CONTENTS

• Definition of NCSE
• Epidemiology and causes of NCSE
• Various clinical presentations
• General clues to the diagnosis of NCSE
• Common differential diagnostic considerations
• EEG:
  • Indications to obtain an EEG
  • Duration of continuous EEG monitoring
• Antiepileptic trial for ictal/interictal continuum abnormalities
• Management of NCSE
• Subtypes of NCSE
  • NCSE with coma
  • Absence NCSE with onset in adulthood
  • Focal NCSE with impaired consciousness
  • Focal NCSE without impaired consciousness
• Epilepsia Partialis Continua (EPC)
• Podcast
• Questions & discussion
• Pitfalls

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definition of NCSE

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preamble: some basic concepts

• Nonconvulsive status epilepticus (NCSE) is defined as status epilepticus without a prominent (clinically obvious) motor component. NCSE may have zero motor components, or it may correlate with subtle movements (e.g., subtle facial twitching).
• NCSE may be diagnosed on the basis of either electrographic or electroclinical seizures: (33475321)
  • Electrographic seizures (or electrographic status epilepticus) refers to patients who are having unequivocal electrographic seizures 📖 on their EEG.
  • Electroclinical seizures (or electroclinical status epilepticus) refers to patients who show a combination of EEG abnormalities plus clinical manifestations.

electrographic nonconvulsive status epilepticus

• Electroencephalographic status epilepticus is defined as one of the following abnormalities.
  • (1) >10 minutes of continuous seizure activity (continuous epileptiform discharges which average >2.5 Hz).
  • (2) Seizure activity occurring >20% of the time over the space of an hour.
    • Isolated seizures, or recurrent seizures with a seizure burden <20% may not correlate with worse outcomes. Although suppressing such seizures may be reasonable if it can be done safely, low-level seizure activity may not merit aggressive therapies.(31886441)
• In the absence of a prominent motor correlate, these EEG abnormalities would be classified as electrographic nonconvulsive status epilepticus.(33475321)

electroclinical nonconvulsive status epilepticus

• An electroclinical seizure is defined as either an electrographic seizure or an ictal-interictal continuum abnormality on EEG plus either of the following:(33475321)
  • (1) Definite clinical correlate time-locked to the pattern (e.g., facial twitching, eye deviation, or nystagmus).
  • (2) EEG and clinical improvement following parenteral antiseizure medication.
• The EEG pattern does not need to meet the criteria of an electrographic seizure (i.e., epileptiform discharges >2.5 Hz for 10 seconds). For example, many EEG abnormalities on the ictal-interictal continuum 📖 (e.g., periodic discharges) may have clinical correlates – so these would qualify as electroclinical seizures.
• Electroclinical nonconvulsive status epilepticus is defined as an electroclinical seizure lasting >10 minutes, or intermittently occurring for >20% of the time over the span of an hour.

integrated clinical definition of nonconvulsive status epilepticus

• The schema below shows a unified clinical approach to diagnose either electrographic or electroclinical nonconvulsive status epilepticus.(27571157)
• Some patients will have unequivocal seizure activity 📖 on EEG, which immediately meets the criteria for nonconvulsive status epilepticus (left end of the spectrum).
• Many patients will have EEG findings lying along the ictal-interictal continuum 📖 (epileptiform discharges with frequency <2.5 Hz, or rhythmic delta activity). These EEG patterns alone are ambiguous and do not meet criteria for NCSE. The diagnosis of NCSE may be reached if there are time-locked symptoms, or if there is clinical improvement following therapy with antiseizure medication.

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epidemiology and causes of NCSE

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epidemiology

• Seizures are common, being detected in ~15% of patients undergoing video EEG monitoring (including SICU or MICU patients with stupor/coma). These are predominantly nonconvulsive seizures. Roughly a third of patients with seizures meet criteria for nonconvulsive status epilepticus.
• Presenting problem to hospital: Seizures may be the initial reason for hospital admission:
  • Patient presenting with altered mental status due to NCSE.
  • Patient presenting with convulsive status epilepticus which rapidly transitions to NCSE (among patients who stop having obvious motor seizures, it's common to transition into NCSE).
• New problem arising in the hospital: NCSE is a common complication encountered among critically ill patients who were admitted for a primary neurologic or systemic disorder. For example, NCSE is especially frequent among patients with one or more of the following diagnoses:
  • Intracerebral or subarachnoid hemorrhage.
  • CNS infection (especially encephalitis).
  • Autoimmune encephalitis.
  • Traumatic brain injury.
  • Brain tumor.
  • Status post neurosurgery.
  • Hypoxic/ischemic brain injury.
  • Septic shock.

general causes of NCSE

• The range of causes of NCSE is broad. Overall, these resemble the range of causes of convulsive status epilepticus (explored further here 📖, with discussion of appropriate investigations here 📖).
• To narrow down this differential diagnosis a bit, some additional considerations may be helpful:
  • (1) Specific subtypes of NCSE may be associated with specific causes (discussed further below).
    • NCSE with coma
    • Absence NCSE with onset in adulthood
    • Focal NCSE with impaired consciousness
    • Focal NCSE without impaired consciousness
  • (2) Specific EEG findings may be associated with certain etiologies, for example:
    • GPDs (generalized periodic discharges). 📖
    • LPDs (lateralized periodic discharges). 📖
    • BIPDs (bilateral independent periodic discharges). 📖
    • LRDA (lateralized rhythmic delta activity). 📖

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potential clinical findings in NCSE

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NCSE may manifest in a variety of ways, which will often be mistaken for other disorders. Some more common manifestations are:(29650639, LaRoche 2018)

impaired mental status

• Confusion, obtundation, or coma.
• Unexplained fluctuations in mental status.

speech/language abnormality

• Aphasia, paraphasic errors.
• Mutism, reduced verbal fluency.
• Echolalia.
• Stuttering.

psychiatric/behavioral disturbance

• Psychosis.
• Mood disturbance.
• Fear/agitation.

movement/motor abnormality

• Subtle rhythmic twitching (especially involving the face or eyes).
• Automatisms (e.g., lip smacking, chewing).(31557430)
• Catatonia (more on this in the section below).
• Gaze deviation.
• Limb paralysis.

perceptual/sensory disturbances

• Hallucinations (olfactory, gustatory, auditory, visual).
• Blindness.
• Sensory disturbance and pain (including headache).

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general clues to the diagnosis of NCSE

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epidemiological/historical clues

• Epilepsy or prior seizures (especially status epilepticus followed by a prolonged or unusual postictal period with lingering neurological abnormalities).
• Otherwise unexplained stupor/coma, especially with fluctuating mental status.
• Known supratentorial structural brain disorder (especially patients admitted for subarachnoid hemorrhage, subdural hematoma, or traumatic brain injury).

clues on examination

• Ocular abnormality:
  • Subtle blinking or eyelid twitching. This may be unmasked by gentle, partial opening of the eyelids.(Dunser 2019)
  • Pupil dilation, sometimes associated with hippus (fluctuations in pupil size).
  • Horizontal nystagmus.
  • Gaze deviation.
• Subtle motor activity, often involving the face or eyelids.
  • NCSE tends to cause facial or synchronous myoclonus with synchronized activity of multiple muscles (whereas toxic/metabolic encephalopathy tends to cause asynchronous, multifocal myoclonus).
  • Among the various indications for EEG monitoring, facial and periorbital twitching is especially likely to correlate with an actual seizure.(27571047)
• Automatisms (e.g., lip smacking, chewing).(31557430)
• Autonomic disturbances (e.g., mydriasis, diaphoresis, hypertension, flushing).(31557430)
• Inability to follow any commands.

clues on neuroimaging

• CT perfusion or MRI may be helpful, as discussed further here: 📖

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common differential diagnostic considerations

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NCSE vs. postictal state

• Postictal state can persist for days in some patients, especially if there is underlying cerebral dysfunction.
• EEG is indicated for patients not returning to baseline within an hour. In postictal states, EEG should show background slowing or suppression.(29650639)

NCSE vs. toxic/metabolic encephalopathy

• NCSE and toxic/metabolic encephalopathy are both extremely common pathologies in the ICU. They may appear similar clinically, and may also simultaneously coexist. Even with complete EEG and laboratory evaluation, it may sometimes be difficult to determine precisely what is going on.(26013921)
• EEG findings expected in encephalopathy include diffuse slowing or a burst-suppression pattern (more on this here: 📖). Alternatively, EEG findings revealing seizures or ictal-interictal continuum abnormalities suggest NCSE.

NCSE vs. catatonia

• NCSE and catatonia may share similar clinical features. To confuse matters further, NCSE may cause catatonia in some patients (e.g., catatonia is one clinical manifestation of absence SE 📖).
• 💡 Patients with either NCSE or catatonia may improve dramatically following therapy with benzodiazepine.
  • Benzodiazepine challenge for the diagnosis of catatonia: 📖
  • Benzodiazepine challenge for the diagnosis of NCSE: 📖
• Diagnosis of NCSE and/or catatonia requires a combination of clinical and EEG monitoring.

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antiepileptic trial for ictal-interictal continuum abnormalities

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factors to consider when approaching EEGs along the ictal-interictal continuum

• (1) What is the category of EEG activity (e.g., LPDs 📖, LRDA 📖, and BIPDs 📖 are most strongly correlated with seizure and potentially the most worrisome).
• (2) How angry the EEG is overall:
  • Higher frequencies may be more concerning (e.g., periodic discharges >2 Hz likely merit therapy).(Hirsch 2022; 28097330) Alternatively, periodic discharges <1 Hz without associated motor manifestations are usually not aggressively treated.(LaRoche 2018)
  • The presence or absence of other worrisome findings (“+ modifiers”), such as fast activity or sharp waves/spikes.
• (3) Any clinical correlate:
  • Note that time-locked symptoms which occur with ictal-interictal discharges indicate the presence of electroclinical nonconvulsive status epilepticus – so this definitely warrants therapy.
  • Neurological deterioration that coincided with the initiation of EEG abnormalities may suggest that EEG abnormalities could be causing deterioration.
• (4) Clinical context:(LaRoche 2018)
  • If the patient is improving, then more conservative management may be reasonable.
  • If there is a clear explanation for the EEG findings which is treatable (e.g., hepatic encephalopathy), this might argue for holding antiepileptic therapy while observing whether the patient responds to treatment of the underlying disorder.
  • If the patient has altered mental status without an alternative explanation, this may favor treatment.
  • Prior history of epilepsy or recent clinical seizure favors treatment.
  • Acute neurologic disorder with high risk of seizures favors treatment (e.g., traumatic brain injury, intracranial hemorrhage).
• (5) Other modalities of neuromonitoring may help clarify whether EEG activity is causing clinical harm (e.g., an increased blood flow on PET scan, or diffusion abnormality on a MRI could suggest a need for more aggressive therapy).(LaRoche 2018)

various potential treatment goals

• (1) Seizure prophylaxis:
  • In some situations, the main concern may be that further deterioration could occur, leading to an unequivocal seizure.
  • Seizure prophylaxis can generally be achieved by using a single antiepileptic agent at a standard dose (e.g., levetiracetam 💉).
• (2) Elimination of periodic discharges or LRDA (lateral rhythmic delta activity):
  • In some situations, it may be suspected that the periodic discharges or LRDA themselves are causing clinical deterioration.
  • Elimination of periodic discharges may be more difficult than seizure prophylaxis, as this can require escalating doses of multiple antiepileptic therapies.
  • If it is uncertain whether the patient would benefit from elimination of periodic discharges or LRDA, a trial of antiepileptic therapy may be reasonable (more on these below).

benzodiazepine trial

• Small doses of benzodiazepine are provided, along with monitoring of the EEG and neurological examination (e.g., incremental doses of IV midazolam up to a maximal cumulative dose of 10 mg, if lower doses are ineffective and sedation doesn't occur).
• A positive trial requires improvement in both the background EEG and the clinical condition.
• Limitations of a benzodiazepine trial:
  • (1) Benzodiazepine-induced sedation may cloud the clinical examination and potentially cause harm (e.g., among patients who are not intubated).
  • (2) Clinical improvement may lag several hours after EEG improvement.(29666958) Thus, lack of clinical improvement following a single dose of benzodiazepine doesn't exclude the potential for clinical benefit.

antiepileptic medication trial

• Conventional antiepileptics may be therapeutically trialed (e.g., valproic acid, levetiracetam, phenytoin, lacosamide).
• This has the advantage of avoiding the confounding sedating effect of benzodiazepines.(29666958)
• Clinical improvement may lag behind EEG improvement, as the patient recovers from a postictal state. Therefore, a trial of 1-2 days may be reasonable (rather than expecting immediate improvement).
• In patients with the most worrisome EEG findings, it could be reasonable to initiate continuous anesthetic agents (e.g., propofol or midazolam) – especially if the patient is already intubated.

general approach

• A general approach to patients with ictal-interictal EEG patterns is shown below. However, individual patient management should be personalized based on consideration of various factors, as listed above.(LaRoche 2018) Specific treatment considerations are also discussed pertaining to various ictal-interictal EEG patterns (GPDs 📖; LPDs 📖; BIPDs 📖; LRDA 📖).

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management of NCSE

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lack of evidence / guidelines

• There is no level-I evidence nor detailed guideline regarding the management of NCSE.
• Many components of NCSE therapy are evidence-free zones.

risks vs. benefits of aggressive therapy

• A key question is:  to what extent are seizures causing harm, versus to what extent are seizures merely a reflection of underlying brain disease.  This is often quite unclear.
• Seizures may cause harm in various ways, for example:
  • In some situations, status epilepticus may cause direct neuronal injury or necrosis (e.g., by causing cellular energy failure and glutaminergic neurotoxicity).  Patients with pre-existing brain injury (e.g., traumatic brain injury or intracranial hemorrhage) may be more susceptible to further injury due to NCSE.
  • In some situations, nonconvulsive status epilepticus could delay awakening from mechanical ventilation, and thereby extend ICU and hospital length of stay.  This could cause iatrogenic harm due to deconditioning and the accumulation of nosocomial complications.
  • Among patients with severe brain injury, seizures may exacerbate abnormal physiology (e.g., causing further elevation of intracranial pressure).
• Aggressive therapies for status epilepticus may also cause harm, for example:
  • The most aggressive therapies involve continuous anesthetic infusions, which may require prolonged intubation.  This exposes patients to risks involved with ongoing intubation.
  • All antiepileptic agents have some side effects (e.g., even levetiracetam may promote agitation or SIADH (syndrome of inappropriate antidiuretic hormone secretion)).

individualized approach

• The approach to any individual patient may depend on a careful weighing of risks vs. benefits for individual therapies.  There is no one-size-fits-all therapy for NCSE.
  • 💡 It's important to recognize that merely the presence of NCSE does not necessarily mandate very aggressive therapy (unlike convulsive status epilepticus).
• Treatment varies depending on the clinical types of NCSE, as discussed further below.  For example:
  • Patients with generalized convulsive status epilepticus who subsequently transition into NCSE should generally be treated in an aggressive fashion (essentially identical to treatment of ongoing convulsive status epilepticus).
  • Patients with absence seizures or preserved consciousness may often be treated less aggressively.

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NCSE with coma

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causes & associations

• Two main subtypes:
  • (1) NCSE in coma with preceding convulsive status epilepticus (“subtle status epilepticus”).
  • (2) NCSE in coma without any preceding convulsive seizure.

clinical features

• Patient is comatose.
• Clinical findings may include:
  • Pupillary hippus, autonomic disturbances may be seen.
  • Myoclonus (facial, limb, perioral), teeth grinding.(29650639)
  • Nystagmus.

EEG features

• Various EEG patterns may be seen.
• Generalized periodic discharges (GPDs) are frequent, and may be interspersed with isoelectric suppression for several seconds.(29650639)

management

• Optimal management may depend on the context and EEG findings, for example:
  • (1) For comatose patients with convulsive status epilepticus who progress to develop NCSE (“subtle status epilepticus” or “postconvulsive nonconvulsive status epilepticus”), the treatment is essentially identical to the management of refractory convulsive status epilepticus (discussed further here) 📖 .(30921018)
  • (2) For patients who are comatose and found to have ictal-interictal EEG abnormalities, the optimal level of aggressiveness is unclear. Many of these patients may have NCSE and would benefit from antiepileptic therapy. However, in some cases the EEG abnormality may not be causing unconsciousness – in which case aggressive therapy with anesthetic infusions could cause harm without potential benefit.
• When the optimal management is unclear, a trial of antiepileptic therapy may be helpful (more on this above).📖
• As with convulsive status epilepticus, all causative factors should be sought out and any reversible causes treated aggressively (e.g., electrolyte abnormalities, medications that reduce seizure threshold). More on the causes of seizures here.📖

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de novo absence status epilepticus in adulthood

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causes & associations

• This occurs mostly in middle-aged or elderly women.(29650639)
• Usually there is no history of seizure.
• The most common causes are toxic/metabolic, especially:(29650639; 28144933)
  • Benzodiazepine or alcohol withdrawal.(31557430)
  • Initiation of psychotropic medications.
  • Antibiotics, chemotherapy, and even antiepileptic medications.
  • Sepsis.
  • Metabolic disturbance.

clinical features

• Consciousness and memory are variably affected. Patients may be catatonic and bedridden.(29650639) In milder cases patients may have reduced decision-making ability, but still be able to eat and drink.(29650639)
• Patients can appear perplexed and indifferent, disoriented, or with psychomotor slowing (e.g., hesitant speech).(29650639)
• Motor manifestations:
  • Half of patients have myoclonus, mostly around the eyes (which may coincide with spike-wave discharges on EEG).(29650639)
  • Automatisms, frontal release signs in some cases, or bilateral Babinski sign may be seen.(29650639)
  • Slow, ataxic gait may occur.(29650639)
  • Bilateral, tonic-clonic seizures can occur.(29650639)
• Overall good prognosis, with a low likelihood of recurrence (if triggers are treated).(29650639)

EEG features

• EEG generally shows irregular spike-wave discharges from 0.5-4 Hz.(28144933)

management

• The physiology of absence status epilepticus may involve excess GABA-receptor activation (unlike most other seizure types). This has several implications:
  • (1) Some antiepileptic medications may paradoxically exert pro-convulsive effects in this context (phenytoin, carbamazepine, oxcarbazepine, gabapentin, tiagabine, or vigabatrin).(28144933)
  • (2) Absence status epilepticus generally isn't believed to cause neuropathological damage (unlike other forms of NCSE). Therefore, there may be somewhat less urgency to immediately controlling it. Escalation to the ICU is generally not required.(28144933)
• Benzodiazepine is the front-line therapy, with consideration of valproate as a second-line therapy (in patients without contraindications to valproate).(31557430) Other treatments may include levetiracetam, topiramate, and possibly lacosamide.(28144933; 31557430)

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focal NCSE with impaired consciousness

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causes & associations

• There is increased incidence in younger people with epilepsy that is poorly controlled.(28144933) However, this is frequently caused by a focal lesion as well.

clinical features of frontal NCSE

• Typically lasts days, frequently recurrent.(29650639)
• Stuttering, severe dysarthria, or aphasia may occur.(29650639)
• Frontal disinhibition, smiling, laughter, or confabulation may be observed.(29650639)
• Potential signs include adverse eye movements, ictal paralysis, or myoclonus of the eyelids/limbs/perioral area.(29650639)
• May be either unilateral or bilateral. Bilateral NCSE may cause obtundation and more notable amnesia.

clinical features of temporal NCSE

• May last hours or days (or longer, if there is an acute symptomatic cause); can be recurrent.
• Overall, patients may vary from from mildly altered to comatose, with variable degrees of amnesia.
• Psychiatric features are prominent:
  • Psychotic hallucinations.
  • Feelings of fear, anxiety, negativism, irritability/aggression, depression.(29650639)
  • Capgras syndrome (belief that someone else has been replaced by an imposter).(29650639)
• Complex automatisms may occur, including oroalimentary automatisms or perseveration.(29650639) Patients may wander.
• Speech arrest and aphasia can occur.

EEG features

• EEG is more sensitive than in focal NCSE without altered consciousness.
• Potential patterns include:
  • Rhythmic spike-waves or high-voltage slow waves.
  • Rhythmic delta or theta activity.
• Abnormalities are often lateralized to one side.

management

• Benzodiazepine is often tried initially (or possibly clobazam). Second-line treatments include fosphenytoin, valproate, levetiracetam, or phenobarbital.
• In more protracted cases, very rarely an antiepileptic infusion may be required (e.g., propofol or midazolam). Overall, escalation to ICU is rarely required.(28144933)

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focal NCSE without impaired consciousness

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causes & associations

• Focal lesion, usually remote.(29650639)
• Usually spontaneous (without nonspecific triggers).

clinical features

• Presentation may be quite diverse, depending on which area of the brain is involved. May last days to weeks, often with recurrent episodes.
• Symptoms may include:
  • Aphasia (most often global) and alexia.(29650639)
  • Sensory, olfactory, gustatory, auditory, or autonomic abnormalities.
  • Visual abnormalities (including size misperceptions, hallucinations, blindness, streaks of light and color – which have been termed “aura continua”).
  • Emotional or psychic symptoms (including isolated fear).
  • Inhibitory focal status epilepticus may cause hemiparesis, alien hand syndrome, or hemispatial neglect.
• May evolve into bilateral convulsive status epilepticus.

EEG features

• Unilateral rhythmic spike-waves or high-voltage slow waves may be seen.(29650639)
• Scalp EEG may commonly be normal.(29650639)

management

• Benzodiazepine is often tried initially.
• Other treatments include valproate, fosphenytoin, levetiracetam, or phenobarbital.(28144933)
• In refractory cases, topiramate or lacosamide may be used.(31557430)

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Epilepsia Partialis Continua (EPC)

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basics

• Epilepsia partialis continua (EPC) is also known as focal motor status epilepticus. It involves persistent focal motor seizures, without an alteration of consciousness.
• Technically EPC is not a form of nonconvulsive status epilepticus, because it involves obvious convulsive seizure activity. However, EPC is fundamentally similar to focal NCSE without impaired consciousness (discussed further above 📖).
  • Compared to other forms of focal NCSE without impaired consciousness, EPC is often more obvious clinically and thus easier to diagnose.

clinical findings

• Prolonged repetitive stereotyped clonic or myoclonic jerking of part or all of one side of the body (e.g.,a group of muscles, a limb, or the hemibody).(29650639) This frequently involves the distal arm. Activity may be regional, with marching from one muscle group to another. (Louis 2021)
• Jerking may be rhythmic or arrhythmic, but muscle jerks should occur at least every ten seconds.(29650639)
• Epilepsia partialis continua can last for hours, days, weeks, or years. It should last for >1 hour to be considered focal motor status epilepticus. Recurrent episodes may occur.
• Symptoms may fluctuate in intensity, but persist during sleep.
• Consciousness is not impaired.

causes of focal motor status epilepticus

• Vascular (e.g., ischemic stroke venous sinus thrombosis, hemorrhage).
• Infection (e.g., HSV encephalitis, HIV, Russian tick-borne encephalitis).
• Tumors.
• Metabolic disorders (e.g., hyponatremia, hyperglycemic hyperosmolar nonketotic state).
• Focal cortical dysplasia.
• Traumatic brain injury (including subdural hematoma).

investigations

• Neuroimaging usually identifies a lesion involving the motor cortex or subcortical structures.
• EEG findings: (29650639)
  • Epileptiform discharges or periodic discharges in 65% of patients.
  • Focal slowing in 20%.
  • No EEG correlate in 20%.

mimics of focal motor status epilepticus (29650639; LaRoche 2018)

• Asterixis.
• Spontaneous clonus.
• Shivering.
• Tremor.
• Hemiballismus/hemichorea.
• Myoclonus (brainstem, spinal).
• Posturing movements (decerebrate and decorticate).
• Psychogenic nonepileptic seizures.
• Spinal reflexes.
• Dystonia.

treatment

• Any underlying disease process should be identified and treated (see the possible causes above).
• Epilepsia partialis continua is generally resistant to therapy.
  • Benzodiazepines may interrupt it, but they aren't a good long-term treatment.(28029552)
  • Some success been reported with levetiracetam and topiramate.(28029552)
  • Aggressive interventions (e.g., intubation with general anesthesia) should be avoided, as these are generally more dangerous than the disease itself.

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• Excessively aggressive treatment of epilepsia partialis continua (e.g., with intubation and anesthetic infusions) may be more dangerous than the disorder itself.
• The diagnosis of nonconvulsive status epilepticus is fraught with hazard. Proper diagnosis likely requires application of EEG to a substantial population of altered patients (accepting that most patients will not be diagnosed with seizures).

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