INTRODUCTION • Nonconvulsive status epilepticus (NCSE) is much more common than is generally appreciated. • NCSE constitutes nearly a quarter of SE cases in a moderate-sized series and 3.5 cases of complex partial SE per 100,000 and 15 cases of other nonconvulsive SE per 100,000 population per year in USA • 1.5 cases of NCSE per 100,000 per year in Sweden • certainly under diagnosed, but its presentation may be subtle • Diagnostic criteria and treatment are controversial
NCSE typically occurs following supposedly controlled convulsions or other seizures, but with persistent neurologic dysfunction despite apparently adequate treatment • NCSE may occur in typical situations such as following other seizures or in the setting of acute stroke. Because there are no motor manifestations, the diagnosis is often missed
NCSE is often missed in patients with altered neurologic function because • NCSE arises often in patients with other serious illnesses • diagnosis is often not entertained. • Diagnosis of NCSE is worth making because NCSE impairs the patient’s health significantly, and it is often a treatable and completely reversible condition
Definitions of NCSE • Contraversial in literature because it is a relatively new clinical entity • Absence of substantial motor manifestations in presence of EEG consistent with on going seizure activity • three main features to the diagnostic criteria for NCSE • alterations in alertness and responsiveness( neurologic deficits) • associated EEG findings • a rapid response to AEDs, particularly benzodiazepines • generally been divided into 2 types: • ABSENCE SE • COMPLEX PARTIAL SE
ABSENCE SE: • characterized by generalized spike and slow wave discharges • Confusion but wakefulness, with blinking or occasional myoclonus • Generalised discharges on EEG • May start or end with a generalized convulsion • Can last days • Typical precipitants: benzodiazepine or other medication withdrawal, generalized convulsions, infection, trauma, metabolic aberrations
COMPLEX PARTIAL SE: • a presumed focal onset • usually with focal discharges and considered the equivalent of prolonged or repetitive complex partial seizures. • May include an “epileptic twilight state” with fluctuating mental state, a lack of responsiveness or confusion, and bizarre behavior • Can last up to months; often recurrent
Rapid generalized epileptiform spikes and slow waves following a few seconds of a normal EEG.
Clues to the Recognition of NCSE • Following generalized convulsions or GCSE but still altered mental state • Subtle signs such as twitching, blinking, and nystagmus in a stuporous patient • Otherwise unexplained stupor or confusion • Altered mental status , particularly after benzodiazepine and other AED withdrawal • History of seizures and a new medical or surgical stress
The EEG in NCSE • EEGs usually have epileptiform activity EEG Criteria • 1. Epileptiformsharp waves • 2. Rhythmicityi.e slowing and rapid rhythmic appearance • 3. Rapid discharges: 1–3.5 Hz
Other EEG patterns • SE typically follows a standard evolution through five characteristic stages: • discrete seizures • mergingseizures • continuousseizures • continuousseizures with brief “flat” periods on the EEG • prolonged flat periods with periodic discharges. • The later stages (4 and 5) are often unaccompanied by actual convulsions and could be considered a type of NCSE.
MORBIDITY: DAMAGE FROM NCSE • exact long-term risk from an episode of NCSE is far less certain • Cases of NCSE are rarely fatal unless associated with GCSE or other acute neurologic disorder. • cognitive deterioration • refractory epilepsy • Hippocampal neuronal loss with damage directly related to the duration and intensity of electrographic seizure activity ( animal studies).
TREATMENT • 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 • NCSE remains an underdiagnosed, treatable condition and one well worth both diagnosing and treating.
From case reports and by analogy to GCSE, the more prolonged cases may be worse , and NCSE may last for days without proper diagnosis • Concomitant systemic factors such as infection, metabolic disturbances, hypotension, and medications might increase the likelihood of damage in a synergistic fashion
Why treat NCSE? • Patients with NCSE should be treated quickly with AEDs for several reasons: • They are clearly ill with ongoing seizures and have impaired consciousness and other neurologic deficits that are potentially reversible and certainly treatable. • NCSE, like other forms of SE, entails the attendant morbidity of incidental trauma, aspiration pneumonia • many episodes of NCSE begin with and may end with generalized convulsions, in turn potentially harmful. • possibility that some prolonged episodes might cause lasting damage.
ABSENCE SE • Straightforward absence SE may be terminated by benzodiazepines relatively quickly. Other treatments such as carbon dioxide inhalation, oral barbiturates, benzodiazepines, and ethosuximide can be effective • Absence SE due to benzodiazepine withdrawal usually responds to brief courses of benzodiazepines, although barbiturates may also be helpful
When longer treatment is necessary, valproate has been effective in preventing recurrences • AEDs, including vigabatrin and tiagabine, have been reported to precipitate or worsen generalized NCSE
Complex partial SE • may be interrupted and controlled by traditional intravenous medications, phenytoin,phenobarbital or oral carbamazepine • IV benzodiazepines are used to interrupt the NCSE once it is recognized
REFRACTORY NCSE • 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. • Treatment should be individualized and judicious (2) but should not be delayed