Months after apparent resolution of their encephalitides, both underwent neuropsychological testing, which demonstrated persistent cognitive deficits, primarily in the domains of memory and executive function, for cases 1 and 2, respectively. population [1C3]. 6% constitute amnestic MCI with a high likelihood to advance to Alzheimer’s disease [2]. MCI is a heterogeneous entity and includes some patients on an indolent path to a nonneurodegenerative and potentially treatable encephalopathy, as well as those with lingering deficits from such a disease process presenting in the recovery phase. If the illness evolves rapidly, a variant of AD may still be considered; however, the presence of atypical signs should raise suspicion for an infectious, paraneoplastic, or autoimmune etiology. 51% of ALE patients may be seronegative [4]. Here we report two cases of antivoltage gated potassium channel complex (VGKCC) Tenacissoside G encephalitis that initially presented as MCI with atypical features. Both had early nonconvulsive spells ascribed to limbic or dystonic seizures. After remission, both were left with MCI corresponding to amnestic or dysexecutive syndromes. 2. Case 1 A 71-year-old woman first presented to us for progressive memory complaints over one year in the context of the loss of a loved one and stress in the family. Past medical history included anxiety, lumbago, psoriasis, and multiple drug sensitivities including to a steroid injection. She had a high school Tenacissoside G education and worked as a telecommunication operator until retiring at age 65. Initially she would become confused with directions, missed appointments, and had occasional word finding difficulty but then had increasing problems with calculations and penmanship. She had forgotten her daughter’s recent pregnancy. She began to have infrequent incidents consisting of rising paresthesiae, during which she was seen to tense her body, clench her teeth, become flushed, and look afraid. They resembled panic attacks. These events were associated with amnesia for the event and were followed by confusion. She had also been having myoclonic jerks, though these had subsided by the time of her initial presentation. A first neurologist started her on levetiracetam for suspected seizures, but this was discontinued after causing delirium. A second neurologist recorded a Mini Mental Status Score (MMSE) of 29/30, a Montreal Cognitive Assessment (MOCA) of 24 (1/5 verbal recall), diagnosed depression/anxiety, and initiated donepezil. This too was discontinued soon thereafter for ineffectiveness. On our initial evaluation, her Clinical Dementia Rating (CDR) was 0.5 and MMSE was 28 (1/3 delayed verbal recall). Formal neuropsychological testing showed a largely intact cognitive profile with the exception of inefficient learning and impaired recall of verbal information. The Dementia Rating Scale (DRS) score was 139. The Beck Inventory was 8, Tenacissoside G not suggestive of active depression. MRI brain showed moderate global cerebral atrophy, though not specifically in the mesial temporal lobes, and small vessel ischemic changes. Fluorodeoxyglucose positron emission tomography (FDG PET) of the brain showed no areas of abnormal metabolism. TRA1 She was diagnosed with MCI, amnestic type, and started on galantamine. There was clinical stabilization. A little over a year from her presentation, she developed increasing anxiety, new auditory hallucinations, sleep disturbance, compulsive behaviors, and attacks resembling panic. Escitalopram and alprazolam were prescribed, subsequently changed to sertraline and lorazepam, and quetiapine was added. Memory complaints resurfaced: an MMSE was 27 (0/3 recall). Galantamine was discontinued due to diarrhea, cramps, and weight loss, Tenacissoside G and she was started on rivastigmine, to which memantine was added. Over the next 3 months increasing anxiety led to a brief psychiatric Tenacissoside G evaluation in the ED. Mild hyponatremia (131?meq/L) was noted. A routine electroencephalogram (EEG) around this time showed bitemporal sharp waves. By 18 months after presentation, mental status had sharply deteriorated with a larger number of stereotyped panic-fear attacks. 48-hour ambulatory EEG showed interictal periodic sharp and slow wave discharges in bilateral temporal lobes, and bitemporal electrographic seizures correlated to these clinical events, hereafter referred to as seizures (Figure 1). She was promptly started on phenytoin and lamotrigine and admitted to the hospital. Open in a separate window Figure 1 Sample 24?hr video EEG tracings from case 1. Push button activation processes and video recorded panic/fear attacks corresponding to left (a) alternating with right (b) temporal lobe activations and electrographic seizures. (c) The interictal record showing periodic left anterior sharp wave epileptiform discharges. 1?Hz time.