02007 VOL. 38 NO.1 CLINICAL EEG and NEUROSCIENCE Nonconvulsive Status Epilepticus Causing Prolonged Stupor After lntraventricular Hemorrhage: Report of a Case J. L. Fernandez-Torre, 2. Agirre, R. Puchades, E. Marco De Lucas and A. Oterino onset of treatment with intravenous phenytoin (100 mg18 h), the clinical state of the patient was unmodified for the next 3 days. Three consecutive EEGs carried out over those days revealed generalized continuous epileptiform activity compatible with a secondarily generalized NCSE (Figure 2b). The patient's metabolic status throughout the course of the disease was carefully controlled, and particular interest was paid to avoid metabolic disturbances such as hyponatremia or hypokalemia, which are known predisposing factors of NCSE. Antiepileptic therapy with valproate (1000 mg/24 h) and clonazepam (1.0 mg/24h) was added to her previous treatment. On the following 17 days, her level of consciousness was fluctuant ranging from somnolence to profound stupor. Several EEGs showed the persistence of ongoing generalized epileptiform discharges during these days. On day 23 after admission, she was conscious and able to understand simple commands. At that time, an EEG disclosed features compatible with a moderate diffuse encephalopathy and resolution of NCSE (Figure 2c). Finally, she was discharged to another hospital for chronic pathology. Kev Words Elderly Patients Electroencephalography lntraventricular Hemorrhage Nonconvulsive Status Epilepticus Stupor ABSTRACT We describe the case of an octogenarian woman who experienced a severe alteration of mental state due to nonconvulsive status epilepticus (NCSE) complicating an intraventricular hemorrhage. Our report emphasizes that NCSE may be the cause of unexplained neurological deterioration in elderly patients with acute brain injury. INTRODUCTION Nonconvulsive status epilepticus (NCSE) is a wellknown cause of altered mental state whose diagnosis may be particularly difficult in elderly people.' Cerebrovascular disease is considered a frequent etiology of epilepsy in older patients, however, intraventricular hemorrhage is an unreported condition associated with NCSE. DISCUSSION lntraventricular hemorrhage is a rarely described cause of NCSE.2,3 Recently, Dennis e l al.3 carried out the first investigation studying the frequency and clinical features of NCSE among comatose patients with subarachnoid hemorrhage. Eight out of 26 patients who underwent continuous electroencephalographic monitoring were diagnosed as having NCSE. In 4 patients, a bilateral intraventricular hemorrhage was observed. Evaluation of persistent coma or neurological deterioration was the reason for which continuous EEG monitoring was carried out. Despite the fact that NCSE was controlled in 5 cases, none of those subjects experienced a significant clinical improvement and all CASE REPORT An 88-year-old woman was admitted to our hospital because of acute alteration of consciousness, nausea and vomiting. She had antecedents of hypertension and had suffered from an ischemic infarction in the territory of the left middle cerebral artery that had caused a mild right hemiparesis. On examination, she was slightly confused, oriented in person and disoriented in time and place. Her speech was not fluent and there was a discrete weakness of the right limbs. Plantar responses were flexor. Acomputed tomography (CT) scan of the brain revealed a lefl intraventricular hemorrhage and a small hematoma localized in the left thalamus (Figure 1). During the next 72 hours, her level of consciousness worsened dramatically, and she became stuporous. Although the clinical worsening was thought secondary to rebleeding, cerebral edema or hydrocephalus, an electroencephalogram (EEG) was requested. The EEG showed the existence of continuous epileptiform discharges involving the entire leff hemisphere in keeping with the diagnosis of localization-related (partial) NCSE (Figure 2a). Despite the From the Department of Clinical Neurophysiology(J. L. Fernandez-Torre, MD, Z. Agirre, MD), Internal Medicine (R. Puchades), Radiology (E. Marco De Lucas, MD) and Neurology (A. Oterino, MD); University Hospital "Marques de Valdecilla"; Santander, Cantabria, Spain. Address requests for reprints to Dr. Jose L. Fernandez-Torre, Department of Clinical Neurophysiology, University Hospital "Marques de Valdecilla," Avda. Valdecilla. sln. 39008 Santander, Cantabria. Spain. Email: jlfemandez@humv.es; ftwrenfc@hotmail.com. Received: February 6, 2006: accepted: April 2, 2006. 57 Downloaded from eeg.sagepub.com at GEORGIAN COURT UNIV on May 2, 2015 02007 VOL. 38 NO. 1 CLINICAL EEG and NEUROSCIENCE Figure 1. ACT scan of the brain revealed the existence of a large intraventricular hemorrhage occupying the left ventride. Fp 1-F3 F3-C 3 C3-P3 P3-0 1 Fp 1-FT F’-T3 T3-T5 T5-01 Fp2-FI F4-C I C4-PJ PI-02 Fp 2-FS F8-TI TCT6 T6-02 Fz-CZ EKG Figure 2A. An EEG performed 72 fours after admission showed the presence of continuous epileptiform discharges (arrow) involving the entire left hemisphere. Verlical bar: 100 pV; Horizontal bar: 1 second; Low filter: 0.5, High filter: 30 Hz. of them died. Similarly, a sudden neurological worsening was the reason for performing an EEG in our case, and NCSE was refractory to conventional antiepileptic treatment. Moreover, NCSE remained uncontrolled for several days, and EEG was the unique method to demonstrate the persistence of ongoing epileptic activity. It could be argued that in our case the long period of obtundation may have simply been related to the intraventricular hemorrhage and the electroencephalographic anomalies constituted only an epiphenomenon. Nevertheless, the behavioral improvement was closely associated with the abolition of the epileptiform activity on Downloaded from eeg.sagepub.com at GEORGIAN COURT UNIV on May 2, 2015 CLINICAL EEG and NEUROSCIENCE 02007 VOL. 38 NO. 1 Fp 1-F3 F343 c'3-P3 P3-01 Fp 1-FF--T3 t3-t5 T5-01 Fp 2-F4 F4-C'4 c'4-P4 P4-02 Fp 2-F8 F8-T4 T4-T6 T6-02 Fz-C'Z EKG Figure 28. On the next days, several EEGs revealed generalized continuous epileptiform activity in keeping with a secondarily generalized NCSE. Vertical bar: 100 pV; Horizontal bar: 1 second; Low filter: 0.5. High filter: 30 Hz. Figure 2C. An EEG carried out 23 days after admission showed findings in keeping with a diffuse encephalopathy with resolution of NCSE, but with some scattered spikes maximal on the right anterior temporal region. A significant improvement of the neurological state of the patient was obselved at that time. Vertical bar: 100 pV; Horizontal bar: 1 second; Low filter: 0.5; High filter: 30 Hz. 59 Downloaded from eeg.sagepub.com at GEORGIAN COURT UNIV on May 2, 2015 CLINICAL EEG and NEUROSCIENCE 02007 VOL. 38 NO. 1 the EEG, suggesting strongly that clinical symptoms had a genuine epileptic origin. Some speculation exists in relation to the pathophysiologic mechanism originating the NCSE in this case. Likely, the small hematoma localized in the left thalamus could be the epileptogenic source of the ipsilateral hemispheric continuous epileptiform discharges. However, an intrinsic epileptogenicity associated with the intraventricular hemorrhage per se, or acute hydrocephalus through disruption of cortico-subcortical pathways, may not be completely ruled out. Thus, it is wellknown that the existence of seizures and pathological EEG features in neonates with severe intraventricular hemorrhage are considered markers of brain injury. Our patient had also a previous history of an ipsilateral middle cerebral artery territory infarction, which could have predisposed the occurrence of seizures from left hemispheric origin. Prolonged localization-related (partial) NCSE is a harmless epileptic condition, which may cause, particularly in the setting of acute brain disorders, permanent brain damage.4-6 Therefore, an early diagnosis and rapid treatment will avoid additional deficits. Although the prognosis of our patient was more favorable than described by Dennis et aL,3 the clinical improvement was markedly slow and neurological outcome poor. Unfortunately, it is not possible to perform continuous EEG monitoring in critically ill patients with altered mental status in our hospital. However, we are aware that this rapidly expanding electrophysiologic technique is the method of choice for evaluating subjects with cerebral damage and unexplained persistent confusion or coma.7 To summarize, NCSE is a possible severe neurological complication in older patients suffering from intraventricular hemorrhage. Since an unexplained deterioration of consciousness level may be the sole clinical sign of NCSE in these subjects, a high level of suspicion and an urgent EEG will be the cornerstone of an early and accurate diagnosis. REFERENCES 1. 2. 3. 4. Fernandez-Torre JL, Diaz-Castroverde AG. Non-convulsive status epilepticus in elderly individuals: report of four representative cases. Age Ageing 2004; 33: 78-81, Begemann M, Rowan AJ, Tuhrim S. Treatment of refractory complex-partial status epilepticus with propofol: case report. 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