Legal and Regulatory Aspects of Sleep Disorders.

Sleep disorders may interact with the law, making awareness important. Insufficient sleep and obstructive sleep apnea (OSA) are prevalent and associated with excessive sleepiness. Patients with excessive sleepiness may have civil or criminal liability if they fall asleep and cause a motor vehicle accident. Awareness of screening and treatment of OSA is increasing in certain industries. Parasomnia associated sleep-related violence represents a challenge to clinicians, who may be called on to consider parasomnia as a contributing, mitigating, or exculpatory factor in criminal proceedings. Improving access to sleep medicine care is an important aspect in reducing the consequences of sleep disorders.

Sleep-Disordered Breathing in Duchenne Muscular Dystrophy: An Assessment of the Literature.

STUDY OBJECTIVES: The aim of this review is to review the literature on sleep-disordered breathing in Duchenne muscular dystrophy (DMD). METHODS: PubMed was searched with an array of search terms, including "OSA," "obstructive sleep apnea," "sleep-disordered breathing," "muscular dystrophy," "neuromuscular," "Duchenne muscular dystrophy," "polysomnography," and "portable monitoring." All relevant articles were discussed. RESULTS: Eighteen research articles and 1 consensus statement were reviewed, and assessed with relevant data presented. Three early studies prior to 1990 assessed DMD associated obstructive sleep apnea. Five studies assessed positive airway pressure (PAP) ventilation and/or sleep in varying neuromuscular disorders, including a cohort with DMD. Six studies since 2000 include PSG data in exclusively DMD cohorts. Three studies involved portable monitoring (PM). CONCLUSIONS: PSG with transcutaneous CO2 capnography is an important part of the clinical care for those with DMD. The utility of PM in DMD is unclear with only 1 study to date comparing PSG to PM data. Initiation of PAP therapy using bilevel modality may prevent the need for device switching as the disease progresses.

Manual quantitative assessment of amplitude and sleep stage distribution of excessive fragmentary myoclonus.

INTRODUCTION: Excessive fragmentary myoclonus (EFM) consists of brief, asynchronous, twitch-like movements appearing asymmetrically in sleep. The new AASM Manual for the Scoring of Sleep and Associated Events identifies some EFM scoring criteria but does not provide amplitude criteria for scoring EFM. Older observational series have used 50 µVs. We report data from various amplitude criteria using blinded comparisons. METHODS: EFMs were analyzed on the polysomnograms of 8 patients (7 men and 1 woman, mean age 57 years, range: 47-79) using a standardized protocol for sensitivity, tonus threshold, impedance, amplitude measurements, and sleep stage. The first 20 minutes each of wake, Stage 1-2, SWS, and REM were analyzed. EFMs ≥ 25, ≥ 40, and ≥ 50 microvolts (µVs) in negative deflection above the baseline were counted in tibialis anterior muscle electromyography (EMG) channels bilaterally. RESULTS: The mean EFM index per minute for wake, regardless of impedance, was: 7.19 ± 5.90 for ≥ 25 µV amplitude; 2.43 ± 2.02 for ≥ 40 µVs; and 2.08 ± 2.23 for ≥ 50 µVs. For sleep stages, the EFM index by stage and amplitude criteria used for measurements were: Stage 1-2: 7.38 ± 5.79 for ≥ 25 µVs; 3.13 ± 3.33 for ≥ 40 µVs; and 2.36 ± 2.66 for ≥ 50 µVs; SWS: 10.05 ± 8.04 for ≥ 25 µVs; 2.71 ± 3.13 for ≥ 40 µVs; and 1.38 ± 1.92 for ≥ 50 µVs; Total REM: 15.96 ± 11.32 for ≥ 25 µVs; 6.32 ± 4.25 for ≥ 40 µVs; and 3.94 ± 3.73 for ≥ 50 µVs; Phasic REM: 19.69 ± 15.45 for ≥ 25 µVs; 8.63 ± 7.06 for ≥ 40 µVs; and 5.52 ± 6.44 for ≥ 50 µVs; Non-phasic REM: 13.93 ± 11.31 for ≥ 25 µVs; 5.16 ± 3.57 for ≥ 40 µVs; and 3.20 ± 2.92 for ≥ 50 µVs. CONCLUSION: EFM rates increase with SWS and total REM with the highest EFM rates occurring during phasic REM. EFM rates were increased across all sleep stages when impedance was > 30 KΩ.

Application of hidden Markov random field approach for quantification of perfusion/diffusion mismatch in acute ischemic stroke.

The perfusion/diffusion 'mismatch model' in acute ischemic stroke provides the potential to more accurately understand the consequences of thrombolytic therapy on an individual patient basis. Few methods exist to quantify mismatch extent (ischemic penumbra) and none have shown a robust ability to predict infarcted tissue outcome. Hidden Markov random field (HMRF) approaches have been used successfully in many other applications. The aim of the study was to develop a method for rapid and reliable identification and quantification of perfusion/diffusion mismatch using an HMRF approach. An HMRF model was used in combination with automated contralateral identification to segment normal tissue from non-infarcted tissue with perfusion abnormality. The infarct was used as a seed point to initialize segmentation, along with the contralateral mirror tissue. The two seeds were then allowed to compete for ownership of all unclassified tissue. In addition, a novel method was presented for quantifying tissue salvageability by weighting the volume with the degree of hypoperfusion, allowing the penumbra voxels to contribute unequal potential damage estimates. Simulated and in vivo datasets were processed and compared with results from a conventional thresholding approach. Both simulated and in vivo experiments demonstrated a dramatic improvement in accuracy with the proposed technique. For the simulated dataset, the mean absolute error decreased from 171.9% with conventional thresholding to 2.9% for the delay-weighted HMRF approach. For the in vivo dataset, the mean absolute error decreased from 564.6% for thresholding to 34.2% for the delay-weighted HMRF approach. The described method represents a significant improvement over thresholding techniques.