Vigilance is a term with varied definitions but the most common usage is sustained attention or tonic alertness. This usage of vigilance implies both the degree of arousal on the sleep-wake axis and the level of cognitive performance. There are many interacting neural and neurotransmitter systems that affect vigilance. Most studies of vigilance have relied on states where the sleep-wake state is altered, e.g. drowsiness, sleep-deprivation, and CNS-active drugs, but there are factors ranging from psychophysics to motivation that may impact vigilance. While EEG is the most commonly studied physiologic measure of vigilance, various measures of eye movement and of autonomic nervous system activity have also been used. This review paper discusses the underlying neural basis of vigilance and its assessment using physiologic tools. Since, assessment of vigilance requires assessment of cognitive function this aspect is also discussed.

Objective-Half of the adults in the United States use complementary and alternative medicine with mind-body therapy being the most commonly used form. Neurology patients often turn to their physicians for insight into the effectiveness of the therapies and resources to integrate them into their care. The objective of this article is to give a clinical overview of mind-body interventions and their applications in neurology.Methods-Medline and PsychInfo were searched on mind-body therapies and neurologic disease search terms for clinical trials and reviews and published evidence was graded.Results-Meditation, relaxation, and breathing techniques, yoga, tai chi, and qigong, hypnosis, and biofeedback are described. Mind-body therapy application to general pain, back and neck pain, carpal tunnel syndrome, headaches, fibromyalgia, multiple sclerosis, epilepsy, muscular dysfunction, stroke, aging, Parkinson disease, stroke, and attention deficit-hyperactivity disorder are reviewed.Conclusions-There are several conditions where the evidence for mind-body therapies is quite strong such as migraine headache. Mind-body therapies for other neurology applications have limited evidence due mostly to small clinical trials and inadequate control groups.

Larger studies are necessary to confirm that ictal MEG recordings in patients with frequent or easily provoked neocortical seizures can contribute localizing information equivalent or superior to invasive EEG recording.

Potential mechanisms of Passiflora incarnata extracts and the effect of extraction methods on ingredients and biological effects were explored. Using the same batch of plant material, total flavonoid yields as measured by high performance liquid chromatography coupled to diode array detection (HPLC-DAD) increased substantially with hot vs. cold extraction methods.Whole Passiflora extract induced prominent, dose-dependent direct GABA A currents in hippocampal slices, but the expected modulation of synaptic GABA A currents was not seen. GABA was found to be a prominent ingredient of Passiflora extract, and GABA currents were absent when amino acids were removed from the extract.Five different extracts, prepared from a single batch of Passiflora incarnata, were administered to CF-1 mice for one week in their drinking water prior to evaluation of their behavioral effects. Anticonvulsant effects against PTZ induced seizures were seen in mice that received two of the five Passiflora extracts. Instead of the anxiolytic effects described by others, anxiogenic effects in the elevated plus maze were seen in mice receiving any of the five Passiflora extracts.

SUMMARY Purpose Zinc occurs in high concentration in synaptic vesicles of glutamatergic terminals including hippocampal mossy fibers. This vesicular zinc can be synaptically released during neuronal activity, including seizures. Zinc inhibits certain subtypes of N-methyl-D-aspartate (NMDA) and γ-aminobutyric acid (GABA)A receptors. By blocking NMDA excitation or GABA inhibition, an excess of zinc may alter the excitability of hippocampal circuits, which contribute to the development of seizures. Methods Twenty-one adult Wistar rats were implanted under anesthesia with Alzet pumps releasing vehicle, 10 μM ZnCl2 or 1,000 μM ZnCl2, at a rate of 0.25 μl/h continuously into the hippocampal hilus for 4 weeks. Kindling was performed by daily awake commissural stimulation at 60 Hz and afterdischarges were recorded from a dentate gyrus electrode. Development of behavioral Racine seizure stages was recorded by a blinded investigator. Results The development of behavioral Racine seizure stages was delayed only in rats infused with 1,000 μM ZnCl2 (p < 0.02). With completion of kindling at stimulation number 20, all groups had reached the same maximum level of behavioral seizures. The expected increased progression of afterdischarge duration was inhibited by both 10 μM ZnCl2 and 1,000 μM ZnCl2 infusion compared to control animals (p < 0.01). At stimulation number 18, all groups had reached the same maximum duration of afterdischarges. Discussion We conclude that excess infused zinc delayed the development of behavioral seizures in a kindling model of epilepsy. These data support the hypothesis that zinc synaptically released during seizures may alter hippocampal excitability similar to zinc infused in our experiment.

A quantitative assay for determination of the main bufadienolides bersaldegenin-1-acetate (1), bersaldegenin-3-acetate (2), bryophyllin A (3), and bersaldegenin-1,3,5-orthoacetate (4) in Bryophyllum pinnatum leaves and manufactured products was developed and validated. The assay involved extraction by pressurised liquid extraction, followed by quantification by ultrahigh performance liquid chromatography-tandem mass spectroscopy. The ultrahigh performance liquid chromatography-tandem mass spectroscopy method was applied to various batches of leaves harvested on several dates from plants grown at two locations (Brazil and Germany). In addition, press juices prepared from plants cultivated in Germany and Brazil were analysed. The total bufadienolide content ranged from 16.28 to 40.50 mg/100 g dry weight in leaves from plants grown in Brazil. The total content of these four bufadienolides was significantly lower in plants cultivated in Germany (3.78-12.49 mg/100 g dry weight, resp.). The total amounts of bufadienolides were 0.091-0.163 mg/100 mL and 0.89-1.16 mg/100 mL in press juices obtained from plants cultivated in Germany and Brazil, respectively. When analysing single leaves from individual plants, the content of bufadienolides was markedly higher in young leaves. For comparative purposes, the content of these bufadienolides was also determined in Bryophyllum daigremontianum and Bryophyllum tubiflorum. Bersaldegenin-1,3,5-orthoacetate (4) was predominant in the leaves of B. daigremontianum and in the stems of B. tubiflorum, while the leaves of B. tubiflorum contained very low amounts of 1-4.

The aim of this retrospective study is to describe changes of seizure frequency in epilepsy patients who participated in the Andrews/Reiter behavioral intervention for epilepsy. For this uncontrolled retrospective study, data was extracted from patients’ medical journals. Intention-to-treat-analyses were restricted to patients with sufficient documentation supporting a diagnosis of probable or definite epilepsy. Main outcome variable was a comparison of mean seizure frequency at baseline and towards completion of the program. The seizure frequency of 30 (50%%) patients showed a clinically meaningful improvement (>50% reduction of seizures) towards the end of the intervention. Twenty-two (37%) patients became seizure-free at the end of the intervention. In summary, a clinically meaningful reduction in reported seizure frequency was observed in epilepsy patients who received the Andrews/Reiter intervention for epilepsy. Prospective trials are needed to further investigate the program’s efficacy and to study epileptic seizure triggers.

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