OBJECTIVE:Although bidirectional interactions between obstructive sleep apnea (OSA) and epilepsy have long been recognized, the effects of OSA on interictal epileptiform discharges (IEDs) remain unclear. This study examined how respiratory events (RE) modulate IED activity across sleep stages, sleep cycles, and epilepsy localizations in patients with focal epilepsy using combined video-electroencephalography (VEEG) and polysomnography (PSG). METHODS:Combined VEEG-PSG was performed in 300 consecutive patients, of whom 52 with coexisting focal epilepsy and OSA were included in the analysis. IEDs were visually identified and quantified during apneic, hypopneic, and nonrespiratory periods across wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. Perievent analyses were performed to evaluate IED rate before, during, and after RE. RESULTS:The IED rate during sleep with RE was higher than during wakefulness (p < .05) but lower than during sleep without RE (p < .05). Across all sleep stages, the IED rate was significantly higher during NREM sleep than REM sleep, regardless of RE presence (p < .001). Among respiratory events, hypopneas were associated with higher IED rate than apneas (p < .001), particularly during NREM sleep (p < .001). Perievent analysis demonstrated dynamic modulation of IED activity, with the lowest IED rate observed in the postevent period compared with during the event period. IED rate declined from the first to the last sleep cycle, with the most prominent reduction observed during hypopnea events. These effects were more pronounced among patients with temporal lobe epilepsy (TLE). No statistically significant difference was observed in the IED rate between RE with and without arousals. SIGNIFICANCE:RE are associated with dynamic perievent modulation of IED activity in patients with focal epilepsy, especially those with TLE, providing novel insight into the relationship between OSA and epilepsy.

BackgroundRetroclival subdural hematoma (rcSDH) secondary to spontaneous intracranial hypotension (SIH) is an exceedingly rare clinical entity, characterized by complex and incompletely understood pathophysiological mechanisms.CaseA 24-year-old female presented with acute and persistent orthostatic headache, with no history of trauma or anticoagulant therapy. Neuroimaging revealed subdural hematomas (SDH) located in the retroclival, infratentorial, and right frontal regions. It was hypothesized that veinous rupture, resulting from venous traction due to decreased cerebrospinal fluid (CSF) pressure, was the underlying mechanism. Following epidural blood patch (EBP) therapy, the patient exhibited marked symptomatic improvement and radiological resolution of hematomas on follow-up imaging.ConclusionRcSDH is considered an uncommon complication of SIH, potentially resulting from venous rupture in the retroclival subdural space due to reduced CSF pressure. SIH should be considered in cases of rcSDH. The treatment is typically focused on addressing the underlying etiology, with early diagnosis and timely intervention being essential for achieving favorable outcomes. In cases of severe brainstem compression, hematoma evacuation should be performed in conjunction with EBP.

Medication overuse headache (MOH) is a chronic secondary headache disorder that develops from excessive analgesic use. The prevalence of MOH is estimated 1–2% in the general population, reaching up to 50% among individuals with chronic headache. Although the pathophysiological mechanisms underlying MOH remain incompletely understood, neuroimaging studies have provided valuable insights into its developments. This review synthesizes current evidence demonstrating that MOH is associated with structural and functional alterations in two key neural systems: (1) the pain matrix involved in nociceptive processing, (2) the mesocorticolimbic reward circuitry implicated in addictive behaviors. Importantly, certain structural and functional changes show partial reversibility following medication withdrawal. Nevertheless, longitudinal studies with larger sample sizes are necessary to establish causal relationships between these neurobiological changes and the development/maintenance of MOH, which remains essential for developing targeted interventions.

Purpose Glymphatic function has not been explored in patients with focal cortical dysplasia (FCD)-related epilepsy. This study aimed to investigate the glymphatic system's involvement in these patients and to evaluate its correlation with response patterns to different antiseizure medications (ASMs) using diffusion tensor imaging along the perivascular space (DTI-ALPS). Methods Fifty-two patients with FCD-related epilepsy (10 with drug-responsive epilepsy and 42 with drug-resistant epilepsy) and 24 healthy controls (HC) were included. Bilateral DTI-ALPS index were calculated and compared among drug-responsive epilepsy, drug-resistant epilepsy, and HC groups. Additionally, we analyzed correlations between the DTI-ALPS index and clinical characteristics. Results Compared to HC, patients with FCD-related epilepsy showed significantly lower DTI-ALPS index in the bilateral hemispheres (p < 0.001). Notably, a significant decrease in the DTI-ALPS index was noted in the hemisphere ipsilateral to the epileptogenic foci, compared to the contralateral hemisphere (p < 0.001). Further analysis revealed that, in patients with drug-resistant epilepsy, the ipsilateral DTI-ALPS index was significantly lower than the contralateral DTI-ALPS index (p < 0.001), whereas patients with drug-responsive epilepsy did not show a significant difference between ipsilateral and contralateral DTI-ALPS index. No significant correlations were found between the DTI-ALPS index and clinical characteristics such as age and duration of epilepsy. Conclusion Our findings suggest a correlation between glymphatic system dysfunction and patients with FCD-related epilepsy, particularly in drug-resistant patients.

Malformations of cortical development (MCD) are a group of congenital brain malformation disorders commonly associated with pharmacoresistant epilepsy (PRE). While studies often focus on surgery outcomes, the pharmacological treatment is still imperative and the odyssey to PRE remains underexplored. We aim to investigate the influence of anti-seizure medications (ASMs) on the development of PRE in this specific patient population. We retrospectively included a cohort of epilepsy patients with MRI-confirmed MCD due to abnormal cell proliferation and apoptosis (group I, mainly FCD II), and abnormal neuronal migration (group II, mainly heterotopia, lissencephaly, and polymicrogyria) from March 2013 to June 2023. The clinical features of group I and group II were compared. Factors associated with PRE were analyzed. The time to development of PRE with different ASMs was assessed using Kaplan–Meier survival analysis. Of 259 enrolled patients with epilepsy and MRI-confirmed MCD (group I, n = 121; group II, n = 138), 73.4

AbstractObjectiveThe ictalHarmonicpattern (Hpattern), produced by the non-linear characteristics of EEG waveforms, may hold significant potential for localizing the epileptogenic zone (EZ) in focal epilepsy. However, further validation is needed to establish theHpattern’s effectiveness as a biomarker for measuring the EZ.MethodsWe retrospectively enrolled 131 patients diagnosed with drug-resistant focal epilepsy, all of whom had complete stereo-electroencephalographic (SEEG) data. From this cohort, we selected 85 patients for outcome analysis. We analyzed the morphological and time-frequency (TF) features of theHpattern using TF plots. A third quartile (Q3) threshold was applied to classify channels expressing either dominant (ChanneldHpattern) or non-dominantHpatterns (Channelnon-dHpattern). We then examined associations between the morphological features of theHpattern and patients’ clinical characteristics, as well as the correlations between the extent of channel removal and seizure outcomes.ResultsWe found no significant correlations between the morphological features of the ictalHpattern and clinical factors, including lesional MRI findings, epileptic onset patterns, epilepsy type, pathology, or surgical outcomes. The non-localizableHpattern appeared exclusively in patients with non-focal onset patterns. Notably, the proportion ofChanneldHpatternwas higher in the seizure-onset zone (SOZ) compared to the early propagation zone. The seizure-free group demonstrated significantly higher removal proportions ofChanneldHpattern, both within and outside the SOZ (p= 0.014;p= 0.036), with AUCs of 0.606 and 0.660, respectively, in a seizure freedom prediction model. Survival analysis confirmed that complete removal of these regions correlated with long-term seizure freedom (p= 0.008;p= 0.028). Further subgroup analysis showed a significant correlation in neocortical epilepsy (p= 0.0004;p= 0.011), but not in mesial temporal lobe epilepsy. Additionally, multivariate analysis identified the complete removal ofChanneldHpatternas the only independent predictor for seizure freedom (p= 0.022; OR 6.035, 95% CI 1.291-28.211).ConclusionsOur study supports the notion that the dominance of the ictalHpattern, regardless of its morphology, serves as a novel biomarker for the EZ in focal epilepsy. The non-linearity in EEG waveforms provides new insights into understanding ictal spreading propagation and offers potential improvements for surgical planning in neocortical epilepsy.

Background and purposeRelapsing polychondritis (RP) is a rare rheumatologic disorder that may affect the neurological system with various presentations. In this study, we present a case and summarize the clinical characteristics of RP-associated meningoencephalitis.Case presentationA 48-year-old man presented with first-ever seizures that were well controlled by valproate. Physical examination results were unremarkable, except for binaural deformation. The initial brain magnetic resonance imaging (MRI) without contrast and electroencephalogram (EEG) findings were normal. However, the patient subsequently developed recurrent fever, scleritis, headache, lethargy, and left arm paresis. Repeated brain MRI with contrast demonstrated increased enhancement of the pia mater and abnormal diffusion-weighted imaging (DWI) signals in the bilateral auricles. The cerebrospinal fluid (CSF) analysis showed 2 leukocytes/μL, 736.5 mg/L of protein, and no evidence of infectious disease or autoimmune encephalitis. Meningoencephalitis secondary to RP was considered. The patient's condition improved significantly and quickly with the administration of dexamethasone (10 mg per day). Oral methylprednisolone was continued, and the patient remained well without relapse during the 9-month follow-up period.ConclusionRP-associated meningoencephalitis is rare but fatal. Although symptoms vary, red or deformed ears remain the most common and suggestive features. Non-specific parenchymal changes and/or meningeal enhancement can be observed on brain MRI scans. CSF lymphocytic pleocytosis with mild protein elevation was observed in most patients.

Background: Isolated cortical vein thrombosis (ICVT), a rare type of cerebral venous thrombosis (CVT), is diagnostically challenging in some cases, and intracranial hypotension (IH) is known to cause CVT. Methods: In this study, we reviewed the clinical and imaging characteristics of ICVT in patients with IH caused by spinal cerebrospinal fluid leakage, based on a literature review and investigation of cases from our hospital. Results: Between January 1, 2007, and November 1, 2019, 735 patients were diagnosed with IH at our hospital; three patients developed ICVT (incidence similar to 0.4%, 3/735), and the literature review yielded an additional 23 cases. Therefore, 26 patients (mean age 35.9 +/- 11.4 years old) were included in this study. The most common symptoms were headache (100.0%, 26/26), focal neurological deficits (53.8%, 14/26), and seizure (34.6%, 9/26). The initial headache was orthostatic in 96.2% (25/26) of patients, and 38.5% (10/26) of patients reported a change in the headache pattern following diagnosis of ICVT. Neuroimaging findings associated with ICVT included the cord sign (61.5%, 16/26) and parenchymal brain lesions (46.2%, 12/26), such as intracerebral hemorrhage (30.8%, 8/26), hemorrhagic infarcts (11.5%, 3/26), and localized edema (11.5%, 3/26). The percentage of patients who received anticoagulation and epidural blood patch therapy was similar (69.2% [18/26] vs. 65.4% [17/26]), and most patients recovered completely (92.3%, 24/26). Conclusion: IH should be considered in the differential diagnosis in patients with ICVT. Knowledge of the relevant clinical and neuroimaging features is important to facilitate early diagnosis for favorable prognosis.

Although many neuroimaging studies have reported structural and functional abnormalities in the brains of patients with cognitive impairments following stroke, little is known about the pattern of such brain reorganization in poststroke dementia (PSD). The present study was aimed at investigating alterations in spontaneous brain activity and gray matter volume (GMV) in PSD patients. We collected T1-weighted and resting-state functional magnetic resonance imaging data from 20 PSD patients, 24 poststroke nondementia (PSND) patients, and 21 well-matched normal controls (NCs). We compared the differences among the groups in GMV and the fractional amplitude of low-frequency fluctuations (fALFF). Then, we evaluated the relationship between these brain measures and cognitive assessments and explored the possible distinguisher for PSD by receiver operating characteristic (ROC) curve analysis. PSD patients showed smaller GMV in the right superior temporal gyrus and lower fALFF values in the right inferior frontal gyrus than both PSND patients and NCs, but such differences were not observed between PSND patients and NCs. Moreover, GMV in the left medial prefrontal cortex showed a significant positive correlation with the Mini-Cog assessment in PSD patients, and GMV in the left CPL displayed the highest area under the ROC curve among all the features for classifying PSD versus PSND patients. Our findings suggest that PSD patients show dementia-specific structural and functional alteration patterns, which may help elucidate the pathophysiological mechanisms underlying PSD.

ObjectiveSpontaneous intracranial hypotension is a risk factor for cerebral venous thrombosis. The occurrence of cerebral venous thrombosis in patients with spontaneous intracranial hypotension raises difficult practical questions regarding the management of the 2 conditions. We reviewed our experience and the relevant literature to evaluate these related questions. MethodsWe retrospectively studied the medical records and imaging studies of patients with spontaneous intracranial hypotension at a tertiary center from January 2007 through January 2017. The main search strategy was a literature review of journal articles in PubMed (1966 to January 2017). ResultsAmong 374 patients with spontaneous intracranial hypotension, 4 were also diagnosed with cerebral venous thrombosis. A literature review yielded an additional 31 cases, including 21 men and 14 women with a mean age of 40.6 years. Of the 35 patients, 8 (22.8%) patients received anticoagulation therapy and epidural blood patch. Nineteen (54.3%) patients were given anticoagulant only. Seven (20%) patients were treated with epidural blood patch only. One (2.9%) patient did not receive epidural blood patch or anticoagulation therapy. There is no difference in terms of age, sex, diagnosis interval, association with other complications, and prognosis between the first 3 groups. Of the 19 patients who received anticoagulation therapy, 4 patients (21.1%) had intracranial hemorrhage or hematoma enlargement after anticoagulation, and one of these 4 patients died following further intracranial hemorrhage. Of the 8 patients who received both anticoagulation and epidural blood patch, 1 patient (12.5%, P=0.528) developed subdural hematoma after anticoagulation. Of the 5 cases had intracranial hemorrhage aggravation after anticoagulation, 4 were subdural hematoma occurrence or enlargement. ConclusionCerebral venous thrombosis is a rare but important complication of spontaneous intracranial hypotension. The primary focus of treatment should be the treatment of intracranial hypotension. It could be possible that anticoagulation might increase the risk of intracranial hemorrhage in patients with spontaneous intracranial hypotension, although a firm conclusion could not be drawn based on the limited number of patients currently available. The use of anticoagulation therapy should be prudent and should be monitored carefully if initiated.

A previously healthy 51-year-old man presented with a 1-week history of severe daily bilateral temporal headaches, associated with neck pain and nausea, with no fever or thunderclap-like onset. His symptoms were orthostatic, occurring within several minutes of assuming the upright position, and alleviated within 5 minutes after lying down. He had no history of lumbar puncture or head or spinal trauma. Cranial CT and CT angiography in a local hospital had normal results. Bed rest and hydration for 4 days failed to relieve his symptoms. One day prior to admission at our hospital, he began to experience headaches even when he was lying flat. Upon admission, his neurologic examination was unremarkable except for neck stiffness.

The purpose of this study was to examine whether a single episode of traumatic subarachnoid hemorrhage (tSAH) could cause superficial siderosis of the central nervous system (SS-CNS).This study was approved by the local ethics committee. Thirty-two patients with a history of a single episode of tSAH were enrolled in the study. An episode of tSAH was confirmed in patients based on a CT scan or a lumbar puncture, and a follow-up examination was conducted at least six weeks after the brain trauma. A follow-up MRI examination was performed, using enhanced gradient echo T2 star-weighted angiography (ESWAN) to detect hemosiderin deposition on the cortical surface. The extent to which hemosiderin deposition was associated with several clinical factors was investigated. Various degrees of hemosiderin deposition were detected in 31 of 32 (96.9%) single-episode tSAH patients. Analysis of contingency tables revealed an association between the regions of subarachnoid bleeding based on CT images and the regions of hemosiderin deposition based on ESWAN images (χ2 = 17.73, P<0.05). SS-CNS was determined to be a common consequence after a single episode of tSAH. The extent of hemosiderin deposition is closely correlated with the initial bleeding sites and bleeding volume.

Subdural haematoma (SDH) is a potentially life-threatening complication in patients with spontaneous intracranial hypotension (SIH). In serious cases, SIH patients who present with SDHs develop neurological deficits, a decreased level of consciousness, or cerebral herniation, and may even require an urgent neurosurgical drainage. Despite numerous publications on SDHs, few report its potential risk factors in patients with SIH. In this study, we retrospectively investigated 93 consecutive SIH patients and divided them into an SDH group (n = 25) and a non-SDH (NSDH) group (n = 68). The clinical and radiographic characteristics of these 93 patients were analyzed, and then univariate analysis and further multiple logistic regression analysis were performed to identify the potential risk factors for the development of SDHs. The univariate analysis showed that advanced age, male gender, longer clinical course, dural enhancement, and the venous distension sign were associated with the development of SDHs. However, multivariate analysis only included the latter three factors. Our study reveals important radiological manifestations for predicting the development of SDHs in patients with SIH.

BACKGROUND:Subdural hematoma (SDH) is a common complication of spontaneous intracranial hypotension (SIH). To date, the management of SDH caused by SIH remains controversial. In this paper, we reviewed the clinical course of SDH in patients with SIH, and discuss the underlying mechanism and attributing factors for rapid resolution of subdural hematomas after epidural blood patch (EBP) surgery.METHODS:We retrospectively reviewed a cohort of seventy-eight SIH patients diagnosed and treated with targeted EBP in our neurology center. Patients who received early CT/MRI follow-up after EBP operation were included.RESULTS:A series of four cases of SIH complicated with SDHs were evaluated. Early follow-up neuroimages of these patients revealed that SDHs could be partially or totally absorbed just two to four days after targeted epidural blood patch treatment.CONCLUSION:Targeted epidural blood patch can result in rapid hematoma regression and good recovery in some patients with a combination of SDH and SIH.

Syncope is a common presentation in the neurology clinic and emergency room. However, pulmonary embolism (PE) as a cause of syncope is not common or well recognized. Four aged patients presented to our clinic with episodic syncope, and PE was finally identified as the underlying cause. The significant clinical presentations included transient loss of consciousness and hypoxemia on admission. Syncope with hypoxia should therefore be highlighted as an important clue to the diagnosis of PE in aged patients. A negative D-dimer test will be encountered in patients with a very short history. Repeated D-dimer testing is necessary.

We report three cases of superficial siderosis of the central nervous system examined with MR susceptibility-weighted imaging (SWI) technique additional to the conventional SE sequence. Deposition of hemosiderin on SWI images is thicker and far more conspicuous compare with conventional T2-weighted images. Additional intracerebral bleeds are evidenced on susceptibility-weighted images in all three cases, which provide possible clues to the underlining etiology of superficial siderosis.

Objective To assess the value of dual-energy computed tomography myelography (CTM) on detecting leaks of cerebrospinal fluid (CSF) in patients with spontaneous intracranial hypotension (SIH). Methods Six patients with SIH underwent spinal CTM on a 2nd generation dual-source CT with tube voltage set at 100 and 140 kVp(with tin filter). The virtual non-contrast (VNC) and iodine map images were calculated from dual-energy images. The average weighted (AW) CTM images were mixed from two kVp images with mix factor of 0. 5. Two radiologists evaluated CSF leak using two sets of images respectively: VNC + iodine map images and AW-CTM images. The results from two reading methods were compared. The level of CSF leaks along the nerve roots, C1-2 retrospinal CSF collections, epidural CSF collections and spinal epidural venous plexus were marked. The consensus about leak sites and CSF collections was made by two radiologists in the third session Kappa statistics were used to measure the agreement between the two methods. Results Forty-one leaks were detected using VNC + iodine map images. Forty-three leaks were detected on AW images. The agreement between two methods was excellent (Kappa =0. 997 ,P ＜0. 01). There were no differences in the detection of C1-2 retrospinal CSF collections (n = 2), epidural CSF collections(n = 3) or spinal epidural venous plexus (n = 1). VNC and iodine map images demonstrated superior visual effects than AW images. Conclusion Dual-energy CTM can be used to diagnose spontaneous spinal cerebrospinal fluid leaks in SIH patient.

Spontaneous intracranial hypotension (SIH) is an increasingly recognized disease characterized by postural headache. Subdural hematoma (SDH) is a severe complication of SIH. We describe 2 patients with SIH who developed bilateral SDHs and outline the typical clinical and neuroimaging findings. After failure of conservative treatment, one patient received epidural blood patch (EBP) and neurosurgical drainage of hematomas and the other was successfully managed by EBP alone without hematoma evacuation. SIH patients with SDH that suffered focal neurological deficits, decreased level of consciousness, or SDH with maximum thickness more than 1 cm were recommended to be treated with surgical drainage, followed by EBP to prevent SDH recurrence.