) in Alzheimer's disease (AD) have rarely included control participants, or participants with very mild levels of cognitive impairment. Furthermore, there is little data to indicate whether or not mildly impaired patients can provide self-report QOL data or if informant reports are needed. OBJECTIVES: This study compared QOL ratings from informants and patients with mild AD (n = 26), Mild Cognitive Impairment (MCI, n = 30), and elderly controls (n = 23). METHODS: Participants (aged 60-91 years) were recruited from an outpatient memory disorder clinic. Elderly controls were recruited from the community. Measures about patients were the Dementia Quality of Life scale, the Neuropsychiatric Inventory-Questionnaire, Instrumental of Activities of Daily Living, and Mini-mental State Exam. Informant depression was assessed with the Geriatric Depression Scale. RESULTS: Results indicated that overall patient-informant agreement for MCI (M=0.24), AD (M=0.48), and controls (M=0.49) did not differ significantly. Self-reported QOL did not differ significantly across the 3 groups. For caregiver-reports, QOL in MCI again did not differ from controls but was significantly greater than QOL in AD for 2 of 6 scales, and QOL in controls was greater than AD for 4 of 6 scales. Regression analyses indicated that neuropsychiatric symptoms were the most consistent predictors of QOL. CONCLUSIONS: In summary, informant- and self-perceptions of QOL differed substantially. Results suggest that future investigators should carefully consider gathering QOL information from both informants and patients because they provide unique information regarding patient QOL and, to date, neither source of information has been established to be superior.     

Energy failure in astrocytes increases the vulnerability of neurons to spreading depression

A neuroprotective role of astrocytes has been hypothesized, but the mechanism is debated and in vivo evidence is limited. To test this hypothesis, a sublethal stressor (spreading depression) and fluorocitrate (FC), a selective inhibitor of the astrocytic Krebs cycle, were used in urethane-anaesthetized adult rats. Neuronal damage was assessed 24 h after treatment with silver stain and immunoreactivity for a 72-kDa heat-shock protein. ATP levels and mitochondrial aconitase activity, a marker indicating exposure to reactive oxygen species, were measured after 4 and 24 h. Spreading depression alone did not affect ATP levels, mitochondrial aconitase activity, or induce neuronal injury in the cortex. Local or intraventricular injection of FC significantly decreased ATP levels and mitochondrial aconitase activity, but did not produce neuronal damage. In animals receiving injections of FC and then spreading depression, there was evidence of significant neuronal stress and damage. Isocitrate, which bypasses the metabolic inhibition produced by FC, prevented all of the changes seen after the combination of FC and spreading depression. One-hour pretreatment with dimethyl sulfoxide (a scavenger of hydroxyl radicals), deferoxamine (an iron chelator) or fructose-1,6-bisphosphate also blocked inactivation of mitochondrial aconitase, ATP depletion and the neuronal damage induced by FC and spreading depression. These experiments demonstrate that inhibition of the metabolism of astrocytes, with a decrease in ATP levels, will increase the susceptibility of neurons to the stress induced by spreading depression. The neuroprotective effects of dimethyl sulfoxide, deferoxamine and fructose-1,6-bisphosphate suggest that oxidative stress contributes to the neurotoxicity in this situation.     

Bladder and sexual function among women with multiple sclerosis

OBJECTIVE: Genitourinary dysfunction is common in women with multiple sclerosis (MS), yet few studies have evaluated the association between bladder and sexual dysfunction in these women. The aim of this study was to determine factors, including demographic and bladder function, associated with sexual dysfunction in a sample of women with MS. METHODS: One hundred and thirty-three women with MS completed questionnaires related to overall heath status, bladder function and sexual function. Response frequencies and percentages were calculated for questionnaire responses. Multivariate logistic regression analyses were performed to determine predictors of sexual dysfunction. RESULTS: Sixty-one per cent of the sample indicated that they had a problem with bladder control. Forty-seven per cent of respondents indicated that their neurological problems interfered with their sex life. Over 70% of the sample reported that they enjoyed, felt aroused and experienced orgasm during sexual activity. Not having a sexual partner and the indication of bothersome neurological problems were the best predictors of sexual dysfunction. Interestingly, patients bothered by their urge incontinence had higher levels of orgasm compared to women not bothered by urge incontinence. CONCLUSIONS: Although over half of the women reported voiding symptoms, most still enjoyed, felt aroused and could experience orgasm. Neurological symptoms and lacking a sexual partner emerged as the best predictors of sexual dysfunction. Urge incontinence may not be a risk factor for an orgasm. Our findings elucidate the complex nature of sexual dysfunction in women with MS.     

Interacting effects of genetic predisposition and depression on adolescent smoking progression

OBJECTIVE: The goal of the present study was to identify specific genetic associations with smoking progression in adolescents and to determine whether these genetic effects on smoking practices are potentiated by depression symptoms. METHOD: Effects of dopamine transporter (SLC6A3) and dopamine receptor (DRD2) genetic variants on smoking progression were evaluated in a cohort of 615 adolescents, including those who had never smoked, and in a subgroup including only adolescents who had been exposed to nicotine (i.e., smoked at least a puff of a cigarette) (N=292). These adolescents were followed from 9th to 11th grade. Depression symptoms were also assessed. RESULTS: In the model of adolescents with a previous smoking experience, the likelihood of progressing to a higher level of smoking by the 11th grade increased almost twofold with each additional DRD2 A1 allele. The likelihood of smoking progression with each additional A1 allele was more pronounced among adolescents with substantial depression symptoms. The model including never-smokers revealed no significant genetic effects. Neither model revealed effects of SLC6A3. CONCLUSIONS: These results provide the first evidence, to the authors' knowledge, for an association of the DRD2 A1 allele with smoking progression among adolescents. This effect is potentiated by depression symptoms. These effects appear to be specific to adolescents who have had at least some nicotine exposure (i.e., at least a puff of a cigarette).     

Urinary incontinence and ultrasound imaging

After completing this overview of incontinence in women, readers will be able to: Explain why urinary incontinence is an under-reported condition. Describe the urinary tract. Identify risk factors for urinary incontinence. List and describe different classifications of urinary incontinence. Explain the roles of the medical history, physical examination and urinalysis in helping clinicians diagnose and treat urinary incontinence. Describe urinary incontinence diagnostic procedures. Explain the importance of ultrasound in urinary incontinence diagnosis and treatment. Discuss the potential role of ultrasound as a urinary incontinence screening tool. Classify and categorize urinary incontinence treatments from least to most invasive.