Recent research has shown that depression in multiple sclerosis (MS) is associated with deficits on cognitively demanding tasks. One explanation for this relationship is that depressed MS patients may have reduced working memory capacity. The present study was designed to test this hypothesis. Depressed MS patients were compared with nondepressed MS patients and nondepressed healthy controls on a task of working memory capacity (reading span) and a short-term memory task not taxing working memory capacity (word span). In support of the capacity-reduction model, compared with the nondepressed groups, depressed MS patients performed significantly worse on reading span (p<.001) but not on word span. Additionally, reading span was significantly correlated with capacity-demanding tasks shown to be impaired in depressed MS patients in previous reports. Results suggest that depressed MS patients are characterized by limited working memory capacity and that the central executive component of the working memory system may be most affected.

Because it is theorized that depression results in reduced available attentional capacity that, in turn, can explain the impaired performance on capacity-demanding tasks in depressed individuals, the authors predicted that multiple sclerosis (MS) patients with depressed mood would have difficulty with these types of tasks. Twenty depressed mood MS participants were compared with 41 nondepressed mood MS participants and 8 nondepressed mood controls on 5 attentional capacity-demanding clinical memory and attentional tasks and 3 tasks with minimal capacity demands. Depressed mood MS patients performed significantly worse than both nondepressed mood groups on the 3 speeded capacity-demanding attentional measures but not on any of the tasks requiring few capacity demands, supporting the authors' predictions. The possibility that the impaired performance of depressed mood MS patients on speeded attentional tasks was mediated by reduced verbal working memory capacity, impaired deployment of executive strategies that access working memory capacity, or psychomotor slowing is explored.

This study examined if individuals who are at increased risk for drowsy-driving because of obstructive sleep apnea syndrome (OSAS), have impairments in driving performance in the moments during microsleep episodes as opposed to during periods of wakefulness. Twenty-four licensed drivers diagnosed with OSAS based on standard clinical and polysomnographic criteria, participated in an hour-long drive in a high-fidelity driving simulator with synchronous electroencephalographic (EEG) recordings for identification of microsleeps. The drivers showed significant deterioration in vehicle control during the microsleep episodes compared to driving performance in the absence of microsleeps on equivalent segments of roadway. The degree of performance decrement correlated with microsleep duration, particularly on curved roads. Results indicate that driving performance deteriorates during microsleep episodes. Detecting microsleeps in real-time and identifying how these episodes of transition between wakefulness and sleep impair driver performance is relevant to the design and implementation of countermeasures such as drowsy driver detection and alerting systems that use EEG technology.

Because the cause and natural history of amaurosis fugax and ocular infarction are unknown in most younger patients, we reviewed the records of 83 patients who had become symptomatic before the age of 45. Cerebral transient ischemic attacks had occurred in 9 of these patients but no case of stroke was found. A striking feature of these patients was that 41% had headache or orbital pain accompanying their amaurotic spells and an additional 25.3% had severe headaches independent of the visual loss. Results of laboratory studies were rarely abnormal and echocardiography disclosed that only 1 patient had previously unknown heart disease. Mitral valve prolapse was detected in 6.5%, a figure similar to that expected for the general population. Of the original 83 patients, 42 were reexamined after a mean period of 5.8 years. None of the patients in this group had had a stroke, and the clinical status at follow-up was not found to correlate with the duration of the visual loss (amaurosis fugax versus ocular infarction), frequency (single versus recurrent episodes), sex, presence of headache or heart disease, cigarette smoking, use of oral contraceptives, or abnormal findings on echocardiograms or laboratory studies. We conclude that amaurosis fugax and ocular infarction occurring in the younger patient are probably associated with a more benign clinical course than that seen in older persons and that migraine is a likely cause for the episodes of visual loss in a majority of this group. Because of this, we believe that a conservative approach to the evaluation of such patients seems warranted.

Objective-To determine the effects of obstructive sleep apnea (OSA) on visual vigilance during simulated automobile driving.Methods-Twenty-five drivers with OSA and 41 comparison drivers participated in an hour-long drive in a high fidelity driving simulator. Drivers responded to light targets flashed at seven locations across the forward horizon. Dependent measures were percent correct (hit rate, HR), and reaction time (RT). Self-assessment of sleepiness used the Stanford Sleepiness Scale (SSS) before and after the drive and the Epworth Sleepiness Scale (ESS).Results-OSA drivers showed reduced vigilance based on lower HR than comparison drivers, especially for peripheral targets (80.7 +/− 14.8% vs. 86.7 +/− 8.8%, p = 0.03). OSAS drivers were sleepier at the end of the drive than comparison drivers (SSS = 4.2 +/− 1.2 vs. 3.6 +/− 1.2, p = 0.03), and increased sleepiness correlated with decreased HR only in those with OSA (r = −0.49, p = 0.01). Lower HR and higher post-drive SSS predicted greater numbers of driving errors in all subjects. Yet, ESS, pre-drive SSS, and most objective measures of disease severity failed to predict driving and vigilance performance in OSA.Conclusions-Reduced vigilance for peripheral visual targets indicates that OSA drivers have restriction of their effective field of view, which may partly explain their increased crash risk. This fatigue-related decline in attention is predicted by increased subjective sleepiness during driving. These findings may suggest a means of identifying and counseling high-risk drivers, and aid in the development of in-vehicle alerting and warning devices.

Summary We evaluated naturalistic driving in 65 drivers with obstructive sleep apnea (OSA) before and after positive airway pressure (PAP) therapy and in 43 comparison drivers. Driving performance metrics included speed (mean, variability), and lateral, and longitudinal acceleration (g’s). Driver state measures included sleepiness and attention to the driving task based on sampled trigger and baseline video clips. OSA drivers showed less variability in speed and lateral g’s compared to control drivers before and after PAP treatment when vehicle speed was <45mph. There were no driving performance differences when vehicle speed exceeded 45 mph. OSA drivers remained less alert than comparison drivers before and after PAP. Average hours of nightly PAP-use predicted improved alertness and lower levels of sleepiness among OSA drivers. The findings suggest increased crash risk among OSA drivers may result from lower levels of attention to the driving task that result in performance lapses that may lead to crashes, rather than to clear and specific patterns of performance deficits in vehicle control.

People spend a significant amount of time behind the wheel of a car. Recent advances in data collection facilitate continuously monitoring this behavior. Previous work demonstrates the importance of this data in driving safety but does not extended beyond the driving domain. One potential extension of this data is to identify driver states related to health conditions such as obstructive sleep apnea (OSA). We collected driving data and medication adherence from a sample of 75 OSA patients over 3.5 months. We converted speed and acceleration behaviors to symbols using symbolic aggregate approximation and converted these symbols to pattern frequencies using a sliding window. The resulting frequency data was matched with treatment adherence information. A random forest model was trained on the data and evaluated using a held-aside test dataset. The random forest model detects lapses in treatment adherence. An assessment of variable importance suggests that the important patterns of driving in classification correspond to route decisions and patterns that may be associated with drowsy driving. The success of this approach suggests driving data may be valuable for evaluating new treatments, analyzing side effects of medications, and that the approach may benefit other drowsiness detection algorithms.

Objective Some patients with obstructive sleep apnea (OSA) remain sleepy despite positive airway pressure (PAP) therapy. The mechanisms by which this occurs are unclear but could include persistently disturbed sleep. The goal of this study was to explore the relationships between subjective sleepiness and actigraphic measures of sleep during the first three months of PAP treatment. Methods We enrolled 80 patients with OSA and 50 comparison subjects prior to treatment and observed them through three months of PAP therapy. PAP adherence and presence of residual respiratory events were determined from PAP machine downloads. Epworth Sleepiness Scale (ESS), Functional Outcomes of Sleep Questionnaire (FOSQ), and actigraphic data were collected before and at monthly intervals after starting PAP. Results OSA subjects were sleepier and showed a greater degree of sleep disruption by actigraphy at baseline. After three months of PAP, only ESS and number of awakenings normalized, while wake after sleep onset (WASO) and sleep efficiency (SE) remained worse in OSA subjects. For OSA subjects, FOSQ improved but never reached the same level as comparison subjects. ESS and FOSQ improved slowly over the study period. Conclusions As a group, OSA patients show actigraphic evidence of persistently disturbed sleep and sleepiness related impairments in day-to-day function after three months of PAP therapy. Improvements in sleepiness evolve over months with more severely affected patients responding quicker. Persistent sleep disruption may partially explain residual sleepiness in some PAP adherent OSA patients.