Our growing understanding of the brain basis of mind has seen an interest in evolutionarily ancient structures, most notably the brainstem. This paper offers an interesting example of this underexplored territory, by considering the mesencephalic component of the trigeminal nucleus. This largely uncelebrated brainstem structure is central to control of the jaw, and for the foundational acts of eating, oral exploration, and biting. This paper explores the interesting anatomy of the mesencephalic trigeminal: unique in the nervous system as a centrally located sensory ganglion, which combines sensory and motor function for the jaw. An unexplored aspect of its anatomy is that the mesencephalic component of the nucleus lies directly adjacent to the brain's core system for the experience of emotion, the peri-acqueductal gray (PAG). The data suggest a role for the jaw, and more broadly the oral cavity, in relation to a range of feeling states, from pleasure to aggression. This is supported by behavioural and classic neuropsychological findings, such as the Klüver-Bucy syndrome. However, the proposal is not well-supported by findings of direct connections between the trigeminal nucleus and the PAG. While these contrasting findings present a conundrum, there may be a role for non-synaptic signalling, of the sort increasingly understood to be important for interoception and homeostasis.

The ability to override prepotent actions is critical to control impulses and adjust behavior depending on goals and contextual needs. In this study, we investigate the inhibitory control abilities of a patient diagnosed with Klüver-Bucy Syndrome following a left temporal resection. The patient presented with disruptive hypersexuality symptoms akin to compulsions, leading to the inability to control and suppress inappropriate actions. The patient was recruited for the current research study while undergoing intracranial monitoring for epilepsy, to investigate the cognitive and neural processes underlying the patient's inhibitory control symptoms. We formulated the hypothesis that an inhibitory control deficit emerges in response to provocative triggers, and we designed a personalized paradigm pairing arousing images with a classic inhibitory control task. We not only confirmed disrupted performance following exposure to triggering, provocative material, but we also leveraged the simultaneously recorded neural data to identify a biomarker reflecting inhibitory control failures. Next, we repeated the experimental paradigm during and after personalized neuromodulation via direct high-frequency stimulation of the right inferior frontal cortex. The patient displayed a marked improvement in his behavior during neuromodulation, mirrored by changes in neural activity, spanning spectral features, event-related potentials and functional connectivity. Altogether, our study revealed that the patient's symptoms were not due to a global inhibition deficit, but to a specific control issue triggered by exposure to provocative material. Overall, our work showcases a feasible, effective approach towards data-driven personalized neuromodulation, which could be leveraged to mitigate specific inhibitory control deficits and potentially other symptoms of executive dysfunction.

The ability to override prepotent actions is critical to control impulses and adjust behavior depending on goals and contextual needs. In this study, we investigate the inhibitory control abilities of a patient diagnosed with Klüver-Bucy Syndrome following a left temporal resection. The patient presented with disruptive hypersexuality symptoms akin to compulsions, leading to the inability to control and suppress inappropriate actions. The patient was recruited for the current research study while undergoing intracranial monitoring for epilepsy, to investigate the cognitive and neural processes underlying the patient's inhibitory control symptoms. We formulated the hypothesis that a reactive inhibitory control deficit emerges in response to provocative triggers, and we designed a personalized paradigm pairing arousing images with a classic inhibitory control task. We not only confirmed disrupted performance following exposure to triggering, provocative material, but we also leveraged the simultaneously recorded neural data to identify a biomarker reflecting inhibitory control failures. Next, we repeated the experimental paradigm during and after personalized neuromodulation via direct high-frequency stimulation of the right inferior frontal cortex. The patient displayed a marked improvement in his behavior during neuromodulation, mirrored by changes in neural activity, spanning spectral features, event-related potentials and functional connectivity. Altogether, our study revealed that the patient's symptoms were not due to a global inhibition deficit, but to a specific control issue triggered by exposure to provocative material. Overall, our work showcases a feasible, effective approach towards data-driven personalized neuromodulation, which could be leveraged to mitigate specific inhibitory control deficits and potentially other symptoms of executive dysfunction.

Herpes simplex virus type 1 (HSV-1) is the leading cause of sporadic fatal encephalitis, typically presenting with temporal lobe abnormalities. It usually manifests as fever, headache, seizure, altered sensorium, and focal neurological deficit. Hyperphagia as a sole complication of HSV-1 encephalitis is a rare presentation. We report a 25-year-old woman with a 10-day history of fever, headache, and vomiting, progressing to confusion, visual hallucinations, and drowsiness. She had a history of meningoencephalitis at age 8 and well-controlled focal seizures. Upon admission, magnetic resonance imaging showed T2/fluid-attenuated inversion recovery hyperintensities in both temporal lobes with diffusion restriction. Electroencephalography indicated generalized slowing and cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis with elevated protein levels. Viral encephalitis was suspected, and intravenous acyclovir was initiated. CSF polymerase chain reaction (PCR) confirmed HSV-1. With treatment, she gradually improved but developed hyperphagia during hospital stay. Hyperphagia, a rare complication of herpes simplex virus (HSV) encephalitis, is a part of Kluver-Bucy syndrome typically associated with other cognitive dysfunctions. Despite early treatment, voracious appetite remained partially, emphasizing the need for rapid diagnosis and treatment to prevent severe outcomes. The case highlights that acute onset hyperphagia can be an isolated complication of HSV encephalitis, requiring tailored therapeutic strategies. Follow-up showed significant weight gain with partial improvement in hyperphagia, underscoring the challenges in managing this condition.

Klüver-Bucy syndrome (KBS) is a rare neuropsychiatric disorder, and it can be associated with a variety of neurological disorders. It is characterized by visual agnosia, placidity, hyperorality, hypersexuality, dietary changes, amnesia, and hypermetamorphosis. KBS is mainly a clinical diagnosis, with at least three symptoms sufficient to diagnose the condition. The case describes a 49-year-old Filipino woman with a history of hypertension who presented with symptoms strongly suggesting KBS following subarachnoid hemorrhage, including behaviors such as hyperorality, hypermobility, placidity, hypermetamorphosis, and hypersexuality along with memory disturbance. She was managed as a case of brief psychotic disorder initially with olanzapine, then on the second presentation as a case of delirium with risperidone. Among many symptoms of KBS, only three symptoms are required for the diagnosis clinically. Numerous neurological conditions can cause KBS. Symptomatic treatment is the mainstream treatment currently for KBS.[3] While different differential diagnoses are present, neurologists, psychiatrists, neurosurgeons, and radiologists should collaborate and be vigilant for the diagnosis of KBS, especially with the presence of one of its etiologies.