Episodes Of Status Epilepticus Research Articles

Prevention of organophosphate-induced chronic epilepsy by early benzodiazepine treatment

Poisoning with organophosphates (OPs) may induce status epilepticus (SE), leading to severe brain damage. Our objectives were to investigate whether OP-induced SE leads to the emergence of spontaneous recurrent seizures (SRSs), the hallmark of chronic epilepsy, and if so, to assess the efficacy of benzodiazepine therapy following SE onset in preventing the epileptogenesis. We also explored early changes in hippocampal pyramidal cells excitability in this model. Adult rats were poisoned with the paraoxon (450μg/kg) and immediately treated with atropine (3mg/kg) and obidoxime (20mg/kg) to reduce acute mortality due to peripheral acetylcholinesterase inhibition. Electrical brain activity was assessed for two weeks during weeks 4-6 after poisoning using telemetric electrocorticographic intracranial recordings. All OP-poisoned animals developed SE, which could be suppressed by midazolam. Most (88%) rats which were not treated with midazolam developed SRSs, indicating that they have become chronically epileptic. Application of midazolam 1min following SE onset had a significant antiepileptogenic effect (only 11% of the rats became epileptic; p=0.001 compared to non-midazolam-treated rats). Applying midazolam 30min after SE onset did not significantly prevent chronic epilepsy. The electrophysiological properties of CA1 pyramidal cells, assessed electrophysiologically in hippocampal slices, were not altered by OP-induced SE. Thus we show for the first time that a single episode of OP-induced SE in rats leads to the acquisition of chronic epilepsy, and that this epileptogenic outcome can be largely prevented by immediate, but not delayed, administration of midazolam. Extrapolating these results to humans would suggest that midazolam should be provided together with atropine and an oxime in the immediate pharmacological treatment of OP poisoning.

Melas, Stroke-Like Episodes and Ketogenic Diet

Investigators at University of Toronto and McMaster University, Canada, report a 22-year-old woman with multiple episodes of status epilepticus and migratory cortical stroke-like lesions.

Neuroimaging in status epilepticus secondary to paraneoplastic autoimmune encephalitis

To describe the characteristic magnetic resonance imaging (MRI) findings of paraneoplastic autoimmune encephalitis in patients with new-onset status epilepticus. The neuroimaging and clinical data of five patients with paraneoplastic autoimmune encephalitis debuting as status epilepticus were retrospectively reviewed. All patients met the criteria for definite paraneoplastic syndrome and all underwent brain MRI during the status epilepticus episode or immediately after recovery. All patients showed hyperintense lesions on T2-weighted imaging (WI) involving the limbic structures, specifically the hippocampus. Three of them showed additional extra-limbic areas of signal abnormalities. The areas of T2 hyperintensity were related to the electroclinical onset of the seizures. In three patients, various techniques were used to study cerebral perfusion, such as arterial spin labelling MRI, single photon-emission computed tomography (SPECT) and 2-[(18)F]-fluoro-2-deoxy-d-glucose (FDG)-positron-emission tomography (PET). Arterial spin labelling showed hyperperfusion overlapping the inflammatory lesions, whereas PET and SPECT disclosed increased perfusion and increased metabolism. The subtraction SPECT co-registered to MRI (SISCOM) demonstrated hypermetabolism outside the areas of encephalitis. After clinical recovery, follow-up MRI revealed the development of atrophy in the initially affected hippocampus. Two patients who had recurrent paraneoplastic autoimmune encephalitis manifesting as status epilepticus showed new T2 lesions involving different structures. The presence of limbic and extra-limbic T2 signal abnormalities in new-onset status epilepticus should suggest the diagnosis of a paraneoplastic syndrome, especially when status epilepticus is refractory to treatment. The lesions are consistently seen as hyperintense on T2WI.

Statins are associated with decreased mortality risk after status epilepticus

Statins display anti-inflammatory and anti-epileptogenic properties in animal models, and may reduce the epilepsy risk in elderly humans; however, a possible modulating role on outcome in patients with status epilepticus (SE) has not been assessed. This cohort study was based on a prospective registry including all consecutive adults with incident SE treated in our center between April 2006 and September 2012. SE outcome was categorized at hospital discharge into 'return to baseline', 'new disability' and 'mortality'. The role of potential predictors, including statins treatment on admission, was evaluated using a multinomial logistic regression model. Amongst 427 patients identified, information on statins was available in 413 (97%). Mean age was 60.9 (±17.8) years; 201 (49%) were women; 211 (51%) had a potentially fatal SE etiology; and 191 (46%) experienced generalized-convulsive or non-convulsive SE in coma. Statins (simvastatin, atorvastatin or pravastatin) were prescribed prior to admission in 76 (18%) subjects, mostly elderly. Whilst 208 (50.4%) patients returned to baseline, 58 (14%) died. After adjustment for established SE outcome predictors (age, etiology, SE severity score), statins correlated significantly with lower mortality (relative risk ratio 0.38, P = 0.046). This study suggests for the first time that exposure to statins before an SE episode is related to its outcome, involving a possible anti-epileptogenic role. Other studies are needed to confirm this intriguing finding.

When is a child with status epilepticus likely to have Dravet syndrome?

To identify clinical risk factors for Dravet syndrome (DS) in a population of children with status epilepticus (SE). Children aged between 1 month and 16 years with at least one episode of SE were referred from 6 pediatric neurology centers in Switzerland. SE was defined as a clinical seizure lasting for more than 30min without recovery of normal consciousness. The diagnosis of DS was considered likely in previously healthy patients with seizures of multiple types starting before 1 year and developmental delay on follow-up. The presence of a SCN1A mutation was considered confirmatory for the diagnosis. Data such as gender, age at SE, SE clinical presentation and recurrence, additional seizure types and epilepsy diagnosis were collected. SCN1A analyses were performed in all patients, initially with High Resolution Melting Curve Analysis (HRMCA) and then by direct sequencing on selected samples with an abnormal HRMCA. Clinical and genetic findings were compared between children with DS and those with another diagnosis, and statistical methods were applied for significance analysis. 71 children with SE were included. Ten children had DS, and 61 had another diagnosis. SCN1A mutations were found in 12 of the 71 patients (16.9%; ten with DS, and two with seizures in a Generalized Epilepsy with Febrile Seizures+(GEFS+) context). The median age at first SE was 8 months in patients with DS, and 41 months in those with another epilepsy syndrome (p<0.001). Nine of the 10 DS patients had their initial SE before 18 months. Among the 26 patients aged 18 months or less at initial SE, the risk of DS was significantly increased for patients with two or more episodes (56.3%), as compared with those who had only one episode (0.0%) (p=0.005). In a population of children with SE, patients most likely to have DS are those who present their initial SE episode before 18 months, and who present with recurrent SE episodes.

Acute dyskinesia: A rare adverse effect of oxcarbazepine in epilepsy with neurobehavioral symptoms

We are reporting an 11-year-old female child of febrile partial seizure since age of 3 months and transient neurobehavioral changes of psychic, gelastic semiology since childhood. She had no history of continued febrile seizure, but had 3 admissions for 3 episodes of status epilepticus in last 3 years. She experienced acute generalized dyskinesia (torticollis, oromandibular dystonia, spasmodic dysphonia, right lower limb eversion plantarflexed type feet dystonia) soon after oxcarbazepine (OXC) therapy from last episode of status epilepsy on 15 April 2013 with similar semiology. We failed to explain the considered infectious, non-convulsive state and hyponatremic extra pyramidal syndrome. We used the Naranjo adverse drug reaction probability scale and stopped OXC. After state intravenous diazepam 2 nd day, she was starting to improve and over a period of 4 days she was asymptomatic. We shifted on clonazepam, sodium valproate for further. She was asymptomatic until 1 month follow-up.

Anesthesia in a child with adrenoleukodystrophy.

X-linked adrenoleukodystrophy (ALD) is rare genetic disorder, and children with ALD are at an increased risk of anesthetic mortality and morbidity [1]. Therefore, they require an individual anesthetic protocol based on their clinical condition. Herein we report the case of a male with childhood-onset X-linked ALD who required general anesthesia for a dental operation. An 11-year-old male (height 143 cm, weight 30 kg) was scheduled for scaling and multiple deciduous tooth extractions under general anesthesia due to his failure to cooperate willingly. He had been diagnosed with childhood-onset X-linked ALD 3 years previously. Other history included an episode of status epilepticus, adrenal insufficiency, aspiration pneumonia, pressure sores and blindness. He was bed-ridden and maintained on a positive-pressure home ventilator via tracheostomy. Physical examination revealed spastic tetraparesis, unresponsiveness to the environment, and cushingoid facies due to chronic steroid supplementation. Preoperative medications including topiramate, divalproex, prednisolone were continued until the morning of the operation. On arrival at the operating room, standard monitoring commenced. For anesthetic induction, 75 mg of pentothal sodium were injected. Anesthesia was maintained using N2O at 2 L/min, O2 at 2 L/min, and sevoflurane. About 5 min after the start of maintenance inhalational anesthesia, the surgeon was unable to open the patient’s mouth so rocuronium 10 mg was injected, after which the mouth could be opened and the surgery commenced. The operation lasted 30 min and was uneventful. Residual neuromuscular blockade was reversed with pyridostigmine 10 mg and glycopyrrolate 0.2 mg, and 15 min after administration of reversal agents, we placed the patient’s home ventilator in pressure-support ventilation (PSV) mode, as it was preoperatively. The patient was observed closely for over 1 h by an anesthesiologist and a pediatrician in the post-anesthesia care unit (PACU). The home ventilator with PSV mode was well tolerated, so we then transferred the patient to the general ward under monitoring with pulse oximetry. X-linked ALD is a progressive neurodegenerative disorder characterized by demyelination of cerebral white matter, axonopathy of the spinal cord, and reduced adrenal response to adrenocorticotropic hormone. The onset age of the condition is between 3 and 10 years, and the patients initially present with behavioral problems and deficits in memory and language. As the disease progresses, vision loss, auditory impairment, hemiparesis and spastic tetraparesis may occur. In the later stages, seizures begin and the patient becomes bedridden, blind, and unable to interact with the environment. Death usually ensues within 2 to 4 years after the onset of symptoms [1]. There are several considerations in anesthetic management for these patients. The anesthetic plan should be formulated based on each individual patient’s condition according to their disease progression. In our case, the anesthetic plan focused on the prevention of seizures and early return to the preoperative condition without any anesthesia-related complications. In an ALD patient with seizure disorders, anticonvulsants should be continued throughout the perioperative period, including the day of surgery, and the anesthesiologist should consider the altered pharmacokinetics of anesthetics due to hepatic microsomal enzyme induction secondary to chronic antiseizure

Parkinson's disease: Less epileptic seizures more status epilepticus

We compared the rate of epilepsy and status epilepticus (SE) in patients with and without Parkinson's disease (PD). Out of 1215 patients with idiopathic PD, 31 had epilepsy and 19 of these had at least one episode of SE (61.3%) compared to 298 of 2537 patients (11.7%; p<0.001) with epilepsy and without concomitant PD. This clinical finding supports the hypothesis that the functional impairment of the basal ganglia in PD patients makes SE more likely.

Etiology, characteristics and outcome of seizures after pediatric hematopoietic stem cell transplantation

PurposeEpileptic seizures are frequent manifestations after hematopoietic stem cell transplantation (HSCT). In this retrospective single-center study we evaluated electroclinical features and analyzed etiologies and outcome of seizures after pediatric HSCT. MethodsOf 261 children transplanted between 2000 and 2010, we identified and analyzed data of 28 patients with seizures within a year from HSCT. ResultsMost frequent etiologies were posterior reversible encephalopathy syndrome (PRES, 14 patients) and central nervous system (CNS) infections (4 patients). Seizures were the presentation of the underlying complications in 22 patients. Sixteen episodes of status epilepticus were identified. Seizures secondary to PRES were usually longer and associated with non-convulsive signs. Early neuroimaging and EEG monitoring proved to be crucial to diagnose and treat seizures and their causes. No patients developed epilepsy suggesting that chronic antiepileptic therapy is not necessary in these patients. Overall survival was 32.3% over 5 years in patients with seizures and 45.8% in patients without seizures (p<0.05). Multivariate statistical analysis identified as independent risk factors for seizures a diagnosis of non-oncological disease and cord blood stem cell transplantation. ConclusionsSeizures in transplanted children are a severe event and are associated with high morbidity and poor outcome. In particular, patients with non-oncological diseases and cord blood stem cell transplantation have to be considered at high risk of seizures. Moreover, this study underlines the importance of early recognition of non-convulsive clinical signs and of EEG monitoring for a prompt diagnosis and an appropriate management of seizures and their causes.

Early onset absence epilepsy with onset in the first year of life: A multicenter cohort study

Absence epilepsy with onset before age 4 years, or early onset absence epilepsy (EOAE), has been rarely reported, and children with onset in the first year of life are considered almost exceptional. We aimed to report the clinical and electrophysiologic features of a cohort of children with absence epilepsy starting within the first year of life. This was a multicenter study including patients with absence epilepsy starting within the first year of life and identified over a 20-year period (1991-2011). We identified 16 patients with absence epilepsy starting within the first year of life with a mean follow-up of 6.4 years. Mean age at seizure onset was 10.3 ± (standard deviation)1.4 months (range 8-12). Two patients experienced rare tonic-clonic seizures that started later than the absences. None of the subjects had episodes of absence status epilepticus. Eleven subjects were seizure-free with the first antiepileptic drug. In eight children, therapy was withdrawn after a mean 3.2 years of treatment. None evolved into a different form of idiopathic generalized epilepsy. SLC2A1 gene analysis in 12 children (75%) failed to reveal glucose transporter 1 deficiency. EOAE, including patients with onset within the first year of life, should be no more considered a distinct idiopathic generalized epilepsy (IGE) syndrome, as it shows electroclinical features, response to therapy, and prognosis similar to childhood absence epilepsy. Moreover, early age of onset is not predictive of GLUT-1 deficiency and genetic analysis may be therefore avoided in patients meeting strict inclusion criteria.

Experimental Models of Status Epilepticus and Neuronal Injury for Evaluation of Therapeutic Interventions

This article describes current experimental models of status epilepticus (SE) and neuronal injury for use in the screening of new therapeutic agents. Epilepsy is a common neurological disorder characterized by recurrent unprovoked seizures. SE is an emergency condition associated with continuous seizures lasting more than 30 min. It causes significant mortality and morbidity. SE can cause devastating damage to the brain leading to cognitive impairment and increased risk of epilepsy. Benzodiazepines are the first-line drugs for the treatment of SE, however, many people exhibit partial or complete resistance due to a breakdown of GABA inhibition. Therefore, new drugs with neuroprotective effects against the SE-induced neuronal injury and degeneration are desirable. Animal models are used to study the pathophysiology of SE and for the discovery of newer anticonvulsants. In SE paradigms, seizures are induced in rodents by chemical agents or by electrical stimulation of brain structures. Electrical stimulation includes perforant path and self-sustaining stimulation models. Pharmacological models include kainic acid, pilocarpine, flurothyl, organophosphates and other convulsants that induce SE in rodents. Neuronal injury occurs within the initial SE episode, and animals exhibit cognitive dysfunction and spontaneous seizures several weeks after this precipitating event. Current SE models have potential applications but have some limitations. In general, the experimental SE model should be analogous to the human seizure state and it should share very similar neuropathological mechanisms. The pilocarpine and diisopropylfluorophosphate models are associated with prolonged, diazepam-insensitive seizures and neurodegeneration and therefore represent paradigms of refractory SE. Novel mechanism-based or clinically relevant models are essential to identify new therapies for SE and neuroprotective interventions.

Surgical treatment of status epilepticus: A palliative approach

Although status epilepticus (SE) does not resemble a domain for neurosurgical indications in single occasions, a microneurosurgical procedure in patients with catastrophic epilepsy and status epilepticus should be considered as an ultimate ratio-choice in these patients. From a personal series of >600 epilepsy surgery procedures in a period from August 1, 1993 until March 13, 2013, 22 patients were identified with catastrophic epilepsy and all of them with at least one episode of status epilepticus. Five of the patients had surgery under ongoing status epilepticus. Twelve patients became seizure-free, two patients had >90% seizure reduction, seven patients >50% seizure reduction, and one patient was unchanged. No surgery-related complications in terms of permanent morbidity were ascertained in the presented series. In the subgroup of the five patients operated in the acute phase of SE one patient became seizure-free (Engel class. I), one showed Engel class II, two Engel class III, and one Engel class IV with no worthwhile improvement. Patients with catastrophic epilepsy including status epilepticus can benefit from resective epilepsy surgery, even with incomplete resection of the epileptogenic lesion.

P.1.20 GOSR2: A novel form of Congenital Muscular Dystrophy

We describe an 36week male who was born with mild hypotonia and subsequently found to have severe developmental delay. There is also reported optic nerve atrophy. Serum creatine kinase (CK) was 5582. MRI of the brain demonstrated periventricular white matter loss, ventriculomegaly, and a thin corpus callosum. His muscle biopsy demonstrated severe non-specific dystrophic changes. Staining with VIA4-1, however, demonstrated normal levels of glycosylated alpha-dystroglycan, and genetic testing for genes known to cause Walker-Warburg Syndrome (WWS) was negative. Whole exome sequencing was performed, which demonstrated compound heterozygous mutations in <i>GOSR2</i>, including a previously described mutation c.430G>T as well as a novel splice site mutation c.336+1G>A. Previous reports have described homozygous c.430G>T mutations as causative of progressive myoclonus epilepsy (PME), a syndrome characterized by myoclonus, seizures, and progressive cognitive decline. Patients with this <i>GOSR2</i> mutation also have areflexia, tremors, ataxia, and mildly elevated CK levels, suggesting a possible subclinical myopathy. Muscle biopsies on these PME patients, however, have been normal. Interestingly, at 28months of age, the patient began to experience clinical seizures with one episode of status epilepticus. <i>GOSR2</i> encodes for a SNARE involved with protein transport from the endoplasmic reticulum to the <i>trans</i>-Golgi apparatus. Our studies suggest that <i>GOSR2</i> may play a role in the transport of critical membrane glycoprotein complexes of myocytes.

Treatment and course of different subtypes of status epilepticus

Since randomized controlled trials are difficult to perform for ethical reasons in a potentially deadly condition like status epilepticus (SE), a retrospective database analysis may be welcome to broaden the evidence for the treatment of SE. In this retrospective study we evaluated every SE treatment at the neurological department of the University of Rostock from January 2000 to December 2009 in order to determine the efficacy of different antiepileptic drugs (AEDs) in terminating different kinds of SE. We analyzed the frequency of refractory courses in different types of SE, at which time which AED was administered and at which time which AED was effective to terminate the different epileptic conditions. A second aim of this study was to evaluate the course and the outcome of different kinds of SE. Statistical comparisons were performed with the χ(2)-test. 167 episodes of SE in 118 patients could be evaluated. The efficacy rates of AEDs differed significantly, mainly due to the superior efficacy of clonazepam (CZP). CZP seemed to be more effective than DZP, LEV, MDM and VPA in terminating generalized convulsive status epilepticus (GCSE), whereas there was no significant difference in the efficacy for terminating nonconvulsive status epilepticus (NCSE) and epilepsia partialis continua (EPC) between the used AEDs. Anaesthesia and CZP both terminated GCSE more effectively than NCSE and EPC. Concerning the course of the different kinds of SE the following results were obtained: 13 patients died during hospital treatment. Treatment in NCSE and EPC started significantly later than in GCSE. There was no significant difference in mortality between the types of SE. However the frequency of refractory courses differed between the types of SE. At the time of SE termination without the administration of anaesthesia a combination therapy using 2 or more AEDs was established in most episodes.

Hemiconvulsion–hemiplegia syndrome revisited: longitudinal MRI findings in 10 children

Hemiconvulsion-hemiplegia syndrome (HHS) is a rare severe epilepsy of infancy consisting of unilateral convulsive status epilepticus immediately followed by transient or lasting ipsilateral hemiplegia. HHS may occur either in patients with previous brain pathology or without any identified cause, so-called 'idiopathic HHS'. We retrospectively analysed clinical and MRI longitudinal findings of a series of 10 patients (six females, four males) presenting with HHS. Age at the study inclusion ranged from 2 years 6 months to 15 years (mean of 5 y 10 mo, median 4 y 2 mo). After defining magnetic resonance imaging (MRI) features as 'typical', i.e. strictly unilateral involvement, and 'atypical', i.e. bilateral, we compared clinical data from both groups. Cognitive level was assessed using Brunet-Lézine or Wechsler scales. HHS occurred at a mean age of 20.5 months (range 8-48 mo). In all cases, status epilepticus lasted for more than 1 hour and was characterised by unilateral clonic seizures followed by ipsilateral hemiplegia (persistent in five patients). Two patients in this series died: the first from multi-organ failure 2 weeks after the status epilepticus and the other from a second episode of ipsilateral intractable febrile status epilepticus 3 years after the first episode. Early MRI (days 1-7 from status epilepticus) showed hemispheric cytotoxic oedema in all, extending to the contralateral side for one. T2 hyperintensity in the basal ganglia was disclosed in 70% of patients and in the hippocampus in 60%. After 1 month (in intermediate and chronic phases), all surviving patients but one showed hemispheric cortical atrophy corresponding to the regions involved during the early stage. Comparing clinical features of patients presenting with 'typical' features, to those with 'atypical' findings, the second group presented psychomotor delay before status epilepticus. This series underlines the major value of early MRI for the prompt diagnosis of HHS, and shows that involvement of subcortical structures has been underestimated. Hippocampal involvement is not constant.

Serum Levels of Cardiac Troponin I in Patients with Status Epilepticus and Healthy Cardiovascular System

Status epilepticus (SE) is accompanied by acute and intense activation of the sympathetic nervous system, which might result in myocyte damage. However, there is insufficient evidence to assess cardiac biomarkers in SE patients. As a highly specific and sensitive biomarker of acute myocardial infarction, serum concentration of cardiac troponin I (cTnI) has been assessed in this study in a sample of SE patients without evidence of previous cardiovascular diseases. In this analytical cross-sectional study, a total number of 30 patients with SE and no history of baseline cardiovascular disorders, aged between 12 and 60 years have been evaluated. Baseline, demographic characteristics and laboratory measurements including cTnI, creatine kinase (CPK) and CPK-MB were recorded for all of patients. cTnI was quantified using ELISA method with the precision of 0.01 ng/mL. All cases had a cardiac troponin level <0.01 ng/mL except for one 60- year-old female with a history of seizure 3 years prior. The last seizure was 60 days prior and the patient had a reported cTnI level as 0.04 ng/mL, within normal limits. The mean serum levels of CPK and CK-MB were 202.20 (SD= 14.46) μg/l and 14.54 (SD= 1.49) ng/mL, respectively. This investigation is one of the few to evaluate serum concentration of cTnI in generalized convulsive SE patients where no detectable elevation was observed in serum concentration of cTnI following SE episode. However, it is very important to take into account that all recruited SE patients included in this study had a healthy cardiovascular system.

Early Developmental Outcome Following Convulsive Status Epilepticus

Investigators at the Developmental Cognitive Neurosciences Unit, Institute of Child Health, London, other centers in the UK, and Dartmouth School of Medicine, NH, USA, prospectively recruited children aged between 1 and 42 months from North London who had at least one episode of convulsive status epilepticus (CSE) and classified them as prolonged febrile seizures (PFS) or nonfebrile CSE.

Transient Inhibition of TrkB Kinase after Status Epilepticus Prevents Development of Temporal Lobe Epilepsy

Temporal lobe epilepsy is the most common and often devastating form of human epilepsy. The molecular mechanism underlying the development of temporal lobe epilepsy remains largely unknown. Emerging evidence suggests that activation of the BDNF receptor TrkB promotes epileptogenesis caused by status epilepticus. We investigated a mouse model in which a brief episode of status epilepticus results in chronic recurrent seizures, anxiety-like behavior, and destruction of hippocampal neurons. We used a chemical-genetic approach to selectively inhibit activation of TrkB. We demonstrate that inhibition of TrkB commencing after status epilepticus and continued for 2 weeks prevents recurrent seizures, ameliorates anxiety-like behavior, and limits loss of hippocampal neurons when tested weeks to months later. That transient inhibition commencing after status epilepticus can prevent these long-lasting devastating consequences establishes TrkB signaling as an attractive target for developing preventive treatments of epilepsy in humans.

Benzodiazepine overtreatment in status epilepticus is related to higher need of intubation and longer hospitalization

Benzodiazepine (BDZ), a widely recognized first-line status epilepticus (SE) treatment, may lead to respiratory depression. This cohort study investigates the effect of BDZ doses in SE patients in terms of morbidity and mortality. It considers incident SE episodes from a prospective registry (2009-2012), comparing patients receiving standard BDZ dose to those receiving exceeding doses (>30% above recommended dose), in terms of likelihood to receive intubation, morbidity, and mortality. Duration of hospitalization was assessed for subjects needing intubation for airways protection (not for refractory SE treatment) versus matched subjects not admitted to the intensive care unit (ICU). We identified 29 subjects receiving "excessive" and 173 "standard" BDZ dose; 45% of the overtreated patients were intubated for airways protection, but only 8% in the standard-dose group (p < 0.001). However, both groups presented similar clinical outcomes: 50% returned to baseline, 40% acquired a new handicap, and 10% died. Orotracheal intubation due to airways protection was associated with significantly longer hospitalization (mean 2 weeks vs. 1 week, p = 0.008). In conclusion, although administration of excessive BDZ doses in SE treatment does not seem to influence outcome, it is related to higher respiratory depression risk and longer hospitalization, potentially exposing patients to additional complications and costs.

A Case of Severe, Persistent Amnesia Following an Episode of Prolonged Status Epilepticus

The role of the hippocampus in memory loss has been well established. We present a case of persistent and profound amnesia in a patient with a prolonged episode of status epilepticus complicated by a history of alcohol abuse. Serial brain MRI ’ s showed concomitant evolution of profound hippocampal damage. doi: http://dx.doi.org/10.4021/jmc1177w