Epilepsia, 44(8):1122–1126, 2003 Blackwell Publishing, Inc. C  2003 International League Against Epilepsy Confirmation of Nonconvulsive Limbic Status Epilepticus with the Sodium Amytal Test ∗ Jorge G. Burneo, ∗ Robert C. Knowlton, †Camilo Gomez, ∗ Roy Martin, and ∗ Ruben I. Kuzniecky ∗ Epilepsy Center and †Comprehensive Stroke Center, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, U.S.A. Summary: Is it a seizure? This question can be difficult for a clinician to answer, and it may be more critical if the possible seizure lasts >30 min. Long-duration questionable seizure ac- tivity changes the question to, “Is it status epilepticus?” Status epilepticus (SE) can be divided into convulsive and non- convulsive types. Convulsive SE is the most easily recognized, whereas nonconvulsive SE is more clinically variable and con- troversial. The term nonconvulsive SE is more often applied to patients who are severely obtunded or comatose with minimal or no motor movements, or in a stupor of altered conscious- ness reflecting generalized ictal activity. Nonconvulsive SE also can be caused by focal seizure activity, sometimes restricted to deep small volumes of brain in which scalp EEG may not be diagnostic. We present the case of a patient who had dominant limbic hip- pocampal SE, but in whom the diagnosis could not be confirmed until a modified novel use of the sodium amytal test was per- formed. Key Words: Epilepsy. Seizures. Status Epilepticus. Amobarbital. CASE REPORT A 19-year-old left-handed woman was transferred to the University of Alabama at Birmingham (UAB) Epilepsy Center with a 2-week history of 15-min events (one to two per week), characterized by numbness of the right up- per extremity occasionally associated with dysarthria and fear. An initial outside evaluation included normal mag- netic resonance imaging (MRI). Because of prolonged stereotypical events, the patient was taken to a local emer- gency room. An initial EEG revealed “questionable left temporal sharp activity.” She was admitted to a local hos- pital. During hospitalization the patient had what was described as a generalized tonic–clonic seizure and was started on phenytoin (PHT). Cerebrospinal fluid (CSF) analysis, MRI, MR angiography (MRA), and subsequent EEG were normal. Because of an increment in the fre- quency of the events of fear, the patient also was given valproic acid (VPA) and was transferred to UAB. Her medical history was remarkable for an episode of abor- tion without complication 2 months before the onset of symptoms. She did not have any history of perinatal dis- ease, febrile seizures, head trauma, or central nervous sys- Accepted April 20, 2003. Address correspondence and reprint requests to R.C. Knowlton, M.D. at UAB-Epilepsy Center, CIRC-312, 1719 6th Avenue South, Birming- ham, AL 35243, U.S.A. E-mail: knowlton@uab.edu tem infections. She had no family history of seizures or epilepsy. Her social history was unremarkable. On ad- mission, she was found with mild dysarthria, hesitant speech, but no clear aphasia. Mild end-gaze nystagmus and ataxia were present. The rest of the examination was normal. She was initially admitted to the video-EEG unit, and VPA was discontinued (VPA level, 106μ/ml). Initial in- terictal (day 1) recordings revealed the presence of rhyth- mic delta slowing over the left hemisphere (Fig. 1). Ictal recordings revealed episodes of fear, unresponsiveness, restlessness, and screaming, without EEG changes. On day 2, an MRI study demonstrated signal changes con- fined to the hippocampus (Fig. 2). CSF analysis was un- remarkable, including polymerase chain reaction (PCR) for herpesvirus. Oxcarbazepine (OXC) was added to her regimen already containing PHT (PHT level, 19.5μ/ml). At day 4, the patient remained clinically unchanged, al- though the EEG showed improvement, with a relative ab- sence of left hemispheric slowing. An “interictal” single- photon emission computed tomography (SPECT) with 31 mCi was done, revealing hyperperfusion of the entire left hemisphere, more prominent in the neocortical left temporal region (Fig. 3). The patient was given 1–2 mg of lorazepam (LZP), i.v., around the clock for 24 h. Initially some ques- tionable improvement was followed by intermittent but 1122