Arielle Crespel

Background: Triphasic waves (TWs), now termed generalized periodic discharges with triphasic morphology, may be mistaken for nonconvulsive status epilepticus (NCSE), particularly in critically ill patients. Changes in vigilance over time can help distinguish encephalopathic patterns from ictal activity. Case Presentation: A 69‐year‐old woman with breast cancer and leptomeningeal metastases developed progressive mutism and impaired consciousness. Cerebrospinal fluid analysis showed atypical cells and markedly elevated protein, while brain MRI demonstrated bilateral sulcal hyperintensities, most prominent in the posterior regions. An EEG performed 1 week after bevacizumab and paclitaxel were discontinued showed only mild background slowing without epileptiform discharges. A repeat EEG 1 week later showed nearly continuous TWs. The discharges disappeared during spontaneous sleep and recurred periodically, consistent with a cyclic alternating pattern of encephalopathy during sleep (CAPE). In the absence of significant metabolic and toxic derangements, these features favored an encephalopathic rather than ictal pattern. Given the advanced disease and poor prognosis, care remained supportive and palliative. Conclusion: This case highlights the importance of interpreting TWs within their clinical context and in relation to the state of vigilance. Their disappearance at sleep onset, with periodic recurrence during sleep producing a CAPE, supports an encephalopathic rather than ictal interpretation, helping to avoid misdiagnosis of NCSE and unnecessary administration of antiseizure medications.

Background Some studies have indicated that deep brain stimulation (DBS) of the thalamus targeting the centromedian nucleus (CMN) may reduce the frequency of seizures in Lennox–Gastaut syndrome (LGS), albeit with incomplete results. DBS targeting of the anterior nucleus of the thalamus (ANT) has demonstrated efficacy in refractory focal epilepsies and is currently FDA-approved for adult treatment. Additionally, the ANT nucleus is morphologically larger than the CMN, facilitating precise targeting and with potentially higher implantation success rates. Patients and methods Three adult patients (one male, two females), all experiencing daily seizures that included episodes of falling, underwent ANT-DBS, one at the age of 22 years, and two at 28 years. Two electrodes were implanted under general anesthesia, using intra-operative MRI and a micro-endoscope. The clinical data regarding seizure frequency and severity, as well as cognitive function and adaptive behaviors, were collected prospectively. Results One patient achieved seizure freedom 3 years post-surgery. This was confirmed by a current follow-up of 8 years after DBS, which represents a total seizure-free period of 5 years. Two patients were followed for 18 and 24 months, respectively; both achieved a seizure reduction of over 75%. All three patients demonstrated considerable improvements in adaptive behavior. No side effects (in particular psychiatric disorders) were observed with the applied therapeutic stimulation parameters. Conclusion This series showed promising results in adult patients with LGS for both improvement of seizure frequency and adaptive behavior. The current use of pediatric thalamic stimulation is limited but the benefits shown in adults present promising prospects for its future application.

Nonconvulsive status epilepticus (NCSE) was initially described in patients with typical and atypical absence status epilepticus (ASE) characterized by states of confusion varying in severity and in focal epilepsies with or without alteration of consciousness. Continuous EEG monitoring of critically ill patients has further refined the classification of NCSE into two main categories: with coma and without coma. Hypnotic, soporific or somniferous epileptic seizures do not exist. On the contrary, patients usually awaken when seizures occur during sleep, and their eyes remain open during ASE. Excessive sleepiness and coma alone are not ictal signs but are observed in the postictal phase of convulsive seizures. On the other hand, excessive sleepiness evolving into coma is a cardinal sign of metabolic/toxic encephalopathies with triphasic waves evolving to burst suppression patterns and ultimately to cerebral inactivity and death. NCSE alone does not directly cause coma. Comas are related to the underlying etiology, patient age and comorbidities, as well as the administration of intravenous sedative drugs to control epileptic seizures. In cases of severe brain injury, NCSE can explain the failure to awaken after the withdrawal of anesthetics and is only an aggravating factor of the neurological condition. In typical ASE, which is characterized by sustained, rhythmic, bilateral, synchronous and unreactive discharges with evolving spatiotemporal patterns (the best example of NCSE), there is no vigilance impairment. This contrasts with metabolic/toxic encephalopathies, which exhibit monomorphic generalized periodic discharges in which patients may become comatose and die. The extended concept of NCSE in comatose patients may lead to an inflated assessment of NCSE, implying a potentially worse prognosis compared to convulsive status epilepticus.