Objective: Post-stroke cognitive impairment is common, but mechanisms and risk factors are poorly understood. Frailty may be an important risk factor for cognitive impairment after stroke. We investigated the association between pre-stroke frailty and acute post-stoke cognition. Methods: We studied consecutively admitted acute stroke patients in a single urban teaching hospital during three recruitment waves between May 2016 and December 2017. Cognition was assessed using the Mini-Montreal Cognitive Assessment (min=0; max=12). A Frailty Index was used to generate frailty scores for each patient (min=0; max=100). Clinical and demographic information were collected, including pre-stroke cognition, delirium, and stroke-severity. We conducted univariate and multiple-linear regression analyses with covariates forced in (covariates included were: age, sex, stroke severity, stroke-type, pre-stroke cognitive impairment, delirium, previous stroke/transient ischemic attack) to investigate the association between pre-stroke frailty and post-stroke cognition. Results: Complete data were available for 154 stroke patients. Mean age was 68 years (SD=11; range=32–97); 93 (60%) were male. Median mini-Montreal Cognitive Assessment score was 8 (IQR=4–12). Mean Frailty Index score was 18 (SD=11). Pre-stroke cognitive impairment was apparent in 13/154 (8%) patients. Pre-stroke frailty was significantly associated with lower post-stroke cognition (Standardized-Beta=−0.40; p<0.001) and this association was independent of covariates (Unstandardized-Beta=−0.05; p=0.005). Additional significant variables in the multiple regression model were age (Unstandardized-Beta=−0.05; p=0.002), delirium (Unstandardized-Beta=−2.81; p<0.001), pre-stroke cognitive impairment (Unstandardized-Beta=−2.28; p=0.001), and stroke-severity (Unstandardized-Beta=−0.20; p<0.001). Conclusions: Pre-stroke frailty may be a moderator of post-stroke cognition, independent of other well-established post-stroke cognitive impairment risk factors. (JINS, 2019, 25, 501–506)

Canadian contributions to cerebrovascular neurosurgery have been disproportionately large and, with some exceptions, relatively unrecognized. In this review, some of the efforts in the advancement of cerebrovascular neurosurgery by Canadian neurologists and neurosurgeons are described.

The recent decline in cardiovascular disease mortality in Western countries has been linked with changes in life style and treatment. This study considers periods of decline before effective medical interventions or knowledge about risk factors. Trends in annual age-standardized death rates from cerebrovascular disease, heart disease and circulatory disease, and all cardiovascular disease are reviewed for three phases, 1881–1916, 1920–1939, and 1940–2000. There was a consistent decline in the cerebrovascular disease death rate between 1891 and 2000, apart from brief increases after the two world wars. The heart disease and circulatory disease death rate was declining between 1891 and 1910 before cigarette smoking became prevalent. The early peak in cardiovascular mortality in 1891 coincided with an influenza pandemic and a peak in the death rate from bronchitis, pneumonia and influenza. There is also correspondence between short-term fluctuations in the death rates from these respiratory diseases and cardiovascular disease. This evidence of ecological association is consistent with the findings of many studies that seasonal influenza can trigger acute myocardial infarction and episodes of respiratory infection are followed by increased risk of cardiovascular events. Vaccination studies could provide more definitive evidence of the role in cardiovascular disease and mortality of influenza, other viruses, and common bacterial agents of respiratory infection.

This study explored effects of the metabolic syndrome (MetS) on language in aging. MetS is a constellation of five vascular and metabolic risk factors associated with the development of chronic diseases and increased risk of mortality, as well as brain and cognitive impairments. We tested 281 English-speaking older adults aged 55–84, free of stroke and dementia. Presence of MetS was based on the harmonized criteria (Alberti et al., 2009). Language performance was assessed by measures of accuracy and reaction time on two tasks of lexical retrieval and two tasks of sentence processing. Regression analyses, adjusted for age, education, gender, diabetes, hypertension, and heart disease, demonstrated that participants with MetS had significantly lower accuracy on measures of lexical retrieval (action naming) and sentence processing (embedded sentences, both subject and object relative clauses). Reaction time was slightly faster on the test of embedded sentences among those with MetS. MetS adversely affects the language performance of older adults, impairing accuracy of both lexical retrieval and sentence processing. This finding reinforces and extends results of earlier research documenting the negative influence of potentially treatable medical conditions (diabetes, hypertension) on language performance in aging. The unanticipated finding that persons with MetS were faster in processing embedded sentences may represent an impairment of timing functions among older individuals with MetS. (JINS, 2015, 21, 116–125)

The diagnosis of dysthymic disorder was created in DSM-III and maintained in DSM-IV to describe a depressive syndrome of mild to moderate severity of at least two years’ duration that did not meet criteria for major depressive disorder. The prevalence of dysthymic disorder is approximately 2% in the elderly population where subsyndromal depressions of lesser severity are more common. Dysthymic disorder was replaced in DSM-V by the diagnosis of “persistent depressive disorder” that includes chronic major depression and dysthymic disorder. In older adults, epidemiological and clinical evidence supports the use of the term “dysthymic disorder.” In contrast to young adults with dysthymic disorder, older adults with dysthymic disorder commonly present with late age of onset, without major depression and other psychiatric disorders, and with a low rate of family history of mood disorders. They often have stressors such as loss of social support and bereavement, and some have cerebrovascular or neurodegenerative pathology. A minority has chronic depression dating from youth with psychiatric comorbidity similar to young adults with dysthymic disorder. In older adults, both dysthymic disorder and subsyndromal depression increase disability and lead to poor medical outcomes. Elderly patients with dysthymic disorder are seen mainly in primary care where identification and treatment are often inadequate. Treatment with antidepressant medication shows marginal superiority over placebo in controlled trials, and problem-solving therapy shows similar efficacy. Combined treatment and collaborative care models show slightly better results, but cost effectiveness is a concern. Further work is needed to clarify optimal approaches to the treatment of dysthymic disorder in elderly patients.

Background: There is growing recognition that apathy is not only a symptom of depression but may be an independent syndrome. This is the first study to investigate the relationship of apathy and depression longitudinally following stroke and to examine the association with dementia.

Method: 106 consecutive eligible participants following stroke received extensive medical, psychiatric and neuropsychological assessments at three to six months (index assessment) and 15 months (follow-up assessment) after their stroke. A subset of participants received magnetic resonance imaging (MRI) scans at index assessment. Ratings were made for DSM-IV major or minor depression and for apathy using the Apathy Evaluation Scale (AES).

Results: While there was no significant overlap between apathy and depression at index assessment (OR = 1.79, 95% CI 0.48, 6.66), the overlap was significant a year later (OR = 7.75, 95% CI 2.60, 23.13). Dementia at index assessment was a common risk factor for both apathy and depression at follow-up (OR = 12.45, 95% CI 2.98, 52.02 and OR = 10.35, 95% CI 2.84, 37.72, respectively).

Conclusions: Apathy and depression after stroke have a common predictor and overlap longitudinally. The overlap might be due to cumulative vascular pathology and because of the relationship of each of these syndromes to dementia, which was an important, possibly causal, predictor for both.

Background: Both the lesion location hypothesis and the vascular depression hypothesis have been proposed to explain the high incidence of depression in stroke patients. However, research studying both hypotheses in a single cohort is, at present, scarce.

Objective: To test the independent effects of lesion location (left hemisphere, anterior region) and of co-occurring generalized vascular damage on the development of depression in the first year after ischemic stroke, while other risk factors for depression are controlled for.

Methods: One hundred and ninety consecutive patients with a first-ever, supratentorial infarct were followed up for one year. CT was performed in the acute phase of stroke, while in 75 patients an additional MRI scan was also available. Depression was assessed at 1, 3, 6, 9, and 12 months after stroke using self-rating scales as screening tools and the SCID-I to diagnose depression according to DSM-IV criteria.

Results: Separate analyses of the lesion location hypothesis and the vascular depression hypothesis failed to reveal significant support for either of these biological models of post-stroke depression. Similar negative results appeared from one overall, multivariate analysis including variables of both focal and generalized vascular brain damage, as well as other non-cerebral risk factors. In addition, level of handicap and neuroticism were independent predictors of depression in this cohort, as has been reported previously.

Conclusion: This study supports neither the lesion location nor the vascular depression hypothesis of post-stroke depression. A biopsychosocial model including both premorbid (prior to stroke) vulnerability factors, such as neuroticism and (family) history of depression, as well as post-stroke stressors, such as level of handicap, may be more appropriate and deserves further study.

Vascular dementia (VaD) is a disorder with no cure and limited treatment options. Similarities between VaD and Alzheimer's disease (AD) arise on a number of levels. Both involve progressive decline in cognition, functional ability, and behavior, and there is evidence for a central role of reduced cholinergic neurotransmission in the two illnesses. Treatment strategies in VaD have historically focused on prevention, although evidence of cognitive benefits with preventative treatment is scarce. Acetylcholinesterase inhibitors represent a rational treatment possibility for symptomatic therapy of patients with VaD. A recent large-scale trial of galantamine in patients with VaD or AD with cerebrovascular disease (AD + CVD) represents the first placebo-controlled trial showing clinically relevant benefits in these important patient populations.