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ObjectiveThis study aimed to investigate the roles of neurotrophic factors (NTFs), monoamine neurotransmitters, and inflammatory processes in the pathophysiology of the comorbidity of epilepsy and depression.MethodsA retrospective analysis was conducted with 57 epilepsy patients (PWE), 50 patients with epilepsy and comorbid depression (PWECD), and 47 healthy controls (HC) admitted between June 2020 and June 2024. Serum levels of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), 5-hydroxytryptamine (5-HT), norepinephrine (NE), dopamine (DA), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were measured using enzyme-linked immunosorbent assay (ELISA). Additionally, BDNF and GDNF levels in cerebrospinal fluid (CSF) samples were analyzed from selected patients in the PWE and PWECD groups.ResultsSerum BDNF levels were significantly lower in both PWE and PWECD groups compared to HC, while no differences between the former two groups. GDNF levels were lower in PWECD compared to HC, but not between PWE and HC. Serum 5-HT was significantly reduced in PWECD compared to both HC and PWE groups. No significant differences were observed in serum DA, NE, and IL-6 levels across the groups. Serum IL-1β levels were elevated in the PWECD group compared to the HC group. The Self-Rating Depression Scale (SDS) score negatively correlated with serum 5-HT and GDNF levels. In terms of predictive ability, serum BDNF demonstrated higher accuracy for the diagnosis of epilepsy [area under the curve, AUC = 0.701, 95% confidence intervals (95% CI) 0.601 ~ 0.801], while serum 5-HT was the best marker for predicting the development of depression in epilepsy patients (AUC = 0.727, 95% CI 0.632 ~ 0.821). No significant correlation was found between serum and CSF BDNF levels within the same subject (r = 0.155; p = 0.221; Spearman correlation), and CSF GDNF levels were too low to be clinically informative.ConclusionThe findings suggest the involvement of NTFs, monoamine neurotransmitters, and inflammatory processes in the pathogenesis of epilepsy and depression. Decreased serum BDNF levels correlate with epilepsy but not necessarily with comorbid depression, while serum GDNF and 5-HT show potential clinical value in diagnosing this comorbidity. However, the deficient levels of NTFs in CSF suggest a need for more sensitive detection methods.

Abstract Background Painful ophthalmoplegia can be caused by various etiologies, and broad differential diagnosis is needed. Carotid-cavernous fistula (CCF) is a rare cause of painful ophthalmoplegia, and early diagnosis is quite difficult. Case presentation Here, we present a case of paroxysmal painful ophthalmoplegia caused by CCF. The episodic symptoms were nonstereotypical and lasted minutes to hours. Magnetic resonance imaging (MRI) and computed tomography angiography (CTA) results were normal, which confounded efforts to determine a diagnosis. Subsequently, digital subtraction angiography (DSA) revealed a posterior-draining CCF. The CCF was treated at an early stage without residual symptoms. Conclusions We propose that symptoms could be relapsing or remitting during an early stage of CCF and that posterior-draining CCF is prone to misdiagnosis due to atypical manifestations. Normal CTA results cannot exclude carotid-cavernous fistula, and DSA should be performed once CCF is suspected.

Purpose: Focal cortical dysplasia (FCD) is a major cause of drug-resistant epilepsy; however the underlying epileptogenic mechanisms of FCD metabolism in epilepsy patients remain unclear. The aim of this study is to detect alterations of γ-aminobutyric acid (GABA), glutathione (GSH), and the composite of glutamate and glutamine (Glx) in MRI-typical and neuropathologically confirmed FCD-associated epilepsy using Hadamard Encoding and Reconstruction of Mega-Edited Spectroscopy (HERMES). Materials and methods: Fourteen epileptic patients suspected to be caused by FCD and 14 healthy controls were enrolled prospectively in this study; all subjects underwent a 3 T MRI scan, including 3D T1 weighted imaging and HERMES. The GABA signal detected by HERMES also contains signals from macromolecules and homocarnosine, so it is referred as GABA+. Signals of GABA+, GSH and Glx detected by HERMES from tumor foci, contralateral cerebral regions, and healthy controls were quantified using Gannet. Fitting errors and signal to noise ratios (SNRs) of GABA + signals were also recorded. Differences of GABA+, GSH, Glx, fitting error and SNR of GABA + among three groups were analyzed using linear mixed effects models. Results: Twelve FCD-associated epilepsy patients (7 females, aged 21.9 ± 9.3 years) and 12 matched healthy controls (7 females, aged 22.8 ± 9.8 years) were finally enrolled in this study. ANOVA results indicated that GABA levels were significantly increased in FCD foci compared with contralateral regions (p = 0.008) and with healthy controls (p = 0.003), while no difference was found in GSH and Glx levels. No difference of fitting errors or SNR of GABA + was found among FCD foci, contralateral regions and healthy controls. Conclusions: Increased GABA levels were found in FCD foci that indicated GABA may play a central role in the pathophysiology of FCD patients with epilepsy.