The finding: In a thorough review of the literature on post-stroke depression (PSD), the authors note the following:

• PSD risk factors : The most robust risk factor is a personal history of a depressive or anxiety disorder preceding stroke.
• Stroke severity and type of stroke: There is a significant association between the severity of stroke and PSD but no significant association between development of PSD and the type of stroke (hemorrhagic or embolic/thrombotic)
• Lesion location: The authors contend that there is an association between left frontal or left basal ganglia strokes however, this risk is restricted to the first 2 months after stroke only.
• Functional and cognitive impairment: The factor most consistently associated with PSD is the severity of impairment of ADLs after stroke.
• Treatment: Antidepressants (medications in reviewed trials included fluoxetine, citalopram, escitalopram, and nortriptyline) vs placebo significantly improved motor recovery (at 12 weeks), long-term survival (7 year follow up) and the rates and severity of depressive symptoms (9 double-blind, placebo-controlled randomized controlled trials included).

The follow-up periods ranged from 3 months to over 7 years with sustained recovery with antidepressants at each time point. Based on these findings, the American Heart Association recommends treatment with antidepressants in PSD to be continued after recovery of depressive symptoms for at least 6 months.

Strength and weaknesses: This is a torough review by experts in the field including the latest pooled data on incidence/prevalence, risk factors, recovery, mortality, and putative pathophysiological mechanisms. This paper thus brings together information from a multitude of studies, across various patient populations, and includes relevant meta-analyses and randomized-controlled trials. The results do not appear to contradict other findings in the post-stroke depression literature and highlight the complexity of this condition. The authors highlight many of the methodological flaws inherent in much of the literature, providing a solid basis to understand much of the controversy that has existed, especially with PSD development and lesion location.

Relevance: There is a high prevalence of depression in stroke patients and many psychiatrists will be responsible for treating these patients in a variety of treatment settings. Additionally, decreases in ADLs, motor functioning, and cognitive functions, whether related to comorbid depression or not, are also prevalent and shown to be significantly decreased with antidepressant medications. These findings allow practitioners to utilize treatments they are familiar with (i.e., SSRIs) to treat symptoms that may otherwise go unrecognized.

The finding:1) Duration of posttraumatic amnesia correlated with functional outcome at the end of inpatient rehabilitation.  2) Duration of posttraumatic amnesia and functional outcome at the end of inpatient rehabilitation correlated with severity of amnesia at the time of presentation as measured by the Galveston Orientation and Amnesia Test (GOAT).  2) At a gross level, parietal lobe lesions were associated with worse functional outcomes.  3)  Stimulant use (amantadine, methylphenidate, amantadine + methylphenidate, modafinil) did not reduce duration of posttraumatic amnesia.

Strength and weaknesses:The pattern of posttraumatic amnesia (i.e., a combined anterograde and retrograde amnesia with graded recovery of the former, and a stepwise [from remote to recent] recovery of the latter, often leaving a window of permanent amnesia) is not a colossal mystery, but how its magnitude and trajectory may affect overall functional outcome is an important area of inquiry.  This was a retrospective study, only had an n of 40, and excluded patients with a history of premorbid neurologic or psychiatric illness (including addictions and cognitive disorders).  The latter excludes a major subset of the TBI population.  The stimulant finding is expressed as “neurostimulant use did not improve outcome,” but the authors only note that it did not improve (i.e., reduce) the length of posttraumatic amnesia.  Stimulant use was not randomly assigned.  Given the frequent use of stimulant use in this population, further, dedicated study on this front is needed.

Relevance:This study provides some guidance for clinicians to use when prognosticating in the highly prevalent but still-nebulous world of traumatic brain injury.

The finding:The presumed relationship between chronic traumatic encephalopathy (CTE) and suicide is just that – presumed.  Available data is inconclusive in drawing a link between these two phenomena, let alone a causal one.

Strength and weaknesses:This is an excellent review that methodically identifies the flawed assumptions masquerading as facts regarding a very important issue.  The author does not seek to debunk the link between suicide and CTE, but rather to point out that it is not yet sufficiently substantiated.  The article may get bogged down in details at times (e.g., the well-trod ground of suicide risk factors), but overall it accomplishes its goal quite succinctly and directly.

Relevance:Highly relevant merely by virtue of media exposure, this review effectively covers an aspect of CTE that most psychiatrists, and especially neuropsychiatrists and psychosomatic medicine specialists would be expected to know well.