SW percent of change from baseline.

<p>SW amplitude (panel A), SW slope (panel B) and SW positive phase duration (panel C) are shown for young subjects (black dots) and middle-aged subjects (open squares). Stars indicate differences between young subjects and middle-aged subjects in each derivation (contrast analysis: *: p<0.05). A) Young subjects showed higher percent of increase in SW amplitude only in Fp1 (F(1,61) = 7.31, p<0.01) and F3 derivations (F(1,61) = 4.28, p<0.05). B) Effect of age group on percent of increase in SW slope tended to be significant. C) Percent of decrease in SW positive phase duration showed significant effect of age group.</p

Data_Sheet_1_How Is the Norepinephrine System Involved in the Antiepileptic Effects of Vagus Nerve Stimulation?.pdf

Vagus Nerve Stimulation (VNS) is an adjunctive treatment for patients suffering from inoperable drug-resistant epilepsy. Although a complete understanding of the mediators involved in the antiepileptic effects of VNS and their complex interactions is lacking, VNS is known to trigger the release of neurotransmitters that have seizure-suppressing effects. In particular, norepinephrine (NE) is a neurotransmitter that has been associated with the clinical effects of VNS by preventing seizure development and by inducing long-term plastic changes that could restore a normal function of the brain circuitry. However, the biological requisites to become responder to VNS are still unknown. In this review, we report evidence of the critical involvement of NE in the antiepileptic effects of VNS in rodents and humans. Moreover, we emphasize the hypothesis that the functional integrity of the noradrenergic system could be a determining factor to obtain clinical benefits from the therapy. Finally, encouraging avenues of research involving NE in VNS treatment are discussed. These could lead to the personalization of the stimulation parameters to maximize the antiepileptic effects and potentially improve the response rate to the therapy.</p

SW characteristics.

<p>SW frequency (number of cycles per sec), SW amplitude (difference in voltage between negative peak-B and positive peak-D of unfiltered signals expressed in µV), SW negative phase duration (number of sec between A and C), SW positive phase duration (number of sec between C and E), and SW slope between B and D expressed in µV/sec.</p

SW characteristics showing significant interactions between age group and sleep conditions.

<p>SW density (panel A) and SW positive phase duration (panel B) are shown for young subjects (black dots) and middle-aged subjects (open squares). Stars indicate differences between baseline sleep and daytime recovery sleep in young and middle-aged subjects (Contrast analysis: *: p<0.0001; **: p<0.00001).</p

SW characteristics showing significant interactions between age group, sleep condition and derivations.

<p>SW amplitude (panel A) and SW slope (panel B) are shown for Fp1 (upper panel) and F3 derivations (lower panel) and for young subjects (black dots) and middle-aged subjects (open squares). Stars indicate differences between baseline sleep and daytime recovery sleep in young and middle-aged subjects (contrast analysis: *: p<0.0001; **: p<0.00001). A) Post-hoc analyses showed significant interactions between age group and sleep condition only in Fp1 (F(1,61) = 10.93, p<0.01) and F3 (F(1,61) = 7.11, p<0.01) derivations. B) Post-hoc analyses showed significant interactions between age group and sleep condition were found only on Fp1 (F(1,61) = 16.31, p<0.001) and F3 (F(1,61) = 8.19, p<0.01) derivations.</p

SW amplitude showing significant interaction between age group, sleep condition and NREMP.

<p>SW amplitude (panel A) and SW slope (panel B) are shown for young subjects (black dots) and middle-aged subjects (open squares), for baseline and recovery sleep during the first NREMP. Stars indicate differences between baseline and recovery sleep (Contrast analysis: *: p<0.05; **: p<0.001; ***: p<0.00001). A) After sleep deprivation, young subjects showed higher SW amplitude enhancement compared to middle-aged subjects during the first NREMP only (interaction age group * sleep condition: F(1,61) = 6.55; p = 0.05). B) After sleep deprivation, young subjects tended to show higher slope enhancement compared to middle-aged subjects during the first NREMP only (interaction age group * sleep condition: F(1,61) = 3,71; p = 0.06).</p

Polysomnographic variables for young and middle-age in both sleep condition.

<p>Untransformed mean (standard deviation); Y: Young, MA: Middle-aged, B: Baseline nocturnal sleep, R: Daytime recovery sleep.</p

SW durations showing significant interactions between age group and sleep pressure.

<p>SW density (panel A), negative phase (panel B) and positive phase (panel C) on F3 derivation are shown for young subjects (black dots), middle-aged subjects (open squares) for the first and last NREMP averaged on the two sleep condition. Star indicates difference between young and middle-aged subjects for SW density and between the first and the last NREMP for SW durations (*: p<0.001; **: p<0.0001). A) Contrast analysis showed higher SW density in young than in middle-aged subjects during the first NREMP only (F(1,61) = 12.15; p<0.001). B) Contrast analysis showed significant SW negative phase duration increase between the first and last NREMP in young subjects (F(1,61) = 15.12; p<0.001) and no significant modification in middle-aged subjects. C) Contrast analysis showed higher SW positive phase duration increase between the first and last NREMP in young subjects (F(1,61) = 120.04; p<0.0001) compared to middle-aged subjects (F(1,61) = 37.48; p<0.001).</p

SW characteristics showing significant interactions between sleep condition and derivations.

<p>SW density (panel A), negative phase (panel B), and positive phase duration (panel C) are shown for baseline sleep (black triangles) and daytime recovery sleep (open circles). Stars indicate differences between baseline sleep and daytime recovery sleep for each derivation (Contrast analysis*: p<0.0001; **: p<0.00001; ***: p<0.000001).</p

Image_1_Plasticity in the Sensitivity to Light in Aging: Decreased Non-visual Impact of Light on Cognitive Brain Activity in Older Individuals but No Impact of Lens Replacement.PDF

Beyond its essential visual role, light, and particularly blue light, has numerous non-visual effects, including stimulating cognitive functions and alertness. Non-visual effects of light may decrease with aging and contribute to cognitive and sleepiness complaints in aging. However, both the brain and the eye profoundly change in aging. Whether the stimulating effects light on cognitive brain functions varies in aging and how ocular changes may be involved is not established. We compared the impact of blue and orange lights on non-visual cognitive brain activity in younger (23.6 ± 2.5 years), and older individuals with their natural lenses (NL; 66.7 ± 5.1 years) or with intraocular lens (IOL) replacement following cataract surgery (69.6 ± 4.9 years). Analyses reveal that blue light modulates executive brain responses in both young and older individuals. Light effects were, however, stronger in young individuals including in the hippocampus and frontal and cingular cortices. Light effects did not significantly differ between older-IOL and older-NL while regression analyses indicated that differential brain engagement was not underlying age-related differences in light effects. These findings show that, although its impact decreases, light can stimulate cognitive brain activity in aging. Since lens replacement did not affect light impact, the brain seems to adapt to the progressive decrease in retinal light exposure in aging.</p