NCSE can occur in a variety of disorders, including hypoxia, metabolic disturbances, and after convulsive seizures [3]. Clinically patients may display subtle, intermittent focal or multifocal rhythmic movements suggestive of seizures; there may not be movements [3]. The wide overlap between the clinical symptoms of NCSE and many other disorders causing change in mental status limits the usefulness of clinical measures for diagnosis [4]. Therefore, the condition can be difficult to diagnose, especially in the obtunded/comatose patient in which comorbid condition are often present [5].
Treatment recommendations between GCSE and NCSE differ significantly. The preferred treatment pathway for GCSE is intravenous administration of lorazepam or diazepam directly followed by phenytoin or equivalent fosphenytoin. Patient with refractory GCSE should be treated in an intensive care units by anaesthetic doses of midazolam, propofol or barbiturates; the anaesthetics are titrated against a burst suppression pattern on EEG monitoring [6]. The initial therapy of NCSE depends on the type and the cause. In most cases of absence NCSE, a small intravenous (i.v.) dose of lorazepam or diazepam will terminate the attack. Complex partial NCSE is initially treated such as GCSE, however, when refractory further non-anaesthetising substances should be given instead of anaesthetics. In subtle SE i.v. anaesthesia may be required [7]. Regarding treatment, comatose NCSE patients treated with benzodiazepines may worsen, whereas generalized nonconvulsive status epilepticus patients may suffer iatrogenically from aggressive treatment (hypotension and respiratory depression) necessitating balancing the potential neurologic morbidity of NCSE against the possible morbidity of IV antiepileptic drugs. Therefore, less aggressive treatment with oral antiepileptics (e.g., Valproic acid) may be considered in clinically mild cases [2, 7]. Determining the prognosis in nonconvulsive status epilepticus (NCSE) is complicated by several factors: under-recognition of NCSE with its spontaneous resolution; incorrect diagnosis of NCSE based on misinterpretation of EEG patterns as NCSE and grouping of different populations that have markedly different co-morbidities [5],9]. There are almost no prospective studies with premorbid neuropsychometric studies, and retrospective studies typically include isolated cases, or case series that include conditions in which the cause of NCSE itself causes cognitive morbidity. Larger, prospective studies will be needed to truly determine the prognosis in the different types of NCSE, stratified according to associated degrees of impairment [2].