If this is the number one survivor reported disability where the fuck is the solution? Describing a problem without a solution is useless.
Poststroke Neurocognitive Disorders Are Mostly Defined by Strategic Lesions
Originally published4 Oct 2018Stroke. 2018;49:2563–2564
See related article, p 2666
Neurocognitive disorders account for a significant proportion of poststroke disabilities and are among the most distressing long-term consequences.1 When stroke survivors were ranked according to their most disabling disturbances, impairment within the cognitive domain was ranked first.2 Recently, poststroke cognitive deterioration has been included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) fifth revision under the new diagnostic category “mild neurocognitive disorder,” while the term “vascular dementia” has been substituted by “major neurocognitive disorder” following a vascular insult.3 This has far-reaching consequences as research can now be directed at assessing and treating a defined disease entity instead of a variable and ill-fitting descriptive condition, which was available before.
Mild neurocognitive disorders after stroke have been investigated both in terms of profiling neuropsychological deficits, as well as in terms of circumscript or general brain damage due to stroke. Only recently, both issues have been looked at together in larger samples of patients allowing a more general structure—function analysis.4,5
In this issue of Stroke, Puy L et al6 investigate 356 mostly ischemic stroke patients 6 months after their stroke according to their cognitive status using detailed cognitive testing, as well as extensive magnetic resonance imaging investigations. A total of 50.8% were found to have a neurocognitive disorder. The patients were diagnosed according to the Vascular Behavioural and Cognitive Disorders criteria7 and were assessed with a global cognitive score, which included the 3 domains language, executive function, and action speed. The patients also underwent 3 Tesla magnetic resonance imaging investigations and the stroke lesions, markers of small vessel disease, medial temporal lobe atrophy, and global cerebral atrophy were documented. In addition, strategic infarcts were listed, and the definitions for these infarcts were predetermined according to previous studies and studies from the literature. Statistical analysis of cognitive scores was adjusted for age, sex, and educational level and calculated with linear and multiple regression models to identify magnetic resonance imaging markers related with the global cognitive score.
Multivariate analysis showed that strategic infarcts had the largest influence and accounted for 22.5% of the variance in the global cognitive score while medial temporal atrophy, stroke volume, and total normalized brain volume together accounted only for an additional 11.8%. Also surprisingly, white matter hyperintensities and microhemorrhages did not show up as independent contributors.
The patients in this sample were young (63 years median), the median Rankin Scale score after 6 months was 2, reflecting a benign course in this cohort, and only one patient had prestroke dementia thought to be because of a previous stroke. Although the selection criteria used in this study minimize the risk of an associated neurodegenerative process, it cannot be ruled out in some cases.
This investigation tackles a difficult and multidimensional issue and helps to describe not only the extent but also the location of brain lesions as they are known to be involved in major functional networks of brain functions. It contributes to a clinically useful and comprehensive approach to the analysis of neurocognitive disorders after stroke.
What are the immediate consequences? It must be recognized that a routine assessment of important cognitive domains is an essential part of the clinical workup. When clinical exam and neuroimaging show that there is involvement of strategic locations of the brain, assessment of function for major brain networks should also be made. These include the domains for language, attention and spatial orientation, object recognition, memory, and motor planning and control.
In the future, more emphasis must be given to the temporal trends of cognitive deterioration. It is unclear how the temporal profiles develop. It has been shown that neurocognitive disorders can develop in a delayed fashion thus suggesting an indirect, more gradual onset rather than a direct, sudden onset. These different time trajectories allow, in principle, to define a therapeutic time window, which could be used as an opportunity for behavioral and other interventions.8,9
Neurocognitive disorders account for a significant proportion of poststroke disabilities and are among the most distressing long-term consequences.1 When stroke survivors were ranked according to their most disabling disturbances, impairment within the cognitive domain was ranked first.2 Recently, poststroke cognitive deterioration has been included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) fifth revision under the new diagnostic category “mild neurocognitive disorder,” while the term “vascular dementia” has been substituted by “major neurocognitive disorder” following a vascular insult.3 This has far-reaching consequences as research can now be directed at assessing and treating a defined disease entity instead of a variable and ill-fitting descriptive condition, which was available before.
Mild neurocognitive disorders after stroke have been investigated both in terms of profiling neuropsychological deficits, as well as in terms of circumscript or general brain damage due to stroke. Only recently, both issues have been looked at together in larger samples of patients allowing a more general structure—function analysis.4,5
In this issue of Stroke, Puy L et al6 investigate 356 mostly ischemic stroke patients 6 months after their stroke according to their cognitive status using detailed cognitive testing, as well as extensive magnetic resonance imaging investigations. A total of 50.8% were found to have a neurocognitive disorder. The patients were diagnosed according to the Vascular Behavioural and Cognitive Disorders criteria7 and were assessed with a global cognitive score, which included the 3 domains language, executive function, and action speed. The patients also underwent 3 Tesla magnetic resonance imaging investigations and the stroke lesions, markers of small vessel disease, medial temporal lobe atrophy, and global cerebral atrophy were documented. In addition, strategic infarcts were listed, and the definitions for these infarcts were predetermined according to previous studies and studies from the literature. Statistical analysis of cognitive scores was adjusted for age, sex, and educational level and calculated with linear and multiple regression models to identify magnetic resonance imaging markers related with the global cognitive score.
Multivariate analysis showed that strategic infarcts had the largest influence and accounted for 22.5% of the variance in the global cognitive score while medial temporal atrophy, stroke volume, and total normalized brain volume together accounted only for an additional 11.8%. Also surprisingly, white matter hyperintensities and microhemorrhages did not show up as independent contributors.
The patients in this sample were young (63 years median), the median Rankin Scale score after 6 months was 2, reflecting a benign course in this cohort, and only one patient had prestroke dementia thought to be because of a previous stroke. Although the selection criteria used in this study minimize the risk of an associated neurodegenerative process, it cannot be ruled out in some cases.
This investigation tackles a difficult and multidimensional issue and helps to describe not only the extent but also the location of brain lesions as they are known to be involved in major functional networks of brain functions. It contributes to a clinically useful and comprehensive approach to the analysis of neurocognitive disorders after stroke.
What are the immediate consequences? It must be recognized that a routine assessment of important cognitive domains is an essential part of the clinical workup. When clinical exam and neuroimaging show that there is involvement of strategic locations of the brain, assessment of function for major brain networks should also be made. These include the domains for language, attention and spatial orientation, object recognition, memory, and motor planning and control.
In the future, more emphasis must be given to the temporal trends of cognitive deterioration. It is unclear how the temporal profiles develop. It has been shown that neurocognitive disorders can develop in a delayed fashion thus suggesting an indirect, more gradual onset rather than a direct, sudden onset. These different time trajectories allow, in principle, to define a therapeutic time window, which could be used as an opportunity for behavioral and other interventions.8,9
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