A systematic literature review of health disparities among rural people with epilepsy (RPWE) in the United States and Canada.

BACKGROUND: Epilepsy is a leading cause of global disease burden, with people with epilepsy (PWE) experiencing adverse health outcomes related to the psychiatric comorbidities and socioeconomic consequences of the disorder. Rural populations are more likely to be impoverished or uninsured, which could impact health outcomes for rural-dwelling PWE (RPWE). AIMS: This systematic literature review identified original research studying health disparities and outcomes among RPWE in the United States and Canada to (1) characterize the disparities faced by RPWE and (2) elucidate the effects of these disparities upon clinical outcomes. METHODS: We performed a systematic search of six electronic databases: Pubmed, Cochrane, PsychInfo, Web of Science, Scopus, and Ovid. Articles considered were original research reports conducted in Canada or the United States before August 2020. A modified Newcastle Ottawa Scale was used to assess the quality of the included studies. RESULTS: Our search returned 2093 articles that examined the health disparities of RPWE, of which six met criteria for this review. Outcome measures of health disparity included in these papers were mortality (2; 33%), use of health resources (2; 33%), and epilepsy prevalence (2; 33%). Only one paper (16%) concluded that RPWE experienced worse health outcomes relative to urban-dwelling PWE, while 5 (84%) found no difference. CONCLUSION: Our study did not find sufficient evidence that RPWE in the US and Canada experience significant health disparities compared to similar urban populations of PWE. More research using prospective studies and datasets allowing better characterization of rurality is required.

The effect of prophylactic antiepileptic medications in aneurysmal subarachnoid hemorrhage patients: A retrospective review.

OBJECTIVE: The current literary evidence suggests but does not heavily endorse the use of prophylactic antiepileptic drugs (AEDs) after aneurysmal subarachnoid hemorrhage. Literature continues to emerge suggesting not only a lack of efficacy but associated poor outcomes. This study is a retrospective review comparing seizure incidence in aneurysmal subarachnoid patients between those given prophylactic AEDs and those not. METHODS: With IRB approval, a retrospective chart review was performed on all aneurysmal subarachnoid patients from 2012 to 2019 at the University of Mississippi Medical center. Univariate and Multivariate analysis was performed using SAS. Primary outcome was seizure incidence between groups. Factors associated with seizure and poor outcome were also investigated. RESULTS: 348 patients were identified: 120 in the AED group, and 228 patients in the non-AED group. There was no significant difference in mean age, gender, ethnicity, HH scores, treatment modality, or mean aneurysm size. The AED group had a higher history of prior aneurysmal rupture (6.7% vs. 1.3%, p = 0.01) and associated intracranial hemorrhage (22.5% vs. 10.5%, p = 0.0004). There was no significant difference in seizure incidence between the two groups (8.3% vs. 4.8%, p = 0.24). On multivariate analysis, aneurysm clipping compared to coiling (OR 3.8, p = 0.012) and delayed cerebral ischemia (OR 2.77, p = 0.023) were associated with seizures. DCI (OR 8.34), HH grade, Age (OR 1.07), Seizure (8.34), and AED use (1.7) were significantly associated with poor outcome. CONCLUSION: This retrospective review adds to the evidence that prophylactic AED use in aneurysmal subarachnoid hemorrhage patients has not been proven to improve seizure rates and may result in worse patient outcomes.

Effects of antidepressant treatment on mice lacking brain-derived neurotrophic factor expression through promoter IV.

Brain-derived neurotrophic factor (BDNF) is implicated in the pathophysiology of major depression; mice lacking BDNF expression through promoter IV (BDNF-KIV) exhibit a depression-like phenotype. We tested our hypothesis that deficits caused by promoter IV deficiency (depression-like behavior, decreased levels of BDNF, and neurogenesis in the hippocampus) could be rescued by a 3-week treatment with different types of antidepressants: fluoxetine, phenelzine, duloxetine, or imipramine. Each antidepressant reduced immobility time in the tail suspension test without affecting locomotor activity in the open field test in both BDNF-KIV and control wild type mice, except that phenelzine increased locomotor activity in wild type mice and anxiety-like behavior in BDNF-KIV mice. The antidepressant treatments were insufficient to reverse decreased BDNF levels caused by promoter IV deficiency. No antidepressant treatment increased the hippocampal progenitors of either genotype, whereas phenelzine decreased the surviving progenitors in both genotypes. The antidepressant treatments differently affected the dendritic extension of hippocampal immature neurons: fluoxetine and imipramine increased extension in both genotypes, duloxetine increased it only in BDNF-KIV mice, and phenelzine decreased it only in wild type mice. Interestingly, a saline-only injection increased neurogenesis and dendrite extensions in both genotypes. Our results indicate that the behavioral effects in the tail suspension test by antidepressants do not require promoter IV-driven BDNF expression and occur without a detectable increase in hippocampal BDNF levels and neurogenesis but may involve increased dendritic reorganisation of immature neurons. In conclusion, the antidepressant treatment demonstrated limited efficacy; it partially reversed the defective phenotypes caused by promoter IV deficiency but not hippocampal BDNF levels.