Nonconvulsive Status Epilepticus

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What is nonconvulsive status epilepticus, and what are its subtypes?

In each of these clinical situations, patients exhibit clinical symptoms associated with ongoing activity on the EEG, which could be interpreted as NCSE.

Beware ictal activity that mimics psychiatric illness | MDedge Psychiatry

The question arises to what extent the symptoms are therefore the consequence of this electrographic disturbance and therefore due to NCSE. The alternative explanation is that the EEG disturbance is an independent aspect perhaps reflecting physiological events, which are not primarily epileptic in other words the EEG findings are simply an epiphenomenon. To complicate further the conceptualization of these syndromes, in some cases of epileptic encephalopathy the ictal EEG changes may be similar to the interictal changes, and in some cases of epileptic behavioral change or psychosis the EEG changes can be detected only in limbic structures and not on the scalp EEG.

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Summary Prolonged nonconvulsive seizures have been recognized at least since the 19th century, although their inclusion within the rubric of status epilepticus was only formalized by Gastaut and colleagues after the Xth Marseilles Colloquium, held in Gastaut et al.

Definition of Nonconvulsive Status Epilepticus NCSE The definition of NCSE favored by this author is: Nonconvulsive status epilepticus is a term used to denote a range of conditions in which electrographic seizure activity is prolonged and results in nonconvulsive clinical symptoms Table 1. Nonconvulsive status epilepticus NCSE is a term used to denote a range of conditions in which electrographic seizure activity is prolonged and results in nonconvulsive clinical symptoms.

Note: 1. The electrographic activity can take various forms. NCSE occurring in the neonatal and infantile epilepsy syndromes 1a. West syndrome 1b. Ohtahara syndrome 1c. NCSE in other forms of neonatal or infantile epilepsy 2. NCSE occurring only in childhood 2a. NCSE in other forms of childhood epileptic encephalopathies, syndromes and etiologies, e. Electrical status epilepticus in slow wave sleep ESES 2d. Atypical absence status epilepticus ii. Tonic—status epilepticus 3b. Typical absence status epilepticus in idiopathic generalized epilepsy 3d. Complex partial status epilepticus: i.

Limbic ii. Nonlimbic 3e. Aura continua with: i. NCSE occurring in late adult life 4a. De novo absence status epilepticus of late onset 5. Some cases of epileptic encephalopathy. Some cases of coma due to acute brain injury with epileptiform EEG changes. Some cases of epileptic behavioral disturbance or psychosis. Some cases of drug induced or metabolic confusional state with epileptiform EEG changes. Masson , Paris Google Scholar. Crossref Google Scholar. Citing Literature. Volume 48 , Issue s8 November Pages References Related Information.

Close Figure Viewer. Browse All Figures Return to Figure. Previous Figure Next Figure. Email or Customer ID. Forgot password? Old Password. New Password. Password Changed Successfully Your password has been changed. These may be included within two or more electrographic seizures with a discrete onset of typical ictal discharges or with continuous discharges throughout the recording. Recurrent electrographic seizures without clinical recovery between them clearly indicate status epilepticus.

Continuous discharges are more controversial. Slower discharges constitute PLEDs or PEDs as discussed above , but faster discharges would be read by most electroencephalographers as an ongoing seizure. Another study found that continuous and intermittent seizures in all forms of SE not just NCSE had no difference in outcome For purposes of diagnosis, there appears. ESE should be considered as "true" status though treatment is often unsuccessful in effecting a clinical improvement.

As always, the clinical outcome is determined primarily by the etiology. Many cases are caused by anoxia or sepsis with multiple medical problems, and the outcome is usually poor. Nevertheless, considering such cases as not representing SE because of the inadequate response to medication is analogous to insisting on a successful outcome with antibiotics before diagnosing an infection.

Several clinical series have demonstrated that the response to AEDs in NCSE is often delayed or very slow such that clinical decisions must be made long before this evidence is available 30, 33, ESE should be considered a type of SE for several reasons. First, the EEG discharge appearance, rhythmicity, and frequency are characteristic for many clinical reports of SE and similar to those from the study of Granner and Lee 17 below.

Second, the very large majority of patients with ESE have had clinical seizures recently, and most will have clinical seizures following the ESE recording 18, 19, 46 , indicating that this is not simply a sign of "burnt out" seizures. For example, patients with ESE, on emergence from pentobarbital treatment, will usually go on to have clinically evident seizures Finally, while many patients with ESE have catastrophic neurologic and medical illness and may not respond to AEDs, many others especially those without anoxia will have EEG and clinical improvement on medication So.

In the end, it makes most sense to consider ESE as a manifestation of status epilepticus usually NCSE and treat accordingly keeping in mind that some of the causative illnesses are devastating rather than stating that something is not an epileptic seizure because we might fail to fix it. Finally, rather than debate what should be seen with NCSE, we can be guided by the EEG patterns actually found in patients with a secure clinical diagnosis. EEG waveform morphologies were quite variable and included typical and atypical spike wave discharges, multiple or polyspike wave discharges, and rhythmic delta activity with intermixed spikes.

Discharge frequency was always 1 to 3. In trying to discern the longerlasting risks one must consider both experimental and clinical information. Their landmark studies laid the foundation for our understanding of the neuronal and neurologic effects of convulsive status. They induced episodes of GCSE lasting up to 5 hours in baboons After hours of seizures it still showed rapid epileptiform discharges punctuated by flat periods. Subsequent pathologic studies showed neuronal damage in the neocortex, cerebellar Purkinje and basket cells, and hippocampus Much of the damage appeared to correlate with the associated hyperpyrexia, hypotension, hypoxia, acidosis, and hypoglycemia.

Paralysis and artificial ventilation in baboons with similar seizures and EEG activity led to reduced neuronal damage, indicating that control of systemic factors provided some protection Nevertheless, even with maintenance of normal homeostasis, SE led to hippocampal neuronal loss, suggesting that the elec-. These latter experiments also provided a model of NCSE, but with persistent and very rapid epileptiform discharges. Lothman and colleagues found that kainic acid whether applied systemically or locally in the hippocampus particularly affected limbic structures, producing seizures that could be nonconvulsive 51, To overcome concern that the neuronal injury was a direct toxic effect they also used electrodes implanted in the rat hippocampus 53, Rapid repetitive stimulation for 30 to 90 minutes led to seizures and self-sustaining SE persisting for 12 to 24 hours after the stimulation ceased.

Electrographic seizures included rapid discharges, often over 10 Hz. Animals with frequent limbic seizures or SE sustained hippocampal neuronal loss, but those with briefer and less frequent seizures did not Chemical and electrical methods of inducing SE may damage neurologic tissue independent of the subsequent seizures, leaving open the question of whether it is the seizures and SE or the precipitant itself that damages neurons.

To address this, Sloviter 56 showed that indirect electrical stimulation via the perforant pathway the primary afferent excitatory pathway to the hippocampus induced damage restricted to hippocampal neurons in rats.

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The typical stimulations used to provoke experimental SE have been intense, and the intensity of the resulting epileptiform discharges appears to correlate with the likelihood of neuronal damage. Lowenstein and colleagues 57 used flurothyl to induce seizures in paralyzed ventilated rats and found evidence of neurologic damage in the amygdala and pyriform cortex strongly associated with prolonged, "high-frequency" ca. Damage was directly related to the duration and intensity of electrographic seizure activity.

The electrical activity of different types of SE varies considerably. Many of these experiments used prolonged, high-frequency stimulation to provoke SE, and the resultant electrographic seizure discharges were also of high frequency and often sustained for hours. Discharges greater than 3 Hz are common in generalized clinical seizures 58 , and many of these models produced sustained discharges of 6—15 Hz, possibly more representative of GCSE than of NCSE, with its usually less dramatic electrographic patterns.

It may be sustained for hours or days but seldom includes the high-frequency. Many of the models establish a clear correlation between the intensity of the electrical seizure activity on one hand and the extent of neuronal damage on the other. With less intense seizure activity, neuronal damage may be minimal or even absent. If the electrical activity of NCSE is often insufficient to cause lasting neuronal damage, it becomes unclear exactly how well these high-intensity stimulation models can be extrapolated to human NCSE, and we must turn to clinical studies.

Human pathologic studies of the effects of SE have been scarce, in part because fatal cases are often associated with acute, severe brain-injuring illnesses such as ischemic strokes, hemorrhages, and encephalitis, all of which may cause damage independently. One case— control study 59 examined hippocampal cell densities in patients who died after episodes of GCSE in comparison to those of matched patients with epilepsy but no SE and to normal controls.

SE patients had significantly decreased hippocampal densities compared with normals and somewhat less than in epilepsy controls, suggesting that the episodes of SE were responsible for the additional damage.

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Episodes of NCSE are seldom fatal unless they occur in association with GCSE or other acute, severe neurologic illnesses, in which case it is difficult to sort out the offending agent. For the most part, pathologic studies of patients with pure forms of NCSE remain unavailable. Lothman 51 has summarized the many physiologic changes such as acidemia and hypotension that occur during SE, but most apply to GCSE. Studies of the long-term effects of SE must assess clinical consequences, including subsequent seizure frequency and cognitive—neuropsychologic function following an episode of SE.

Seldom can a baseline be assessed before the SE to see if there is a change. Most studies are of GCSE, and it correlates with worsened seizure control, but this may be due to the underlying illness causing SE rather than to the episode itself Nevertheless, there may be a subset of patients with a worsened clinical course following SE. Absence SE. Most authors have found little longterm morbidity from absence SE. Nevertheless, this conclusion usually rests on clinical impressions in moderate-sized series rather than on actual measure.

No long-term sequelae were noted in several prominent series 4—6. Early reports on CPSE included very few patients. Most returned to normal or "baseline cognitive function" 10, 34, 61 , but not all were studied thoroughly with subsequent neuropsychologic tests. In a more recent CPSE series 35 , none of 20 patients had cognitive deterioration, and 5 had meticulous neuropsychologic assessment. Krumholz and colleagues 62 reported 10 patients with CPSE for 36 hours or longer, all of whom had lasting neurologic deficits.

Two patients each had strokes or encephalitis, and another three had multiple medical problems that may have contributed to the deficits. Three patients had refractory epilepsy, and all sustained prolonged memory deficits, lasting 3 to 24 months, but at least 2 improved. CPSE occurred more frequently in medically sick patients, raising the question of synergistic harmful effects of NCSE and medical illnesses. Other individual reports 9, 11 also found prolonged memory deficits after NCSE; it is uncertain whether they are permanent.

They show few long-term sequelae, but most include limited follow-up. That of Guberman and colleagues 63 is exceptional by including 5-year follow- up on 8 patients, showing no intellectual, memory, or behavioral deterioration. Scholtes and colleagues 65 evaluated 65 patients and found good outcomes in all but one. Patients with ESE in the setting of serious medical illness have a terrible prognosis, but it is not possible to dissect out that portion of the long-term harm done by epileptiform discharges or NCSE 18, 19, 46, Most clinical studies of the effects of SE are pediatric and retrospective.

Several have found negative consequences, but it is very difficult to control for many variables. Comprehensive neurologic and neuropsychologic evaluations before and after SE are seldom available. Also, patients with a progressive illness worsen, whether or not related to the SE, and many patients with neurologic deficits fluctuate with time.

Finally, it is difficult to control for the influence of AEDs. Medications, doses, serum levels, and drug interactions may change frequently in patients with refractory epilepsy, including at the time of testing. Dodrill and Wilensky 67 obtained neuropsychologic testing on adults with epilepsy.

Nine had episodes of SE over a 5-year interval, and these patients worsened neuropsychologically while some. Maytal and colleagues 68 studied children with SE, almost all convulsive. Seventeen had cognitive and other deficits after the SE, usually attributed to an acute illness such as a stroke. They concluded that "the major neurologic sequelae are usually due to the underlying insult rather than to the prolonged seizure itself.

Although clinical studies show little evidence of permanent neurologic injury from episodes of NCSE it would be unwise to ignore the prolonged memory dysfunction in several well-reported cases, and NCSE has some similarities to convulsive SE It is possible that a minority of episodes of NCSE might lead to significant deficits. Concomitant systemic factors such as infection, metabolic disturbances, hypotension, and medications might increase the likelihood of damage in a synergistic fashion Episodes associated with focal lesions such as strokes may involve two processes, with a greater chance of lasting harm Finally, by extrapolation from experimental studies 57 episodes of NCSE with more rapid and presumably excitatory epileptiform discharges may be more worrisome.

They are clearly ill with ongoing seizures and have impaired consciousness and other neurologic deficits that are potentially reversible and certainly treatable. Additionally, many episodes of NCSE begin with and may end with generalized convulsions, in turn potentially harmful.

Finally, we must remain alert to the possibility that some prolonged episodes might cause lasting damage. NCSE remains an underdiagnosed, treatable condition and one well worth both diagnosing and treating. Treatment of NCSE is often easier than diagnosis, but when the initial treatment is unsuccessful subsequent treatment can become far more complicated and difficult. Straightforward absence SE may be terminated by benzodiazepines relatively quickly.

Other treatments such as carbon dioxide inhalation, oral bar-. Intravenous phenytoin can also help 3. Absence SE due to benzodiazepine withdrawal e. With such an acute precipitant, long-term treatment may be unnecessary. When longer treatment is necessary, valproate has been effective in preventing recurrences 72 , but this does not mean that other medications would be ineffective, especially given the overlap syndromes and the possibility that many episodes of absence SE are actually focal-onset, secondarily generalized seizures.

Complex partial SE may be interrupted and controlled by traditional intravenous medications, phenytoin and phenobarbital 9 or oral carbamazepine More frequently, intravenous benzodiazepines are used to interrupt the NCSE once it is recognized Nevertheless, CPSE is often recurrent 35 , and patients are much less likely to remain off medication. In occasional cases of NCSE, patients recover spontaneously Benzodiazepines are used nearly uniformly in the attempt to interrupt NCSE in the rest of patients, and they are often successful 16, Lorazepam may be the preferable drug Nevertheless, there are clearly many cases in which the NCSE proves resistant 35, In a recent series of patients with NCSE where the foci were found to be primarily in frontal areas 45 there was often a delay of 2 days before diagnosis.

In most of these refractory patients, intravenous benzodiazepines were unsuccessful in breaking the SE. Most responded to intravenous phenytoin, but one required pentobarbital. Benzodiazepines often improve the EEG without leading to clinical improvement. Higher doses of longacting intravenous medication such as phenytoin and phenobarbital 30, 77 or increasing levels of already used AEDs 33 may be helpful. In the end, even patients with periodic discharges or PEDs whether considered SE or not actually did reasonably well, as long as anoxia was not the cause 78 , and most returned to baseline.

In the idealized case, any form of NCSE is diagnosed readily and responds immediately to intravenous benzodiazepines. This is not a rare scenario, but. Fortunately, given the relatively minimal evidence of ongoing damage and rapid establishment of lasting neurologic deficits due to NCSE, treatment probably need not be as aggressive as for continuing convulsive SE.

Many of the treatments cited above occurred over days though this is not the recommended plan. It is relatively rare that patients will need such aggressive treatment as pentobarbital- induced coma or treatment with such substitutes as propofol, ketamine, and much higher doses of benzodiazepines such as lorazepam and midazolam. Still, there are many reasons for treating NCSE expeditiously. Treatment should be individualized and judicious 2 but should not be delayed. NCSE presents in remarkably varied ways but often in typical situations such as following other seizures or in the setting of acute stroke.

Because there are no motor manifestations, the diagnosis is missed frequently, but it is also made frequently by astute neurologists and other clinicians. The mission of the Epilepsy Foundation is to lead the fight to overcome the challenges of living with epilepsy and to accelerate therapies to stop seizures, find cures, and save lives. Skip to main content. Sign In Register find us donate. Nevertheless, its presentation is protean and it may be mistaken for many other 1 To whom correspondence should be addressed.

Indi- TABLE 1 Absence Status Epilepticus: Clinical Features Confusion but wakefulness, with blinking or occasional myoclonus May start or end with a generalized convulsion Can last days Minimal focal features; generalized discharges on EEG Often prior absence, myoclonic, or convulsive seizures Typical precipitants: benzodiazepine or other medication withdrawal, generalized convulsions, infection, trauma, metabolic aberrations.

TABLE 2 Complex Partial Status Epilepticus: Clinical Features Confusion to unresponsiveness "Epileptic twilight state" with fluctuating mental status Recurrent or prolonged complex partial seizures Observed or presumed focal onset, often temporal or frontal; focal slowing and discharges on EEG Often prior epilepsy and vascular disease in the elderly Can last up to months; often recurrent May produce severe amnesia following Other forms of focal NCSE are discussed later with respect to their presentations.

There are additional confused, stuporous, or comatose patients found to have rapid, rhythmic, continuous epileptiform discharges on the EEG, with or without clinically evident seizures, in the setting of severe medical illnesses or, perhaps most commonly, following clinically evident convulsions or generalized convulsive SE.

Presentation, Evaluation, and Treatment of Nonconvulsive Status Epilepticus

Many of the elderly patients diagnosed with NCSE have not had epilepsy earlier in life but have had benzodiazepine withdrawal or other significant effects of medications on the brain 6. TABLE 4 Clues to the Recognition of NCSE Following generalized convulsions or GCSE Subtle signs such as twitching, blinking, and nystagmus in a stuporous patient Otherwise unexplained stupor or confusion, especially in the elderly Altered mental status in the elderly, particularly after benzodiazepine withdrawal History of seizures and a new medical or surgical stress "Stroke plus" elderly should always prompt a consideration of medication toxicity or medication withdrawal.

EEG Stages in Status Epilepticus From experimental animal studies and clinical samples from patients with generalized convulsive SE GCSE , Treiman and colleagues 36 proposed that the EEG in GCSE typically follows a standard evolution through five characteristic stages: discrete sei- zures, merging seizures, continuous seizures, continuous seizures with brief "flat" periods on the EEG, and prolonged flat periods with periodic discharges.

For purposes of diagnosis, there appears to be no clear difference between continuous and intermittent electrographic seizure activity. Electrographic Status Epilepticus ESE ESE should be considered as "true" status though treatment is often unsuccessful in effecting a clinical improvement. Clinical Guidance Finally, rather than debate what should be seen with NCSE, we can be guided by the EEG patterns actually found in patients with a secure clinical diagnosis. Clinical Morbidity Lothman 51 has summarized the many physiologic changes such as acidemia and hypotension that occur during SE, but most apply to GCSE.

Nevertheless, this conclusion usually rests on clinical impressions in moderate-sized series rather than on actual measure ment. Other treatments such as carbon dioxide inhalation, oral bar- biturates, benzodiazepines, and ethosuximide can be effective 5. The petit mal epilepsies: their treatment with tridione. JAMA ; — Kaplan PW. Nonconvulsive status epilepticus. Semin Neurol ;— Schwab RS. A case of status epilepticus in petit mal. Electroenceph Clin Neurophysiol ;—2. Niedermeyer E, Khalifeh R.

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