Objective: Obstructive sleep apnea (OSA) causes hypoxemia and fragmented sleep, which lead to neurocognitive deficits. We hypothesised that focal loss of cortical gray matter generally within areas ...associated with memory processing and learning and specifically within the hippocampus would occur in OSA.
Methods: Voxel-based morphometry, an automated processing technique for magnetic resonance images, was used to characterise structural changes in gray matter in seven right handed, male patients with newly diagnosed OSA and seven non-apneic, male controls matched for handedness and age.
Results: The analysis revealed a significantly lower gray matter concentration within the left hippocampus (
p=0.004) in the apneic patients. No further significant focal gray matter differences were seen in the right hippocampus and in other brain regions. There was no difference in total gray matter volume between apneics and controls.
Conclusion: This preliminary report indicates changes in brain morphology in OSA, in the hippocampus, a key area for cognitive processing.
For individuals with epilepsy in the United States and other countries, stigma can be one of the most distressing consequences of having seizures, along with the unpredictability of future seizures ...and the inability to drive. The impact of stigma on the lives of epilepsy patients is far reaching, frequently including effects on interpersonal relationships, general health, employment opportunities, and overall quality of life. Education about epilepsy directed at the broader community, as well as at the individual with epilepsy, is the most effective means of addressing misperceptions and fear. Epilepsy advocacy organizations, such as the Epilepsy Foundation, are important allies in this effort.
Adults taking antiepileptic drugs (AEDs) have an augmented risk for osteopenia and osteoporosis because of abnormalities of bone metabolism associated with AEDs. The increased fracture rates that ...have been described among patients with epilepsy may be related both to seizures and to AEDs. The hepatic enzyme–inducing AEDs phenytoin, phenobarbital, and primidone have the clearest association with decreased bone mineral density (BMD). Carbamazepine, also an enzyme-inducing drug, and valproate, an enzyme inhibitor, may also adversely affect bone, but further study is needed. Little information is available about specific effects of newer AEDs on bone. Physicians are insufficiently aware of the association between AEDs and bone disease; a survey found that fewer than one-third of neurologists routinely evaluated AED-treated patients for bone disease, and fewer than 10% prescribed prophylactic calcium and vitamin D. Physicians should counsel patients taking AEDs about good bone health practices, and evaluation of bone health by measuring BMD is warranted after 5 years of AED treatment or before treatment in postmenopausal women.
Detecting sleep latency during the Multiple Sleep Latency Test (MSLT) using electroencephalogram (scalp-EEG) is time-consuming. The aim of this study was to evaluate the efficacy of a novel in-ear ...sensor (in-ear EEG) to detect the sleep latency, compared to scalp-EEG, during MSLT in healthy adults, with and without sleep restriction.
We recruited 25 healthy adults (28.5±5.3 years) who participated in two MSLTs with simultaneous recording of scalp and in-ear EEG. Each test followed a randomly assigned sleep restriction (≤5 hours sleep) or usual night sleep (≥7 hours sleep). Reaction time and Stroop test were used to assess the functional impact of the sleep restriction. The EEGs were scored blind to the mode of measurement and study conditions, using American Academy of Sleep Medicine 2012 criteria. The Agreement between the scalp and in-ear EEG was assessed using Bland-Altman analysis.
Technically acceptable data were obtained from 23 adults during 69 out of 92 naps in the sleep restriction condition and 25 adults during 85 out of 100 naps in the usual night sleep. Meaningful sleep restrictions were confirmed by an increase in the reaction time (mean ± SD: 238±30 ms vs 228±27 ms;
=0.045). In the sleep restriction condition, the in-ear EEG exhibited a sensitivity of 0.93 and specificity of 0.80 for detecting sleep latency, with a substantial agreement (κ
0.71), whereas after the usual night's sleep, the in-ear EEG exhibited a sensitivity of 0.91 and specificity of 0.89, again with a substantial agreement (κ
0.79).
The in-ear sensor was able to detect reduced sleep latency following sleep restriction, which was sufficient to impair both the reaction time and cognitive function. Substantial agreement was observed between the scalp and in-ear EEG when measuring sleep latency. This new in-ear EEG technology is shown to have a significant value as a convenient measure for sleep latency.
The symptom burden resulting from sleep-disordered breathing (SDB) in patients with mild-to-moderate congestive heart failure (CHF) is unclear. The current authors monitored 24-h activity levels and ...compared subjective and objective measures of daytime sleepiness in 39 CHF patients, New York Heart Association class 2-3, on optimal medication. A total of 22 patients were classified as SDB (apnoea/hypopnoea index (AHI) median (range) 22.3 (16.6-100) events.h-1), and 17 as no SDB (NoSDB; AHI 3.7 (0-12.3) events.h-1). SDB was defined as AHI>or=15 events.h-1. Patients were assessed by 24-h activity monitoring (actigraphy) for a period of up to 14 days, a single objective sleepiness test (Oxford Sleep Resistance test) and Epworth Sleepiness Scale. The duration of daytime activity was significantly shorter in the SDB group compared with the NoSDB group. The SDB group also had increased time in bed and poorer sleep quality, as shown by the fragmentation index. Objectively the SDB group when compared with the NoSDB group were significantly sleepier, subjectively the groups did not differ. The amount of napping was similar for both groups. Despite the lack of subjective symptoms of daytime sleepiness, congestive heart failure patients with sleep-disordered breathing were objectively sleepier during the day and had reduced daytime activity with longer periods in bed and poorer sleep quality when compared with those without sleep-disordered breathing.
Sexual dysfunction may arise more frequently in men and women with epilepsy than with other chronic illnesses, manifesting primarily as diminished sexual desire and potency. Studies using ...retrospective self-report of sexual attitude and behavior find an incidence of sexual dysfunction ranging from 14-66%. Sexual dysfunction may be more common in partial than in generalized epilepsies. Sexual dysfunction in epilepsy may result from a disturbance in social or psychological factors affecting sexual responsiveness. Alternatively, epileptiform discharges may disrupt the function of structures mediating sexual behavior, particularly the limbic cortex, or alter the release of hypothalamic or pituitary hormones. Antiepileptic drugs modulate hormone release from the hypothalamic-pituitary-gonadal axis and may have direct inhibitory effects on sexual behavior. Evidence both supports and refutes each of these etiologies in the sexual dysfunction seen with epilepsy. Specific evaluation and treatment protocols for patients with sexual dysfunction are available.
Epilepsy is a common neurological disorder that may be affected by reproductive hormones and may complicate reproductive health. Many women with epilepsy experience changes in seizure frequency and ...severity with changes in reproductive cycles, including at puberty, over the menstrual cycle, with pregnancy and at menopause. Ovarian steroids alter neuronal excitability at the membrane and in the genome. Altered protein synthesis as a consequence of changes in RNA mediated gene transcription is one mechanism for steroid mediated effects on excitability. These genomic effects are delayed and sustained. In contrast, membrane effects are immediate and short duration. These effects are mediated at both the GABA-A and NMDA receptors. Estrogen also dynamically alters synaptic connectivity. Estrogen enhances excitability and lowers the seizure threshold, whereas progesterone enhances inhibition and increases the seizure threshold. In experimental models of epilepsy, estrogen is proconvulsant and progesterone is anticonvulsant. The net effect of these steroid actions is to alter neuronal excitability over physiological cycles. Some epilepsy syndromes are expressed or worsened at puberty. One third to one half of women with epilepsy have catamenial seizure patterns, with seizures most likely to occur in the perimenstrual period and at ovulation. More research is needed to understand the effects of menopause on epilepsy. Antiepileptic drugs may exacerbate the risk of reproductive endocrine disorders in women with epilepsy. Fertility rates are lower for women with epilepsy. Women with epilepsy are more likely to have anovulatory menstrual cycles, abnormal pituitary LH release and altered ovarian steroid concentrations. Polycystic ovaries are detected more often in women with epilepsy, particularly those on valproate. Treatment of hormone sensitive seizures relies on standard AEDs. Small trials suggest that adjunctive progesterone therapy is sometimes helpful. The newer AEDs, gabapentin and lamotrigine may have some advantages for women with epilepsy. These drugs do not alter levels of steroid hormones and do not interfere with effectiveness of hormonal contraception. Experience in pregnancy is limited. The dynamic effects of hormones on seizure expression and of seizures on reproductive health complicate the management of epilepsy in women. Newer AEDs may offer advantages for women with epilepsy in the reproductive years.
Antiepileptic drug (AED) selection in women of reproductive age should consider efficacy, tolerability, interactions with contraceptive medications, and teratogenicity. Women planning a pregnancy ...should be counseled regarding the need for compliance with therapy and the risk for birth defects. All women with epilepsy who are of childbearing potential should receive folate supplementation. Vitamin K supplementation is recommended during the final month of pregnancy. Withdrawal of AED therapy in seizure-free women can be considered before conception. Women who require AED therapy should receive AED monotherapy rather than polytherapy when at all possible. Medication changes post conception do not significantly reduce the risk for major fetal malformations and may compromise seizure control. Breastfeeding is generally safe for women taking AEDs. Menstrual disorders, reproductive endocrine disorders, ovulatory dysfunction, and infertility appear to be relatively common in women with epilepsy.
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