Dear Editor, We thank Primavera and Audenino for their interest in our case report [1, 2]; in fact, they raise three intriguing issues which deserve some comments. First, we agree with them that our patient experienced one episode of non-convulsive status epilepticus (NCSE); however, this should not be viewed as an alternative diagnosis with respect to metabolic encephalopathy, as Primavera and Audenino seem to imply. In fact, both phenomena may be present in the same patient, especially in case of hepatic encephalopathy [3], with NCSE representing one of its more severe manifestations [4]. Increased ammonia levels may reduce the critical activity threshold in brain, triggering abnormal electric bursts, and possibly resulting in a SE. Consistently, a large spectrum of EEG patterns may be observed in these cases, including TWs with epileptiform characteristics, as Primavera and Audenino wisely remark as a second point in their letter. Thus, we proceeded exactly in the direction suggested by these authors, extensively searching for factors responsible for mental status impairment, and identifying it in a rapidly cycling hyperammoniemic state due to the previous procedure of ureterosigmoidostomy, performed several years before. These are the reasons why we proposed a causal diagnosis of hyatrogenic hyperammoniemic encephalopathy as the solution to this quiz case, whose clinical expression, during the period of hospitalization, cycled from a minimal encephalopathy, to a progressive depression of consciousness, to a full NCSE. Still, a differential diagnosis between these two entities remains of value, especially when thinking to therapeutic options, as Primavera and Audenino correctly raise as their last comment. A causal therapy of the underlying condition may be sufficient for metabolic encephalopathy per se; additional symptomatic treatment is mandatory when metabolic encephalopathy is complicated by SE. Benzodiazepine administration, such as lorazepam, is a well-established firstline therapy, but our patient did not respond to it. For subsequent steps, there are many reasonable options, including intravenous phenytoin, valproate, midazolam, propofol, and barbiturates. Choice depends also on the type of NCSE which includes complex partial (or focal) SE, absence SE, and SE in comatose patients [5]. In particular, treatment algorithms for NCSE in a comatose patient with potentially good prognosis, as it was our case, suggest either IV phenytoin or valproate [6]. Valproate is usually preferred, due to its superior tolerability and ease of use. However, the hyperammoniemic state of our patient represented a contraindication to valproate, given the possibility that this drug might further worsen her metabolic derangement, even in the presence of normal liver-associated enzymes [7, 8]. Thus, we resorted to IV phenytoin, with ECG and blood pressure monitoring, which proved to be safe and effective.