The effects of high-dose corticosteroids for multiple sclerosis relapse on blood pressure: A pilot study.

BACKGROUND: Multiple sclerosis (MS) relapses are often treated with short pulses of high dose corticosteroids. Previous literature demonstrates corticosteroids can increase blood pressure (BP). There are few studies regarding effects of high dose, pulse corticosteroids on BP when treating MS relapses. OBJECTIVE: To investigate the effect of high dose pulse corticosteroids for MS relapses on BP and determine factors that may influence development of acute hypertension. METHODS: In this open-label pilot study, adult patients with a diagnosis of MS were enrolled if determined to be having a relapse that would meet criteria for corticosteroid treatment. BP was monitored sequentially over the course of their corticosteroid treatment and correlations were made with demographic data, including past medical and family history. RESULTS: 22 subjects contributed data. Higher daytime BP was noted in subjects with a past personal (p = 0.007) or family history of hypertension (p = 0.037). Nighttime BP recordings did not show the normal 10% drop and nocturnal diastolic BP was within a hypertensive range during corticosteroid treatment. CONCLUSION: MS patients may be at risk of increased BP when treated with corticosteroids for relapses. Those with a past or family history of hypertension may be at higher risk and may warrant more frequent monitoring.

Performance monitoring following total sleep deprivation: effects of task type and error rate.

There is a need to understand the neural basis of performance deficits that result from sleep deprivation. Performance monitoring tasks generate response-locked event-related potentials (ERPs), generated from the anterior cingulate cortex (ACC) located in the medial surface of the frontal lobe that reflect error processing. The outcome of previous research on performance monitoring during sleepiness has been mixed. The purpose of this study was to evaluate performance monitoring in a controlled study of experimental sleep deprivation using a traditional Flanker task, and to broaden this examination using a response inhibition task. Forty-nine young adults (24 male) were randomly assigned to a total sleep deprivation or rested control group. The sleep deprivation group was slower on the Flanker task and less accurate on a Go/NoGo task compared to controls. General attentional impairments were evident in stimulus-locked ERPs for the sleep deprived group: P300 was delayed on Flanker trials and smaller to Go-stimuli. Further, N2 was smaller to NoGo stimuli, and the response-locked ERN was smaller on both tasks, reflecting neurocognitive impairment during performance monitoring. In the Flanker task, higher error rate was associated with smaller ERN amplitudes for both groups. Examination of ERN amplitude over time showed that it attenuated in the rested control group as error rate increased, but such habituation was not apparent in the sleep deprived group. Poor performing sleep deprived individuals had a larger Pe response than controls, possibly indicating perseveration of errors. These data provide insight into the neural underpinnings of performance failure during sleepiness and have implications for workplace and driving safety.

Sleep deprivation lowers reactive aggression and testosterone in men.

The role of sleep deprivation in aggressive behavior has not been systematically investigated, despite a great deal of evidence to suggest a relationship. We investigated the impact of 33 h of sleep loss on endocrine function and reactive aggression using the Point Subtraction Aggression Paradigm (PSAP) task. PSAP performance was assessed in 24 young men and 25 women who were randomly assigned to a sleep deprivation or control condition. Sleep deprivation lowered reactive aggression and testosterone (but not cortisol) in men, and disrupted the positive relationship between a pre-post PSAP increase in testosterone and aggression that was evident in rested control men. While women increased aggression following provocation as expected, no influence of sleep deprivation was found. This is the first experimental study to demonstrate that sleep deprivation lowers reactive aggression in men. Testosterone, but not cortisol, played a role in the relationship between sleep and reactive aggression in men.