The clinical presentation of NCSE is heterogeneous and
the EEG is an essential diagnostic tool [23,24]. In patients with moderate or
severe mental retardation, with psychiatric disorders and especially in
critically ill patients, a high degree of clinical suspicion is often necessary
to establish the diagnosis of NCSE within the shortest possible time. Many
reports use the term “NCSE” in an all-encompassing manner, applying this
definition for patients with varied clinical manifestations and etiologies, in
a way that impairs the distinction between focal and generalized forms, as well
as the assessment of prognosis in different situations, thus, taking into
consideration data such as etiology, age, clinical and electrographic
presentation is of importance, given the fact that the course and prognosis of focal and generalized forms
are quite different and possibly dependent on those aspects.
Figure
3:
EEG trace of Typical Absence NCSE
Figure
4:
EEG trace of Atypical Absence NCSE.
Figure 5: EEG trace of complex partial NCSE
Figure 6: Generalized periodic epileptiform discharge.
In our study, NCSE occurs in children with or without a history of
epilepsy, but most are known epileptics. Presumed Perinatal and pediatric
strokes are frequent etiology of NCSE, so prolonged follow up in those groups
of patients to early detect NCSE is mandatory. EEG can differentiate between
subtypes when clinical presentation is non-decisive, that confirms the golden
role of EEG in diagnosis and classification [20-24]. Clinical manifestations of
NCSE in our study children include cognitive and/or behavioral impairments;
symptoms characteristically fluctuate in intensity over time. Alteration of the
conscious level characteristic of the syndrome can range from slowing of
ideation to complete loss of awareness. Children are usually able to carry out
simple tasks and even complex daily life activities. Speech may be slurred,
incoherent, sometimes with echolalia and palilalia. Children may show
behavioral, language and cognitive deterioration. Pediatric populations are at increased risk
of NCSE development than adults, due to the addition of typical and atypical
absence status epilepticus portion. Several neurological conditions, among them
metabolic encephalopathy, drug intoxication, prolonged postictal status, and
transitory global amnesia, require differential diagnosis with NCSE [7].
Behavioral changes that may occur in these cases can lead to an erroneous
diagnosis of psychiatric conditions such as depression, psychosis, and
hysteria; however, the most difficult differential diagnosis is by far between
these two main types of NCSE, i.e., generalized with absence seizures and focal
with complex partial seizures [26]. This distinction is especially difficult
when dealing with focal NCSE of frontal origin, when the discharges tend to
propagate in a relatively diffuse pattern [27]. A previous history of partial
epilepsy and focal or lateralized EEG finding is of help for the diagnosis of
complex partial SE, whereas the presence of generalized idiopathic epilepsy and
generalized discharges supports the diagnosis of absence SE. The NCSE patients’ EEGs in our work showed
focal, multifocal, generalized, or periodic lateralized epileptiform
discharge. Periodic lateralized epileptiform discharges are mainly recorded
from patients with CPSE, previous vascular insults or simple partial NCSE
presented by disturbed behavior and other psychiatric manifestations [10].
Table 1: Classification of study
subjects according to dominant type of Non-convulsive Status Epilepticus.
|
NCSE Types
|
Typical absence NCSE
|
Atypical absence NCSE
|
Simple Partial NCSE
|
Complex Partial NCSE
|
|
Number & %
|
8 (7%)
|
34 (31%)
|
6 (5%)
|
64 (57%)
|
Table
2: Etiology
of non-convulsive status epilepticus.
|
NCSE
|
Cryptogenic etiology
|
Vascular Insult
|
Acute symptomatic
|
Remote symptomatic
|
Acute precipitant
|
|
No.=112
|
52 (47%)
|
20 (18%)
|
16 (14%)
|
14 (12%)
|
10 (9%)
|
