Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died suddenly and unexpectedly under 6 months of age. Of these, 26 died from sudden infant death syndrome (SIDS), 5 from congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 from a prolonged seizure, 1 from prolonged neonatal hypoxemia, and 1 from meningitis and brain infarction. The frequency and duration of apneas recorded some 3-12 weeks prior to the infants' death were analyzed. The brainstem materials were collected and studied in an attempt to elucidate the relationship between sleep apnea, and prone sleep position and gliosis in some nuclei associated with cardiorespiratory characteristics, such as nucleus ambiguus in the medulla oblongata and the solitary nucleus, as well as structures associated with arousal phenomenon, such as the reticular formation, the superior central nucleus and the nucleus raphe magnus in the pons, the dorsal raphe nuclei in the midbrain and medulla oblongata, periaqueductal gray matter in midbrain, and locus ceruleus. Gliosis was estimated as the density of glial fibrillary acidic protein (GFAP)-positive reactive astrocytes. Variant-covariant analyses were carried out using the characteristics of apnea as an independent variable and sleep position and gliosis as dependent variables. A significant association was found only in the frequency of obstructive apnea and prone position (P<0.001) and gliosis in the raphe nuclei in the midbrain (P<0.001). Although prone position is a well-known risk factor for SIDS, the frequency of obstructive apnea has not been associated with the prone sleep position. The observed relation between prone sleep and the density of gliosis does not relate to epidemiological findings. Further studies are needed to investigate the unexpected statistical association.
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PMID:Interaction between apnea, prone sleep position and gliosis in the brainstems of victims of SIDS. 1235 Mar

Obstructive sleep apnea can affect an individual with epilepsy profoundly. These relatively common disorders can coexist and potentially exacerbate each other. The identification and appropriate treatment of OSA may have far-reaching consequences in improving a patient's quality of life and recurrence of seizures. Clinicians must be aware of the relationship of these disorders and keenly question epilepsy patients, regardless of their body habitus, regarding potential symptoms of sleep apnea. Although the underlying pathogenic mechanisms are unclear, we can model the information gained from the observations to further the understanding of the relationship between sleep and epilepsy.
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PMID:Obstructive sleep apnea in epilepsy. 1280 Jul 81

In recent years, sleep medicine has become a rapidly advancing field filled with exciting new discoveries. Many sleep disorders are diagnosed by clinical history alone. Sleep disorders such as sleep apnea, narcolepsy, periodic limb movement disorder, parasomnias, and nocturnal seizures usually require evaluation in the sleep laboratory. Sleep studies are used for diagnostic purposes, to assess disease severity, and to evaluate treatment efficacy. Sleep testing should be tailored to answer the specific clinical question at hand. This article reviews the techniques most commonly performed in the sleep laboratory and their indications, interpretation, and limitations. These include the polysomnogram, the multiple sleep latency test, and the maintenance of wakefulness test. The accurate interpretation of these studies requires a comprehensive sleep and medical history.
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PMID:The use of sleep studies in neurological practice. 1544 17

One of every 15 adults in the United States has at least moderate sleep apnea. The true prevalence is higher, as approximately 0.3 to 5% of adults with sleep apnea are undiagnosed. Sleep apnea has major health consequences; therefore, neurologists must recognize and treat sleep apnea syndromes appropriately. There are three main categories of sleep apnea: obstructive sleep apnea (OSA), central sleep apnea (CSA), and mixed sleep apnea. OSA results from upper airway obstruction, and CSA is due to lack of inspiratory muscle effort; mixed apnea results from a combination of these factors. Sleep apnea syndromes can present within the spectrum of "typical" neurological complaints, including forgetfulness, headaches, sleepiness, fatigability, seizures, and muscle and nerve weakness. A good sleep history, a nocturnal polysomnogram, and multiple sleep latency test are important in elucidating the diagnosis and validating the complaints of sleepiness. The gold standard for treatment of OSA is positive airway pressure, although some patients may benefit from surgical interventions designed to bypass the site of airway obstruction. With CSA, treatment is directed toward the underlying disorder. Patients with CSA may also benefit from several types of nasal positive airway pressure treatment, while some require mechanical ventilation.
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PMID:Neurological perspective on obstructive and nonobstructive sleep apnea. 1544 19

A 34-year-old man developed posttraumatic epilepsy and a disinhibited orbitofrontal syndrome following severe head trauma at age 22. After an 11-year prison term marked by repeated impulsive aggression, he was transferred to a state psychiatric hospital. Replacement of phenytoin by valproic acid resulted in a 100-lb weight gain, exacerbation of sleep apnea, and right heart failure. Despite replacement of valproate with topiramate, he died of a cardiorespiratory arrest during a seizure. This case illustrates the potential risks associated with valproate therapy in the obese brain-damaged population.
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PMID:Lethal obesity associated with sodium valproate in a brain-injured patient. 1597 Jul 28

Pro AED: The central issue in medical decision-making is risk-benefit assessment. Surgery of any type is still considered to be a major undertaking. To warrant these risks, the patient has a right to expect that they have a greater chance of a good outcome with an invasive therapy than with a non-invasive one. The main question is when, if ever, this becomes the case when comparing implantation of a VNS Therapy System versus adding an antiepileptic drug (AED)? After the first drug? The second? After all AEDs have failed? To date, no randomized trial comparing the addition of an AED against vagus nerve stimulation (VNS Therapy) has been undertaken, although several are currently being contemplated. Without this information, it is more difficult to make a case for early implementation of VNS Therapy. Unfortunately, few data are available regarding the potential for patients to become seizure-free after implantation of a VNS Therapy System. Another issue is side effects. It is important to remember that VNS Therapy also produces adverse events, albeit very different in character than those associated with AEDs, to which physicians have become accustomed. These include cough, dyspnea, pharyngitis, voice alteration and sleep apnea. A less frequently discussed, potentially negative consequence of VNS Therapy relates to the ability to obtain imaging of the patient. Patients who have undergone VNS Therapy System implantation are not candidates for imaging of the chest, breast, or abdomen. A second issue is that imaging of the brain can only be performed with MRI scanners that meet certain requirements, and as MRI technology develops, scanners meeting these requirements may become harder to find. However, to summarize, VNS Therapy is an excellent and useful treatment choice. Fortunately, the choice between AEDs and VNS Therapy is not an "either/or" decision. Each has a role in the treatment of patients with epilepsy, and the advantages and disadvantages of each should be kept in perspective. Pro VNS Therapy: VNS Therapy is no longer a new treatment for patients with refractory epilepsy. The first implant was performed in l988, and since then more than 30,000 patients have received this therapy. It is no longer considered an unusual or dangerous procedure, but it is still used almost exclusively for refractory epilepsy patients and it has not been generally accepted for use as a first line or even second line therapy. However, compared to the new AEDs, VNS Therapy has similar efficacy results in clinical trials and in many epilepsy syndromes and the long-term efficacy results are even more positive, with continued improvement in seizure reduction for up to two years. Two of the major reasons for not using VNS Therapy early are that it is a surgical procedure, and its safety during MRI procedures, especially with 3 Tesla, has not yet been elucidated. The safety profile of VNS Therapy is very favorable; the side effects being totally different from those seen with AEDs. The most important aspects are that there have been no pharmacological interactions, cognitive or sedative side effects reported, and it is safe for use in all age groups. Side effects are restricted to local irritation, hoarseness, coughing and, in a few cases, swallowing difficulties when the stimulator is on, but these tend to disappear with time. No idiosyncratic side effect has emerged during the 16 years of use. Compliance is guaranteed. The cost of the implantation of the VNS Therapy System, when spread out over 8 years (battery life), is actually less than the cost of using a new AED over an eight-year period, and real savings as regards hospital costs due to seizures can be expected.
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PMID:VNS Therapy versus the latest antiepileptic drug. 1612 Apr 90

The aim of the study was to assess sleep-wake habits and disorders and excessive daytime sleepiness (EDS) in an unselected outpatient epilepsy population. Sleep-wake habits and presence of sleep disorders were assessed by means of a clinical interview and a standard questionnaire in 100 consecutive patients with epilepsy and 90 controls. The questionnaire includes three validated instruments: the Epworth Sleepiness Scale (ESS) for EDS, SA-SDQ for sleep apnea (SA), and the Ullanlinna Narcolepsy Scale (UNS) for narcolepsy. Sleep complaints were reported by 30% of epilepsy patients compared to 10% of controls (p=0.001). The average total sleep time was similar in both groups. Insufficient sleep times were suspected in 24% of patients and 33% of controls. Sleep maintenance insomnia was more frequent in epilepsy patients (52% vs. 38%, p=0.06), whereas nightmares (6% vs. 16%, p=0.04) and bruxism (10% vs. 19%, p=0.07) were more frequent in controls. Sleep onset insomnia (34% vs. 28%), EDS (ESS >or=10, 19% vs. 14%), SA (9% vs. 3%), restless legs symptoms (RL-symptoms, 18% vs. 12%) and most parasomnias were similarly frequent in both groups. In a stepwise logistic regression model loud snoring and RL-symptoms were found to be the only independent predictors of EDS in epilepsy patients. In conclusion, sleep-wake habits and the frequency of most sleep disorders are similar in non-selected epilepsy patients as compared to controls. In epilepsy patients, EDS was predicted by a history of loud snoring and RL-symptoms but not by SA or epilepsy-related variables (including type of epilepsy, frequency of seizures, and number of antiepileptic drugs).
Seizure 2006 Jul
PMID:Sleep-wake habits and disorders in a series of 100 adult epilepsy patients--a prospective study. 1654 7

We present a case of laryngospasm in a 12-year-old male who experienced sudden, nocturnal episodes of breathing difficulties and agitation. Apart from laryngospasm, the main differential diagnoses included frontal seizures, sleep-related choking syndrome, sleep asthma, sleep apnoea and REM sleep behaviour disorder. The video and the EEG recordings supported the diagnosis of laryngospasm. The pH-metry confirmed the existence of reflux. Its treatment successfully controlled the episodes. This case illustrates, with a typical video recording, this infrequent type of paroxysmal event with an important differential diagnosis.[Published with video sequences].
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PMID:Sleep-related laryngospasm: a video-polysomnographic recording. 1656 30

A few publications documented the coexistence of epilepsy and obstructive sleep apnea (OSA). The extent, nature, and clinical relevance of this association remain poorly understood. We retrospectively reviewed the database of our sleep center to identify patients with both sleep apnea and epilepsy. Characteristics of epilepsy, sleep history, presence of excessive daytime sleepiness [Epworth Sleepiness Scale (ESS)] and polysomnographic data were assessed. The effect of continuous positive airway pressure (CPAP) on seizure reduction was prospectively analyzed after a median interval of 26 months (range: 2-116 months) from the diagnosis of OSA. OSA was found in 29 epilepsy patients (25 men and 4 women) with a median age of 56 years (range: 37-79). The median apnea hypopnea index was 33 (range: 10-85), the oxygen desaturation index was 12 (range 0-92), and 52% of the patients had an ESS score >10. In 27 patients, epilepsy appeared 1 month to 44 years prior to the diagnosis of OSA. In 21 patients, the appearance of OSA symptoms coincided with a clear increase in seizure frequency or the first appearance of a status epilepticus. Treatment with CPAP was continued with good compliance in 12 patients and led to a significant reduction of both ESS scores and seizure frequency in 4 patients. Our data suggest the importance of considering diagnosis and treatment of OSA in epilepsy patients with poor seizure control and/or reappearance of seizures after a seizure-free interval.
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PMID:Epilepsy and obstructive sleep apnea. 1656 44

A sleep history should be taken routinely in patients with epilepsy. Treatment of sleep disorders and improvement in sleep hygiene may improve seizure control, daytime cognitive functioning, and quality of life. Patients with recurrent sleepiness interfering with daily activities or an Epworth Sleepiness Scale score more than 10 should be considered for additional evaluation by a sleep specialist. Treatment options for insomnia include improvements in sleep hygiene, cognitive behavior therapies, and sedative or hypnotic drugs. Alterations in the timing or type of antiepileptic drugs (AEDs) may be helpful (for example, using sedating medications before bedtime and avoiding evening use of drugs that may exacerbate insomnia ). Improvements in sleep hygiene alone are less effective than cognitive behavioral therapy or pharmacologic therapy. Cognitive behavioral therapy is more efficacious and its effects longer lasting than pharmacologic treatments. Sedative and hypnotic drugs may exacerbate AED cognitive adverse effects during the day and should be used only after other therapies have failed. Excessive daytime sleepiness (EDS) in patients with epilepsy may be secondary to AEDs, nocturnal seizures, or a concomitant sleep disorder such as sleep apnea or restless leg syndrome. Sedating AEDs should be minimized during the day, and activating AEDs should be used as appropriate. Video electroencephalogram polysomnography should be performed when EDS interferes with daily activities and the etiology of sleepiness is unclear. AEDs that are associated with weight gain should be avoided in patients with sleep apnea. AEDs that may promote weight loss should be considered for obese patients with sleep apnea. Continuous positive airway pressure is the treatment of choice for sleep apnea.
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PMID:Epilepsy and sleep. 1694 70


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