Archive for category Epilepsy

[WEB SITE] The Relationship Between Epilepsy and Sleep

The Thomas Haydn Trust in an aid to understanding Epilepsy and Sleep has published this mobile article. This article is not extensive and should not be used as medical advice; it’s intended for information purposes only. This dictionary is also available for download from http://www.thomashaydntrust.com/publications.htm in .pdf format. [Please note that this is version 1 and further updates may be availalbe]
 Written by M C Walker, S M Sisodiya

Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, Queen Square, London, and National Society for Epilepsy, Chalfont St Peter, Bucks. London, and National Society for Epilepsy, Chalfont St Peter, Bucks. September 2005. This article can be reproduced for educational purposes.

Introduction

Epilepsy has a complex association with sleep. Certain seizures are more common during sleep, and may show prominent diurnal variation. Rarely, nocturnal seizures are the only manifestation of an epileptic disorder and these can be confused with a parasomnia. Conversely, certain sleep disorders are not uncommonly misdiagnosed as epilepsy. Lastly, sleep disorders can exacerbate epilepsy and epilepsy can exacerbate certain sleep disorders. This chapter is thus divided into four sections: normal sleep physiology and the relationship to seizures; the interaction of sleep disorders and epilepsy; and the importance of sleep disorders in diagnosis.

Normal sleep physiology and the relationship to seizures

Adults require on average 7 – 8 hours sleep a night. This sleep is divided into two distinct states – rapid eye movement (REM) sleep and non-REM sleep. These two sleep states cycle over approximately 90 minutes throughout the night with the REM periods becoming progressively longer as sleep continues. Thus there is a greater proportion of REM sleep late on in the sleep cycles. REM sleep accounts for about a quarter of sleep time. During REM sleep, dreams occur; hypotonia or atonia of major muscles prevents dream enactment. REM sleep is also associated with irregular breathing and increased variability in blood pressure and heart rate. Non-REM sleep is divided into four stages (stages I – IV) defined by specific EEG criteria. Stages I/II represent light sleep, while stages III/IV represent deep, slow-wave sleep.

Gowers noted that in some patients, epileptic seizures occurred mainly in sleep. Sleep influences cortical excitability and neuronal synchrony. Surveys have suggested that 10 – 45% of patients have seizures that occur predominantly or exclusively during sleep or occur with sleep deprivation. EEG activation in epilepsy commonly occurs during sleep, so that sleep recordings are much more likely to demonstrate epileptiform abnormalities. These are usually most frequent during non-REM sleep and often have a propensity to spread so that the epileptiform discharges are frequently observed over a wider field than is seen during the wake state. Sleep deprivation (especially in generalised epilepsies) can also ‘activate’ the EEG, but can induce seizures in some patients. Thus many units perform sleep EEGs with only moderate sleep deprivation (late night, early morning), avoidance of stimulants (e.g. caffeine-containing drinks) and EEG recording in the afternoon. Sleep-induced EEGs in which the patient is given a mild sedative (e.g. chloral hydrate) are also useful.

Sleep and generalised seizures

Thalamocortical rhythms are activated during non-REM sleep giving rise to sleep spindles. Since similar circuits are involved in the generation of spike-wave discharges in primary generalised epilepsy, it is perhaps not surprising that non-REM sleep often promotes spike-wave discharges. Epileptiform discharges and seizures in primary generalised epilepsies are both commonly promoted by sleep deprivation. Furthermore, primary generalised seizures often occur within a couple of hours of waking, whether from overnight sleep or daytime naps. This is most notable with juvenile myoclonic epilepsy in which both myoclonus and tonic-clonic seizures occur shortly after waking, and the

Διαφήμιση

syndrome of tonic-clonic seizures on awakening described by Janz. Seizure onset in this syndrome is from 6 – 35 years and the prognosis for eventual remission is good.

Certain epileptic encephalopathies show marked diurnal variation in seizure manifestation and electrographic activity. An example is the generalised repetitive fast discharge during slow-wave sleep occurring in Lennox-Gastaut syndrome. Another example is electrical status epilepticus during sleep (ESES). This is characterised by spike and wave discharges in 85 – 100% of non-REM sleep. This phenomenon is associated with certain epilepsy syndromes, including Landau-Kleffner, Lennox-Gastaut syndrome, continuous spikes and waves during sleep and benign epilepsy of childhood with rolandic spikes. ESES can thus be a component of a number of different epilepsy syndromes with agedependent onset, many seizure types, and varying degrees of neuropsychological deterioration. Indeed, ESES has been described in the setting of an autistic syndrome alone with no other

manifestation of epilepsy.

Sleep and partial epilepsies

Inter-ictal epileptiform abnormalities on the EEG occur more frequently during sleep, especially stage III/IV sleep (slow-wave sleep). The discharges have a greater propensity to spread during sleep, and thus are often seen over a wider field than discharges occurring during wakefulness. Temporal lobe seizures are relatively uncommon during sleep, while frontal lobe seizures occur often predominantly (sometimes exclusively) during sleep. Nocturnal frontal lobe seizures can be manifest as: brief stereotypical, abrupt arousals; complex stereotypical, nocturnal movements; or episodic nocturnal wanderings with confusion. Inherited frontal lobe epilepsies can manifest with only nocturnal events that can be confused with parasomnias (see below). Autosomal dominant nocturnal frontal lobe epilepsy is such an epilepsy. This has been associated with mutations in alpha-4 and beta-2 subunits of the neuronal nicotinic acetylcholine receptor. Onset is usually in adolescence with seizures occurring frequently, sometimes every night. The seizures are provoked by stress, sleep deprivation and menstruation, and often respond well to carbamazepine.

The interaction of sleep disorders and epilepsy

Seizures can disrupt sleep architecture. Complex partial seizures at night disrupt normal sleep patterns, decrease REM sleep and increase daytime drowsiness. Daytime complex partial seizures can also decrease subsequent REM sleep, which may contribute to impaired function. Antiepileptic drugs (AEDs) can also disrupt normal sleep patterns, although there are conflicting data (this is partially due to drugs having different short-term and long-term effects). Carbamazepine, for example, given acutely reduces and fragments REM sleep, but these effects are reversed after a month of treatment. The GABAergic drugs can have a profound effect on sleep; phenobarbitone and benzodiazepines prolong non-REM sleep and shorten REM sleep, while tiagabine increases slow-wave sleep and sleep efficiency. Gabapentin and lamotrigine may both increase REM sleep.

Certain sleep disorders are more common in patients with epilepsy. This is particularly so with obstructive sleep apnoea which is more common in patients with epilepsy and can also exacerbate seizures. Indeed, sleep apnoea is approximately twice as common in those with refractory epilepsy than in the general population. The reasons why this is so are unknown, but may relate to increased body weight, use of AEDs, underlying seizure aetiology or the epilepsy syndrome itself.

Patients with obstructive sleep apnoea often find that seizure control improves with treatment of the sleep apnoea. Topiramate may also be a particularly useful drug in these cases.

The importance of sleep disorders in differential diagnosis

On occasions nocturnal seizures can be misdiagnosed as a primary sleep disorder (see above). Conversely, certain sleep disorders can be misdiagnosed as epilepsy and the more common of these will be discussed below. Sleep disorders tend to occur during specific sleep phases and thus usually occur at specific times during the night, while seizures usually occur at any time during the night. There may also be other clues in the history, including age of onset, association with other symptoms (see below) and the stereotypy of the episodes (seizures are usually stereotypical).

In cases where there is some uncertainty, video-EEG polysomnography is the investigation of choice. There are, however, instances in which the diagnosis can be difficult even after overnight video-EEG telemetry as frontal lobe seizures can be brief with any EEG change obscured by movement artefact, and it is often the stereotypy of the episodes that confirms the diagnosis.

Abnormalities of sleep are divided into three main categories: 1) dysomnias or disorders of the sleepwake cycle; 2) parasomnias or disordered behaviour that intrudes into sleep, and 3) sleep disorders associated with medical or psychiatric conditions. Although there is an extensive list of conditions within each of these categories, we will confine ourselves to the clinical features of the more common conditions that can be confused with epilepsy.

Narcolepsy

Narcolepsy is a specific, well-defined disorder with a prevalence of approximately one in 2000. It is a life-long condition usually presenting in late teens or early 20s. Narcolepsy is a disorder of REM sleep and has as its main symptom excessive daytime sleepiness. This is manifest as uncontrollable urges to sleep, not only at times of relaxation (e.g. reading a book, watching television), but also at inappropriate times (e.g. eating a meal or while talking). The sleep is itself usually refreshing. The other typical symptoms are cataplexy, sleep paralysis and hypnagogic/hypnopompic hallucinations. These represent REM sleep phenomena such as hypotonia/atonia, and dreams occurring at inappropriate times. Cataplexy is a sudden decrease in voluntary muscle tone (especially jaw, neck and limbs) that occurs with sudden emotion like laughter, elation, surprise or anger. This can manifest as jaw dropping, head nods or a feeling of weakness or, in more extreme cases, as falls with ‘paralysis’ lasting sometimes minutes. Consciousness is preserved. Cataplexy is a specific symptom of narcolepsy, although narcolepsy can occur without cataplexy. Sleep paralysis and hypnagogic hallucinations are not particularly specific and can occur in other sleep disorders and with sleep deprivation (especially in the young). Both these phenomena occur shortly after going to sleep or on waking.

Sleep paralysis is a feeling of being awake, but unable to move. This can last minutes and is often very frightening, so can be associated with a feeling of panic. Hypnagogic/hypnopompic hallucinations are visual or auditory hallucinations occurring while dozing/falling asleep or on waking; often the hallucinations are frightening, especially if associated with sleep paralysis.

Narcolepsy is associated with HLA type. Approximately 90% of all narcoleptic patients with definite cataplexy have the HLA allele HLA DQB1*0602 (often in combination with HLA DR2), compared with approximately 25% of the general population. The sensitivity of this test is decreased to 70% if cataplexy is not present. The strong association with HLA type has raised the possibility that narcolepsy is an autoimmune disorder. Recently loss of hypocretin-containing neurons in the hypothalamus has been associated with narcolepsy, and it is likely that narcolepsy is due to deficiency in hypocretin (orexin).

Since narcolepsy is a life-long condition with possibly addictive treatment, the diagnosis should always be confirmed with multiple sleep latency tests (MSLT). During this test five episodes of sleep are permitted during a day; rapid onset of sleep and REM sleep within 15 minutes in the absence of sleep deprivation are indicative of narcolepsy.

The excessive sleepiness of narcolepsy can be treated with modafinil, methylphenidate or dexamphetamine and regulated daytime naps. The cataplexy, sleep paralysis and hypnagogic/hypnopompic hallucinations respond to antidepressants (fluoxetine or clomipramine are the most frequently prescribed). People with narcolepsy often have fragmented, poor sleep at night, and good sleep hygiene can be helpful.

Sleep apnoea

Sleep apnoea can be divided into the relatively common obstructive sleep apnoea and the rarer central sleep apnoea. Obstructive sleep apnoea is more common in men than women and is associated with obesity, micrognathia and large neck size. The prevalence may be as high as 4% in men, and 2% in women. The symptoms suggestive of obstructive sleep apnoea are loud snoring, observed nocturnal apnoeic spells, waking at night fighting for breath or with a feeling of choking, morning headache, daytime somnolence, personality change and decreased libido. Although the daytime somnolence can be as severe as narcolepsy, the naps are not usually refreshing and are longer. Obstructive sleep apnoea and central sleep apnoea can be associated with neurological disease, but central sleep apnoea can also occur as an idiopathic syndrome. The correct diagnosis requires polysomnography with measures of oxygen saturations and nasal airflow or chest movements. To be pathological a sleep apnoea or hypopnoea (a 50% reduction in airflow) has to last ten seconds and there need to be more than five apnoeas/hypopnoeas per hour (the precise number to make a diagnosis varies from sleep laboratory to sleep laboratory).

Uncontrolled sleep apnoea can lead to hypertension, cardiac failure, pulmonary hypertension and stroke. In addition, sleep apnoea has been reported to worsen other sleep conditions, such as narcolepsy, and to worsen seizure control.

Treatment of sleep apnoea should include avoidance of alcohol and sedatives and weight reduction. Pharmacological treatment is not particularly effective, although REM suppressants such as protriptyline can be helpful. The mainstays of treatment are surgical and include tonsillectomies, adenoidectomy and procedures to widen the airway, and the use of mechanical devices. Dental appliances to pull the bottom jaw forward can be effective in mild cases, but continuous positive airway pressure administered by a nasal mask has become largely the treatment of choice for moderate/severe obstructive sleep apnoea. In cases associated with neuromuscular weakness intermittent positive pressure ventilation is often necessary.

Restless legs syndrome/periodic limb movements in sleep

Restless legs syndrome (RLS) and periodic limb movements in sleep (PLMS) can occur in association or separately. Most people with RLS also have PLMS, but the converse is not true and most people with PLMS do not have RLS. RLS is characterised by an unpleasant sensation in the legs, often described as tingling, cramping or crawling, and an associated overwhelming urge to move the legs. These sensations are usually worse in the evening, and movement only provides temporary relief. RLS affects about 5% of the population. Periodic limb movements in sleep are brief, repetitive jerking of usually the legs that occur every 20 – 40 seconds. These occur in non-REM sleep and can cause frequent arousals. PLMS occurs in about 50% of people over 65 years. These conditions can also be associated with daytime jerks. Both RLS and PLMS can be familial, but can be secondary to peripheral neuropathy (especially diabetic, uraemic and alcoholic neuropathies), iron deficiency, pregnancy and rarely spinal cord lesions.

Symptomatic relief can be achieved with benzodiazepines, gabapentin and opioids, but L-DOPA and dopamine agonists are the mainstay of treatment.

Sleep-wake transition disorders

The most common of these are hypnic jerks or myoclonic jerks that occur on going to sleep or on waking. They are entirely benign in nature, and require no treatment. They can occur in association with other sleep disorders. Rhythmic movement disorder is a collection of conditions occurring in infancy and childhood characterised by repetitive movements occurring immediately prior to sleep onset that can continue into light sleep. One of the most dramatic is headbanging or jactatio capitis nocturna. Persistence of these rhythmic movements beyond the age of ten years is often associated with learning difficulties, autism or emotional disturbance. Sleep-talking can occur during non-REM and REM sleep, but is often seen with wake-sleep transition and is a common and entirely benign phenomenon.

Nocturnal enuresis

Nocturnal enuresis is a common disorder that can occur throughout the night. Although diagnosis is straightforward, it can recur in childhood, and also occurs in the elderly, with approximately 3% of women and 1% of men over the age of 65 years having the disorder. Thus, on occasions, it can be misdiagnosed as nocturnal epilepsy.

Non-REM parasomnias

Non-REM parasomnias usually occur in slow-wave (stage III/IV) sleep. These conditions are often termed arousal disorders and indeed can be induced by forced arousal from slow-wave sleep. There are three main non-REM parasomnias – sleepwalking, night terrors and confusional arousal. These disorders often have a familial basis, but can be brought on by sleep deprivation, alcohol and some drugs. They can also be triggered by other sleep disorders such as sleep apnoea, medical and psychiatric illness. Patients are invariably confused during the event, and are also amnesic for the event. These conditions are most common in children, but do occur in adults.

Sleepwalking may occur in up to 25% of children, with the peak incidence occurring from age 11 – 12 years. The condition is characterised by wanderings often with associated complex behaviours such as carrying objects, and eating. Although speech does occur, communication is usually impossible. The episode usually lasts a matter of minutes. Aggressive and injurious behaviour is uncommon, and should it occur then polysomnography may be indicated to exclude an REM sleep parasomnia (see below), and to confirm the diagnosis. Night terrors are less common and are characterised by screaming, and prominent sympathetic nervous system activity – tachycardia, mydriasis and excessive sweating. Both these conditions are usually benign and rarely need treatment. If dangerous behaviour occurs, then treatment may be indicated. Benzodiazepines, especially clonazepam, are usually very effective.

REM parasomnias

Nightmares are REM phenomena that can occur following sleep deprivation, with certain drugs (e.g. L-DOPA) and in association with psychological and neurological disease. Sleep paralysis (see narcolepsy) is also an REM parasomnia, and may be familial.

Of more concern are REM sleep behaviour disorders. These consist of dream enactment. They are often violent, and tend to occur later in sleep when there is more REM sleep. These are rare and tend to occur in the elderly. In over one-third of cases, REM sleep behaviour disorders are symptomatic of an underlying neurological disease such as dementia, multisystem atrophy, Parkinson’s disease, brainstem tumours, multiple sclerosis, subarachnoid haemorrhage and cerebrovascular disease. In view of this, a history of possible REM sleep behaviour disorder needs to be investigated by polysomnography, and if confirmed, then possible aetiologies need to be investigated. REM sleep behaviour disorders respond very well to clonazepam.

Further reading

• BAZIL CW (2002) Sleep and epilepsy. Semin Neurol 22(3) , 321-327.

• FOLDVARY-SCHAEFER NJ (2002) Sleep complaints and epilepsy: the role of seizures,

antiepileptic drugs and sleep disorders. Clin Neurophysiol 19(6) , 514-521.

• MALOW BA (2002) Paroxysmal events in sleep. J Clin Neurophysiol 19(6) , 522-534.

• SCHNEERSON J. Handbook of Sleep Medicine . Blackwell Science, Oxford.

[END]

ABOUT THE THOMAS HAYDN TRUST

The Thomas Haydn Trust is The Paediatric Epilepsy Charity that aims to serve the needs of Young People, Parents, Carers and Medical Professionals. But to know who we are you need to know why we are.

Providing local services and sharing the rewards globally is the core of THT’s work, weather newly diagnosed or not, you will find THT a valuable source of support, knowledge and news for the epilepsies.

The Thomas Haydn Trust was set up in the wake of Thomas Haydn Smith’s diagnosis of Lennox-Gastaut Syndrome – One of the Most severe forms of Childhood Onset Epilepsies, affecting 1 in 1,000,000 epilepsy sufferer’s worldwide.

In setting up THT our aim was to combat many of the hurdles that Thomas and his family come across while living with LGS. THT strives to ‘Give Something Back’ to organisations that help families and children with severe epilepsies.

We work towards our goals in the following manner:

Research

Raising the need profile for both basic and clinical research into Lennox-Gastaut Syndrome and other childhood Epilepsies.

Support

By providing a free and open forum for sufferers, family and carers’, allowing them to share experiences, build relationships and facilitate peer learning. THT also provides details of leading specialist support organisations of specific Epilepsy conditions – Supporting the specific needs of the child.

Education

Developing an ever-expending resource of research findings and educational materials for the public and medical professionals.

Funding

Where possible, fund individuals and organisations involved in support, development and care of families with sick children.

Awareness

Raising awareness of childhood Epilepsies through various mediums including the internet, press, radio and television. Highlighting the effects of LGS and other childhood onset Epilepsies through our live events – Raising awareness is the key principle on which THT works.

Empowerment

Promoting the advancement of individuals with Epilepsy to speak out against ignorance, predjudice and bigotry that still surrounds conditions of Epilepsy.

Networking

Developing links with other national and international organisations to create a coalition of information sharing networks.

via The Relationship Between Epilepsy and Sleep – Wattpad

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[WEB SITE] Wristband devices may improve detection and characterization of epileptic seizures

New research published in Epilepsia (http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1528-1167), a journal of the International League Against Epilepsy (ILAE), indicates that wristband devices may improve the detection and characterization of seizures in patients with epilepsy.

New devices are needed for monitoring epileptic seizures, especially those that can lead to sudden death. While rare, “sudden unexpected death in epilepsy” (SUDEP) is the most common cause of death in epilepsy, and it often occurs at night. The gold standard for monitoring seizures-video-electroencephalography- is available in epilepsy monitoring units but is an impractical procedure for daily life use. Therefore, clinicians often rely on patients and caregivers to report seizure counts, which are often inaccurate.

In their attempts to develop a better monitoring method, Giulia Regalia, PhD and Francesco Onorati, PhD, of Empatica Inc. in Milan, Italy and Cambridge, Massachusetts, and their colleagues examined the potential of automated, wearable systems to detect and characterize convulsive epileptic seizures. The researchers used three different wristbands to record two signals-called electrodermal activity and accelerometer signals-that usually exhibit marked changes upon the onset of convulsive seizures, obtaining 5928 hours of data from 69 patients, including 55 convulsive epileptic seizures from 22 patients.

The wristband detectors showed high sensitivity (95% of seizures were detected) while keeping the false alarm rate at a bearable level (on average, one false alarm every four days), which improves a pioneering 2012 study led by MIT professor Rosalind Picard, now chief scientist at Empatica.

In addition to detecting seizures, the method also revealed certain characteristics of the seizures, which may help alert clinicians and patients to seizures that are potentially dangerous and life-threatening.

“The present work provides significant improvements for convulsive seizure detection both in clinical and ambulatory real-life settings,” said Dr. Regalia. “Accurate seizure counts with real-time alerts to caregivers allows an early application of aid, which can be protective against SUDEP risk.” She noted that the wristband detectors do not require caregivers to be near patients continuously, which could significantly improve patients and caregivers’ quality of life.

Source: Wristband devices may improve detection and characterization of epileptic seizures

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[WEB SITE] Findings reveal how seizures can have lasting detrimental effects on memory

October 16, 2017

Although it’s been clear that seizures are linked to memory loss and other cognitive deficits in patients with Alzheimer’s disease, how this happens has been puzzling. In a study published in the journal Nature Medicine, a team of researchers reveals a mechanism that can explain how even relatively infrequent seizures can lead to long-lasting cognitive deficits in animal models. A better understanding of this new mechanism may lead to future strategies to reduce cognitive deficits in Alzheimer’s disease and other conditions associated with seizures, such as epilepsy.

“It’s been hard to reconcile how infrequent seizures can lead to persistent changes in memory in patients with Alzheimer’s disease,” said corresponding author Dr. Jeannie Chin, assistant professor of neuroscience at Baylor College of Medicine. “To solve this puzzle, we worked with a mouse model of Alzheimer’s disease focusing on the genetic changes that seizures might trigger in the memory center of the brain, the hippocampus, that could lead to loss of memory or other cognitive deficits.”

The researchers measured the levels of a number of proteins involved in memory and learning and found that levels of the protein deltaFosB strikingly increase in the hippocampus of Alzheimer’s disease mice that had seizures. DeltaFosB already is well known for its association with other neurological conditions linked to persistent brain activity of specific brain regions, such as addiction. In this study, the researchers found that after a seizure, the deltaFosB protein remains in the hippocampus for an unusually long time; its half-life – the time it takes for the amount of protein to decrease by half – is eight days. Most proteins have a half-life that is between hours and a day or two.

“Interestingly, because deltaFosB is a transcription factor, meaning that its job is to regulate the expression of other proteins, these findings led us to predict that the increased deltaFosB levels might be responsible for suppressing the production of proteins that are necessary for learning and memory,” Chin said. “In fact, we found that when the levels of deltaFosB increase, those of other proteins, such as calbindin, decrease. Calbindin also has been known for a long time to be involved in Alzheimer’s disease and epilepsy, but its mechanism of regulation was not known. We then hypothesized that deltaFosB might be regulating the production of calbindin.”

Further investigations supported the researchers’ hypothesis. The scientists showed that deltaFosB can bind to the gene calbindin suppressing the expression of the protein. When they either prevented deltaFosB activity or experimentally increased calbindin expression in the mice, calbindin levels were restored and the mice improved their memory. And when researchers experimentally increased deltaFosB levels in normal mice, calbindin expression was suppressed and the animals’ memory deteriorated, demonstrating that deltaFosB and calbindin are key regulators of memory.

Connecting pieces of the puzzle

“Our findings have helped us answer the question of how even infrequent seizures can have such lasting detrimental effects on memory,” Chin said. “We found that seizures can increase the levels of deltaFosB in the hippocampus, which results in a decrease in the levels of calbindin, a regulator of memory processes. DeltaFosB has a relatively long half-life, therefore even when seizures are infrequent, deltaFosB remains in the hippocampus for weeks acting like a brake, reducing the production of calbindin and other proteins, and disrupting the consequent brain activity involved in memory. The regulation of gene expression far outlasts the actual seizure event that triggered it.”

The scientists found the same changes in deltaFosB and calbindin levels in the hippocampus of Alzheimer’s disease patients and in the temporal lobe of epilepsy patients. However, they underscore that it is too soon to know whether regulating deltaFosB or calbindin could improve or prevent memory problems or other cognitive deficits in people with Alzheimer’s disease. However, “now that we know that the levels of deltaFosB and calbindin are effective markers of brain activity in the hippocampus and memory function, we propose that these markers could potentially help assess clinical therapies for Alzheimer’s and other diseases with seizures,” Chin said.

Source: Findings reveal how seizures can have lasting detrimental effects on memory

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[WEB SITE] The Relationship Between Epilepsy and Sleep

The Thomas Haydn Trust in an aid to understanding Epilepsy and Sleep has published this mobile article. This article is not extensive and should not be used as medical advice; it’s intended for information purposes only. This dictionary is also available for download from http://www.thomashaydntrust.com/publications.htm in .pdf format. [Please note that this is version 1 and further updates may be availalbe]

Written by

M C Walker, S M Sisodiya

Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, Queen Square, London, and National Society for Epilepsy, Chalfont St Peter, Bucks. London, and National Society for Epilepsy, Chalfont St Peter, Bucks. September 2005. This article can be reproduced for educational purposes.

Introduction

Epilepsy has a complex association with sleep. Certain seizures are more common during sleep, and may show prominent diurnal variation. Rarely, nocturnal seizures are the only manifestation of an epileptic disorder and these can be confused with a parasomnia. Conversely, certain sleep disorders are not uncommonly misdiagnosed as epilepsy. Lastly, sleep disorders can exacerbate epilepsy and epilepsy can exacerbate certain sleep disorders. This chapter is thus divided into four sections: normal sleep physiology and the relationship to seizures; the interaction of sleep disorders and epilepsy; and the importance of sleep disorders in diagnosis.

Normal sleep physiology and the relationship to seizures

Adults require on average 7 – 8 hours sleep a night. This sleep is divided into two distinct states – rapid eye movement (REM) sleep and non-REM sleep. These two sleep states cycle over approximately 90 minutes throughout the night with the REM periods becoming progressively longer as sleep continues. Thus there is a greater proportion of REM sleep late on in the sleep cycles. REM sleep accounts for about a quarter of sleep time. During REM sleep, dreams occur; hypotonia or atonia of major muscles prevents dream enactment. REM sleep is also associated with irregular breathing and increased variability in blood pressure and heart rate. Non-REM sleep is divided into four stages (stages I – IV) defined by specific EEG criteria. Stages I/II represent light sleep, while stages III/IV represent deep, slow-wave sleep.

Gowers noted that in some patients, epileptic seizures occurred mainly in sleep. Sleep influences cortical excitability and neuronal synchrony. Surveys have suggested that 10 – 45% of patients have seizures that occur predominantly or exclusively during sleep or occur with sleep deprivation. EEG activation in epilepsy commonly occurs during sleep, so that sleep recordings are much more likely to demonstrate epileptiform abnormalities. These are usually most frequent during non-REM sleep and often have a propensity to spread so that the epileptiform discharges are frequently observed over a wider field than is seen during the wake state. Sleep deprivation (especially in generalised epilepsies) can also ‘activate’ the EEG, but can induce seizures in some patients. Thus many units perform sleep EEGs with only moderate sleep deprivation (late night, early morning), avoidance of stimulants (e.g. caffeine-containing drinks) and EEG recording in the afternoon. Sleep-induced EEGs in which the patient is given a mild sedative (e.g. chloral hydrate) are also useful.

Sleep and generalised seizures

Thalamocortical rhythms are activated during non-REM sleep giving rise to sleep spindles. Since similar circuits are involved in the generation of spike-wave discharges in primary generalised epilepsy, it is perhaps not surprising that non-REM sleep often promotes spike-wave discharges. Epileptiform discharges and seizures in primary generalised epilepsies are both commonly promoted by sleep deprivation. Furthermore, primary generalised seizures often occur within a couple of hours of waking, whether from overnight sleep or daytime naps. This is most notable with juvenile myoclonic epilepsy in which both myoclonus and tonic-clonic seizures occur shortly after waking, and the

Διαφήμιση

syndrome of tonic-clonic seizures on awakening described by Janz. Seizure onset in this syndrome is from 6 – 35 years and the prognosis for eventual remission is good.

Certain epileptic encephalopathies show marked diurnal variation in seizure manifestation and electrographic activity. An example is the generalised repetitive fast discharge during slow-wave sleep occurring in Lennox-Gastaut syndrome. Another example is electrical status epilepticus during sleep (ESES). This is characterised by spike and wave discharges in 85 – 100% of non-REM sleep. This phenomenon is associated with certain epilepsy syndromes, including Landau-Kleffner, Lennox-Gastaut syndrome, continuous spikes and waves during sleep and benign epilepsy of childhood with rolandic spikes. ESES can thus be a component of a number of different epilepsy syndromes with agedependent onset, many seizure types, and varying degrees of neuropsychological deterioration. Indeed, ESES has been described in the setting of an autistic syndrome alone with no other

manifestation of epilepsy.

Sleep and partial epilepsies

Inter-ictal epileptiform abnormalities on the EEG occur more frequently during sleep, especially stage III/IV sleep (slow-wave sleep). The discharges have a greater propensity to spread during sleep, and thus are often seen over a wider field than discharges occurring during wakefulness. Temporal lobe seizures are relatively uncommon during sleep, while frontal lobe seizures occur often predominantly (sometimes exclusively) during sleep. Nocturnal frontal lobe seizures can be manifest as: brief stereotypical, abrupt arousals; complex stereotypical, nocturnal movements; or episodic nocturnal wanderings with confusion. Inherited frontal lobe epilepsies can manifest with only nocturnal events that can be confused with parasomnias (see below). Autosomal dominant nocturnal frontal lobe epilepsy is such an epilepsy. This has been associated with mutations in alpha-4 and beta-2 subunits of the neuronal nicotinic acetylcholine receptor. Onset is usually in adolescence with seizures occurring frequently, sometimes every night. The seizures are provoked by stress, sleep deprivation and menstruation, and often respond well to carbamazepine.

The interaction of sleep disorders and epilepsy

Seizures can disrupt sleep architecture. Complex partial seizures at night disrupt normal sleep patterns, decrease REM sleep and increase daytime drowsiness. Daytime complex partial seizures can also decrease subsequent REM sleep, which may contribute to impaired function. Antiepileptic drugs (AEDs) can also disrupt normal sleep patterns, although there are conflicting data (this is partially due to drugs having different short-term and long-term effects). Carbamazepine, for example, given acutely reduces and fragments REM sleep, but these effects are reversed after a month of treatment. The GABAergic drugs can have a profound effect on sleep; phenobarbitone and benzodiazepines prolong non-REM sleep and shorten REM sleep, while tiagabine increases slow-wave sleep and sleep efficiency. Gabapentin and lamotrigine may both increase REM sleep.

Certain sleep disorders are more common in patients with epilepsy. This is particularly so with obstructive sleep apnoea which is more common in patients with epilepsy and can also exacerbate seizures. Indeed, sleep apnoea is approximately twice as common in those with refractory epilepsy than in the general population. The reasons why this is so are unknown, but may relate to increased body weight, use of AEDs, underlying seizure aetiology or the epilepsy syndrome itself.

Patients with obstructive sleep apnoea often find that seizure control improves with treatment of the sleep apnoea. Topiramate may also be a particularly useful drug in these cases.

The importance of sleep disorders in differential diagnosis

On occasions nocturnal seizures can be misdiagnosed as a primary sleep disorder (see above). Conversely, certain sleep disorders can be misdiagnosed as epilepsy and the more common of these will be discussed below. Sleep disorders tend to occur during specific sleep phases and thus usually occur at specific times during the night, while seizures usually occur at any time during the night. There may also be other clues in the history, including age of onset, association with other symptoms (see below) and the stereotypy of the episodes (seizures are usually stereotypical).

In cases where there is some uncertainty, video-EEG polysomnography is the investigation of choice. There are, however, instances in which the diagnosis can be difficult even after overnight video-EEG telemetry as frontal lobe seizures can be brief with any EEG change obscured by movement artefact, and it is often the stereotypy of the episodes that confirms the diagnosis.

Abnormalities of sleep are divided into three main categories: 1) dysomnias or disorders of the sleepwake cycle; 2) parasomnias or disordered behaviour that intrudes into sleep, and 3) sleep disorders associated with medical or psychiatric conditions. Although there is an extensive list of conditions within each of these categories, we will confine ourselves to the clinical features of the more common conditions that can be confused with epilepsy.

Narcolepsy

Narcolepsy is a specific, well-defined disorder with a prevalence of approximately one in 2000. It is a life-long condition usually presenting in late teens or early 20s. Narcolepsy is a disorder of REM sleep and has as its main symptom excessive daytime sleepiness. This is manifest as uncontrollable urges to sleep, not only at times of relaxation (e.g. reading a book, watching television), but also at inappropriate times (e.g. eating a meal or while talking). The sleep is itself usually refreshing. The other typical symptoms are cataplexy, sleep paralysis and hypnagogic/hypnopompic hallucinations. These represent REM sleep phenomena such as hypotonia/atonia, and dreams occurring at inappropriate times. Cataplexy is a sudden decrease in voluntary muscle tone (especially jaw, neck and limbs) that occurs with sudden emotion like laughter, elation, surprise or anger. This can manifest as jaw dropping, head nods or a feeling of weakness or, in more extreme cases, as falls with ‘paralysis’ lasting sometimes minutes. Consciousness is preserved. Cataplexy is a specific symptom of narcolepsy, although narcolepsy can occur without cataplexy. Sleep paralysis and hypnagogic hallucinations are not particularly specific and can occur in other sleep disorders and with sleep deprivation (especially in the young). Both these phenomena occur shortly after going to sleep or on waking.

Sleep paralysis is a feeling of being awake, but unable to move. This can last minutes and is often very frightening, so can be associated with a feeling of panic. Hypnagogic/hypnopompic hallucinations are visual or auditory hallucinations occurring while dozing/falling asleep or on waking; often the hallucinations are frightening, especially if associated with sleep paralysis.

Narcolepsy is associated with HLA type. Approximately 90% of all narcoleptic patients with definite cataplexy have the HLA allele HLA DQB1*0602 (often in combination with HLA DR2), compared with approximately 25% of the general population. The sensitivity of this test is decreased to 70% if cataplexy is not present. The strong association with HLA type has raised the possibility that narcolepsy is an autoimmune disorder. Recently loss of hypocretin-containing neurons in the hypothalamus has been associated with narcolepsy, and it is likely that narcolepsy is due to deficiency in hypocretin (orexin).

Since narcolepsy is a life-long condition with possibly addictive treatment, the diagnosis should always be confirmed with multiple sleep latency tests (MSLT). During this test five episodes of sleep are permitted during a day; rapid onset of sleep and REM sleep within 15 minutes in the absence of sleep deprivation are indicative of narcolepsy.

The excessive sleepiness of narcolepsy can be treated with modafinil, methylphenidate or dexamphetamine and regulated daytime naps. The cataplexy, sleep paralysis and hypnagogic/hypnopompic hallucinations respond to antidepressants (fluoxetine or clomipramine are the most frequently prescribed). People with narcolepsy often have fragmented, poor sleep at night, and good sleep hygiene can be helpful.

Sleep apnoea

Sleep apnoea can be divided into the relatively common obstructive sleep apnoea and the rarer central sleep apnoea. Obstructive sleep apnoea is more common in men than women and is associated with obesity, micrognathia and large neck size. The prevalence may be as high as 4% in men, and 2% in women. The symptoms suggestive of obstructive sleep apnoea are loud snoring, observed nocturnal apnoeic spells, waking at night fighting for breath or with a feeling of choking, morning headache, daytime somnolence, personality change and decreased libido. Although the daytime somnolence can be as severe as narcolepsy, the naps are not usually refreshing and are longer. Obstructive sleep apnoea and central sleep apnoea can be associated with neurological disease, but central sleep apnoea can also occur as an idiopathic syndrome. The correct diagnosis requires polysomnography with measures of oxygen saturations and nasal airflow or chest movements. To be pathological a sleep apnoea or hypopnoea (a 50% reduction in airflow) has to last ten seconds and there need to be more than five apnoeas/hypopnoeas per hour (the precise number to make a diagnosis varies from sleep laboratory to sleep laboratory).

Uncontrolled sleep apnoea can lead to hypertension, cardiac failure, pulmonary hypertension and stroke. In addition, sleep apnoea has been reported to worsen other sleep conditions, such as narcolepsy, and to worsen seizure control.

Treatment of sleep apnoea should include avoidance of alcohol and sedatives and weight reduction. Pharmacological treatment is not particularly effective, although REM suppressants such as protriptyline can be helpful. The mainstays of treatment are surgical and include tonsillectomies, adenoidectomy and procedures to widen the airway, and the use of mechanical devices. Dental appliances to pull the bottom jaw forward can be effective in mild cases, but continuous positive airway pressure administered by a nasal mask has become largely the treatment of choice for moderate/severe obstructive sleep apnoea. In cases associated with neuromuscular weakness intermittent positive pressure ventilation is often necessary.

Restless legs syndrome/periodic limb movements in sleep

Restless legs syndrome (RLS) and periodic limb movements in sleep (PLMS) can occur in association or separately. Most people with RLS also have PLMS, but the converse is not true and most people with PLMS do not have RLS. RLS is characterised by an unpleasant sensation in the legs, often described as tingling, cramping or crawling, and an associated overwhelming urge to move the legs. These sensations are usually worse in the evening, and movement only provides temporary relief. RLS affects about 5% of the population. Periodic limb movements in sleep are brief, repetitive jerking of usually the legs that occur every 20 – 40 seconds. These occur in non-REM sleep and can cause frequent arousals. PLMS occurs in about 50% of people over 65 years. These conditions can also be associated with daytime jerks. Both RLS and PLMS can be familial, but can be secondary to peripheral neuropathy (especially diabetic, uraemic and alcoholic neuropathies), iron deficiency, pregnancy and rarely spinal cord lesions.

Symptomatic relief can be achieved with benzodiazepines, gabapentin and opioids, but L-DOPA and dopamine agonists are the mainstay of treatment.

Sleep-wake transition disorders

The most common of these are hypnic jerks or myoclonic jerks that occur on going to sleep or on waking. They are entirely benign in nature, and require no treatment. They can occur in association with other sleep disorders. Rhythmic movement disorder is a collection of conditions occurring in infancy and childhood characterised by repetitive movements occurring immediately prior to sleep onset that can continue into light sleep. One of the most dramatic is headbanging or jactatio capitis nocturna. Persistence of these rhythmic movements beyond the age of ten years is often associated with learning difficulties, autism or emotional disturbance. Sleep-talking can occur during non-REM and REM sleep, but is often seen with wake-sleep transition and is a common and entirely benign phenomenon.

Nocturnal enuresis

Nocturnal enuresis is a common disorder that can occur throughout the night. Although diagnosis is straightforward, it can recur in childhood, and also occurs in the elderly, with approximately 3% of women and 1% of men over the age of 65 years having the disorder. Thus, on occasions, it can be misdiagnosed as nocturnal epilepsy.

Non-REM parasomnias

Non-REM parasomnias usually occur in slow-wave (stage III/IV) sleep. These conditions are often termed arousal disorders and indeed can be induced by forced arousal from slow-wave sleep. There are three main non-REM parasomnias – sleepwalking, night terrors and confusional arousal. These disorders often have a familial basis, but can be brought on by sleep deprivation, alcohol and some drugs. They can also be triggered by other sleep disorders such as sleep apnoea, medical and psychiatric illness. Patients are invariably confused during the event, and are also amnesic for the event. These conditions are most common in children, but do occur in adults.

Sleepwalking may occur in up to 25% of children, with the peak incidence occurring from age 11 – 12 years. The condition is characterised by wanderings often with associated complex behaviours such as carrying objects, and eating. Although speech does occur, communication is usually impossible. The episode usually lasts a matter of minutes. Aggressive and injurious behaviour is uncommon, and should it occur then polysomnography may be indicated to exclude an REM sleep parasomnia (see below), and to confirm the diagnosis. Night terrors are less common and are characterised by screaming, and prominent sympathetic nervous system activity – tachycardia, mydriasis and excessive sweating. Both these conditions are usually benign and rarely need treatment. If dangerous behaviour occurs, then treatment may be indicated. Benzodiazepines, especially clonazepam, are usually very effective.

REM parasomnias

Nightmares are REM phenomena that can occur following sleep deprivation, with certain drugs (e.g. L-DOPA) and in association with psychological and neurological disease. Sleep paralysis (see narcolepsy) is also an REM parasomnia, and may be familial.

Of more concern are REM sleep behaviour disorders. These consist of dream enactment. They are often violent, and tend to occur later in sleep when there is more REM sleep. These are rare and tend to occur in the elderly. In over one-third of cases, REM sleep behaviour disorders are symptomatic of an underlying neurological disease such as dementia, multisystem atrophy, Parkinson’s disease, brainstem tumours, multiple sclerosis, subarachnoid haemorrhage and cerebrovascular disease. In view of this, a history of possible REM sleep behaviour disorder needs to be investigated by polysomnography, and if confirmed, then possible aetiologies need to be investigated. REM sleep behaviour disorders respond very well to clonazepam.

Further reading

• BAZIL CW (2002) Sleep and epilepsy. Semin Neurol 22(3) , 321-327.

• FOLDVARY-SCHAEFER NJ (2002) Sleep complaints and epilepsy: the role of seizures,

antiepileptic drugs and sleep disorders. Clin Neurophysiol 19(6) , 514-521.

• MALOW BA (2002) Paroxysmal events in sleep. J Clin Neurophysiol 19(6) , 522-534.

• SCHNEERSON J. Handbook of Sleep Medicine . Blackwell Science, Oxford.

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Source: The Relationship Between Epilepsy and Sleep – Wattpad

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[BLOG POST] You Probably Didn’t Aware Of These Surprising Epileptic Seizure Causes

Epileptic Seizure Causes

Epileptic Seizure has no known cause in about half of those with the condition. In the other, the condition may be traced to various factors.

Genetic influence. Some types of epilepsy, which are categorized by the type of seizure you experience or the part of the brain that is affected, run in families. In these cases, it’s likely that there’s a genetic effect.

Researchers have associated some types of this disorder to specific genes that Epileptic Seizure Causes, also include genes though it’s estimated that up to 500 genes could be tied to the condition. For most people, genes are only part of the cause of this disorder. Certain genes may make a person more sensitive to environmental conditions that provoke seizures.

Head trauma. Epileptic Seizure Causes by Head trauma as a result of a car accident or other traumatic injury.

Brain conditions. Brain conditions that cause damage to the brain, such as brain tumors or strokes, can cause Epileptic Seizure. Stroke is a leading cause of epilepsy in adults older than age 35.

Infectious diseases. Infectious diseases, such as meningitis, AIDS and viral encephalitis, can cause epilepsy.

Prenatal injury. Before birth, babies are sensitive to brain damage that could be caused by several factors, such as an infection in the mother, poor nutrition or oxygen deficiencies. This brain damage can result in epilepsy or cerebral palsy.

  • Different epilepsies are due to many different underlying Epileptic Seizure Causes.Epileptic Seizure Causes can be complex, and sometimes hard to identify. A person might start having seizures because they have one or more of the following.
  • A genetic tendency that is not inherited, but is a new change in the person’s genes.
  • A structural (sometimes called ‘symptomatic’) change in the brain, such as the brain not developing properly, or damage caused by a brain injury, infections like meningitis, a stroke or a tumour. A brain scan, such as Magnetic Resonance Imaging (MRI), may show this.
  • Structural changes due to genetic conditions such as tuberous sclerosis, or neurofibromatosis, which can cause growths affecting the brain.Developmental disorders. Epilepsy can sometimes be associated with developmental disorders, such as autism and neurofibromatosis
  • A genetic tendency, passed down from one or both parents (inherited). source

Source:  You Probably Didn’t Aware Of These Surprising Epileptic Seizure Causes

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[WEB SITE] New method uses advanced noninvasive neuroimaging to localize and identify epileptic lesions

Epilepsy affects more than 65 million people worldwide. One-third of these patients have seizures that are not controlled by medications. In addition, one-third have brain lesions, the hallmark of the disease, which cannot be located by conventional imaging methods. Researchers at the Perelman School of Medicine at the University of Pennsylvania have piloted a new method using advanced noninvasive neuroimaging to recognize the neurotransmitter glutamate, thought to be the culprit in the most common form of medication-resistant epilepsy. Their work is published today in Science Translational Medicine.

Glutamate is an amino acid which transmits signals from neuron to neuron, telling them when to fire. Glutamate normally docks with the neuron, gives it the signal to fire and is swiftly cleared. In patients with epilepsy, stroke and possibly ALS, the glutamate is not cleared, leaving the neuron overwhelmed with messages and in a toxic state of prolonged excitation.

In localization-related epilepsy, the most common form of medication-resistant epilepsy, seizures are generated in a focused section of the brain; in 65 percent of patients, this occurs in the temporal lobe. Removal of the seizure-generating region of the temporal lobe, guided by preoperative MRI, can offer a cure. However, a third of these patients have no identified abnormality on conventional imaging studies and, therefore, more limited surgical options.

“Identification of the brain region generating seizures in location-related epilepsy is associated with significantly increased chance of seizure freedom after surgery,” said the new study’s lead author, Kathryn Davis, MD, MSTR, an assistant professor of Neurology at Penn. “The aim of the study was to investigate whether a novel imaging method, developed at Penn, could use glutamate to localize and identify the epileptic lesions and map epileptic networks in these most challenging patients.”

“We theorized that if we could develop a technique which allows us to track the path of and make noninvasive measurements of glutamate in the brain, we would be able to better identify the brain lesions and epileptic foci that current methods miss,” said senior author Ravinder Reddy, PhD, a professor of Radiology and director of Penn’s Center for Magnetic Resonance and Optical Imaging.

Reddy’s lab developed the glutamate chemical exchange saturation transfer (GluCEST) imaging method, a very high resolution magnetic resonance imaging contrast method not available before now, to measure how much glutamate was in different regions of the brain including the hippocampi, two structures within the left and right temporal lobes responsible for short- and long-term memory and spatial navigation and the most frequent seizure onset region in adult epilepsy patients.

The study tested four patients with medication-resistant epilepsy and 11 controls. In all four patients, concentrations of glutamate were found to be higher in one of the hippocampi, and confirmatory methods (electroencephalography and magnetic resonance spectra) verified independently that the hippocampus with the elevated glutamate was located in the same hemisphere as the epileptic focus/lesion. Consistent lateralization to one side was not seen in the control group.

While preliminary, this work indicates the ability of GluCEST to detect asymmetrical hippocampal glutamate levels in patients thought to have nonlesional temporal lobe epilepsy. The authors say this approach could reduce the need for invasive intracranial monitoring, which is often associated with complications, morbidity risk, and added expense.

“This demonstration that GluCEST can localize small brain hot spots of high glutamate levels is a promising first step in our research,” Davis said. “By finding the epileptic foci in more patients, this approach could guide clinicians toward the best therapy for these patients, which could translate to a higher rate of successful surgeries and improved outcomes from surgery or other therapies in this difficult disease.”

Source: Penn Medicine

Source: New method uses advanced noninvasive neuroimaging to localize and identify epileptic lesions

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[ARTICLE] Electroencephalography in the Diagnosis of Genetic Generalized Epilepsy Syndromes – Full Text

Genetic generalized epilepsy (GGE) consists of several syndromes diagnosed and classified on the basis of clinical features and electroencephalographic (EEG) abnormalities. The main EEG feature of GGE is bilateral, synchronous, symmetric, and generalized spike-wave complex. Other classic EEG abnormalities are polyspikes, epileptiform K-complexes and sleep spindles, polyspike-wave discharges, occipital intermittent rhythmic delta activity, eye-closure sensitivity, fixation-off sensitivity, and photoparoxysmal response. However, admixed with typical changes, atypical epileptiform discharges are also commonly seen in GGE. There are circadian variations of generalized epileptiform discharges. Sleep, sleep deprivation, hyperventilation, intermittent photic stimulation, eye closure, and fixation-off are often used as activation techniques to increase the diagnostic yield of EEG recordings. Reflex seizure-related EEG abnormalities can be elicited by the use of triggers such as cognitive tasks and pattern stimulation during the EEG recording in selected patients. Distinct electrographic abnormalities to help classification can be identified among different electroclinical syndromes.

Introduction

Genetic generalized epilepsy (GGE) encompasses several electroclinical syndromes diagnosed and classified according to clinical features and electroencephalographic (EEG) characteristics (13). The EEG hallmark of GGE is bilateral synchronous, symmetrical, and generalized spike-wave (GSW) discharges. Polyspikes and polyspike-wave discharges are also commonly seen in GGE. Fixation-off sensitivity (FOS), eye-closure sensitivity, photoparoxysmal response (PPR), epileptiform K-complexes/sleep spindles, and occipital intermittent rhythmic delta activity (OIRDA) are among the spectrum of abnormalities described in GGE (4).

In this review, we will be discussing the ictal and the interictal EEG abnormalities in GGE. We will also focus on the electrographic differences among different GGE syndromes, factors affecting the yield of EEG, and diagnostic pitfalls.[…]

Continue —> Frontiers | Electroencephalography in the Diagnosis of Genetic Generalized Epilepsy Syndromes | Neurology

 

Figure 1. Typical interictal epileptiform discharges in genetic generalized epilepsy. Note bilateral, symmetrical, and synchronous spike-wave discharges (A), polyspike-wave discharges (B), and polyspikes (C).

 

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[WEB SITE] Monitor stress, seizures, activity, sleep

Embrace it’s wearable device designed to improve the lives of the people with epilepsy.

 

“Embrace is glorious in design, very sleek and attractive. Living in a world of seizure helmets and wheelchairs it is nice to have such an unobtrusive and attractive device.

 

A gorgeous smart watch for you

The case is made of strong, polished metal with either an elegant leather or an elastic fabric band. Embrace is the thinnest smart watch of this kind ever made. It snaps on, then tightens with a magnet for perfect fit. […]

Source: Monitor stress, seizures, activity, sleep

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[WEB SITE] Status Epilepticus | Epilepsy Foundation

CONTENT HIGHLIGHTS
  • Status epilepticus is when a seizure lasts longer than 5 minutes or when seizures occur close together and the person doesn’t recover between seizures.
  • There are different types of status epilepticus: convulsive and non-convulsive.
  • Convulsive status epilepticus requires emergency treatment by trained medical personnel in a hospital setting. It can be life-threatening.

What is status epilepticus?

Status epilepticus is said to occur when a seizure lasts too long or when seizures occur close together and the person doesn’t recover between seizures. Just like there are different types of seizures, there are also different types of status epilepticus.

Over the last several decades, the length of seizure that is considered as status epilepticus has shortened. Years ago, a seizure needed to last longer than 20 minutes to be considered status epilepticus. In the last few years, it is now defined as any seizure greater than 5 minutes. This makes sense because most seizures do not last longer than 2 minutes. The longer a seizure lasts, the less likely it will stops on its own without medication. Very long seizures (i.e., status epilepticus) are dangerous and even increase the chance of death. It is important that these long seizures are identified early, so they can be treated early.

Epilepsy.com Seizure Emergency Editor Matthew Hoerth MD speaks with Dr. Christopher Kramer, a neurointensive care specialist from the Mayo Clinic, about the importance of recognizing and treating status epilepticus. A paper published in the Neurocritical Care Journal from 2012 nicely outlined guidelines for treating this neurologic emergency. This paper detailed the subtypes of status epilepticus, emphasized the high mortality rates of this condition, and summarized the best medical evidence for treatment.

Convulsive Status Epilepticus

This term is used to describe the more common form of emergency situation that can occur with prolonged or repeated tonic-clonic (also called convulsive or grand mal) seizures. Most tonic-clonic seizures end normally in 1 to 2 minutes, but they may have post-ictal (or after-effects) symptoms for much longer. This makes it hard to tell when a seizure begins and ends.

Status epilepticus occurs when….

  • The active part of a tonic-clonic seizure lasts 5 minutes or longer.
  • A person goes into a second seizure without recovering consciousness from the first one.
  • A person has repeated seizures for 30 minutes or longer.

This type of status epilepticus requires emergency treatment by trained medical personnel in a hospital setting.This situation can be life-threatening and getting treatment started fast is vital. The outlook for this type of status may vary depending on the cause of the emergency and if other medical problems or complications occur.

  • Status epilepticus requires urgent medical treatment to lessen the chance of serious complications.
  • Medical treatment needs to be started as soon as possible. Oxygen and other support for breathing, intravenous fluids (fluid given into a blood vessel), and emergency medications are needed.
  • At times, medicines called anesthetics are used in the hospital to put a person into a coma to stop the seizures.
  • Continuous EEG (electroencephalogram) monitoring may be needed to monitor the seizures and how a person responds to treatment.
  • Tests may also be needed to find the cause of the seizure emergency so it can be treated correctly. People with a known cause, such as a brain infection, brain tumor, or stroke, may have a worse outlook than those with no other medical problems or known cause.

Nonconvulsive Status Epilepticus

This term is used to describe long or repeated absence or focal impaired awareness (complex partial) seizures.

  • The person may be confused or not fully aware of what is going on, but they are not “unconscious,” like in a tonic-clonic seizure.
  • These situations can be harder to recognize than convulsive seizures. Symptoms are more subtle and it’s hard to tell seizure symptoms from the recovery period.
  • There is no consistent time-frame on when these seizures are called an emergency. It depends in part on how long a person’s typical seizures are and how often they occur.

When nonconvulsive status epilepticus occurs or is suspected, emergency medical treatment in a hospital setting is needed. EEG testing may be needed to confirm the diagnosis first. People with this type of status are also at risk for convulsive status epilepticus, thus quick treatment is required.

Source: Status Epilepticus | Epilepsy Foundation

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[WEB SITE] How Ketogenic Diets Curb Inflammation 

Summary: The neurological benefits experienced by those with epilepsy who follow ketogenic diets may be a result of the low carb diet lowering brain inflammation, researchers report.

Source: UCSF.

Ketogenic diets — extreme low-carbohydrate, high-fat regimens that have long been known to benefit epilepsy and other neurological illnesses — may work by lowering inflammation in the brain, according to new research by UC San Francisco scientists. The UCSF team has discovered a molecular key to the diet’s apparent effects, opening the door for new therapies that could reduce harmful brain inflammation following stroke and brain trauma by mimicking the beneficial effects of an extreme low-carb diet

“It’s a key issue in the field — how to suppress inflammation in brain after injury,” said Raymond Swanson, MD, a professor of neurology at UC San Francisco, chief of the neurology service at the San Francisco Veterans Affairs Medical Center, and senior author of the new study.

In the paper, published online September 22, 2017 in the journal Nature Communications, Swanson and his colleagues found the previously undiscovered mechanism by which a low carbohydrate diet reduces inflammation in the brain. Importantly, the team identified a pivotal protein that links the diet to inflammatory genes, which, if blocked, could mirror the anti-inflammatory effects of ketogenic diets.

“The ketogenic diet is very difficult to follow in everyday life, and particularly when the patient is very sick,” Swanson said. “The idea that we can achieve some of the benefits of a ketogenic diet by this approach is the really exciting thing here.”

Low-Carb Benefits

The high-fat, low-carbohydrate regimen of ketogenic diets changes the way the body uses energy. In response to the shortage of carb-derived sugars such as glucose, the body begins breaking down fat into ketones and ketoacids, which it can use as alternative fuels.

In rodents, ketogenic diets — and caloric restriction, in general — are known to reduce inflammation, improve outcomes after brain injury, and even extend lifespan. These benefits are less well-established in humans, however, in part because of the difficulty in maintaining a ketogenic state.

In addition, despite evidence that ketogenic diets can modulate the inflammatory response in rodents, it has been difficult to tease out the precise molecular nuts and bolts by which these diets influence the immune system.

Intricate Molecular Waltz

In the new study, the researchers used a small molecule called 2-deoxyglucose, or 2DG, to block glucose metabolism and produce a ketogenic state in rats and controlled laboratory cell lines. The team found that 2DG could bring inflammation levels down to almost control levels.

This image shows hippocampal slices.

Immunostaining for Iba1 and iNOS identify activated microglia in mouse hippocampal slice cultures after 24 h incubation with LPS (10 μg/ml) or LPS + 2DG (1 mM) NeuroscienceNews.com image is credited to Swanson et al./Nature Communications.

“I was most surprised by the magnitude of this effect, because I thought ketogenic diets might help just a little bit,” Swanson said. “But when we got these big effects with 2DG, I thought wow, there’s really something here.”

The team further found that reduced glucose metabolism lowered a key barometer of energy metabolism — the NADH/NAD+ ratio — which in turn activated a protein called CtBP that acts to suppress activity of inflammatory genes.

In a clever experiment, the researchers designed a drug-like peptide molecule that blocks the ability of CtBP to enter its inactive state —essentially forcing the protein to constantly block inflammatory gene activity and mimicking the effect of a ketogenic state.

Peptides, which are small proteins, don’t work well themselves as drugs because they are unstable, expensive, and people make antibodies against them. But other molecules that act the same way as the peptide could provide ketogenic benefits without requiring extreme dietary changes, Swanson said.

The study has applications beyond brain-related inflammation. The presence of excess glucose in people with diabetes, for example, is associated with a pro-inflammatory state that often leads to atherosclerosis, the buildup of fatty plaques that can block key arteries. The new study could provide a way of interfering with the relationship between the extra glucose in patients with diabetes and this inflammatory response.

Source: How Ketogenic Diets Curb Inflammation – Neuroscience News

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