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ORIGINAL ARTICLE
Year : 2003  |  Volume : 51  |  Issue : 4  |  Page : 453-454

Nonconvulsive status epilepticus: An under diagnosed and potentially treatable condition


Department of Neurology, The Institute of Neurological Sciences, CARE Hospitals, Nampally, Hyderabad - 500001,

Correspondence Address:
The Institute of Neurological Sciences, Exhibition Road, Nampally, Hyderabad - 500001
jmkmurthy@satyam.net.in



How to cite this article:
Murthy J M. Nonconvulsive status epilepticus: An under diagnosed and potentially treatable condition. Neurol India 2003;51:453-4


How to cite this URL:
Murthy J M. Nonconvulsive status epilepticus: An under diagnosed and potentially treatable condition. Neurol India [serial online] 2003 [cited 2014 Oct 31];51:453-4. Available from: http://www.neurologyindia.com/text.asp?2003/51/4/453/5012


Nonconvulsive status epilepticus (NCSE) is an important status epilepticus (SE) type and is defined as a mental status changes from baseline of at least 30 to 60 minutes duration associated with continuous or near continuous ictal discharges on EEG.[1] NCSE is not rare but it is clearly under diagnosed. In a prospective, population based study of status epileptic, NCSE represented approximately 5% of SE cases presenting in Richmond, Virginia.[2] NCSE constitutes approximately 20 to 23% of status epilepticus cases,[3],[4] occurring in about 8% of all comatose patients without signs of seizure activity,[5] and persisting in 14% of patients after controlling generalized convulsive status epilepticus (GCSE).[4] There is hardly any data on NCSE from India. This partly is related to lack of facilities like continuous monitoring in intensive care units. To diagnose NCSE there has to be, at the very least, EEG evidence of seizures. Without EEG, one can only guess at the cause of behavioral or cognitive change and the diagnosis of a NCSE remains speculative. In our neurological intensive care unit with the availability of continuous EEG monitoring we were able to diagnose NCSE in 15 patients over a period of one year (unpublished data).
The diagnosis of NCSE is difficult to establish. Making a diagnosis of NCSE traditionally involves the clinical picture of an abnormal mental status with diminished responsiveness, a supportive EEG, and often a responsive to antiepileptic drug medication. In the broadest sense, this only requires establishing a seizure pattern on EEG. NCSE has a pleomorphic clinical presentation and may present as absence, complex partial, or electrographic SE.[7],[8],[9],[10] Several classification systems have been proposed. Conventional classification divides NCSE into absence status epilepticus (ASE) and a lateralization-related NSCE - complex partial status epilepticus (CPSE), mostly by electroencephalographic (EEG) criteria. However the mortality in NCSE is largely a function of NCSE etiology, rather than to a particular type or pattern of EEG.[11] An emerging unifying hypothesis has been to divide NCSE based on whether there is a primary epileptic encephalopathy in which mental status changes are due to seizure activity, versus electrographic NCSE in which the electrographic pattern of NCSE is present but encephalopathy is most likely due to some other brain insult. Kaplan[1] developed a more detailed classification utilizing clinical characteristics to categorize patients, especially mental status 1) localization-related NCSE, 2) generalized NCSE (GNSE), and 3) indeterminate or intermediate NCSE. GNSE is further divided into: 1) ASE associated with childhood absences or more rarely in the setting of juvenile myoclonic epilepsy (JME), 2) patients with childhood-onset, secondary generalized epilepsy, often with mental retardation, often with greater confusion and myoclonus; 3) elderly patients without epilepsy who present de novo, usually with toxic or metabolic dysfunction, intake of psychotropic drugs or benzodiazepine withdrawal, and 4) generalized nonconvulsive status secondary to partial epileptic status of temporal or frontal lobe origin. Recently Shneker and Fountain[11] categorized patients based on the easily observable characteristics of etiology, mental status, and presence of complications, thus relying less on the interpretation necessary for traditional classification. Such an approach helps the clinician to predict the probable outcome in a particular clinical setting and also to decide the appropriate therapeutic options.
ASE in patients with idiopathic generalized epilepsies as reported by Chemmanam et al[12] in this issue of the journal; is not infrequent.[13],[14] Of the thirty-two patients with NCSE studied by Tomson et al,[15] eighteen had generalized seizure activity on EEG, but only six of these had a history of absence epilepsy or juvenile myoclonic epilepsy. Generalized idiopathic epilepsies, and JME in particular, are clear candidates for drug-induced worsening of seizures including status epilepticus,[16],[17],[18],[19] JME is a frequent form of idiopathic generalized epilepsy and is often misdiagnosed.[20],[21],[22] Of the 28 patients with JME who received carbamazepine, two had myoclonic status and vigabatrin in association with carbamazepine provoked a mixed absence and myoclonic status.[19]
The natural history of NCSE is not well defined, especially mortality and morbidity. This is partly due to methodological issues, such as not giving due weight-age to the underlying etiology, mental status changes and associated complications and also lack of uniform accurate definition of NCSE. NCSE is likely to include status epilepticus of diverse pathophysiology. Higher mortality rates of 50 to 52% have been reported for NCSE in critically ill patients,[23],[24] and in patients who had NCSE after GCSE.[6] Most studies of NCSE in the critically ill have also found mental status to be an important contributor to mortality.[8],[25],[26] In the study by Shneker and Fountain[11] mortality rates were higher in patients 1) in the acute medical group (27%) vs the epilepsy (3%) and the cryptogenic (18%) groups (P < 0.02), 2) with severe mental status impairment (39%) compared to those with mild impairment (7%) (P < 0.0002). Mental status impairment and etiology were independently associated with mortality (P < 0.001).
Randomized controlled trials of treatments for NCSE are lacking. A few small case series have reported success with valproate.[26] Most conventional antiepileptic drugs (AEDs) have been reported to be effective for some patients. Refractory NCSE has been reported to respond to midazolam, propofol or pentobabrbitola.[27] It will be appropriate to monitor the patients with continuous EEG monitoring.
The treatment of NCSE needs to be tailored to the perceived urgency and morbidity of the condition. Patients with epilepsy as the only cause of NCSE should probably not be routinely treated very aggressively. The rationale is that they are unlikely to die from NCSE.[11] Conventional AEDs are the drugs of first choice. Patients with ASE related to idiopathic generalized epilepsies, absence epilepsy and JME respond well with benzodiazepine. However the appropriate drug of choice may be valporate infusion. No long-term morbidity from absence SE.[13],[28]
Patients with NCSE of cryptogenic etiology are at a moderate risk of death, may develop epilepsy, and are typically in otherwise good health.[11] These patients should be treated aggressively. Parenrtal anesthetic therapy should be considered if they fail a benzodiazepine and a parentral load of an AED.
If NCSE is due to an acute medical illness treatment with pentobarbital, propofol, or midazolam to attain EEG background suppression, may be more effective than other strategies.[27] In this systemic review of treatment of refractory status epilepticus, NCSE was most often treated with midazolam. Of the 16 patients with NCSE, only in one patient (6%) NCSE could not be ultimately controlled with midazolam. The mortality was 75% (12/16). Except for one patient all the other patients had encephalopathy due to some other brain insult.[29]
In conclusion, NCSE can be under-recognized because of the pleomophic clinical features. EEG is the diagnostic cornerstone, and electroclinical correlation allows rapid diagnosis and appropriate management. 

  »   References Top

1.Kaplan PW. Nonconvulsive status epilepticus. Seminars in Neurology 1996;16:33-40.  Back to cited text no. 1  [PUBMED]  
2.Towne AR, Waterhouse EJ, Morton LD, Kopee Garnett L, Brown AJ, DeLorenzo RJ. Unrecognized nonconvulsive status epilepticus in comatose patients. Epilepsia 1998;39:K07.  Back to cited text no. 2    
3.Celesia GG, Modern concepts of status epilepticus. JAMA 1976;235:1571- 4.  Back to cited text no. 3    
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5.Towne AR, Waterhouse EJ, Boggs JG, et al. Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology 2000;54:340-5.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.DeLorenzo RJ, Waterhouse EJ, Towne AR, et al. Persistent nonconvulsive status epilepticus after control of convulsive status epilepticus. Epilepsia 1998;38:833-40.  Back to cited text no. 6    
7.DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of status epilepticus. J Clin Neurophysiol 1995;12:316-25.  Back to cited text no. 7    
8.Towne AR, Pellock JM, Ko D, et al. Determinants of mortality in status epilepticus: a retrospective study of 292 adult patients. Epilepsia 1994;35:27-34.  Back to cited text no. 8  [PUBMED]  
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12.Chemmanam T, Pandian JD, Singh YP, Pandhi M. Non convulsive status epilepticus - A rare presentation of juvenile myoclonic epilepsy. Neurology India 2003;51:  Back to cited text no. 12    
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19.Genton P, Gelisse P, Thomas P, Dravet C. Do carbamazepine and phenytoin aggravate juvenile myoclonic epilepsy? Neurology 2000;55:1106-9.  Back to cited text no. 19    
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