Non-convulsive Status Epilepticus Presenting Research Articles

Cognitive Biases to Consider in Non-convulsive Status Epilepticus Presenting in a Hematologic Malignancy.

Cognitive Biases to Consider in Non-convulsive Status Epilepticus Presenting in a Hematologic Malignancy.

Non-convulsive status epilepticus presenting as acute confusional state in a young adult

Nonconvulsive status epilepticus (NCSE) can occur in a variety of clinical conditions and is characterized by prolonged electrographic seizures without clinically discernible seizure activity. It may be one of the most frequently missed diagnoses in patients with altered neurologic function because it is often seen in patients with other serious illnesses. For accurate diagnosis of NCSE, an alteration in baseline cognition or behavior and a concurrent epileptiform seizure pattern on electroencephalography (EEG) must be present. This case of a young adult male presented to our emergency room with an acute onset of confusional state and behavioral changes with no clue for its etiology on initial clinical or after routine investigations including CT brain until EEG picked up continuous epileptic discharges. He responded dramatically to antiepileptic drugs without any recurrence during follow-up of 4 months. Many cases like this are being diagnosed with the use of continuous EEG monitoring (cEEG) in Neurological Intensive Care Units. The advent of cEEG is instrumental in the diagnosis as well as monitoring the response to treatment of this condition with antiepileptic drugs. Increased awareness and a high index of suspicion are needed for timely diagnosis of NCSE if a patient presents with acute onset of unexplainable cognitive or behavioral change of at least 30–60 min duration. Patients with NCSE need to be managed exactly as convulsive SE, using EEG as a guide rather than clinical observations as the determinant of response to treatment.

Challenge of diagnosing non-convulsive status epilepticus presenting as delirium.

Nonconvulsive status epilepticus (NCSE) is relatively common in older people. Although NCSE is a known cause of delirium, diagnosis is often delayed or missed. We report three cases where NCSE was identified as the cause of delirium in older people that illustrate the challenge of diagnosis. The cases illustrate that clinical manifestations such as slight twitching of the eyelids or periorally, eye signs, automatisms and disorders of speech and language are often very subtle. Electroencephalography (EEG), and monitoring the clinical and EEG effects of intravenous anticonvulsants, are crucial to diagnosis. Increased availability of portable EEG machines will facilitate early diagnosis. In situations where an EEG is not easily available, a trial of treatment is warranted. Hypoactive delirium is the main variant seen in NCSE but psychosis may also occur. Clinicians should maintain a high index of suspicion for NCSE in patients with delirium especially when no other obvious cause is identified.

EEG in adults in the laboratory or at the patient's bedside

Electroencephalogram (EEG) recording in the laboratory lasts at least 20 minutes and uses 19 active electrodes. It includes rest periods, stimulation procedures, a 3-mn hyperventilation period and intermittent photic stimulation (IPS). Recorded at the bedside, the EEG uses at least eight electrodes; the stimulation procedures, duration of the EEG and need to repeat the examination depend on the indication. Simultaneous video recording is recommended. The EEG report describes the basic rhythm, its reactivity and pathological activities, whether epileptic or not, and their organization. The synthetic conclusion interprets the results while taking into account the clinical context and contributes, if possible, diagnostic and/or therapeutic help in patient management. EEG performed as soon as possible after a seizure is essential for the diagnosis and initial management of epilepsy. It is helpful to characterize the epileptic syndrome in order to initiate optimal treatment. EEG is also useful in managing the withdrawal of antiepileptic drugs. EEG is also extremely useful in case of impaired consciousness, confusional state or even acute or subacute cognitive disorders. It is the only available tool able to validate the diagnosis of non-convulsive status epilepticus presenting with confusional state. EEG helps in the diagnosis of toxic or metabolic encephalopathy and can assess its severity, especially in hepatic encephalopathy. Except in rare exceptions, EEG is not routinely indicated for the evaluation of typical vasovagal syncope, headaches, dizziness, typical transient global amnesia and transient ischemic attack. EEG is irreplaceable in the diagnosis and management of certain severe and frequent pathologies involving the cerebral cortex.

A case of nonconvulsive status epilepticus presenting as dissociative fugue

<p><span>Nonconvulsive status epilepticus is characterised by changes in behaviour, memory, affect or level of consciousness. We report a case of nonconvulsive status epilepticus precipitated by carbamazepine that presented as dissociative fugue. The patient was a 49-year-old man. He first experienced a tonic-clonic seizure nine years previously and was diagnosed with <em>grand mal</em> epilepsy. He had been using carbamazepine 800 mg daily for the last eight years. He had not had any tonic-clonic seizures since carbamazepine was introduced but began to display behavioural disturbances periodically. He also left home many times, and remembered nothing about the period he had been away after he returned. He was hospitalised with a preliminary diagnosis of dissociative fugue. He had recurrent episodes with dissociative symptoms during his stay in the hospital. An electroencephalogram (EEG) and a 24-hour video EEG revealed nothing abnormal. An EEG recording taken during an episode indicated complex partial status epilepticus. Carbamazepine was substituted with valproate, and the patient was discharged in remission. </span></p>

A case of nonconvulsive status epilepticus presenting as dissociative fugue

Nonconvulsive status epilepticus is characterised by changes in behaviour, memory, affect or level of consciousness. We report a case of nonconvulsive status epilepticus precipitated by carbamazepine that presented as dissociative fugue. The patient was a 49-year-old man. He first experienced a tonic-clonic seizure nine years previously and was diagnosed with grand mal epilepsy. He had been using carbamazepine 800 mg daily for the last eight years. He had not had any tonic-clonic seizures since carbamazepine was introduced but began to display behavioural disturbances periodically. He also left home many times, and remembered nothing about the period he had been away after he returned. He was hospitalised with a preliminary diagnosis of dissociative fugue. He had recurrent episodes with dissociative symptoms during his stay in the hospital. An electroencephalogram (EEG) and a 24-hour video EEG revealed nothing abnormal. An EEG recording taken during an episode indicated complex partial status epilepticus. Carbamazepine was substituted with valproate, and the patient was discharged in remission.

Non-convulsive status epilepticus presenting with catatonia and suicidal behavior

Non-convulsive status epilepticus (NCSE) is an uncommon clinical entity. An electroencephalogram (EEG) helps in diagnosis of NCSE, in cases without overt motor manifestations of seizures such as automatisms. We describe an 18-year-old patient with NCSE, who had presented with catatonia and suicidal attempts. There were no automatisms or eye signs indicative of seizure. He had an episode of tonic neck deviation followed by incontinence, which first alerted us to the possibility of epilepsy. An abnormal EEG and a clinical response along with correction of EEG abnormalities with diazepam clarified the diagnosis. Management and hospital course are described in brief. The patient had residual symptoms, suggestive of a postictal state at discharge. The case shows the importance of keeping NCSE as a differential diagnosis, in cases presenting with catatonic symptoms, perplexity, and confusion. The presence of fleeting hallucinations and behavioral disturbances indicate limbic seizures in such cases, presenting in a catatonic state.

Nonconvulsive Status Epilepticus Presenting as Epileptic Nystagmus in a Patient With Herpes Encephalitis

Epileptic nystagmus (EN) is characterized by rhythmic ocular oscillations or quick, repetitive eye movements secondary to seizure activity. The fast component of EN is known to be contralateral to the epileptogenic focus. There are few reports EN occurring patients in nonconvulsive status epilepticus (NCSE). We report such a patient in the setting of herpes encephalitis.

Cognitive dysfunction with complex visual hallucinations due to focal nonconvulsive status epilepticus: A neuropsychological study and SISCOM

A 74-year-old woman with left hemiparesis due to a previous stroke presented with the sudden development of cognitive impairment and episodic complex visual hallucinations as manifestations of nonconvulsive status epilepticus (NCSE). Neuropsychological tests performed during NCSE demonstrated deficits encompassing several cognitive domains. The short-lasting complex visual hallucinations were stereotypical, vivid, and accompanied by intense fear. The seizure activity in the right temporo–parieto–occipital region, as documented by SISCOM and electroencephalogram (EEG) recording, was thought to be due to an unusual clinical presentation of NCSE. Subcortical cerebromalacia likely blocked the propagation route, restricting the ictal activities within this area.

Bálint‐like syndrome as an unusual representation of non‐convulsive status epilepticus

The clinical signs of posterior cortex dysfunction are, due to their paucity and subtlety, very often ignored as non-specific during clinical evaluation of non-convulsive status epilepticus. Therefore, focal non-convulsive status epilepticus emerging from the posterior cortex, and especially the parietal lobes, can be fairly under-recognised. We report a 66-year-old patient with focal non-convulsive status epilepticus presenting as isolated Bálint-like syndrome, successfully treated to full clinical and electrophysiological recovery. The diagnostic and pathophysiological features are discussed. Focal non-convulsive status epilepticus can be associated with negative phenomena such as neuropsychological deficits mimicking those detected more often in degenerative and vascular brain diseases. [Published with video sequences].

A Case of Nonconvulsive Status Epilepticus Presenting with Triphasic Waves

A Case of Nonconvulsive Status Epilepticus Presenting with Triphasic Waves

Upbeat nystagmus as a clinical sign of physostigmine-induced right occipital non-convulsive status epilepticus

The main indication for use of physostigmine is treatment of anticholinergic coma after anaesthesia and intoxication. Generalized epileptic seizures are known complications of physostigmine, whereas focal seizures and non-convulsive status epilepticus (NCSE) have not been described as complications in this setting [1]. Epileptic nystagmus (EN) is a rare clinical sign of seizures defined as repetitive jerking of the eyes secondary to epileptic activity. EN usually occurs as horizontal nystagmus with its fast phase beating away from the epileptogenic hemisphere [2]. Purely vertical beating EN on the contrary is unusual and has been described only a few times in the setting of bilateral epileptic activity [3]. We present a patient in whom cholinergic treatment with physostigmine resulted in right occipital NCSE presenting with upbeat nystagmus and prolonged impairment of consciousness documented on video electroencephalogram (EEG). A 66-year-old woman with history of drug abuse for analgetics and hypnotics but no history of epilepsy was admitted to our intensive care unit presenting with coma [Glasgow Coma Score (GCS) 8, eye 2/verbal 2/motor 4]. Initial computed tomography (CT) scan, CT angiography and perfusion CT revealed no causative abnormalities. An immediate EEG showed severe encephalopathy. On physical examination, signs suggestive of an anticholinergic syndrome (dry skin, dilated pupils and urinary retention) were found, and drug intoxication was suspected. Under continuous EEG recordings, two repeated doses of 1 mg intravenous physostigmine were administered, leading to a right occipital EEG status pattern associated with upbeat nystagmus, as shown in the figure and animation (Fig. 1, online resources 1 and 2). The time relationship between the occipital spikes and the fast phase of the nystagmus was constant at about 100 ms. The patient remained unresponsive. With another 2 mg lorazepam, nystagmus ceased, paralleled by remission of the right occipital EEG status pattern. The patient regained consciousness and was amenable to further treatment (GCS 14, eye 4/verbal4/motor 6). Systemic application of physostigmine may typically lead to generalized epileptic seizures. Our patient showed focal seizure activity. Interestingly, consciousness remained impaired, although physostigmine is expected to raise the level of consciousness immediately in case of anticholinergic coma. We think that NCSE at this moment prevented full recovery in the present case, because GCS improved to nearnormal values after termination of NCSE by lorazepam. The clinical presentation of NCSE generally depends on the cortical area(s) involved. Symptoms may range from very discrete alterations in normal behaviour to alterations in the level of consciousness [4]. Impairment of consciousness may result from widespread unilateral and bilateral seizure discharge. However, there are reports of complete loss of consciousness with lateralized epileptic discharge only (for review, see [5]). It is important to note that epileptic discharge did not occur strictly unilaterally in the present case. However, this does not equate to generalized epileptic seizure. Just in the occipital lobe, epileptic discharge spreads rapidly to contralateral homologous areas via the corpus callosum with predominance on one side [6]. Electronic supplementary material The online version of this article (doi:10.1007/s00415-011-6257-9) contains supplementary material, which is available to authorized users.

Non-Convulsive Status Epilepticus Presenting as Recurrent Hypersomnia

Back to table of contents Previous article Next article LETTERFull AccessNon-Convulsive Status Epilepticus Presenting as Recurrent HypersomniaAkhilesh Sharma M.B.B.S.Shubh Mohan Singh M.D.Sandeep Grover M.D.Savita Malhotra M.D., Ph.D., F.A.M.S.,Manish Modi M.D., D.M.,Akhilesh Sharma M.B.B.S.Search for more papers by this authorShubh Mohan Singh M.D.Search for more papers by this authorSandeep Grover M.D.Search for more papers by this authorSavita Malhotra M.D., Ph.D., F.A.M.S.Search for more papers by this author,Manish Modi M.D., D.M.Search for more papers by this author,Published Online:1 Apr 2010https://doi.org/10.1176/jnp.2010.22.2.247.e5AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: In most of the literature of Kleine-Levin syndrome, epileptiform activity in the EEG has been rarely described and is considered to be of no clinical significance. The EEG activities reported include isolated spike discharges, 1 self-limited photoparoxysmal response 2 and sharp waves. 3We describe a patient presenting with recurrent hypersomnia suggestive of Kleine-Levin syndrome who was subsequently diagnosed as having complex partial seizure.Case ReportA 13-year-old boy presented with a 4-year history of recurrent episodes of hypersomnolence. Exploration of history revealed that onset of the sleep episodes was immediately preceded by low-grade fever. The first sleep episode was characterized by an irresistible urge to sleep, and when family members tried to keep him awake, he was irritable and wept like a small child. The first episode of sleep lasted for 18 hours during which he woke up for urinating and passing stools and in between also consumed sugar rich confectionaries in large quantities.Over the next 2 months the patient had three more similar episodes, each lasting for 5–7 days. During these episodes he also exhibited intermittent focal clonic movements of limbs, lip smacking, tongue protrusion, and blinking eye movements lasting for a few minutes. The patient had complete amnesia of the episodes. After the fourth episode, he was treated with clobazam, 10 mg/day, with which the patient remained asymptomatic for 2 years. Although he continued to take the medication, the patient had a relapse of symptoms. Over the next 2 years, the patient continued to have similar episodes (six such episodes), each lasting for 8–15 days. During the interepisodic period, he appeared to be healthy except for a decline in scholastic performance.The patient’s EEG revealed widely generalizing spike and slow-wave complexes with right temporal lobe preponderance while the patient was experiencing a strong urge to sleep along with intermittent clonic movements. Video EEG revealed generalized epileptiform discharges followed by diffuse slowing.With the above clinical picture and investigation findings, the patient was diagnosed with complex partial seizure and was treated with carbamazepine, 600 mg/day, and clobazam, 10 mg/day, with which the symptoms disappeared. A video EEG performed after the resolution of symptoms showed interictal record.Later, he had one similar episode, during which the repeat EEG again showed generalizing spike and slow-wave complexes. Following this, levetiracetam, 1,000 mg/day, was added to the previous regimen.Discussion Our patient presented with an illness that was apparently precipitated by fever and was characterized by episodes of hypersomnolence, hyperphagia, and irritability followed by amnesia for the episode. Clinically, these episodes were suggestive of Kleine-Levin syndrome. 4 , 5 However, investigations revealed the presence and resolution of complex partial seizure that was effectively treated with antiepileptics and was associated with the amelioration of the symptoms of Kleine-Levin syndrome. Though complex partial seizure is known to have protean manifestations, to the best of our knowledge, complex partial seizure presenting with Kleine-Levin syndrome-like symptoms has not been reported before. On the other hand, though nonspecific EEG changes are common in Kleine-Levin syndrome, epileptiform activity is conspicuous by its absence in reported cases. 4Our case thus represents a rare finding of the association of Kleine-Levin syndrome-like symptoms and complex partial seizure. This case also demonstrates the importance of getting an EEG done in all cases of Kleine-Levin syndrome.Department of Psychiatry, Postgraduate Institute of Medical Education & Research, Chandigarh, IndiaDepartment of Neurology, Postgraduate Institute of Medical Education & Research, Chandigarh

Non-Convulsive Status Epilepticus Presenting as Recurrent Hypersomnia

Non-Convulsive Status Epilepticus Presenting as Recurrent Hypersomnia

Nonconvulsive Status Epilepticus Presenting with Throat Clearing as Part of Clinical Seizure Semiology

Oro-alimentary automatisms such as chewing movements, lip-smacking, repeated snuffling, swallowing and retching have been reported with seizures usually of temporal lobe origin. Throat clearing, usually along with other vegetative signs, has been reported in patients with temporal and rarely extra-temporal lobe epilepsy. We report a case of a 93-year-old woman admitted with acute right temporo-occipital stroke. Repeated throat clearing episodes raised suspicion for complex partial seizures. Video-EEG recording confirmed frequent right hemispheric focal seizures originating from the right posterior temporal area concordant with her cortical stroke. The value of throat clearing as a sign of complex partial seizures of temporal lobe origin and its lateralizing and localizing value is discussed.

Non-convulsive status epilepticus in adults - an overview

Status epilepticus (SE) is the most frequent neurological emergency requiring admission on the intensive care unit (ICU). The classification of status epilepticus may be dichotomised into the and the form. Whereas the diagnosis of generalised convulsive status epilepticus (GCSE) is easily made in view of the evident manifestation, the diagnosis of non-convulsive status epilepticus (NCSE) may become very difficult according to its non-spectacular and protean presentation. Non-convulsive status epilepticus is a common cause of altered mental status and delirium; and a substantial number of comatose patients in the intensive care unit may suffer from NCSE. The most important part of making a diagnosis of NCSE is to think of it at all. The definite diagnosis of NCSE is dependent on electroencephalographic (EEG) confirmation. Repetitive or, optimally, continuous EEG recording may help to closely monitor seizure activity and to guide the therapy in order to protect the patient from under- and/or over-treatment. The interpretation of EEG recordings of NCSE may become challenging because of numerous artifacts caused by the patient, caregivers and devices, and because of trace elements of ambiguous significance and of waveforms mimicking epileptic activity. Non-convulsive status epilepticus was historically subdivided into the groups of complex-partial status epilepticus (focal; CPSE) and absence status (generalised; AS). Most recently, a classification proposed by the International League Against Epilepsy (ILAE) has subdivided focal NCSE into aura continua (non-convulsive simple partial with maintained consciousness) and into dys-cognitive (with impaired consciousness) of mesial temporal or neocortical origin. Several patients with focal NCSE or AS were known for pre-existing epilepsy. In addition, other types of NCSE have been reported, like subtle where convulsions in patients with GCSE clinically stop, but the continuous epileptic activity electroencephalographically still persists. Another variant belongs to those patients with critical illness where the serious disorder and/or medications may trigger an acute, prolonged and all too often very-hard-to-treat epileptic condition (critical illness SE [CISE]). The majority of these patients will never have had seizures before. Of note, none of the currently proposed classifications has gained broad acceptance and official approval. Since the need for immediate and intensive treatment of GCSE is beyond debate, the insidiously calm presentation of NCSE may mislead to a much less aggressive therapeutic approach. However, experimental and clinical data suggest that continuous epileptic activity in the brain during NCSE associated with consecutive (glutamatergic) hyperexcitation triggers neurotoxicity and proapoptotic mechanisms which eventually may lead to irreversible brain damage and the onset of a chronic epileptic disorder or to an irreversible neurological deficit. Thus, recent national and international guidelines and reviews recommend immediate and intensive treatment for NCSE as well as for GCSE. With a few exceptions, the first drug is an intravenous benzodiazepine, mainly lorazepam; intravenous phenytoin or valproate should be started without delay. Persistence of NCSE after administration of these two classes of drugs heralds refractory (RSE) where single or combinations of drugs in anaesthetic dosages requiring intubation and enteral antiepileptics may be added except for the cases of AS or an underlying terminal disease. The outcome of NCSE is mainly determined by the type, duration, cause and the severity of concomitant diseases.

Monday July 3, 2006 7:30-9:00 Hall 5B Teaching Session To treat or not to treat the EEG in paediatric epilepsy syndromes

Abstract 1 R. Pressler ( 1 Department of Clinical Neurophysiology, National Hospital for Neurology, UK ) Treatment of interictal discharges can improve behaviour in children with epilepsy Increased behavioural problems in children with epilepsy are a consequence of various factors including underlying brain lesion, age of onset, antiepileptic drugs, psychosocial issues, seizure type and frequency, and interictal EEG abnormalities. Suppression of discharges will improve behaviour in children with nonconvulsive status epilepticus presenting as pseudo-dementia or more subtle behavioural changes, and in children with prolonged nocturnal discharges such as ESES. The effect of intermittent interictal EEG discharges on behaviour and cognition is still controversial. Whether cognitive and behavioural problems can be directly caused by discharges or are a coexisting phenomenon can be determining through improvement of cognition and behaviour, if EEG discharges are suppressed. In children with drug resistant epilepsy and learning difficulties suppression of discharges was associated with improvement in global rating of psychosocial function. In children showing interictal discharges but without epilepsy, suppression of discharges showed no definite effect. In children with well-controlled or mild epilepsy, improved behaviour was only observed in children who showed a reduction of discharges during active treatment, but not in patients without a change in discharge rate. The issue of ‘treating the EEG’ remains controversial. The question is not whether to treat the EEG, but whether seizures, so subtle as to be recognisable only by EEG and behavioural monitoring, produce disability sufficient to justify treatment.

Nonconvulsive status epilepticus presenting as a subacute progressive aphasia

We report a 62-year-old man with non-convulsive status epilepticus (NCSE) presenting as a progressive aphasia that developed insidiously over 5 weeks. On video-EEG monitoring, aggravation of the aphasia coincided with occurrence of seizure activities arising from the left fronto-temporal area. Brain MRI was noncontributory but a fluorodeoxyglucose-PET scan revealed a hypometabolism in the left anterior temporal area. Following anticonvulsant treatment, aphasia recovered gradually over several weeks despite prompt resolution of epileptic discharges on EEG. Our patient’s findings, gradual onset of isolated aphasia with gradual resolution after initiation of treatment, may differ from previously reported cases with aphasic status epilepticus because their aphasia showed abrupt onset and rapid resolution with anticonvulsant medication.

Nonconvulsive Status Epilepticus in a Patient with Mental Status Changes

ABSTRACT.We report a case of nonconvulsive status epilepticus presenting as recurring episodes of altered mental status before and after bone marrow transplantation for multiple myeloma. Early recognition of nonconvulsive status epilepticus as a cause of altered mental status is important, because prompt treatment with antiepileptic medications may improve neurologic outcome. EEG is the essential diagnostic test in the evaluation of the disturbance of the level of consciousness in patients undergoing the transplantation procedure.

Nonconvulsive Status Epilepticus in the Emergency Room

The study reviewed emergent cases of nonconvulsive status epilepticus (NCSE) to evaluate causes of diagnostic and management delay and examined frequent diagnostic features suggestive of NCSE. In a retrospective study, we assessed the clinical presentation of 23 patients with one or more NCSE episodes, their medical history, EEG, and antiepileptic drug (AED) treatment. We also evaluated causes of diagnostic delay in patients referred to the emergency room (ER) in confusional states. There was considerable overlap in clinical features of patients with complex partial SE (CPSE) and generalized nonconvulsive SE (GNSE). Delays in seeking medical attention were common. Diagnosis was significantly delayed in 10 patients. Three cases illustrate the possible markedly different presentations of NCSE. NCSE often goes unrecognized or is mistaken for behavioral or psychiatric disturbance. The pleomorphic clinical presentation of NCSE indicates that EEG and a therapeutic trial of AEDs afford the best diagnostic measures in acute waxing and waning confusional states associated with agitation, bizarre behavior, staring, increased tone, mutism, or subtle myoclonus.