井林 賢志

BACKGROUND: Chronic inflammation of the thorax, as in tuberculosis-related pyothorax, can cause secondary malignant lymphomas. However, primary malignant lymphoma of the central nervous system, specifically of the dura mater, developing after intracranial infection or inflammation has rarely been reported. Herein, the authors describe a case of primary dural lymphoma that developed secondary to subdural empyema, with an initial presentation mimicking a chronic subdural hematoma. OBSERVATIONS: A 51-year-old man had undergone single burr hole drainage for subdural empyema 2 years prior. The patient subsequently underwent multiple craniotomy and drainage procedures, with successful remission of the subdural empyema. He was subsequently referred to the authors' hospital approximately a year after his initial treatment because of a recollection of subdural fluid, which was suspected to be recurrent empyema. After another single burr hole drainage, which revealed only a subdural hematoma, a histopathological diagnosis of B-cell lymphoma of the dural/subdural membrane was made. Subsequent radiation therapy was completed, with good local control and no recurrence of the subdural hematoma confirmed at 2 months posttreatment. LESSONS: Intracranial lymphoma triggered by chronic inflammation is rare but should be considered a differential diagnosis in subdural hematomas for which the background pathology is unclear. https://thejns.org/doi/10.3171/CASE24153.

The efficacy of surgical treatment for drug-resistant epilepsy has been proven based on accumulated evidence, such as several randomized controlled trials. There are emerging treatment modalities, including less invasive surgical techniques and neuromodulation devices, which have also been proven to benefit patients by improving seizure control. A recent methodological shift from subdural electrocorticography recordings to stereo-encephalography recordings for intracranialelectroencephalography (iEEG) monitoring has also positively impacted clinical decision-making. Although some of these newer modalities are yet to be implemented in Japan, this article provides updated evidence and a summary of the currently available options for surgical treatment of patients with drug-resistant epilepsy. We hope that this summary will widen the treatment opportunities for patients with this highly impactful disease.

OBJECTIVE: Endovascular electroencephalography (evEEG) uses the cerebrovascular system to record electrical activity from adjacent neural structures. The safety, feasibility, and efficacy of using the Woven EndoBridge Aneurysm Embolization System (WEB) for evEEG has not been investigated. METHODS: Seventeen participants undergoing awake WEB endovascular treatment of unruptured cerebral aneurysms were included. After WEB deployment and before detachment, its distal deployment wire was connected to an EEG receiver, and participants performed a decision-making task for 10 minutes. WEB and scalp recordings were captured. RESULTS: All patients underwent successful embolization and evEEG with no complications. Event-related potentials were detected on scalp EEG in 9/17 (53%) patients. Of these 9 patients, a task-related low-gamma (30-70 Hz) response on WEB channels was captured in 8/9 (89%) cases. In these 8 patients, the WEB was deployed in 2 middle cerebral arteries, 3 anterior communicating arteries, the terminal internal carotid artery, and 2 basilar tip aneurysms. Electrocardiogram artifact on WEB channels was present in 12/17 cases. CONCLUSIONS: The WEB implanted within cerebral aneurysms of awake patients is capable of capturing task-specific brain electrical activities. Future studies are warranted to establish the efficacy of and support for evEEG as a tool for brain recording, brain stimulation, and brain-machine interface applications.

BACKGROUND: We previously found that vagus nerve stimulation (VNS) strengthened stimulus-evoked activity in the superficial layer of the sensory cortex but not in the deep layer, suggesting that VNS altered the balance between the feedforward (FF) and feedback (FB) pathways. Band-specific oscillatory activities in the cortex could serve as an index of the FF-FB balance, but whether VNS affects cortical oscillations along sensory pathways through neuromodulators remains unclear. HYPOTHESIS: VNS modulates the FF-FB balance through the cholinergic and noradrenergic systems, which modulate stimulus gain in the cortex. METHODS: We investigated the effects of VNS using electrocorticography in the auditory cortex of 34 Wistar rats under general anesthesia while presenting click stimuli. In the time-frequency analyses, the putative modulation of the FF and FB pathways was estimated using high- and low-frequency power. We assessed, using analysis of variance, how VNS modulates auditory-evoked activities and how the modulation changes with cholinergic and noradrenergic antagonists. RESULTS: VNS increased auditory cortical evoked potentials, consistent with results of our previous work. Furthermore, VNS increased auditory-evoked gamma and beta powers and decreased theta power. Local administration of cholinergic antagonists in the auditory cortex selectively disrupted the VNS-induced increase in gamma and beta power, while noradrenergic antagonists disrupted the decrease in theta power. CONCLUSIONS: VNS might strengthen the FF pathway through the cholinergic system and attenuate the FB pathway through the noradrenergic system in the auditory cortex. Cortical gain modulation through the VNS-induced neuromodulatory system provides new mechanistic insights into the effect of VNS on auditory processing.

Gamma oscillations are physiological phenomena that reflect perception and cognition, and involve parvalbumin-positive γ-aminobutyric acid-ergic interneuron function. The auditory steady-state response (ASSR) is the most robust index for gamma oscillations, and it is impaired in patients with neuropsychiatric disorders such as schizophrenia and autism. Although ASSR reduction is known to vary in terms of frequency and time, the neural mechanisms are poorly understood. We obtained high-density electrocorticography recordings from a wide area of the cortex in 8 patients with refractory epilepsy. In an ASSR paradigm, click sounds were presented at frequencies of 20, 30, 40, 60, 80, 120, and 160 Hz. We performed time-frequency analyses and analyzed intertrial coherence, event-related spectral perturbation, and high-gamma oscillations. We demonstrate that the ASSR is globally distributed among the temporal, parietal, and frontal cortices. The ASSR was composed of time-dependent neural subcircuits differing in frequency tuning. Importantly, the frequency tuning characteristics of the late-latency ASSR varied between the temporal/frontal and parietal cortex, suggestive of differentiation along parallel auditory pathways. This large-scale survey of the cortical ASSR could serve as a foundation for future studies of the ASSR in patients with neuropsychiatric disorders.