Noninvasive Ventilation in Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis is a progressive neurodegenerative disease involving upper and lower motor neurons and has limited treatment options. The weakness progresses to involve the diaphragms, resulting in respiratory failure and death. Home noninvasive ventilation has been shown to improve survival and quality of life, especially in those with intact bulbar function. Once initiated, close monitoring with nocturnal oximetry, remote downloads from the home noninvasive ventilation machine, and measurement of serum bicarbonate should be conducted. Additionally, transcutaneous CO2 monitoring can be considered if available. This article discusses the indications, timing, initiation, and management of noninvasive ventilation in amyotrophic lateral sclerosis.

Portable Monitoring for the Diagnosis of OSA.

In-laboratory, attended polysomnography has long been the gold standard for the diagnosis of sleep-disordered breathing (SDB). In recent years, economic pressures and long wait times have driven interest in home sleep testing, which has, in turn, led to the development of algorithms that bypass the sleep laboratory in favor of portable monitoring studies and in-home initiation of positive airway pressure therapy. For appropriately selected outpatients, evidence is accumulating that portable monitors are a reasonable substitute for in-laboratory polysomnography. In the inpatient setting, in which SDB is both highly prevalent and associated with adverse outcomes in certain populations, the literature is evolving on the use of portable monitors to expedite diagnosis and treatment of SDB. This review discusses society guidelines and recent research in the growing field of portable monitoring.

Behavioral evaluation of rats following low-level inhalation exposure to sarin.

We evaluated the effects, in rats, of single and multiple low-level inhalation exposures to sarin. Rats were trained on a variable-interval, 56 s (VI56) schedule of food reinforcement and then exposed to sarin vapor (1.7-4.0 mg/m(3) x 60 min) or air control. The exposures did not produce clinical signs of toxicity other than miosis. Subsequently, performance on the VI56 and acquisition of a radial-arm maze spatial memory task was evaluated over approximately 11 weeks. Single exposures did not affect performance on the VI56 and had little effect on acquisition of the radial-arm maze task. Multiple exposures (4.0 mg/m(3) x 60 min/day x 3) disrupted performance on the VI56 schedule during the initial post-exposure sessions. The disruption, however, resolved after several days. Multiple exposures also produced a deficit on the radial-arm maze task in that sarin-exposed rats tended to take it longer to complete the maze and to make more errors. The deficit, however, resolved during the first three weeks of acquisition. These results demonstrate that in rats, inhalation exposure to sarin at levels below those causing overt signs of clinical toxicity can produce cognitive and performance deficits. Furthermore, the observed deficits do not appear to be persistent.