Progress in Elucidating Biomarkers of Antidepressant Pharmacological Treatment Response: A Systematic Review and Meta-analysis of the Last 15 Years.

BACKGROUND: Antidepressant drugs are widely prescribed, but response rates after 3 months are only around one-third, explaining the importance of the search of objectively measurable markers predicting positive treatment response. These markers are being developed in different fields, with different techniques, sample sizes, costs, and efficiency. It is therefore difficult to know which ones are the most promising. OBJECTIVE: Our purpose was to compute comparable (i.e., standardized) effect sizes, at study level but also at marker level, in order to conclude on the efficacy of each technique used and all analyzed markers. METHODS: We conducted a systematic search on the PubMed database to gather all articles published since 2000 using objectively measurable markers to predict antidepressant response from five domains, namely cognition, electrophysiology, imaging, genetics, and transcriptomics/proteomics/epigenetics. A manual screening of the abstracts and the reference lists of these articles completed the search process. RESULTS: Executive functioning, theta activity in the rostral Anterior Cingular Cortex (rACC), and polysomnographic sleep measures could be considered as belonging to the best objectively measured markers, with a combined d around 1 and at least four positive studies. For inter-category comparisons, the approaches that showed the highest effect sizes are, in descending order, imaging (combined d between 0.703 and 1.353), electrophysiology (0.294-1.138), cognition (0.929-1.022), proteins/nucleotides (0.520-1.18), and genetics (0.021-0.515). CONCLUSION: Markers of antidepressant treatment outcome are numerous, but with a discrepant level of accuracy. Many biomarkers and cognitions have sufficient predictive value (d ≥ 1) to be potentially useful for clinicians to predict outcome and personalize antidepressant treatment.

[Acute bilateral deafness and facial diplegia as a presentation of occlusion of the basilar artery]. / Surdité bilatérale suivie d'une diplégie faciale révélatrice d'une occlusion du tronc basilaire.

INTRODUCTION: Sudden bilateral deafness and facial weakness are unusual presentations of brain stem stroke. OBSERVATION: We report the case of a patient who presented successively sudden bilateral deafness and facial diplegia in correlation with a brain stem stroke but without any ischemic pontine lesion. DISCUSSION: Unlike our case, all of the earlier publications, have reported the presence of ischemic pontine lesions in patients with bilateral deafness and facial diplegia. Selective vulnerability of inner ear to ischemia has been hypothesized but cannot explain the facial diplegia. CONCLUSION: Our case would suggest extra-neuraxis failure by ischemia of the acoustico-facial nerve.

Psychomotor retardation is a scar of past depressive episodes, revealed by simple cognitive tests.

The cumulative duration of depressive episodes, and their repetition, has a detrimental effect on depression recurrence rates and the chances of antidepressant response, and even increases the risk of dementia, raising the possibility that depressive episodes could be neurotoxic. Psychomotor retardation could constitute a marker of this negative burden of past depressive episodes, with conflicting findings according to the use of clinical versus cognitive assessments. We assessed the role of the Retardation Depressive Scale (filled in by the clinician) and the time required to perform the neurocognitive d2 attention test and the Trail Making Test (performed by patients) in a sample of 2048 depressed outpatients, before and after 6 to 8 weeks of treatment with agomelatine. From this sample, 1140 patients performed the TMT-A and -B, and 508 performed the d2 test, at baseline and after treatment. At baseline, we found that with more past depressive episodes patients had more severe clinical level of psychomotor retardation, and that they needed more time to perform both d2 and TMT. When the analyses were performed again after treatment, and especially when the analyses were restricted to patients with clinical remission, the cognitive tests were the only ones correlated with past depressive episodes. Psychomotor retardation tested at a cognitive level was therefore systematically revealing the burden of past depressive episodes, with an increased weight for patients with less remaining symptoms. If prospectively confirmed, interventions such as cognitive remediation therapy could benefit from a more specific focus on neurocognitive retardation.