nonconvulsive status epilepticus ( ncse ) can be classified as absence status or complex partial status . absence status is characterized by bilateral synchronized spike and wave complex bursts and a variety of conscious disturbances ( niedermeyer and ribeiro 2000 ) . possible precipitating factors for ncse include benzodiazepine withdrawal , excessive use of the psychotropic drugs , and electrolyte imbalances . hyponatremia is a rare precipitating factor ( lee 1985 ; thomas et al 1992 ; tomson et al 1992 ) . primavera et al reported that a case of ncse resulting from hyponatremia , was improved with saline solution treatment ( primavera et al 1995 ) . absence seizures are also characterized by generalized spike and slow wave complexes , and cases with focal lesion - associated absences have been reported ( millan et al 2001 ) . however , absence seizure and absence status are distinct conditions that should be considered separately . interestingly , we observed a case of de novo absence status associated with a region of focal brain activity , suspected of being an epileptogenic zone and hyponatremia caused by polydipsia . since x-2 year , a 57-year - old man had been treated for primary insomnia at a psychiatric clinic , and psychotropics were administered . he had developed the habit of drinking large amounts of water , about 23 liters per day at that time . he had no family history of seizure disorder , and no history of hypertension , diabetes , perinatal difficulty , stroke , or trauma . in april of x year , the patient began vomiting and could not say his own name , address , or the date . the next day he and his family presented at our psychiatric clinic . at first examination he showed poor orientation , memory disturbances , a decrease in spontaneous speech , bradykinesia , confusion , and was suspected to have a subacute consciousness disturbance . he was admitted to our psychiatric ward for further examination on that day . on admission he had taken etizolam 2 mg , sulpiride 150 mg , promethazine 12.5 mg , chlorpromazine 12.5 mg , and phenobarbital 15 mg . electrolyte analysis revealed hyponatremia ( 118 meq / l)(138146 ) , urine osmolarity 369 mosm / kg ( 501300 ) , urine sodium 0.85 g / day ( 46 ) , serum osmolarity 268 mosm / kg ( 275290 ) , and antidiuretic hormone ( adh ) was 8.4 pg / ml ( 0.33.5 ) , and we suspected the syndrome of inappropriate secretion of antidiuretic hormone ( siadh ) . electroencephalogram ( eeg ) was recorded by the usual routine settings for about one hour . eeg revealed bilateral spike and slow wave complexes during the recording on admission ( figure 1a ) . we treated the patient with 10001500 ml / day saline infusion and intravenous 5 mg of diazepam , slowly injected without eeg recording ; his consciousness improved temporarily , but became disturbed again . the next day we confirmed irregular spike and slow wave complexes , and during drowsy and light sleep some focal spikes in the left anterior area ( figure 1b ) . on the third day , the spike and slow wave complexes disappeared . his conscious disturbance improved , as shown in eeg changes . after he recovered from disturbed consciousness , he had amnesia and could not remember anything from one to two days before his admission . magnetic resonance imaging ( mri ) showed small lacunars in the left basal ganglia and slight atrophy in the left temporal area . single photon emission tomography ( spect ) during the interictal period showed an area of hypoperfusion in the left frontal and anterior - temporal area . neuropsychological examination showed that mini - mental status examination and raven colored progressive matrices were 27/30 and 24/36 , respectively , when the patient was alert . after admission we suspected drug - induced polydipsia , and stopped other medications apart from benzodiazepine , brotizolam 0.25 mg , and flunitrazepam 1 mg for his insomnia . thereafter , however , the patient often suffered from insomnia and had further difficulty controlling the polydipsia . two weeks after admission , serum sodium , adh , and serum osmolarity were at normal levels . therefore we diagnosed the patient as ncse , as a result of polydipsia - induced hyponatremia . a on the first day of the first episode , continuously spike and slow wave complexes were seen in frontal area . b on the second day of the first episode , some spikes were seen in left front - temporal area during drowsy state . he came to our hospital by ambulance and was admitted in the early morning . on admission , serum sodium was 126 meq / ml . we administered saline infusion 1500 ml / day . we considered that hyponatremia indirectly induced the onset of ncse through the epiletpogenic zone in the left front - temporal area , and assumed that an anticonvulsant would be needed for ncse . thus we used phenytoin 200 mg after the second episode , and the patient has had no recurrence of seizures and episodes of hyponatremia for five years . we diagnosed this case as nsce , specifically , classical de novo absence status ( niedermeyer and ribeiro 2000 ) . eeg revealed continuously bilateral spike and slow wave complexes in the frontal area in both episodes , and showed some spikes in the left frontal area after recovery from absence status . researchers have reported that benzodiazepines are effective for treating the clinical manifestations and eeg paroxysmal activity associated with absence status ( niedermeyer and ribeiro 2000 ) . we used benzodiazepine in the first episode , but we felt that correcting sodium levels was more clearly effective , because his consciousness disturbance was not clearly improved by diazepam in the first episode . primavera and colleagues ( 1995 ) reported a case of de novo absence status with no focal signs in repeated episodes , which was treated effectively by correcting sodium levels . our case was de novo absence status showing continuously symmetrical frontal spike and slow wave complexes . after recovery from absence status , eeg showed some spikes in the left front - temporal area , mri showed lacunar infarctions in the left basal ganglia , and spect showed hypoperfusion in the left anterior - frontal area . however , we clearly could not affirm the etiology of this region , for example , congenital or cryptogenic . we could not confirm that the onset of absence status started from this focal region , but suspected the left front - temporal region to be an epileptogenic zone . kudo and colleagues ( 1995 ) reported that complex partial status mimicking absence status originates from the frontal area in unclassified ncse . and millan and colleagues ( 2001 ) reported cases of frontal localization of absence seizure . as a matter of course , absence seizure and absence status are distinct conditions that should not be considered together . however we considered that hyponatremia induced by polydipsia precipitated epileptogenicity in the left frontal area , and then focal activity secondarily generalized and resulted in absence status . in conclusion , we reported a case of de novo absence status associated with two rare factors : a region of focal activity suspected of being an epileptogenic zone , and hyponatremia caused by polydipsia . in this case , the metabolic imbalance of hyponatremia , and the suspected left front - temporal epileptogenic zone , appeared to be involved in the onset of absence status . the answer to the controversy over the onset of ncse awaits the elucidation of the origin of generalized spike and slow wave complexes .
we report a case of de novo absence status associated with focal discharge and polydipsia - induced hyponatremia . 
 nonconvulsive status epilepticus ( ncse ) is classified as absence status or complex partial status . 
 absence status is characterized by bilateral synchronized spike and wave complex bursts and a variety of conscious disturbances . 
 possible precipitating factors for ncse include benzodiazepine withdrawal , excessive use of psychotropic drugs , and electrolyte imbalances . 
 hyponatremia is a rare precipitating factor . in this case , the patient was 59 years old and had suffered from primary insomnia but had no history of epilepsy . 
 ncse improved by means of saline infusion . however after recovery from ncse eeg revealed some spikes in the left frontal area . 
 absence seizures can also show generalized spike and slow waves , and cases of focal lesion - associated absence seizures have been reported . 
 although absence seizures and absence status are two distinct conditions , they should not be considered together . 
 we assumed that hyponatremia induced by polydipsia precipitated epileptogenicity in the left frontal area , and then focal activity secondarily generalized and resulted in absence status .