Anoxic Seizures Research Articles

Katılma Nöbetlerinde Demir ve Pirasetam ile Anoksik Epileptik Nöbetlerde Levetirasetamın Etkinliği

Introduction: In this study, the patients diagnosed with breath holding spell (BHS) or anoxic epileptic seizures and initiated at least one out of iron or piracetam or levetiracetam therapies were evaluated. Material and Methods: We retrospectively evaluated 194 BHS patients. Iron therapy was initiated in case of iron deficiency anemia or case of ferritin values under 12 ng/dl even if there was no anemia. The patients having no iron deficiency anemia, low ferritin and anoxic epileptic seizures were administered piracetam and the patients diagnosed with anoxic epileptic seizures were administered levetiracetam. Results: One hundred and eight patients (55.7%) were male. The mean age was 21.39±12.78 months. Iron therapy was initiated in 87 patients, piracetam to 96, and levetiracetam in 11 patients. Seizure numbers were manifestly decreased in all groups by the end of the first month after treatment concerning pretreatment levels (p<0.05). Conclusions: We determined that the spells were reduced or completely stopped in all groups. Levetiracetam seems to be considerably effective in patients developing anoxic epileptic seizures after BHS.

Approach to the pre-school child with sudden loss of consciousness

Abstract There are several causes for sudden loss of consciousness in pre-school children. These include Transient Loss of Consciousness (T-LOC), which encompasses a group of disorders with the following characteristics: abnormal motor control, loss of responsiveness, amnesia for the period of unconsciousness, and a short duration. There are three main categories of T-LOC in pre-school children: syncope, resulting from a sudden and reversible lack of oxygenated blood supplied to the brain, often caused by transient impairment of cardiac output or systemic arterial hypotension. Secondly, epileptic seizures due to excessive and hypersynchronous cortico-neuronal electrical activity in the brain, and thirdly, “unexplained T-LOC,” which includes cases not yet diagnosed fully, and those for which a pathophysiological mechanism has not yet been identified, despite thorough investigations. Reflex Anoxic Seizures (RAS) are important in the differential diagnosis of non-epileptic paroxysmal events in infants and pre-school children. Parents and carers who witness these episodes are understandably anxious, and the mainstay of management is ensuring that the correct diagnosis is made, reassurance is given, and both the patient and parents are educated about the condition. Diagnosis can be made based off a detailed history, including an eyewitness account of the episode, as well as clinical examinations. This review aims to describe an approach to the diagnosis and management of T-LOC in pre-school children.

Recognition and nursing management of reflex anoxic seizures in children.

Reflex anoxic seizures (RAS) present with a transient loss of consciousness and are triggered by an unexpected stimuli. These are paroxysmal, short-lived episodes of pronounced bradycardia or transient asystole; the episodes are self-limiting, lasting between 15 seconds and 1 minute. RAS are an important differential diagnosis of transient loss of consciousness but they are commonly misdiagnosed as epileptic events. An accurate and focused history is key to the diagnosis. They are mostly managed by performing an ECG to rule out other causes of arrhythmia, with subsequent explanation of the condition and reassurance given to parents. Nurses play an important role in eliciting the history and providing support to parents following the diagnosis. This article addresses the epidemiology and pathophysiology of RAS, with suggestions for management. An illustrative case study is included to highlight some of the challenges that health professionals working in different clinical set-ups are likely to come across while managing a child with RAS.

Compression of a giant pseudomeningocele causing transient anoxic seizures—a case report

Transient anoxic seizure upon application of pressure on a giant pseudomeningocele has never been reported in the literature; such abrupt changes in intracranial pressure due to large volume of cerebrospinal fluid (CSF) translocation, if left untreated may lead to permanent cerebral hypoxic injury and death. Here we describe a case of a 26-year-old woman who had undergone lumbar disc surgery in another unit few months ago and developed a large lump around her back. Any pressure on the lump resulted in headaches and at times episodes of seizures. Clinical examination revealed a very large fluid-filled lump consistent with a giant pseudomeningocele, confirmed by an MRI. A video EEG while applying pressure on the lump was recorded. The patient developed a typical seizure attack with a characteristic pattern of cerebral anoxia, and a paired ECG showed irregular rhythm with junctional and ventricular ectopic beats during the latter part of the attack, raising a suspicion of asystole. Upon relieving the pressure off the lump, the patient gradually regained consciousness with no permanent neurological deficit. We then discuss the pathophysiology of anoxic seizures and highlight the need to be vigilant in managing patients with such lesions in order to prevent permanent cerebral hypoxic injury and death.

Can syncope cause convulsive seizures in adults?

Convulsive epileptic seizures triggered by transient cerebral hypoperfusion 'reflex anoxic seizures' are well-described in children but are not commonly recognized in adults. We report a case series of 12 adults who presented acutely after generalized tonic-clonic seizures with a clear syncopal phase before the convulsion. We describe the aetiology, semiology and natural history of these events. Four patients (33.3%) had relevant risk factors for development of seizures/active epilepsy. Five patients (41.7%) had recurrent events prior to initial review by an epileptologist, but when anti-syncope measures were instituted there were no seizure recurrences over a median follow-up period of 34.5 (interquartile range 29.3-41.8)months. Syncope may be an under-recognized trigger for convulsive acute symptomatic seizures. Avoidance of syncope may be more effective than anti-seizure medications in preventing reflex anoxic seizures.

Reflex Anoxic Seizure in a 13-Year-Old Healthy Girl by Performing the “Mess Trick” and “Fainting Lark”

“Mess Trick” is the process of simultaneous squatting with hyperventilation followed by sudden erect posturing to induce syncope. “Fainting Lark” is the “mess trick” combined with forced valsalva while erect. This rare behavior, when identified, has been isolated to autistic, cognitively impaired children. More unlikely is this behavior discovered in the cognitively-well population. A 13-year-old healthy girl presented with a first episode of seizure. The seizure was unprovoked according to the history provided by the patient and an eyewitness. Routine radiology and laboratory analysis could not reveal an etiologic source. After speaking with the adolescent in the absence of her parents, she admitted playing a “black-out” game performing the “mess trick” and “fainting lark.” The resultant myoclonic jerks were the result of intentionally provoked syncope. Therefore, high-risk behaviors should be included in the differential of first episode of unprovoked seizure in a healthy adolescent.

Breath holding spells

The terminology is confusing and there is no internationally agreed nomenclature for Breath Holding Spells and related disorders. In North America, the term generally includes Reflex Anoxic Seizures (RAS) [1] or “Pallid Breath-Holding Spells” (see chapter on RAS) and Expiratory Apnea Syncope (EAS) or “Cyanotic Breath-Holding Spells” [2]. The mechanisms and treatment options are so different that I believe the distinction is important.

Anoxic-epileptic seizures

Although this special issue is devoted to paroxysmal non-epileptic events, we think the inclusion of anoxicepileptic seizures (AES) is justified because almost all affected children do not have epilepsy. However, they do have epileptic seizures, but usually only when provoked by a syncope [1]. This chapter assumes that the reader knows that most syncopes are convulsive [2] and that this does not imply AES but rather that when there is acute cerebral hypoxia or ischemia, that leads to an anoxic (non-epileptic) seizure, with non-epileptic spasms, non-epileptic tonic extensions, non-epileptic myoclonus and so forth. The syncopes known to have been associated with AES are mainly neurally-mediated, in particular RAS (reflex anoxic seizures/reflex asystolic syncope), prolonged expiratory apnea (PEA – otherwise known as, cyanotic or blue breath-holding spells), mixed types with both cardiac inhibition and expiratory grunts, and more typical vasovagal syncope [1]. Compulsive Valsalva manoeuvres are also well known to trigger epileptic seizures [1] and obstructive apnea has been the mechanism in at least one child patient [3]. To date, AES have not been reported in the syncopes associated with long QT syndrome and other cardiac conduction defects, neonatal hyperekplexia, paroxysmal extreme pain disorder or imposed upper airways obstruction.

Neurally mediated syncope

Syncope and autonomic failure are defined. Then the symptoms are described. There are three types of neurally mediated syncope; situational, carotid sinus hypersensitivity, and vasovagal syncope, which is the commonest form. The diagnosis can most often be made by taking a detailed history, but the tilt table test will help to confirm this. Details of the test are given. The different terms that have been used to describe this form of syncope have caused confusion, but neurally mediated syncope seems to be the best. There may often be difficulties in differentiating neurally mediated syncope from epilepsy, with all the problems a wrong diagnosis may cause, both personal and social, especially in the case of reflex anoxic seizures. The ocular compression test can help in making a definite diagnosis. Management will include reassurance, and advice on avoiding situations, which may result in an attack. Drugs are of limited value, and if syncope occurs frequently, cardiac pacemakers may have to be considered. This is justified, not only by the distress the attacks can cause to the individual, but also by such problems as driving and working with machinery.

Intractable or refractory epilepsy

The prognosis for those suffering from frequent seizures will be closely linked to their etiology (1). If there is extensive brain damage, whether this results from trauma, disease, or brain tumors, there is likely to be a poor response to whatever treatment is given. The more diffuse the lesions the worse this will be: and localisation is also a factor, for example mesial temporal sclerosis causing complex partial seizures. For these reasons patients who are mentally handicapped often have the additional handicap of epilepsy (2). The best chance of controlling the fits lies in making an accurate diagnosis and applying appropriate treatment, whether this is surgery to remove a tumor or the identification of a metabolic disorder which can be controlled, such as pyridoxine dependency or biotinidase deficiency (3). It is important to identify epileptic syndromes, often genetically determined, so that at least an accurate prognosis can be given, even if this does not effect treatment. For example the prognosis for infantile spasms and the Lennox-Gastaut syndrome are well known (4). Tuberous sclerosis is another diagnosis to be viewed with concern. Even within the field of epilepsy there are important diagnostic issues; for instance differentiating minor seizures from reflex anoxic seizures, and absence epilepsy and pseudoseizures from complex partial seizures (5). EDITORIAL

Bath-induced paroxysmal events - response to letter from Stephenson.

To the Editor Thank you for your interest in our case report. What we describe is our process of thinking in this case, in a child with episodes of impaired consciousness, colour change, and hypotonia which were apparently precipitated by water. We believe a systematic approach is important in such situations and disagree that this case report is misleading or factually incorrect. Firstly, reflex anoxic seizures (RAS) in children can be precipitated by distressing events, and if bathing is distressing (for whatever reason), it is possible that a reflex anoxic seizure could be precipitated. Furthermore, splashing of (cold) water on the face is a well recognised cause of vagal overstimulation which can also result in RAS. We did not conclude that it was RAS in this case, nor was this the focus of our case report. We recognise that in your paper, RAS was not thought to be a cause of bath-induced paroxysmal disorders. Secondly, it has been recognised that syncopal events in relation to water can be associated with long QT syndrome [1]. Although the majority of events in this case series were related to submersion and/or swim racing, these factors were not present in all cases [1]. There is another report of a cardiac sinus arrest (in an adult) from bathing diagnosed on a loop recorder [2]. These cases highlight the importance of at least considering cardiac causes including long QT syndrome when investigating children with paroxysmal events apparently triggered by water, as we did in this case with a simple ECG. Thirdly, you mentioned that you have only found 4 causes of bath-induced events. This is incorrect. In your review, although discussed, you discounted the case of histamine release-induced events. Water-induced anaphylaxis/events are a well recognized complication and can present in a similar fashion to our case [3], [4], [5]. The EEG tracing is indeed in microvolts, and the inaccuracies in the references are acknowledged.

Bath-induced paroxysmal events - Notes on a case report.

To the Editor I was interested to read the case report of bathing epilepsy published by Stutchfield and Loh [1] and wish to comment on several misleading statements and factual errors. As the authors would know, we have published a comprehensive review of bath-induced events [2]. Since then, three further papers on bathing epilepsy have been published [3], [4], [5], [6] together with a letter [6] confirming that what was originally reported as neonatal-onset bathing epilepsy is in fact alternating hemiplegia of childhood. Stutchfield and Loh [1] begin their Abstract by writing that “Bath-induced events in infants and children can be triggered by various etiologies, including cardiological, neurological, and metabolic causes.” This statement reflects the general message of the paper and its conclusion that “There is a wide differential diagnosis for reduced conscious level triggered by bathing” [1]. This contradicts the findings of our very careful review [2], which found only four conditions triggered by bathing in infants, these being bathing epilepsy — by far the commonest [2], [3], [4], [5], alternating hemiplegia of childhood [6], hyperekplexia, and paroxysmal extreme pain disorder [2]. Stutchfield and Loh [1] stated that reflex anoxic seizures (reflex asystolic syncope), cyanotic breath-holding spells (prolonged expiratory apnea), and cardiac syncope from long QT syndrome might be triggered by bathing in infancy, but to my knowledge, no such reports have been published. With regard to the authors' EEG findings, readers should note that the unit of measurement for the amplitudes of the interictal background activity as well as the “slow build-up of irregular high amplitude (530 mV) delta activity” should be microvolts and not millivolts: indeed, the calibration at the top of Fig. 1. confirms this. Finally, the authors' list of references deserves comment as well. Their reference [1] – De Keyzer et al. – describes a case of bathing epilepsy (bath water was at 37 °C) and not hot water epilepsy, despite its title. Their reference [3] – Fertleman et al. – was not published in JAMA Neurol (the new name for Archives of Neurology) but rather in the journal Neurology. Lastly, their reference [4] – Mikati et al. – was published in Pediatr Neurol and not J Pediatr Neurol. Conflict of interest None.

Prolonged Sinus Pauses Revealing A Paroxysmal Extreme Pain Disorder: Is It A Frequent Situation? A Case Report

Title : Paroxysmal extreme pain disorder (PEPD) is an autosomal dominant painful neuropathy with many,but not all, cases linked to gain-of-function mutations in SCN9A which encodes voltage-gated sodium channel Na.1.7. It is a very rare condition featured by flushing of the lower half of the body and excruciating burning pain caused by any stimulus below the waist or in the perianal region. PEPD may be associated with cardiovascular instability, especially prolonged sinus pauses, and thus has anesthetic implications. Pacemaker implantation is the alternative therapeutic option, but its indications have not been clarified yet. Background: This condition is well described in neurological literature, but to our knowledge, this is the first case report of a patient with paroxysmal extreme pain disorder with prolonged sinus pauses requiring anesthesia for an epicardial pacemaker even with the peri-operative risk of the pathology.This clinical observation can help for a better management and understanding of the cardiac risk complications of PEPD especially for an infant whose diagnostic is frequently made at the stage of complication This clinical observation can put the item on the necessity of establishing recommendations for management of cardiac complications during PEPD. Case report : We extensively searched the literature on cardiac pacing in patients with PEPD and we described a new case of a 9 month old infant who was admitted in the emergency department for an episode of malaise apnea and hemifacial cyanosis relevant to PEPD. The neurologic exploration was normal. The diagnostic was confirmed by genetic study. The 24 hours recording demonstrated long pauses of 15 seconds during the crisis justifying the implantation of epicardial pacemaker without peri-operatory complications due to the high anesthetic risk of this pathology. Conclusion : Paroxysmal extreme pain disorder is a highly distinctive sodium channelopathy with incompletely carbamazepine-sensitive bouts of pain and sympathetic nervous system dysfunction. It is most likely to be misdiagnosed as epilepsy and, particularly in infancy, as hyperekplexia and reflex anoxic seizures. Clinicians must evocate this diagnostic even any clinical suspicion given the severity of cardiac complications.

Management of Reflex Anoxic Seizures

Investigators at the Roald Dahl EEG Unit, Alder Hey Children’s NHS Foundation, Liverpool, UK, review the definition, pathophysiology, clinical presentation, and management of reflex anoxic seizures (RAS) in children.

Glycopyrrolate and Theophylline for the Treatment of Severe Pallid Breath-holding Spells

Severe pallid breath-holding spells (BHSs) are based on parasympathetic hyperactivity, leading to cardiac asystole, pallor, brain ischemia, loss of consciousness, and reflex anoxic seizures. In recent years, an increasing number of patients with severe pallid BHSs have been successfully treated with pacemaker implantation. We present the case of a 13-month-old girl suffering from repeated severe pallid BHSs, causing asystole, loss of consciousness, and generalized anoxic seizures. She underwent treatment with oral glycopyrrolate, an anticholinergic drug, and an oral retard preparation of theophylline. The aim of the treatment was to decrease cardiac inhibition with glycopyrrolate and to bring about a positive chronotropic effect with theophylline. In our case, the combined therapy was effective in suppressing syncope and reflex anoxic seizures associated with BHSs This avoided the need for ventricular pacemaker implantation.

Diverse Presentation of Breath Holding Spells: Two Case Reports with Literature Review

Breath holding spells are a common and dramatic form of syncope and anoxic seizure in infancy. They are usually triggered by an emotional stimuli or minor trauma. Based on the color change, they are classified into 3 types, cyanotic, pallid, and mixed. Pallid breath holding spells result from exaggerated, vagally-mediated cardiac inhibition, whereas the more common, cyanotic breathholding spells are of more complex pathogenesis which is not completely understood. A detailed and accurate history is the mainstay of diagnosis. An EKG should be strongly considered to rule out long QT syndrome. Spontaneous resolution of breath-holding spells is usually seen, without any adverse developmental and intellectual sequelae. Rare cases of status epilepticus, prolonged asystole, and sudden death have been reported. Reassurance and education is the mainstay of therapy. Occasionally, pharmacologic intervention with iron, piracetam; atropine may be of benefit. Here we present 2 cases, one of each, pallid and cyanotic breath holding spells.

Successful Treatment of Pallid Breath-Holding Spells With Fluoxetine

Pallid breath-holding (PBH) is a childhood condition that presents with recurrent syncope. Although typically benign, severe cases can lead to asystole and anoxic seizures. Previous studies have advocated pacemaker placement to abbreviate symptoms. This was a retrospective study of patients treated with fluoxetine for PBH spells. Clinical response, side effects and avoidance of pacemaker implantation were reviewed in six patients (12-60 months) treated with fluoxetine for PBH. Patients were referred because of concern of arrhythmia and failed medical treatment strategies. Two patients had previously implanted loop recorders, 5 patients had documented episodes of asystole, and 2 patients had generalized seizures. Fluoxetine resulted in alleviation of syncope in 5 of 6 patients. Time to symptomatic improvement symptoms ranged from 2 days to 1 month (median, 2 weeks). Median duration of treatment with fluoxetine was 12 months (12-24 months). One patient demonstrated no improvement and had a pacemaker implanted. There were no reported side effects to fluoxetine. Fluoxetine can be used to treat childhood PBH spells and may obviate the need for permanent pacing in a significant subset of this population. Considering its safe side-effect profile it is a worthwhile first-line agent to treat this disorder.

Reflex anoxic seizure: an important diagnosis to remember

Children may present with a sudden collapsing episode, and the paramedic team is often requested to attend such emergencies. It is important that these episodes are correctly categorised as being either epileptic or non-epileptic events. A reflex anoxic seizure (RAS) is one such presentation. RAS is a paroxysmal, spontaneously-reversing, brief episode of asystole triggered by pain, fear or anxiety. RAS occur due to a brief stoppage of the heart caused by overactivity of the vagus nerve. This is usually triggered by an unpleasant stimulus, following which the child may appear pale and lifeless. The diagnosis is usually made by a paediatrician but it is important that the paramedic team are aware of this condition. A child with a diagnosis of RAS may be managed by reassurance from paramedic practitioners if the child is judged to be well after an episode.

A pallid paroxysmal event in children: it is vagal anoxic seizure, it is treatable, and it is not “epilepsy”

A pallid paroxysmal event in children: it is vagal anoxic seizure, it is treatable, and it is not “epilepsy”

A nurse-led ‘first fitter’ clinic in a paediatric emergency department: an experience

BackgroundThe diagnoses of a child who presents to an Accident and Emergency (A&E) department with ‘jerking’ or loss of consciousness include an epileptic seizure, vasovagal event, cardiac syncope or other...