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Background: The co-occurrence of Rathke cleft cysts (RCCs) and meningiomas in the sellar and parasellar regions represents an exceedingly rare clinical entity. Achieving maximal resection through a single operative approach while minimizing adverse events is challenging, often necessitating multiple surgical approaches, as suggested by previous reports., Observations: The authors report the case of a 49-year-old female with a history of kidney transplant who presented with headaches and was diagnosed with coexisting RCC and meningioma in the sellar and planum sphenoidale regions, respectively. Given the prolonged, refractory nature of her symptoms and based on her treatment preferences, a two-stage surgical approach was planned. This involved an endoscopic transnasal transsphenoidal approach followed by a right craniotomy to achieve maximal tumor resection while minimizing potential complications. No residual disease or tumor remnants were present at the 6-month follow-up. The pituitary gland was preserved, and the patient's preoperative symptoms had fully resolved., Lessons: The preoperative diagnosis of concurrent skull base tumors is essential for effective management planning and determining the optimal surgical approach. The proximity of these tumors to critical neurovascular structures necessitates meticulous surgical planning to minimize adverse effects while ensuring maximal tumor resection. https://thejns.org/doi/10.3171/CASE24551.

Neuroinflammation is potentiated by early degeneration of the locus coeruleus noradrenergic pathway (LC-NE) commonly seen in aging-related neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In animal models, lipopolysaccharide (LPS) induces strong peripheral immune responses that can cause cognitive changes secondary to neuroinflammation. The influence of the peripheral immune response on cognition might be exacerbated by LC-NE degeneration, but this has not been well characterized previously. In this study, we investigated how systemic inflammation affects neuroinflammation and cognition in aged rats that have had either normal or damaged LC-NE transmitter systems. Rats were first exposed to the selective noradrenergic (NE) neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) to induce degeneration of central NE pathways. Two weeks later, the rats received a low dose of LPS. This resulted in 3 treatment groups (Control, LPS-, and DSP4+LPS-treated rats) studied at 4 hours (short-term subgroup) and 7 days (long-term subgroup) following the LPS injection. DSP4+LPS-treated rats exhibited increased serum levels of several pro-inflammatory cytokines, increased astroglial and microglial activation in the hippocampus, and poorer performance in the novel object recognition task (NORT) compared to controls and LPS-treated rats. Additionally, serum and brain tissue levels of brain-derived neurotrophic factor (BDNF) were modulated over time in the DSP4+LPS group compared to the other two groups. Specifically, DSP4+LPS-treated rats in the short-term subgroup had lower hippocampal BDNF levels (~25%) than controls and LPS-treated rats, which negatively correlated with hippocampal astrogliosis and positively correlated with hippocampal IL-1β levels. Serum and hippocampal BDNF levels in the DSP4+LPS-treated rats in the long-term subgroup returned to levels similar to the control group. These results show that systemic inflammation in LC-NE-lesioned aged rats promotes an exacerbated systemic and central inflammatory response compared to LC-NE-intact rats and alters BDNF levels, indicating the important role of this neurotransmitter system in response to neuroinflammation.

Behavioral, neuropsychological, and neuroimaging evidence has suggested that categories can often be learned via either an explicit rule-based (RB) mechanism critically dependent on medial temporal and prefrontal brain regions, or via an implicit information-integration (II) mechanism relying on the basal ganglia. In this study, participants viewed sine-wave gratings (Gabor patches) that varied on two dimensions and learned to categorize them via trial-by-trial feedback. Two different stimulus distributions were used; one was intended to encourage an explicit RB process and the other an implicit II process. We monitored brain activity with scalp electroencephalography (EEG) while each participant: (1) passively observed stimuli represented of both distributions; (2) categorized stimuli from one distribution, and, 1 week later; (3) categorized stimuli from the other distribution. Categorization accuracy was similar for the two distributions. Subtractions of Event-Related Potentials (ERPs) for correct and incorrect trials were used to identify neural differences in RB and II categorization processes. We identified an occipital brain potential that was differentially modulated by categorization condition accuracy at an early latency (150-250 ms), likely reflecting the degree of holistic processing. A stimulus-locked Late Positive Complex (LPC) associated with explicit memory updating was modulated by accuracy in the RB, but not the II task. Likewise, a feedback-locked P300 ERP associated with expectancy was correlated with performance only in the RB, but not the II condition. These results provide additional evidence for distinct brain mechanisms supporting RB vs. implicit II category learning and use.