Otoacoustic emissions as a screening test for hearing impairment in children recovering from acute bacterial meningitis

OBJECTIVES: To study the efficacy of otoacoustic emissions (OAEs) as a screening test for hearing impairment in children with acute bacterial meningitis. Hearing tests were performed before discharge from the hospital in an attempt to improve coverage and avoid delays in the diagnosis of postmeningitic hearing loss. METHODS: Children with bacterial meningitis were recruited from 21 centers. In the 48 hours before discharge from the hospital, all patients underwent a thorough audiologic assessment consisting of transient evoked OAEs, auditory brainstem responses (ABRs), otoscopy, and tympanometry. Hearing loss was defined as ABR threshold >/=30 dB. The results of OAE screening were compared with the gold standard of ABR threshold. RESULTS: Of 124 children recruited, we were able to perform both OAEs and ABRs on 110 children. Seven (6.3%) of the 110 children had ABR threshold >/=30 dB; 2 had sensorineural hearing loss and 5 had conductive hearing loss. At follow-up, hearing loss persisted in both cases of sensorineural hearing loss and no new cases were identified. All 7 children with hearing loss failed the OAE screening test. Ninety-four children with normal hearing thresholds passed the test, and 9 failed. Thus, the screening test had a sensitivity of 1.00 (95% confidence interval, 0.59 to 1.00), a specificity of 0.91 (0.85 to 0.97), a positive predictive value of 0. 44 (0.20 to 0.70), and a negative predictive value of 1.00 (0.96 to 1.00). CONCLUSIONS: OAE screening in children recovering from meningitis was found to be feasible and effective. The test was highly sensitive and reasonably specific. Inpatient OAE screening should allow early diagnosis of postmeningitic hearing loss and prompt auditory rehabilitation.     

Screening for medium chain acyl-CoA dehydrogenase deficiency using electrospray ionisation tandem mass spectrometry

OBJECTIVE: To establish criteria for the diagnosis of medium chain acyl-CoA dehydrogenase (MCAD) deficiency in the UK population using a method in which carnitine species eluted from blood spots are butylated and analysed by electrospray ionisation tandem mass spectrometry (ESI-MS/MS). DESIGN: Four groups were studied: (1) 35 children, aged 4 days to 16.2 years, with proven MCAD deficiency (mostly homozygous for the A985G mutation, none receiving carnitine supplements); (2) 2168 control children; (3) 482 neonates; and (4) 15 MCAD heterozygotes. RESULTS: All patients with MCAD deficiency had an octanoylcarnitine concentration ([C8-Cn]) > 0.38 microM and no accumulation of carnitine species > C10 or < C6. Among the patients with MCAD deficiency, the [C8-Cn] was significantly lower in children > 10 weeks old and in children with carnitine depletion (free carnitine < 20 microM). Neonatal blood spots from patients with MCAD deficiency had a [C8-Cn] > 1.5 microM, whereas in heterozygotes and other normal neonates the [C8-Cn] was < 1.0 microM. In contrast, the blood spot [C8-Cn] in eight of 27 patients with MCAD deficiency > 10 weeks old fell within the same range as five of 15 MCAD heterozygotes (0.38-1.0 microM). However, the free carnitine concentrations were reduced (< 20 microM) in the patients with MCAD deficiency but normal in the heterozygotes. CONCLUSIONS: Criteria for the diagnosis of MCAD deficiency using ESI-MS/MS must take account of age and carnitine depletion. If screening is undertaken at 7-10 days, the number of false positive and negative results should be negligible. Because there have been no instances of death or neurological damage following diagnosis of MCAD deficiency in our patient group, a strong case can be made for neonatal screening for MCAD deficiency in the UK.     

Is there a final common neural pathway in delirium? Focus on acetylcholine and dopamine

This article reviews the literature relevant to improving our understanding of the neural underpinnings of delirium. That the characteristic symptoms of delirium occur as a result of a wide diversity of causes supports the concept of a "final common pathway. " What constitutes this may involve certain brain regions or circuits and certain neurotransmitters. Neuroanatomical data derived from neuroimaging and lesion reports suggest the importance of pathways in prefrontal cortex, thalamus, fusiform cortex, posterior parietal cortex, and basal ganglia. Neurotransmitters most implicated in delirium that could be candidates to mediate the characteristic symptoms of delirium, as well as the electroencephalogram changes, are acetylcholine and dopamine. Acetylcholine deficiency and dopamine excess---absolute and/or relative to each other---appear to be critical in the final common pathway. These neurotransmitters affect each other, depending on the receptor subtype, and their receptor distribution among layers of cortex in areas such as prefrontal cortex and temporal lobe suggests that cholinergic and dopaminergic neurons could interact with each other during delirium. Electroconvulsive therapy is described as a special situation in which excess dopamine and delirium may have a therapeutic effect on depression recovery, in contrast with the usual association of delirium with negative effects.     

A Randomized Controlled Trial Comparing the Effects of Yoga With an Active Control on Ambulatory Blood Pressure in Individuals With Prehypertension and Stage 1 Hypertension

The purpose of this study was to compare the effects of yoga with an active control (nonaerobic exercise) in individuals with prehypertension and stage 1 hypertension. A randomized clinical trial was performed using two arms: (1) yoga and (2) active control. Primary outcomes were 24‐hour day and night ambulatory systolic and diastolic blood pressures. Within‐group and between‐group analyses were performed using paired t tests and repeated‐measures analysis of variance (time × group), respectively. Eighty‐four participants enrolled, with 68 participants completing the trial. Within‐group analyses found 24‐hour diastolic, night diastolic, and mean arterial pressure all significantly reduced in the yoga group (?3.93, ?4.7, ?4.23 mm Hg, respectively) but no significant within‐group changes in the active control group. Direct comparisons of the yoga intervention with the control group found a single blood pressure variable (diastolic night) to be significantly different (P=.038). This study has demonstrated that a yoga intervention can lower blood pressure in patients with mild hypertension. Although this study was not adequately powered to show between‐group differences, the size of the yoga‐induced blood pressure reduction appears to justify performing a definitive trial of this intervention to test whether it can provide meaningful therapeutic value for the management of hypertension.