Prospective Cohort Study

Secret History: Return of the Black Death Channel 4, 7-8pm In 1348 the Black Death swept through London, killing people within days of the appearance of their first symptoms. Exactly how many died, and why, has long been a mystery. This Secret History documentary follows experts as they pick through the evidence and reveal why the plague killed on such a scale. And they ask, what might be coming next?

Medscape

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(00)02490-9.pdf

The importance of selenium to human health

The essential trace mineral, selenium, is of fundamental importance to human health. As a constituent of selenoproteins, selenium has structural and enzymic roles, in the latter context being best-known as an antioxidant and catalyst for the production of active thyroid hormone. Selenium is needed for the proper functioning of the immune system, and appears to be a key nutrient in counteracting the development of virulence and inhibiting HIV progression to AIDS. It is required for sperm motility and may reduce the risk of miscarriage. Deficiency has been linked to adverse mood states. Findings have been equivocal in linking selenium to cardiovascular disease risk although other conditions involving oxidative stress and inflammation have shown benefits of a higher selenium status. An elevated selenium intake may be associated with reduced cancer risk. Large clinical trials are now planned to confirm or refute this hypothesis. In the context of these health effects, low or diminishing selenium status in some parts of the world, notably in some European countries, is giving cause for concern.

The importance of selenium to human health.

Because depression and painful symptoms commonly occur together, we conducted a literature review to determine the prevalence of both conditions and the effects of comorbidity on diagnosis, clinical outcomes, and treatment. The prevalences of pain in depressed cohorts and depression in pain cohorts are higher than when these conditions are individually examined. The presence of pain negatively affects the recognition and treatment of depression. When pain is moderate to severe, impairs function, and/or is refractory to treatment, it is associated with more depressive symptoms and worse depression outcomes (eg, lower quality of life, decreased work function, and increased health care utilization). Similarly, depression in patients with pain is associated with more pain complaints and greater impairment. Depression and pain share biological pathways and neurotransmitters, which has implications for the treatment of both concurrently. A model that incorporates assessment and treatment of depression and pain simultaneously is necessary for improved outcomes.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/216320/ira30040_2433_2445.pdf

Depression and pain comorbidity: a literature review.

Objectives To investigate the clinical correlates of visual symptoms in patients with migraine. Method Patients with migraine that attended our headache clinics were enrolled. Headache profiles, disability, and comorbidities were acquired with structured questionnaires. A semi-structured visual phenomenon questionnaire was also used to assess the characteristics of visual symptoms, including visual aura in patients with migraine with aura and transient visual disturbance in patients with migraine without aura. Headache specialists interviewed with the participants for the ascertainment of diagnosis and verification of the questionnaires. Result Migraine with aura patients with visual aura (n = 743, female/male = 2.3, mean age: 34.7 ± 12.2 years) and migraine without aura patients with non-aura transient visual disturbance (n = 1,808, female/male = 4.4, mean age: 39.4 ± 12.6 years) were enrolled. Patients with transient visual disturbance had higher headache-related disability and more psychiatric comorbidities. Chronic migraine was more common in migraine without aura than migraine with aura patients (41.9% vs. 11.8%, OR = 5.48 [95% CI: 4.33–7.02], p < 0.001). The associations remained after adjusting confounding factors. Conclusion Presence of non-aura transient visual disturbance may suggest a higher migraine-related disability and is linked to higher risk of chronic migraine than typical migraine aura in migraine patients. Further studies are needed to elucidate the potential mechanism.

Non-aura visual disturbance with high visual aura rating scale scores has stronger association with migraine chronification than typical aura

We appreciate DeSouza et al.’s interest in and comments (1) on our study (2) and find the results from their recent study of great interest (3). In their study, in addition to conventional volume and thickness-based measures, a graph-theoretical approach was used to delineate differences in structural covariance networks between patients with chronic migraine (CM) and healthy controls (HC). While DeSouza et al. did not find any between-group differences using the conventional volume or thickness-based measures, we showed that cortical thickness was decreased in several painrelated cortical regions in CM patients (2). Their finding of significant differences in structural network measures leads DeSouza et al. to suggest that such measures may provide a more sensitive means to detect structural differences in CM (3). While we agree with DeSouza et al. on the importance of using structural covariance network analysis, as it provides complementary information, we want to emphasize with our study (2) that homogeneity of the patient population is of utmost importance in order to reveal subtle differences, even if those differences appear to be shared with other chronic pain conditions. Hence, if medication overuse, psychiatric comorbidities, and ongoing preventive medication are not controlled for then, irrespective of the structural measure used, it is difficult to ascribe the presence or absence of findings to CM pathophysiology alone. For example, it has previously been demonstrated by our group that medication overuse is associated with specific structural and neurochemical differences (4,5). Additionally, depression itself is known to affect brain morphology and connectivity, as revealed by graph theory-based brain network analysis (6). As for the discrepancy between DeSouza et al.’s study (3) and ours (2), differences in the abovementioned factors possibly account for this. Furthermore, DeSouza et al. measured the averaged cortical thickness in 68 cortical regions of interest (ROIs) (34 in each hemisphere) parcellated according to the Desikan-Killiany atlas, rather than using a vertex-based approach. The subtle differences within a sub-ROI area between groups could theoretically be averaged out by such an ROI analysis. Further studies applying all of the above-mentioned structural measures in a more homogenous patient population are warranted and may provide additional novel insights into CM-specific pathophysiology.

Reply to letter to the editor: Insights into chronic migraine pathophysiology – what measures of gray matter reveal:

In this issue, Prakash and colleagues present this thought-provoking report on four patients each with cluster headaches which responded favourably within 2 weeks to a relatively high dosage of indomethacin (1). After a thorough literature review, they identified three relevant groups of such patients: (i) those with cluster headache responsive to indomethacin; (ii) those with cluster headache wrongly diagnosed as paroxysmal hemicrania (PH) because of apparent response to indomethacin; and (iii) patients with co-existent cluster headache and PH. They also note that physicians tended to diagnose patients as having PH if patients were responsive to indomethacin even though the clinical profiles of the patients were compatible with cluster headache (1). This paper inspires us to re-think the diagnostic criteria of trigeminal autonomic cephalalgias (TACs) in the International Classification of Headache Disorders, 2nd edn (ICHD-2) (2).

Can response to indomethacin exclude the diagnosis of cluster headache

Editorial Screening of Dementia

Dear Editor, We thank Professor Kawada for his comments and interest in our article.1 We agree that clinical stage of chronic kidney disease (CKD) would be closely related to the progress of cognitive performance. Helmer et al.2 collected longitudinal data from the ThreeCity populationbased cohort study reported that global cognitive decline and incident dementia were associated with eGFR decline rather than low eGFR level. Nevertheless Miwa et al.3 conducted a longitudinal study (OSACA2) to evaluate the association between CKD at baseline and incident dementia and found CKD was independently associated with the risk of dementia in patients with vascular components.2 Mild CKD was related to increased risk of all cause dementia, whereas moderatesevere CKD showed borderline difference. Furthermore, a recent metaanalysis found that some crosssectional and longitudinal studies have demonstrated a significantly increased risk of cognitive impairment in patients with CKD.4 Although one of limitations of our study is crosssection study design, according to OSACA2 and previous metaanalysis, the baseline state of CKD might be associated with cognitive decline and might be served as a predictor of cognition impairment. However, as in the article cited by Dr. Kawada,5 fluctuations in attention and executive function within haemodialysis cycle were present in only a minority of patients and were associated moderately with intradialytic hypotensive episodes. We believe this is not the case in our patients who are all nonhaemodialysis patients and have relatively stable hemodynamic status. Finally, we appreciate Professor Kawada for his comments on our multivariate regression model. Indeed, as we mentioned in our article, the sample size is small and more subjects with followup data would make the results more stable and solid.

Jong Ling Fuh

Papers

Non-aura visual disturbance with high visual aura rating scale scores has stronger association with migraine chronification than typical aura

Reply to letter to the editor: Insights into chronic migraine pathophysiology – what measures of gray matter reveal:

Can response to indomethacin exclude the diagnosis of cluster headache

Editorial Screening of Dementia

Cognitive impairment and chronic kidney disease: Risk assessment.