It has been observed that the serum of patients with epilepsy shows more reactivity against the carboxy or C terminal domain (21, 25C27). (5). Several etiologies have been described in addition to classic causes of EPC as well (vascular, neoplastic, systemic autoimmune) (6). A systematic review (5) described additional etiologies such as tick-borne encephalitis, unspecified encephalitis, brain trauma, multiple sclerosis, systemic etiologies, mitochondrial diseases, and metabolic disorders. Interestingly, in this review, all forms of epilepsy were described, including those with non-motor symptoms. An additional description of EPC is in current use, including patient’s auras. These are described as (AC) and include somatosensory, proprioceptive, visual, auditory, musical, olfactory, gustatory, epigastric/autonomic, anxiety, and dysmnesic episodes. Timeframe of symptoms is of essence, and as suggested by an European epilepsy study group (7), a subclassification aids in the diagnosis and workup; this impacts the prognosis as well (8). Roughly, the classification divides EPC into four subgroups: type 1, a single episode of EPC; type 2, chronic recurrent and non-progressive EPC; type 3, chronic persistent and non-progressive; and type 4, chronic progressive EPC (5). The following case depicts a young woman that had an epilepsy onset with AC, with chronic persistent and non-progressive EPC, misdiagnosed initially as a non-neurological entity and finally found to be an immune-mediated epilepsy. Case Description A right-handed 27-year-old female, 2nd year Internal Medicine resident had no relevant family history. In her past medical history, she had an event of right optic neuritis with amaurosis that resolved without sequelae 3 years before present medical history. At that time, she was treated with intravenous steroids and was followed up by a neurologist at her hometown. No further investigations or antimyelin oligodendrocyte glycoprotein (anti-MOG) antibodies testing were performed; the optic neuritis was a single self-limited event. She began 2 years ago with a sudden feeling of joy that lasted for 40s, followed by paresthesia in both inferior extremities with loss of awareness and manual automatisms with the right hand that ended with a tonic posture of the four extremities. Phenytoin (PHT) was initiated, with a diminished frequency of seizures, about once per week. One month later, during a flight, the patient experienced transient symptoms of inability to recognize faces (prosopagnosia) and incapacity to interpret words (she describes an event where she saw the word Mexico but read Comiex). Her symptoms were brief (about 1 min each) and occurred many times during that day. A diagnosis of non-motor was made with an electroencephalogram (EEG), oxcarbazepine (OXC) was initiated, PHT was discontinued, and patient became seizure free. Six months later, she developed hyponatremia due CCT239065 to OXC, and her antiepileptic treatment was again modified to levetiracetam (LEV). During her outpatient follow-up, she still presented with flashing lights in colors predominantly red, blue and green in her lower right visual field, prosopagnosia, and other visual disturbances including seeing her NDRG1 hand as if it were torn in half, finally followed by visual hallucinations characterized by hair invading the faces of people around her with an intense sense of fear. These always occurred in a stepwise manner, and the patient drew her seizures (Figure 1). Lacosamide (LCM) and topiramate (TPM) were added to her antiseizure (AS) treatment. Open in a separate window Figure 1 Patient’s drawing depicting seizure semiology. Numbers placed in the image depict the order of symptoms: (1) flashing colors in the lower right visual field, (2) prosopagnosia, (3) visual disturbance of hand tearing in half, and (4) hair invading people’s faces, fear. Isolated events that did not appear in an orderly fashion: *reading words with incapacity to interpret them; **eye version to the right. In the course of the following year, she was admitted in second-level care centers on four occasions for treatment and observation, with recurrent EPC as described. Due to the lack CCT239065 of improvement in her symptoms, suspicion arose of a diagnosis of a non-neurological entity such CCT239065 as psychogenic non-epileptic seizures (PNES); this was assumed to be secondary to stress.