Seizures due to pyridoxine deficiency in Parkinson's disease.

Parkinson's disease (PD) is a complex neurodegenerative disorder characterized not only by its hallmark motor symptoms but also by a myriad of non-motor manifestations, including cognitive decline, autonomic manifestations, and gastrointestinal disturbances. Amidst these, a lesser-known but critical aspect is the increased risk of functional deficiency of pyridoxine (vitamin B6) in patients with PD, which is linked to an increased risk of seizures. This review investigates the intersection of PD, new-onset seizures, and pyridoxine deficiency, aiming to elucidate the significance of these associations and their contributions to the neurologic burden in PD. Case reports documenting the occurrence of seizures in patients with PD, particularly in the context of high-dose dopaminergic therapy and the subsequent revelation of pyridoxine deficiency were included. These cases, which often featured extensive workups revealing unremarkable findings aside from pyridoxine deficiency, underscore the multifaceted nature of PD and its treatment-related complications. The findings in these case reports suggest that dietary insufficiencies, gastrointestinal dysfunctions, and drug-nutrient interactions may eventually precipitate pyridoxine deficiency, which in turn may lead to seizures by disrupting GABAergic neurotransmission. This sheds the light on the need for increased clinical awareness and routine monitoring of pyridoxine levels in patients with PD, especially those undergoing significant therapeutic adjustments or exhibiting comorbidities that might interfere with their dietary intake such as gastrointestinal manifestations or depression. Such proactive measures could potentially mitigate the impact of this complication in patients with PD, ultimately enhancing patient care and quality of life.

Aneurysmal Subdural Hematoma: A Systematic Review.

BACKGROUND: Aneurysmal subdural hematoma (aSDH) is a rare complication of aneurysm rupture, affecting between 0.5 and 7.9% of patients with aneurysmal subarachnoid hemorrhage (aSAH). The clinical presentation, course, and outcomes of these patients are largely unknown. OBJECTIVE: This study aims to systematically review the literature to evaluate the demographics, clinical presentation, aneurysm location, treatment options, and outcomes of patients with aSDH with and without aSAH. METHODS: In accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, we conducted a systematic review of three databases (PubMed, EMBASE, and Google Scholar). From identified reports, we extracted data on patients' demographics, clinical presentation, imaging findings, surgical interventions, and clinical outcomes. We compared clinical outcomes, need for surgical treatment, and aneurysm location between patients with aSDH with and without concurrent aSAH using χ2 and Fisher's exact tests. We used simple and multivariable logistic regression models to further examine the association between the presence of aSAH and surgical treatment with clinical outcomes. RESULTS: We identified 112 articles with a total of 270 patients (70% women, mean age 52.8 [± 15.5] years). The most common aneurysm locations were the middle cerebral artery, followed by the posterior communicating artery, and the internal carotid artery. Patients with isolated aSDH fully recovered more frequently than those with concomitant aSAH (38% vs. 6%). The presence of aSAH increased the odds of unfavorable outcome (odds ratio [OR] 2.68, 95% confidence interval [CI] 1.34-5.37). Surgical treatment was inversely associated with unfavorable outcome in the univariable (OR 0.48, 95% CI 0.28-0.84) but not in the multivariable analysis (OR 0.76, 95% CI 0.35-1.66). CONCLUSION: aSDH occurs infrequently. Simultaneous presence of both aSDH and aSAH from an aneurysmal source is associated with poor outcomes. Surgical treatment is associated with lower rates of unfavorable outcomes including death and severe disability.

Impact of pre-treatment cerebral microbleeds on the outcomes of endovascular thrombectomy: A systematic review and meta-analysis.

OBJECTIVE/AIM: To investigate the effect of cerebral microbleeds (CMBs) on the functional and safety outcomes of endovascular thrombectomy (EVT) in patients with acute ischemic stroke (AIS) due to large vessel occlusion (LVO). METHODS: This study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines for systematic review and meta-analysis. We included observational studies that recruited AIS-LVO patients, used susceptibility-sensitive magnetic resonance imaging (MRI) to detect CMBs, and examined the association between them and predefined outcome events. The extracted data included study and population characteristics, risk of bias domains, and outcome measures. The outcomes of interest included functional independence, revascularization success, procedural and hemorrhagic adverse events. We conducted a meta-analysis using the Mantel-Haenszel method and calculated the risk ratios. RESULTS: Four studies with a total of 1,514 patients were included. A significant reduction in the likelihood of achieving a favorable functional outcome was observed in patients with CMBs (Risk ratio (RR) 0.69, 95% confidence interval (CI): 0.52 to 0.91, P=0.01). No significant differences were observed between the CMBs and no CMBs groups in terms of successful revascularization, mortality, intracranial hemorrhage (ICH), subarachnoid hemorrhage (SAH), and parenchymal hematoma. CONCLUSIONS: The presence of CMBs significantly reduced the likelihood of achieving functional independence post-EVT in AIS-LVO patients. However, CMBs did not impact the rates of successful revascularization, mortality, or the occurrence of various hemorrhagic events. Future research should explore the mechanisms of this association and strategies to mitigate its impact.

An Ultrastructural Perspective on Cell Death.

In the field of cell death, there is still a wide gap between the molecular models and their ultrastructural phenotypes. Because only very few published works included electron microscopy (EM) images, many ultrastructural features have not yet been incorporated into the descriptions of death modes. Some of the EM features that appear in dying cells have not been incorporated in describing death modes. It includes the accumulation of lipid droplets and glycogen, the appearance of extranuclear chromatin in the cytoplasm, and the various ways mitochondria become damaged. We argue that electron microscopy should be routinely included in these studies because it exposes some new features that molecular studies do not. It has successfully recognized new modes of cell death, such as entosis, methuosis, and paraptosis. Elucidating the precise sequence of events in death modes could be the cornerstone for offering the proper therapy of many diseases by slowing down or stopping the progression of degeneration. This review presents our own experience applying ultrastructural interpretations to death modes and explaining their biochemical implications. We complement the molecular and biochemical data and point out missing features that should be considered and studied.