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Background: Escalating street violence and criminal homicides have an adverse impact on psychological well-being. However, these consequences have been difficult to evaluate. Using a recently validated scale, we aimed to assess the impact of fear of crime on the psychological status of middle-aged and older adults living in a rural setting afflicted by endemic violence. Methods: Participants were selected from Atahualpa residents included in previous studies targeting psychological distress in the population. A validated scale was used to objectively quantify fear of crime in participants. Differences in symptoms of depression and anxiety between baseline and follow-up were used as distinct dependent variables and the continuous score of the fear of crime scale was used as the independent variable. Linear regression models were fitted to assess the association between the exposure and the outcomes, after adjusting for relevant confounders. Results: A total of 653 participants (mean age = 53.2 ± 11.5 years; 57% women) completed the requested tests. We found a 13% increase in symptoms of depression and anxiety during the peak of violence in the village compared with previous years. Linear regression models showed a significant association between the total score on the fear of crime questionnaire and worsening symptoms of depression (β =.24; 95% CI = 0.14-0.35) and anxiety (β =.31; 95% CI = 0.24-0.37), after adjustment for relevant confounders. Conclusions: This study shows a significant aggravating effect of fear of crime on pre-existing symptoms of depression and anxiety and a deleterious effect of these conditions on overall well-being. [ABSTRACT FROM AUTHOR]

Background and Purpose: Recent studies have suggested an association between dysfunction of the choroid plexus and the glymphatic system. However, information is inconclusive. Following a population-based study design, we aimed to assess the association between choroid plexus calcifications (CPCs)—as a surrogate of choroid plexus dysfunction—and severity and progression of putative markers of glymphatic dysfunction, including white matter hyperintensities (WMH) of presumed vascular origin and abnormally enlarged basal ganglia perivascular spaces (BG-PVS). Methods: This study recruited community-dwellers aged ≥40 years living in neighboring Ecuadorian villages. Participants who had baseline head CTs and brain MRIs were included in cross-sectional analyses and those who additional had follow-up MRIs (after a mean of 6.4 ± 1.5 years) were included in longitudinal analyses. Logistic and Poisson regression models, adjusted for demographics and cardiovascular risk factors, were fitted to assess associations between CPCs and WMH and enlarged BG-PVS severity and progression. Results: A total of 590 individuals were included in the cross-sectional component of the study, and 215 in the longitudinal component. At baseline, 25% of participants had moderate-to-severe WMH and 27% had abnormally enlarged BG-PVS. At follow-up, 36% and 20% of participants had WMH and enlarged BG-PVS progression, respectively. Logistic regression models showed no significant differences between CPCs volumes stratified in quartiles and severity of WMH and enlarged BG-PVS. Poisson regression models showed no association between the exposure and WMH and enlarged BG-PVS progression. Baseline age remained significant in these models. Conclusions: Choroid plexus calcifications are not associated with putative markers of glymphatic system dysfunction. [ABSTRACT FROM AUTHOR]

Objective: Abnormal ankle-brachial index (ABI) determinations may be associated with an increased risk of incident strokes. However, the impact of previous strokes in this relationship is unknown. We estimated the role of previous strokes on the association between abnormal ABI determinations and incident stroke risk in community-dwelling older adults. Methods: Atahualpa residents aged ≥60 years received ABI determinations, cardiovascular risk factors assessment, and brain MRIs. ABIs were classified as abnormal if ≤0.9 or ≥1.4. Incident strokes were diagnosed by a certified neurologist with the aid of a post-event MRI. Poisson regression models were fitted to estimate stroke incidence rate ratio (IRR) according to categories of ABI. Results: Analysis included 389 participants (mean age: 68.2 ± 8.1 years). Eighty-six persons (22%) had abnormal ABI determinations. Incident strokes occurred in 38 (9.8%) individuals after a mean follow-up of 6.1 ± 1.9 years. Abnormal ABIs were associated with incident strokes in unadjusted analyses (p = 0.002) as well as in a Poisson regression model adjusted for demographics and clinical covariates (IRR: 2.57; 95% C.I.: 1.29–5.13), but not when the model was adjusted for neuroimaging covariates (IRR: 1.46; 95% C.I.: 0.67–3.20). Interaction models showed that having both abnormal ABI and non-lacunar strokes at baseline made the individual 9.7 times more likely to have an incident stroke (95% C.I.: 3.87–24.4). The risk was reduced to 2.2 (95% C.I.: 0.96–5.13) for those who only had an abnormal ABI. Conclusions: An abnormal ABI is associated with a doubling the risk of incident strokes, but its importance is superseded by history of non-lacunar strokes. [ABSTRACT FROM AUTHOR]

Neurocysticercosis (NCC) is the most common helminthic infection of the nervous system and a frequent cause of reactive seizures and epilepsy worldwide. In many cases, multiple episodes of focal seizures related to an identifiable parenchymal brain cyst (and likely attributable to local damage) continue for years after the cyst resolves. However, cases where seizure semiology, interictal EEG abnormalities, and parasites location do not correlate raise concerns about the causal relationship between NCC and either reactive seizures or epilepsy, as well as the epileptogenic potential of parasites. Neurosurgical series of patients with intractable epilepsy and cross-sectional population-based studies have shown a robust association between NCC and hippocampal sclerosis (HS), which might contribute to the above-referred inconsistencies. Current information does not allow to define whether in patients with NCC, HS could result from recurrent seizure activity from a local or distant focus or from chronic recurrent inflammation. In either case, HS may become the pathological substrate of subsequent mesial temporal lobe epilepsy (MTLE). Longitudinal clinical- and population-based cohort studies are needed to evaluate the causal relationship between NCC and HS and to characterize this association with the occurrence of MTLE. If a cause-and-effect relationship between NCC and HS is demonstrated, NCC patients could be assessed to examine neuronal mechanisms of hippocampal epileptogenesis in comparison with animal models, to identify biomarkers of hippocampal epileptogenesis, and to develop novel interventions to prevent epilepsy in NCC and perhaps in other forms of acquired epilepsy.

This document is a letter published in the journal Vascular Medicine. The study investigates the relationship between the ankle-brachial index (ABI), a marker of peripheral artery disease (PAD), and the progression of white matter hyperintensities (WMH) of presumed vascular origin in older adults. The study found no interrelated progression between ABI and WMH, suggesting that therapies for one vascular condition may not apply to others. The study has limitations, such as a small sample size and potential bias, but provides valuable insights for further research and early recognition of patients in need of medical therapy. [Extracted from the article]