Correspondence
Neuropsychiatric outcomes after stroke In The Lancet Neurology, Maree L Hackett and colleagues1 have written a comprehensive review of neuropsychiatric outcomes of stroke. The authors discuss non-cognitive neuropsychiatric outcomes at length; however, the meaning of noncognitive neuropsychiatric outcomes in this review is equivocal. Do they mean psychiatric reactions to the outcomes of brain damage or direct effects of the damage caused by a stroke? In the review they discuss both scenarios, resulting in a mixed bag. Hackett et al discuss depression, anxiety, emotional lability, and apathy as the most common neuropsychiatric outcomes. Depression in patients with stroke is a good example of a condition with unclear definitions. In the diagnostic criteria for depression of the Diagnostic and Statistical Manual-5,2 in addition to depressed mood and loss of pleasure (anhedonia), at least four other possible symptoms are assumed to be present, including weight loss or gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue or loss of energy, worthlessness or inappropriate guilt, and diminished concentration or indecisiveness. A diagnosis of depression should not include symptoms that are clearly due to a general medical disorder. However, this is exactly what seems to have been done in studies of stroke-related depression. For example, diminished concentration and indecisiveness are typical symptoms of damage to executive functions, whereas weight loss or gain can be caused by disturbance in the thalamic circuits, which can interfere with satiety and normal control of eating and ability to exercise. These symptoms might have nothing to do with the patient’s mood. Insomnia or hypersomnia, and fatigue or loss of energy, can be 1168
caused by damage in the vigilanceupholding-system networks (reticular activation system and associated connections). Likewise the other syndromes described in the Review, in addition to depression, can be caused directly by brain damage or might arise as psychiatric outcomes to the damage, or a mixture of both. Questionnaires used to diagnose these syndromes might lead to even more unclear results than psychiatric interviews. The methods and criteria used to diagnose post-stroke depression and the other syndromes can consequently yield unclear and vague diagnoses at best, or even miss a potential diagnosis. Damage to neural networks caused for example by a stroke, a tumour, or trauma will obviously also damage higher brain functions, whether cognitive or non-cognitive. Consequently the cause of these brain-function-associated symptoms does not need to be speculated.
Hackett and colleagues claim that no clear relation exists between the syndromes and location of brain lesion, which is an obvious conclusion. Mental functions are the result of functioning neural networks and, as such, there cannot be a direct modular localisation. Damage in seemingly similar brain regions might disturb different functions, and damage in different locations can disturb similar functions. What would be helpful to patients would be diagnoses based on clearer understanding of how higher mental functions are organised and how stroke damages them. I have no competing interests.
Merja E Kallio merja.kallio@helsinki.fi Department of Neurology, Helsinki University Central Hospital, Helsinki FI-00029, Finland 1
2
Hackett ML, Köhler S, O’Brien JT, Mead GE. Neuropsychiatric outcomes of stroke. Lancet Neurol 2014; 13: 525–34. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 5th edn. Arlington: American Psychiatric Publishing, 2013.
Authors’ reply Kallio comments that our review1 is a ‘mixed bag’ because we included both the psychiatric reaction to the outcomes of brain damage and the direct effects of damage caused by stroke. We deliberately took a broad and open view and discussed both types of causes, because to separate them clinically is generally impossible. Syndromes such as depression or apathy, and their persistence after stroke, are probably due to a multifactorial interplay of biological, psychological, and social factors. The debate about whether diagnostic criteria for major depression can be translated to stroke has not yet been solved.2 The so-called narrow focus view has led to the construction of depression scales tailored to specific populations. For stroke, there is the post-stroke depression rating scale,3 which is not widely used. Depression after stroke is generally not qualitatively different from depression occurring at any other time, after other health events, or in the general population. However, we need to keep an open mind, and research is needed to explore the specificity of the post-stroke depression phenotype to establish whether it really is a unitary concept. Kallio’s view that damage to neural networks will obviously also damage higher brain functions seems reductionist. For example, that view excludes the possibility of a reactive depression that is only indirectly related to the brain lesion by causing impairment and disability. The notion that the cause is “damage to neural networks” is not informative unless further specified. However, little evidence exists for a direct aetiological role of specific neural structures, urging us, unfortunately, to conclude that the cause of most of these syndromes is unknown. Kallio suggests that, because mental functions are the result of functioning neural networks, there cannot be a direct modular localisation. We agree,
www.thelancet.com/neurology Vol 13 December 2014
Neuropsychiatric outcomes after stroke In The Lancet Neurology, Maree L Hackett and colleagues1 have written a comprehensive review of neuropsychiatric outcomes of stroke. The authors discuss non-cognitive neuropsychiatric outcomes at length; however, the meaning of noncognitive neuropsychiatric outcomes in this review is equivocal. Do they mean psychiatric reactions to the outcomes of brain damage or direct effects of the damage caused by a stroke? In the review they discuss both scenarios, resulting in a mixed bag. Hackett et al discuss depression, anxiety, emotional lability, and apathy as the most common neuropsychiatric outcomes. Depression in patients with stroke is a good example of a condition with unclear definitions. In the diagnostic criteria for depression of the Diagnostic and Statistical Manual-5,2 in addition to depressed mood and loss of pleasure (anhedonia), at least four other possible symptoms are assumed to be present, including weight loss or gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue or loss of energy, worthlessness or inappropriate guilt, and diminished concentration or indecisiveness. A diagnosis of depression should not include symptoms that are clearly due to a general medical disorder. However, this is exactly what seems to have been done in studies of stroke-related depression. For example, diminished concentration and indecisiveness are typical symptoms of damage to executive functions, whereas weight loss or gain can be caused by disturbance in the thalamic circuits, which can interfere with satiety and normal control of eating and ability to exercise. These symptoms might have nothing to do with the patient’s mood. Insomnia or hypersomnia, and fatigue or loss of energy, can be 1168
caused by damage in the vigilanceupholding-system networks (reticular activation system and associated connections). Likewise the other syndromes described in the Review, in addition to depression, can be caused directly by brain damage or might arise as psychiatric outcomes to the damage, or a mixture of both. Questionnaires used to diagnose these syndromes might lead to even more unclear results than psychiatric interviews. The methods and criteria used to diagnose post-stroke depression and the other syndromes can consequently yield unclear and vague diagnoses at best, or even miss a potential diagnosis. Damage to neural networks caused for example by a stroke, a tumour, or trauma will obviously also damage higher brain functions, whether cognitive or non-cognitive. Consequently the cause of these brain-function-associated symptoms does not need to be speculated.
Hackett and colleagues claim that no clear relation exists between the syndromes and location of brain lesion, which is an obvious conclusion. Mental functions are the result of functioning neural networks and, as such, there cannot be a direct modular localisation. Damage in seemingly similar brain regions might disturb different functions, and damage in different locations can disturb similar functions. What would be helpful to patients would be diagnoses based on clearer understanding of how higher mental functions are organised and how stroke damages them. I have no competing interests.
Merja E Kallio merja.kallio@helsinki.fi Department of Neurology, Helsinki University Central Hospital, Helsinki FI-00029, Finland 1
2
Hackett ML, Köhler S, O’Brien JT, Mead GE. Neuropsychiatric outcomes of stroke. Lancet Neurol 2014; 13: 525–34. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 5th edn. Arlington: American Psychiatric Publishing, 2013.
Authors’ reply Kallio comments that our review1 is a ‘mixed bag’ because we included both the psychiatric reaction to the outcomes of brain damage and the direct effects of damage caused by stroke. We deliberately took a broad and open view and discussed both types of causes, because to separate them clinically is generally impossible. Syndromes such as depression or apathy, and their persistence after stroke, are probably due to a multifactorial interplay of biological, psychological, and social factors. The debate about whether diagnostic criteria for major depression can be translated to stroke has not yet been solved.2 The so-called narrow focus view has led to the construction of depression scales tailored to specific populations. For stroke, there is the post-stroke depression rating scale,3 which is not widely used. Depression after stroke is generally not qualitatively different from depression occurring at any other time, after other health events, or in the general population. However, we need to keep an open mind, and research is needed to explore the specificity of the post-stroke depression phenotype to establish whether it really is a unitary concept. Kallio’s view that damage to neural networks will obviously also damage higher brain functions seems reductionist. For example, that view excludes the possibility of a reactive depression that is only indirectly related to the brain lesion by causing impairment and disability. The notion that the cause is “damage to neural networks” is not informative unless further specified. However, little evidence exists for a direct aetiological role of specific neural structures, urging us, unfortunately, to conclude that the cause of most of these syndromes is unknown. Kallio suggests that, because mental functions are the result of functioning neural networks, there cannot be a direct modular localisation. We agree,
www.thelancet.com/neurology Vol 13 December 2014
