Cognition In The Wild Pdf: Fill & Download for Free

Capitalism is morally justifiable to someone whose altitude of moral function is (by almost any standard) immature, delusional or stunted. If someone believes that individuals operate in an antisocial vacuum and according to purely self-serving impulses, then they have invested in a 3-year-old’s rigid emphasis of I/Me/Mine egotism. And this level is where capitalism functions best.On the other hand, as we mature through adolescence into increasingly prosocial expectations and relations, we tend to recognize the importance of sharing, compassion, community, compromise, and indeed altruism. Part of growing up is (usually) coming to appreciate that no one operates in isolation without complex interactions and interdependencies with others, and that the only truly satisfying moments in life are a consequence of these trust relationships and communal experiences. As a consequence, a more mature moral orientation engages the world with empathy, kindness and generosity, and relaxes the self-absorbed and protective I/Me/Mine fixation of ego. Again, this is really about growing up. And once we grow up, we realize that capitalism seems to flourish at a rather banal, childish and emotionally stunted level of moral function – according to a very narrow definition of what is beneficial (i.e. “greed is good”) that doesn’t take into account a broader wealth of human experience, relationships, courage and love.As a consequence of the cognitive bias inherent to willfully childish morality, there is a lot of misleading information, revisionist history and ideological distortion in pro-capitalist rhetoric. I’ll try to set some of it straight.Here are some assumptions expressed in support of capitalism that are factually incorrect:1. Capitalism has improved the quality of life for people all over the Earth. Actually, it was widespread public education (and scientific experimentation and technological innovation driven by that education), in concert with democracy and expanding civil rights, that has improved the quality of life for people all over the Earth. It is the feedback loop of democracy, education and civil liberties supported by the rule of law that created the middle class and stabilized economic opportunity for more and more citizens. Even innovation isn’t mainly from capitalism; if you carefully analyze what has done the most good for the most people – be it a new scientific understanding, a new vaccination, a new technology, etc. – it is almost always a result of academic research at public institutions or government-funded research, not innovation that resulted from free markets. These leaps forward have indeed been made more efficiently and effectively by a single product of capitalism: mass production. But that’s it. That’s the only real contribution capitalism has made to humanity’s progress – the rest came from the Enlightenment and the evolution of democratic civil society thereafter. It can also be confidently argued that even the success of “free markets” in producing wealth was a result of the flourishing of this civil society – for “free markets” don’t exist in the wild, they are created by civic institutions and the rule of law. So again, it is the Enlightenment that really should receive primary credit for amplification of the common good…not capitalism.2. The benefits of profit-driven productivity outweigh its negative externalities. This declaration is as ignorant as it is arrogant. It’s why the rabidly pro-capitalist peeps are still denying climate change (sigh). It’s why that farmer a few years back ate spoonfuls of pesticide every morning to prove how safe it was. It’s why Ayn Rand thought cigarettes were her “Promethean muse,” dismissing any negative health impacts (until she contracted lung cancer). In order for the prevailing strain of growth-dependent global capitalism to keep producing wealth, it requires four things: a) unlimited, easily-accessed natural resources; b) a continuous supply of cheap labor; c) a growing consumer base whose affluence is also increasing; and d) no accountability (and no cost accounting) for negative externalities – and ideally no acknowledgement of them. Unfortunately for the pro-capitalist ideologues, it is extremely likely that none of these conditions will persist for more than another fifty years or so. Why? Well for one, the negative ecological externalities (climate change, loss of biodiversity, resource depletion, disruptive pollution, species extinction, etc.) resulting from human industry are increasingly interfering with productivity – and doing so quite directly. And for another, the affluence that supports a growing consumer base is directly at odds with cheap labor in our global economy, and these two dependencies will inevitably collide. And, finally, large numbers of people are waking up to the fact that the traditional engines of commerce are destroying the planet and need to be more accountable to their impacts – which will change the available opportunities and cost accounting for capitalist enterprise.3. The “tragedy of the commons” has been empirically validated. In reality, it has not. This is a thought experiment in the abstract, and its "inevitability" has been soundly debunked by the work of Elinor Ostrom. Check out her research on successful self-governance of the commons in the real world (common pool resource management) which relies neither on private property nor State management of land and resources, but on local, community-based, self-organized solutions.4. Private property in an exchange economy produces freedom. This is ridiculous. Private property restricts freedom – 99% of everything around us is privately owned and we can’t use it, access it - or sometimes even touch it. That’s not freedom, it’s a world of fences that corral us into the few remaining spaces that are still publicly owned (or the spaces we ourselves privately own). Exchange economies likewise benefit those with the most resources and influence who can game the system for their own benefit, deceiving both consumers and workers into believing that “working and consuming” is what life is all about. But being a wage slave is not freedom. Having Type II Diabetes from eating fast food is not freedom. Becoming addicted to cigarettes is not freedom. Premature disease and death from industrial pollutants is not freedom. Having lots of cool stuff you can buy on the Internet may feel like freedom…but it’s just a poor substitute for the real thing.5. The theory of labor appropriation as a “natural law” is sound. This is laughable. Locke based this on a naïve misconception of Native Americans and other hunter-gatherer societies. In reality – as validated by decades of careful research – hunter-gatherer societies frequently have had no conception of private property or of appropriating property by adding value with labor. Locke was simply wrong.6. Capitalism is not violent, coercive or fraudulent. This is so misinformed it’s just silly. State capitalism has either been directly responsible – or has engineered the perfect conditions – for most of the military actions around the globe since WWII. Industrial capitalism has resulted in the violent, lethal or injurious exploitation of workers since the beginning of the industrial revolution. Capitalist expansion has created endless varieties of forced appropriation of land, resources and indeed labor – from outright slavery to sweat shops. Capitalist commercialism is responsible for defrauding millions of consumers through false advertising, creating artificial demand, outright deception and fear-mongering, and deliberate theft. And to say that corporations haven’t used coercive force to intimidate workers and consumers is to ignore about half of the available history on consumer and worker rights.7. Capitalism is morally neutral. Hogwash. Please see points 1-6.The common thread here, you will notice, is that pro-capitalist idealists tend to avoid more complex and nuanced views of the world, holding rather blindly to a cherished individualism and economic opportunity for the privileged class, and loudly resisting when anyone questions their oversimplified definitions of negative liberty. Again, any moral justification for capitalism invokes a sort of immature blindness to the prosocial realities that likely helped human societies flourish since the dawn of our species (at least that’s what most of the research in group selection and prosocial genetic dispositions seems to indicate). But if we allow capitalism to continue destroying our society and the planet, humans will become a sad footnote in the annals of the extinct.In closing, I recommend you read my latest essay for more clarification on many of these issues: The Goldilocks Zone of Integral Liberty: A Proposed Method of Differentiating Verifiable Free Will from Countervailing Illusions of Freedom (scroll down that page to read it online, or download the PDF here: http://www.tcollinslogan.com/resources/IntegralLiberty.pdf)My 2 cents.

Yup! (Note that this is quite a heated debate, so you’ll get wildly divergent perspectives.)Many scientists have raised issues with the validity of evolutionary psychology. Since the mind does not leave fossils and has no obvious connection with stretches of DNA, there are fewer empirical constraints on evolutionary psychology than on other branches of evolutionary theory.This lack of constraint enables the proliferation of plausible-sounding stories based on hypothetical advantages conferred by a mental trait. The harshest critics of the evo psych approach label these stories ‘just so-stories’[1][1][1][1] . Of course, the proponents of evolutionary psychology are not just pulling stories out of a hat, so they think this is just a form of name-calling. (I disagree with the accusation that the critique is no more than name-calling, for reasons I describe briefly below.)In my own opinion, there is a narrowness to the evolutionary psychology approach. Many human mental traits are assumed to have arisen around the time when anatomically modern human arose, or shortly before. This selection is assumed to have occurred in what is termed the environment of evolutionary adaptedness (EEA). But I think a great deal of work needs to be done to prove that a mental trait has arisen in a particular time and place[2][2][2][2] . More deeply, there seems to be an assumption that the mind itself is a recent phenomenon, rather than something that began forming much earlier than the emergence of humans. Conversely, there is also an assumption that the mind stopped evolving in the ‘Stone Age’, and this is if anything even more misleading.An important style of critique attacks the optimality assumption that is common to fields such as evo psych and Bayesian decision theory[3][3][3][3]:“Much of this research aims to demonstrate that cognitive behavior can be explained from rational principles alone, without recourse to psychological or neurological processes and representations. We note commonalities between this rational approach and other movements in psychology - namely, Behaviorism and evolutionary psychology - that set aside mechanistic explanations or make use of optimality assumptions.”There are serious problems with the strand of rationalism that assumes optimality is always at play in biology. In practice, such assumptions can always be justified by inventing a cost function for which a behavior is optimal. In other words, optimality has free parameters that make the concept quite loose. This looseness allows optimality to be used to explain a behavior as well as the exact opposite behavior. Theories that “explain too much” are in a sense useless if they don’t provide a principled reason for choosing a given cost function (whether for Bayesian optimality or evolutionary fitness).This article in Scientific American captures some of the problems:Four Fallacies of Pop Evolutionary Psychology‘Fallacy 1: Analysis of Pleistocene Adaptive Problems Yields Clues to the Mind's Design’‘Fallacy 2: We Know, or Can Discover, Why Distinctively Human Traits Evolved’‘Fallacy 3: “Our Modern Skulls House a Stone Age Mind”’‘Fallacy 4: The Psychological Data Provide Clear Evidence for Pop EP’If you would like to read more deeply on this topic, perhaps check out David Buller’s essay ‘Evolutionary Psychology: A Critique’ [pdf].Footnotes[1] Just-so story - Wikipedia[1] Just-so story - Wikipedia[1] Just-so story - Wikipedia[1] Just-so story - Wikipedia[2] Buller on Evolutionary Psychology[2] Buller on Evolutionary Psychology[2] Buller on Evolutionary Psychology[2] Buller on Evolutionary Psychology[3] Bayesian Fundamentalism or Enlightenment? On the explanatory status and theoretical contributions of Bayesian models of cognition.[3] Bayesian Fundamentalism or Enlightenment? On the explanatory status and theoretical contributions of Bayesian models of cognition.[3] Bayesian Fundamentalism or Enlightenment? On the explanatory status and theoretical contributions of Bayesian models of cognition.[3] Bayesian Fundamentalism or Enlightenment? On the explanatory status and theoretical contributions of Bayesian models of cognition.

That’s not an easy question to answer.It would seem intuitive that, for a brain disorder such as stroke, clinical assessment should include the examination of memory, thinking, and mood. However, until quite recently, the focus has been on the physical manifestations of stroke, and neuropsychological aspects have received far too little attention. There is now mounting evidence that cognitive impairment after stroke is a significant contributor to disability, and its prevalence tends to increase sharply with advancing age. However, studies on the prevalence, course, and prognosis of poststroke cognitive disorders have produced wildly conflicting results. In fact, the symptoms of poststroke cognitive impairment are not well defined, and are misunderstood and misdiagnosed by many clinicians.This post is quite long, because I'm not sure what you're really asking. It's divided into three main sections, to make it easier to find the information you want:(1) What categories of cognitive impairment can be caused by ischemic brain stroke?Stroke can have a wide range of effects on brain function, from mild poststroke cognitive impairment (PSCI) to overt poststroke dementia (PSD). Our understanding of these effects is undergoing rapid change, This section discusses the current terminology used in the recent research literature, and how each category of impairment is defined.(2) Whether, when, and why will cognitive dysfunction (PSCI and/or PSD) occur after an ischemic stroke?Does ischemic brain stroke always cause cognitive impairment? No. This section discusses the frequency with which each type of impairment is caused in stroke survivors, how soon after stroke the impairment is seen, and some of the factors affecting a given stroke survivor's likelihood of suffering long-term cognitive impairment.(3) What sorts of behavioral changes can be caused by poststroke cognitive impairment?Both sections (1) and (2) might just be technobabble to the layman who's never encountered what stroke can do, other than the obvious physical difficulties such as a paralyzed arm. It occurred to me that you might really be wondering whether the strange behaviors of a loved one were actually caused by stroke, or by something else. This third section describes the more common, and some of the more unusual, behavioral changes that stroke can cause.(1) What categories of cognitive impairment can be caused by ischemic brain stroke?The terminology surrounding poststroke cognitive impairment is changing, so let's start there, for clarity.The term "vascular cognitive impairment (VCI)" has been proposed as an umbrella term to recognize the broad spectrum of cognitive and behavioral changes associated with vascular pathology. The most common causes of VCI are small-vessel disease, large-vessel disease, and strategic infarcts that may be either cortical or subcortical. VCI may also be the result of hypoperfusion, hemorrhage, and hereditary conditions (for example, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, CADASIL). All of these subtypes of VCI may appear poststroke. Even when poststroke dementia (PSD) and poststroke cognitive impairment (PSCI) are not purely vascular in origin, they can at least partly be regarded as categories of VCI.Poststroke dementia (PSD) is defined as any dementia occurring after stroke, including vascular dementia, Alzheimer’s disease, other neurodegenerative dementias, or mixed dementia. (Note that vascular lesions often coexist with Alzheimer's disease pathology and other lesions, and the presence of multiple pathologies greatly increases the odds of dementia.) The concepts PSD and PSCI usually refer to conditions occurring after symptomatic strokes with corresponding ischemic findings on neuroradiological imaging. However, seemingly asymptomatic strokes – a common incidental finding in patients both with and without symptomatic strokes – add to the vascular burden of the brain and can affect cognitive function. Dementia can even be caused by non-focal neurological changes found in patients with transient ischemic attack (TIA).Poststroke cognitive impairment (PSCI) is a common and under-recognised problem that may eventually lead to dementia (PSD). Two major issues hampering PSCI research include the lack of a clear-cut definition and a lack of highly specific and sensitive screening tools that accurately predict PSCI. PCSI is currently defined as failure in any cognitive domain after stroke, including attention and processing speed (sustained attention, divided attention, selective attention, information processing speed); frontal-executive function (planning, decision making, working memory, responding to feedback/error correction, novel situations, overriding habits, mental flexibility, judgment); learning and memory (immediate memory, recent memory -- including free recall, cued recall -- and recognition memory); language (naming, expressive, grammar and syntax, receptive); visuoconstructional-perceptual ability (construction, visual perception, and reasoning); praxis-gnosis-body schema (praxis, gnosis, right/left orientation, calculation ability, body schema, facial recognition); and/or social cognition (recognition of emotions and social cues, appropriate social inhibitions, theory of mind, empathy.)However, studies on the prevalence and progression of PSCI vary wildly as to the number of domains that must be impaired, the number of tests per domain, how domains are defined, and specific cut-offs used to define impairment. Early definitions of PSCI were based on the concept of mild cognitive impairment (MCI), primarily framed as a precursor to Alzheimer’s disease. (Note that there are several different types of MCI; and two-thirds of MCI patients will not progress to Alzheimer's.) The definition of MCI (and, accordingly, earlier definitions of PSCI) often requires intact basic activities of daily living (ADLs). However, stroke patients often have substantial physical impairments that interfere with ADLs, independent of cognitive function. Therefore, it has recently been recommended that requirements for intact ADLs should be specific to instrumental ADLs (IADLs) that are associated with cognition (e.g. managing money). This is consistent with the recent DSM-5 criteria which emphasize impairment in IADLs as a distinguishing factor between major and minor neurocognitive disorders. The new criteria also do not require memory impairment as a core symptom of PSCI or PSD. In stroke, it may be possible to have severely disabling cognitive problems but still retain memory. This latter change will be a major leap forward in studying and understanding poststroke cognitive function.Even without progression to PSD, milder levels of cognitive impairment may result in reduced participation in rehabilitation and poor adherence to treatment. PSCI predicts suboptimal recovery in activities of daily living, which in turn results in a lower quality of life (and a heavier burden on caregivers.)(2) Whether, when, and why will cognitive dysfunction (PSCI and/or PSD) occur after an ischemic stroke?The studies that have been conducted on neuropsychological aspects of stroke have produced conflicting results. Various studies have concluded that some stroke survivors may show no cognitive deficits, whereas the cognitive function of others may decline, initially decline and then improve, decline and then remain stable, and/or may progress to dementia over time. How many stroke survivors follow each of these poststroke profiles is unknown, since different studies reached widely different conclusions. The differences in prevalence and progression reported by different researchers may be related to differences in the diagnostic criteria (see above), the cognitive tests used, the timing of the testing (i.e., how soon after stroke the first cognitive testing is done, and how frequently follow-up testing is done, and long the follow-up period is), history of previous stroke, stroke location, the volume of the lesion, the presence of large‐ and small‐vessel disease, population sample (clinical- versus population-based, ages, gender, etc), inclusion/exclusion criteria for those patients to be tested, ethnicity, and the presence of neurodegenerative pathology. In some patients, the initial poststroke cognitive state may reflect prestroke cognitive decline or delirium. On top of all of this, some researchers have concluded that cognitive outcome following a stroke is dependent on sociodemographic, health, and stroke‐related risk factors, not just on the properties of the stroke itself and the overall pre-stroke vascular burden of the brain.For example, population or sampling characteristics, such as study setting (hospital or community), inclusion of patients with recurrent stroke, or inclusion of patients with pre-stroke cognitive impairment or dementia, can lead to variation in estimates of PSCI or PSD prevalence. Exclusion of patients who have difficulty undergoing cognitive testing (e.g., have severe aphasia due to the stroke) may be unavoidable, but can also effect prevalence estimates. Some publications state that up to 78% of patients show some cognitive deficits within 1 month after the stroke. However, delirium is quite common in the days and weeks immediately following a stroke. (Studies have reported an incidence of delirium as high as 48% in the acute phase of stroke.) Delirium, which has a rapid onset, is a serious disturbance in mental abilities that results in confused thinking and reduced awareness of the environment. Because symptoms of delirium and dementia can be similar, diagnosis of one in the presence of the other can be tricky. Ergo, erroneously high figures for the prevalence of cognitive deficits may be produced by studies that assess cognitive function within a month or two of the stroke; and those that went on to conduct additional assessments months later might have reported initial cognitive decline followed by some degree of recovery, whereas what was actually being observed was the resolution of the delirium. Most of the higher quality studies did not attempt to establish baseline poststroke cognition until three months after the stroke.One of the biggest flaws is the method(s) used to evaluate cognitive function. Even though there is an enormous amount of evidence that domain-specific cognitive tools are essential to capture the impact of PSCI and/or PSD, the vast majority of studies have relied exclusively on short, simple screening tests such as the Mini-Mental State Examination (MMSE) and/or Montreal Cognitive Assessment (MoCA). There are far too many factors that can affect the outcome of these simplistic tests for either one to be used to diagnose cognitive impairment, let alone estimate its severity. Both tests were initially developed to quickly screen for the possibility of Alzheimer's in outpatient settings rather than to identify cognitive defects in stroke patients. These tests have low sensitivity for the most commonly affected cognitive domains after stroke, such as executive function and processing speed. Moreover, PSCI is usually accompanied by additional cognitive deficits, such as aphasia/language dysfunction, vision loss, apraxia and spatial neglect, for which the tests are not sensitive and may greatly underestimate cases of cognitive impairment involving specific neurological deficits (e.g., aphasia). A 2019 systematic review on the cognitive screening tools used in the diagnosis of PSCI concluded that studies on PSCI have relied almost exclusively on nonspecific cognitive screening tools; that it is very well established that they are hopelessly inadequate for this purpose; and that a comprehensive standardized battery of neuropsychological tests is needed to fully capture the effects of stroke on cognitive function; even multidomain screening tools such as the new Oxford Cognitive Screen (OCS) are superior for the diagnosis of PSD and PSCI.Keeping all of this in mind, studies have generally concluded that, six months poststroke, roughly half of stroke survivors have neurocognitive disorders, two-thirds of whom have PSCI, and one-third of whom have PSD. Due to the inadequacies of the assessment tools that have been used, the prevalence of PSCI and PSD are undoubtedly higher. A study involving a population free from pre-stroke cognitive decline found that 57% suffered from cognitive impairment one year after stroke, only one third of whom developed a purely vascular cognitive disease. Poststroke cognitive impairment in the remainder was complex with a high coexistence of vascular and degenerative changes.Temporal aspects of cognitive impairment in patients (e.g., whether patients remain stable, improve, or decline) have often been ignored. Most of the studies that attempted to address this essential feature used screening tools such as the MMSE to judge the severity of cognitive problems. As noted above, the MMSE was never intended for this purpose and is hopelessly inadequate for it, despite its widespread use. Moreover, many studies have been cross-sectional, which are inadequate for addressing temporal aspects -- only longitudinal studies yield accurate information on progression. Finally, as more is learned about poststroke cognitive function, it becomes clear that a relatively long follow-up is needed to fully capture the impact of a stroke on the brain. Acute stroke may cause both a sudden cognitive decline and accelerated cognitive decline that is persistent over time. Very recent studies have concluded that cognitive function can decline in a delayed fashion, suggesting an indirect, more gradual onset rather than (or in addition to) a direct, sudden onset; any study with a short follow-up time period is unlikely to capture the full extent of a delayed decline. Delayed decline has been reported in approximately one‐third of patients. Several reasonably reliable studies with follow-up periods as long as five years have concluded that the delayed development of incident dementia remains up to 9 times greater than among an age-matched population for ≥5 years after stroke. Decline in cognitive function, however, is not inevitable; ~2.7 to 20% stroke survivors with PSCI but no dementia may eventually recover, depending on age and provided there is no recurrent stroke.Studies that combined sophisticated imaging techniques with extensive neuropsychological tests have produced the most reliable information, although these are few and far between. One excellent, and very interesting, example is a 2018 paper on a prospective, hospital-based study used 3-T MRI and a comprehensive standardized battery of neuropsychological tests 6 months after the index event to define the neuroimaging determinants of poststroke cognitive performance and their relative contributions. Data were available for 356 patients, 326 [91.6%] of whom had experienced an ischemic stroke.Half of the patients were found to have cognitive impairment six months poststroke.Of the many different MRI markers, the presence of a lesion within a small "strategic" site (i.e., the right corticospinal tract, left antero-middle thalamus, left arcuate fasciculus, left middle frontal gyrus, or left postero-inferior cerebellum) was the main determinant of poststroke cognitive performance and accounted for 22.5% of the observed variance in the global cognitive score.Stroke volume, total medial temporal lobe atrophy, and brain tissue volume were independent but weaker determinants, together accounting for an additional 11.8% variance in the global cognitive score.The total stroke volume accounted for only a small proportion (4.3%) of the variability in cognitive performance.The white matter hyperintensity (WMH) burden, presence of microbleeds, and dilated perivascular spaces were not independent determinants.This study emphasizes the fact that, regardless of their volume, lesions in strategic areas have a key role in the occurrence of poststroke neurocognitive disorders. Strategic strokes accounted for poor cognitive performance in patients with both a small stroke volume and no cerebral atrophy. 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 the 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.Also, atrophy has been one of the most controversial MRI markers for poststroke cognitive performance. Data from this 2018 study indicate that cerebral atrophy is associated with cognitive impairments. The researchers hypothesize that post-ischemia neurodegeneration in the subcortical region is probably one of the main contributors. Their results also emphasize the role of medial temporal lobe atrophy in poststroke neurocognitive disorders, independently from a potentially associated Alzheimer's disease. Medial temporal lobe atrophy may be related to delayed ischemic injury in hippocampal areas associated with selective vulnerability in a pure vascular process.Unfortunately, the cross-sectional design of this 2018 study made it impossible to investigate the relationship between MRI markers and long-term cognitive performance.The increasing use of MRI is influencing, and may even exaggerate, the estimate of the vascular burden behind cognitive impairment, because vascular changes are more apparent than degenerative ones in neuroradiology. On the other hand, depending on their location, vascular lesions may be more influential than they appear to be, disrupting interconnections between several distal regions. This applies, for example, to lesions in the basal ganglia and to the deep white matter, which damage the frontal-subcortical network and associate with executive dysfunction. The thalamus is another example of a strategic infarct location that may also cause amnestic dysfunction, in addition to executive defects.(3) What sorts of behavioral changes can be caused by poststroke cognitive impairment?I tripped across an interesting paper, Stroke and Behavior by Victor W Mark, describing the more common, and some of the more unusual, behavioral changes that stroke can cause. It's intended for the clinician, but it occurred to me that the answer I've written above might just be gibberish to the layman who's never encountered what stroke can do, other than the obvious physical difficulties, such as a paralyzed arm ... and that you might be asking your question because you wonder whether the changes you're observing in your loved one were actually caused by stroke, or something else. I'll briefly summarized what the paper had to say, but if you want to learn more, I'd suggest you contact Dr Mark to ask for a copy of the full publication: Stroke and Behavior | Request PDFDoctors and researchers primarily assess the impact of stroke in the controlled environment of the clinic or laboratory, using tests and materials that are assumed to simulate daily living activities, but that actually fail to represent the demands of the "real world" on the stroke survivor. Notably, performance is generally evaluated in response to the doctor’s prompting (“on command”), whereas much of real life occurs spontaneously, without prompting, and in a much more familiar environment. These differences can lead to marked differences in behavior between laboratory and home settings that you'll rarely find discussed in the research literature.Also note that behavioral studies of stroke primarily assess its acute effects, i.e., changes that take place shortly after the stroke. However, the severity as well as the quality of the behavioral effects of stroke may change considerably over the long run.In some languages -- for example, Chinese -- tone production during speech is crucial for interpreting individual word meanings in those languages. In addition, stroke survivors who had received less formal education are believed to develop more severe symptoms in many cognitive domains. The paper warns that many researchers have studied adults from industrialized societies who were formally well-educated and whose native language was nontonal (i.e., a language in which a word’s meaning is not affected by its intonation). The behavioral changes after stroke among patients who fall outside of these characteristics -- for example, patients from rural China -- are less well understood. On top of that, stroke survivors with severely impaired speech are usually excluded from studies on the impact of stroke on behavior, even those that involve nonverbal cognition tests. Hence, there is also little understanding of the impact of stroke on nonverbal communication in stroke patients.The following are some of the types of cognitive symptoms that can be caused by stroke. The paper also sometimes provides information on how such symptoms are diagnosed in stroke survivors, and some limited information on rehabilitation.Executive functions: Dr Mark says, "This very broad category refers to processes that regulate other functions, in the same way that a company’s executive controls subsidiary operations (eg, marketing, hiring, promotion, production, support services) without directly being involved with them." Generally speaking, executive functions involve planning (which requires abstraction), initiation, staying mindful of task objectives (working memory), prioritizing goals, sequencing activities for specific goals, and inhibiting attention to irrelevant stimuli (minimizing distraction).Disturbances to executive function after stroke can cause lack of spontaneity, distractibility, performing multistep operations in the wrong order, failure to inhibit behaviors that are inappropriate to a situation (eg, laughing while attending a funeral), or performing actions repeatedly for a goal or in response to stimulation, but needlessly ("perseveration"). In “recurrent perseveration”, a subtype of perseveration that is common in aphasia, patients uncritically repeat a response that they had provided to a previous question, but now, when given a new question, is inappropriate.The presence of executive dysfunction after a stroke is thought to predict limited functional recovery, and to interfere with the patient's ability to respond to rehabilitation efforts. Apparently, executive dysfunction after acute stroke is very common, with figures as high as 50% to 75% having been reported. However, it is very difficult to assess executive dysfunction, because the tests often involve lengthy, laborious procedures and/or require patients to understand complex instructions or give spoken responses. The requirements for understanding and responding to complex instructions often end up with a large number of aphasic patients being excluded from executive function studies.Language: Aphasia, which is one of the most common cognitive disturbances caused by stroke, is difficulty in communicating using language. Language is the ability to encode ideas into words or symbols for communication to someone else, and includes speaking, understanding the speech of others, reading, writing, gesturing (including sign language), and using numbers. Aphasia must be distinguished from speech dysarthria, mutism, aphonia (inability to vocalize), and hearing loss, which affect the physical ability to produce or hear speech, but do not selectively affect the symbolic aspects of speech. For example, stroke survivors with dysarthria experience “slurred” or “mumbled” speech due to limited lip, tongue and jaw movement; and there may be changes in pitch, or vocal quality (e.g., hoarseness or breathiness.)Aphasia occurs in about one-third of acute stroke patients and predicts worse survival than in nonaphasic stroke patients. By six months after stroke onset, aphasia may improve in more than one-half of patients and completely resolve in about 38%.Aphasia primarily results from left hemisphere injury (whether the patient is left- or right-handed.) However, aphasic disorders may rarely be caused by right hemisphere stroke, which is called crossed aphasia. The impairments that follow right hemisphere stroke are often subtle and difficult to recognize, including the patient having impaired interpretation of the social signals in discourse (such as failing to notice when another individual wants to end discussion), misunderstanding ambiguity, and producing meandering topics during speech expression.While aphasia often becomes less severe, the character of the aphasic disturbance may itself change during the patient's recovery. For example, global aphasia (typified by markedly impoverished speech comprehension and production) may change to Wernicke aphasia (fluent but nonsensical speech and poor comprehension); Broca aphasia (good comprehension, poor speech production) may resolve to anomic aphasia (good comprehension and fluency, but with word-finding difficulties). While nonfluent aphasia often gives way to fluent aphasia, fluent aphasia does not change to nonfluent aphasia.Stroke may also affect the use and/or interpretation of speech intonation, called aprosodia. "Affective aprosodia" is the disturbed interpretation or expression of emotional tone in speech; and "linguistic aprosodia" is the disturbance of nonemotional tone, for example, the conveyance of emphasis (“!”) or interrogation (“?”) in a sentence. In such disorders, the problem is not with word selection or sentence construction, but rather with determining the speaker’s social perspective (Is he angry?) or need for information (Is she asking a question?). Aprosodia is not associated with damage to any particular brain area or side. Testing is complicated by the need to rely on contrived situations that may not represent ordinary conditions for communications.Apraxia of speech can also be caused by stroke. This disturbance involves the inconsistent production of speech sounds (particularly consonants, depending on whether they are initial vs later in a word), and is considered a deficit of planning speech movements. This inconsistency thus differs from speech dysarthria. Associated difficulties include slowed rate of speech and abnormal rhythm and intonation. The disorder often is found with concurrent nonfluent aphasia. Reliable diagnosis and treatment have not been well-developed; its incidence in stroke is undetermined.Attention: Attention is the process of enhancing detection of a signal or stimulus from the environment, to the point where it can then be acted upon. Inattention caused by stroke may either be lateralized or nonlateralized with respect to the environment.The lateralized deficit is termed "unilateral spatial neglect" (neglect for short) and is a topic of intense research. This interest may be in part because the disorder, like aphasia, is easily noticed. For example, the patient with acute severe neglect consistently gazes toward the side of hemispheric damage (Vulpian sign), in the absence of oculomotor palsy. When patients with acute neglect combined with hemiplegia (total or partial paralysis of one side of the body) are asked to clap their hands, often they wave only the relatively good hand toward the body midline repeatedly without accommodating the lack of mobility in the other hand. This "one-handed clapping" is known as the Eastchester clapping sign. There is a general decrease in the initiation of action, and in exploring toward the contralateral side of space. Such problems can hamper locomotion (including car or wheelchair navigation), eating, grooming, reading, and protecting the paralyzed limbs from injury during transfers between bed and chair. Unilateral spatial neglect may even occur in one’s imagination, for example, when describing a familiar space that is out of view. Patients are often unaware of their attentional deficit and/or associated unilateral limb paralysis.Neglect is almost invariably opposite the side of hemispheric injury rather than on the same side of injury. It is about equally common after left versus right hemisphere damage, but right unilateral neglect is typically milder and resolves more rapidly.Neglect initially occurs in about one-half of all stroke survivors, but its incidence quickly diminishes, so that by about three months after the stroke, only ~30% of survivors still have neglect. However, standard neglect assessments may underestimate its prevalence. For example, standard pen-and-paper assessments may not detect neglect, whereas requesting the patient to perform everyday activities such as self-grooming or finding one’s way in a wheelchair may produce evidence of neglect.Patients with neglect are also susceptible to nonlateralized deficits of attention, including difficulty sustaining attention (or vigilance) over several minutes, and slowed response times. The finding that acute neglect may be a biomarker for chronic disability or impaired nonlateralized visuospatial processing, even in the absence of demonstrable neglect suggests that it may not be neglect per se that is most disabling, but rather an associated general inattention disorder. Unfortunately, there has been little investigation into nonspatial attentional deficits, their effect on daily living activities, epidemiology, and natural history, let alone controlled trials of rehabilitation.Memory: When referring to memory here, we are not including the “working memory” that was indicated to be an executive function (i.e., remaining constantly mindful of a fact or task requirement), but rather the process of either learning information or reconstituting it whenever necessary without staying mindful of it (episodic memory). Routine screening tests such as the MMSE ask the patient to repeat 3 unrelated words (e.g., apple, penny, table) immediately, to ensure the patient heard and understood the words, and then to recall those words after a few minutes’ delay (typically 5 minutes) as a brief clinical assessment of memory. Most Alzheimer's patients are unable to recall the words, even in the earliest stages of the disease. Impaired memory may occur in only ~11% of acute stroke patients -- and yet, until very recently, stroke survivors were not considered to have dementia unless they had impaired memory. This requirement was based on the hallmark symptom of Alzheimer's disease, not on any understanding of the severity of the impact stroke can have on the human brain. Moreover, to this day, the vast majority of the research literature on the prevalence and severity of cognitive dysfunction caused by stroke relies on brief screening tools such as the MMSE. Note, too, that unlike most cognitive disorders, verbal memory may continually worsen over the years after a stroke, relative to healthy individuals of the same age.Emotion: Stroke can provoke a wide variety of emotional changes which tend to follow a sequence rather than occurring all at once.Initial changes may include the “catastrophic reaction” and pseudobulbar affect. Catastrophic reaction refers to short-term marked irritability, anger, anxiety, or sadness when prompted to perform a task within the first few days of stroke onset. For example, patients with acute fluent aphasia with poor speech comprehension (Wernicke aphasia) may display marked agitation. After recovery from the aphasia, patients have reported that they had felt terrified, yet they believed that they could comprehend speech ordinarily, despite clinical observations to the contrary. Pseudobulbar affect is disinhibited crying or laughter that does not match the patient’s mood. The condition has a large number of synonyms, including emotionalism, emotional incontinence, pathologic affect, pathologic laughter and crying, and pseudobulbar palsy. Pseudobulbar affect has not been studied comprehensively. Its prevalence after stroke has been reported to range from 18% to 58%. The condition can be readily misdiagnosed as depression, with which it may co-occur. Stress can aggravate the pathologic display of affect.True depression emerges a few weeks after stroke onset. In stroke survivors, depression comprises a combination of sad mood, lack of initiative, steady state rather than cyclic emotional changes, lowered self-esteem, and feelings of guilt, particularly after patients have interacted with the complex world outside of the intensive care unit. depression is exceedingly common, ranging from 40% to 60% of patients, depending on the sample. The relationship between stroke and depression is bidirectional: depression itself is a risk factor for subsequent stroke, including fatal stroke, for unclear reasons. depression carries with it an increased risk of suicidal ideation, particularly in the first 2 years. Depression is also a biomarker for general cognitive impairment147,148 and impaired activities of daily living. Fortunately, conventional antidepressant medications are efficacious for poststroke depression. Improvement in depression is associated with improved self-care skills.Poststroke fatigue, which can co-occur with other poststroke conditions such as depression, also develops relatively late after stroke onset. In stroke survivors, "fatigue" refers to declining cognitive ability that is associated with the feeling of physical or mental strain, which can disrupt even simple routine activities. Poststroke fatigue may be found in the absence of pronounced neurologic deficits and is associated with failure to return to employment. It tends to be a chronic disorder. It has a reported prevalence ranging from 23% to 75%.Informal observations noted that the attitude of the stroke survivor toward the paralyzed arm may be affected. For example, patients with right hemiplegia and global (or severe) aphasia may reach over with the left hand and repeatedly mobilize the limp arm in the first few hours after stroke onset. In contrast, patients with left hemiplegia after stroke are more apt to demonstrate marked hatred for the arm, a condition that is called misoplegia.Apathy refers to the combination of lack of goal-directed behaviors and diminished interest and concern. The incidence of poststroke apathy is 20% to 25%. The condition does not occur invariably with depression, but it does place patients at high risk for depression and suicidal ideation. Apathy has not been investigated very thoroughly in stroke patients.Diminished empathy may also follow stroke. Empathy refers to the ability to adopt the perspective of another individual with concern for that person’s goals. The study of empathy is a newly emerging focus in poststroke behavioral changes. According to a recent study, about one-half of the caregivers of patients recovering from right hemisphere stroke regarded the patients’ loss of empathy as one of their greatest stressors. As discussed under "language" above, right hemisphere stroke can make it difficult for a stroke survivor to understand sarcasm, which is one aspect of reduced empathy.Movement: The behavioral regulation of movement, particularly limb movement, can be significantly affected by stroke. As noted above, patients may exhibit unilateral motor neglect; however, another cause is learned nonuse. The difference between the two is that the former is considered to be based on a form of inattention, whereas the latter is thought to emerge from the combination of the inability of the partially paralyzed limb to perform routine self-care activities and the simultaneous compensation for such activities by the opposite, better functioning arm. Thus, learned nonuse is behaviorally conditioned by the circumstances of chronic hemiparesis (slight paralysis or weakness on one side of the body), leading to the persisting inhibition of spontaneous limb use for everyday activities.Motor neglect and learned nonuse of hemiparesis can both be improved with verbal prompting. However, the inverse relationship can also occur, i.e., movement can be inhibited after prompting. The difference depends on the extent of attention paid by the patient. For example, in the Foix-Chavany-Marie syndrome (aka anterior opercular syndrome), stroke survivors may be unable to perform movements of the mouth upon command, yet show normal movements in a more familiar context (which demands less attention), such as when presented food or in response to an emotional stimulus. A limb version of such automatic-voluntary dissociation has been proposed, termed exo-evoked akinesia, but has seldom been reported clinically. Functional movement disorder (aka conversion disorder or psychogenic neurologic disorder) is a different kind of exo-evoked akinesia that manifests as a movement failure when the patient attends to the affected limb or is commanded to move it, but improves with distraction.Ideomotor apraxia (or apraxia for short) is the failure to competently generate the movements that are specific to tool use or gestures, despite (a) having sufficient movement capability to perform nonspecific movements and (b) understanding the task requirements. The term is applied when the stroke survivor is unable to recreate movements specific to learned activities, rather than reflecting part of a more general memory disorder. Ideomotor apraxia is most often reported with respect to upper extremity function, less so for oral movements (eg, soda straw use or blowing out a match), and even less for leg use (eg, kicking a ball, stamping out a cigarette). Roughly 6-7% of stroke survivors exhibit apraxia. Apraxia is important to stroke care because it is a biomarker for impaired functional recovery.Alien hand syndrome is a mostly unilateral disorder that involves seemingly purposeful activities by one hand without the patient’s consciously intending them, as if an alternate personality were guiding them. Although various subtypes have been described, the two most often reported are frontal alien hand and callosal alien hand, named for the brain regions that are characteristically affected. Frontal alien hand involves the disinhibited grabbing of objects that are within reaching distance. Often it is then hard for the patient to release the object. Callosal alien hand involves one hand obstructing, repeating, or undoing the actions of the other hand that is under voluntary control. For example, a callosal alien hand may counteract blouse unbuttoning by the other hand. Alien hand in either form may be frustrating, humiliating, or even dangerous, such as when grasping a hot object or driving a car. Despite numerous case reports, the epidemiology of alien hand has rarely been studied because it is rare, accounting for less than 1% of stroke patients in one series.Sensory processing: Agnosias, in which a given sensory system is functioning normally but the brain misinterprets the signals from the system, are not unusual after stroke, but are not studied as much as the disorders described above, for several reasons. For example, because these disorders mostly arise from damage to posterior parts of the cerebrum, they often occur little or no effect on motor control and therefore are less likely to warrant inpatient rehabilitation. In addition, it is not unusual for patients with these disturbances to be unaware of these problems (the condition of anosognosia). [Speaking from my experience with agnosias in Alzheimer's patients, the caregiver is typically unaware of the problems, as well, and cannot begin to understand why the patient is behaving in a given way. In Alzheimer's, agnosias come and go, which further confuses efforts to figure out what is going on.]Visual agnosias may be chronic in 20% of stroke survivors. Those with loss of visual awareness -- at least for stationary objects -- to one side may initially be unaware of this loss. If they lack pronounced cognitive disorders, they can often readily discover their visual field limitation through interacting with the environment or through clinical education, and may learn to compensate for visual loss by increasing their head or eye movements to one side. However, a large percentage exhibit highly disorganized visual exploration, even in their preserved visual field for unclear reasons, and are vulnerable to accidents at busy traffic intersections or in other cluttered environments. Simple coaching and practice or formal oculomotor training may help to minimize this problem.A rare poststroke symptom of visual agnosia is the inability to recognize objects despite being capable of making elementary judgments about their properties, e.g., size and shape. Similarly, patients with auditory agnosia can point to sounds and describe some of their properties (eg, “clicking” when listening to a thumb moving along a pocket comb) without being able to specify the object responsible. A similar disturbance attends the rarely reported instance of tactile agnosia.A peculiar but little studied disorder involves the difficulty that stroke patients may have with connecting familiar percepts or concepts to each other. In particular, stroke survivors, particularly those with aphasia, were unable to color in line drawings of familiar objects with the expected colors (eg, banana / yellow). Instead, they significantly often chose unexpected colors, even though color blindness was excluded. This, accordingly, is termed color association disorder. A right hemisphere stroke patient without aphasia, however, used just a couple of colors in a line drawing of multiple familiar objects in a single plausible outdoor scene.Although such a disorder would seem to have little clinical relevance, the researchers noted that aphasic patients may also be prone to other abnormalities of percept matching, namely inability to match sounds that they heard to the most likely object in a picture array (eg, meow / cat). They also could not properly simulate object use when they were shown objects (eg, swing the arm when shown a hammer). The latter is a standard assessment of apraxia. The real-life implications of such difficulties when measured under laboratory conditions is not yet clear, but suggest a fundamental difficulty with abstraction.Hallucinations, although rare, can also follow stroke. Typically, the hallucinations are of the visual kind, i.e., seeing something that isn't there. The stroke patient may see simple geometric shapes or complex objects, or have uncontrollable reexperiencing of objects that had just been viewed (palinopsia, or visual perseveration).Still other visual disturbances for which the clinician should be aware include alexia (the inability to interpret writing or print despite being able to see it), achromatopsia (loss of color vision from brain injury), and prosopagnosia (difficulty recognizing familiar faces). The auditory analog of prosopagnosia -- i.e., the impaired ability to recognize familiar voices -- is termed phonagnosia and has been reported in stroke, but rarely studied.For more reading:https://www.researchgate.net/publication/328287207_Neuroimaging_Determinants_of_Poststroke_Cognitive_Performance_The_GRECogVASC_Study to request a copy of the full paperPuy L, Barbay M, Roussel M, Canaple S, Lamy C, Arnoux A, Leclercq C, Mas JL, Tasseel-Ponche S, Constans JM, Godefroy O. Neuroimaging Determinants of Poststroke Cognitive Performance: The GRECogVASC Study. Stroke. 2018 Nov;49(11):2666-73.This large and detailed cross-sectional study used a comprehensive, standardized neuropsychological battery to explore all cognitive domains; and assessed cognitive performance after adjusting for demographic factors to eliminate confusion between demographic factors and MRI determinants. It was not restricted to dementia or to the presence of cognitive impairment but rather analyzed the cognitive score as a continuous variable; this reflects cognitive performance more accurately and is not affected by discretization errors.Poststroke Neurocognitive Disorders Are Mostly Defined by Strategic LesionsBrainin M, Teuschl Y. Poststroke Neurocognitive Disorders Are Mostly Defined by Strategic Lesions. Stroke. 2018;49:2563–2564.These experts published an assessment of the Puy et al study.Prevalence and short‐term changes of cognitive dysfunction in young ischaemic stroke patientsPinter D, Enzinger C, Gattringer T, Eppinger S, Niederkorn K, Horner S, Fandler S, Kneihsl M, Krenn K, Bachmaier G, Fazekas F. Prevalence and short‐term changes of cognitive dysfunction in young ischaemic stroke patients. European journal of neurology. 2018 Nov 29.Most studies on poststroke cognitive impairment involve older patients. In general, the burden of cerebrovascular disease and the severity of cognitive impairment increase with age. Pinter et al studied young ischaemic stroke patients (18-55 years) for the presence and development of neuropsychological deficits.Using the Oxford Cognitive Screen to Detect Cognitive Impairment in Stroke Patients: A Comparison with the Mini-Mental State ExaminationMancuso M, Demeyere N, Abbruzzese L, Damora A, Varalta V, Pirrotta F, Antonucci G, Matano A, Caputo M, Caruso MG, Pontiggia GT. Using the Oxford cognitive screen to detect cognitive impairment in stroke patients: a comparison with the Mini-Mental state examination. Frontiers in neurology. 2018 Feb 28;9:101.ScienceDirectHu GC, Chen YM. Post-stroke dementia: epidemiology, mechanisms and management. International Journal of Gerontology. 2017 Dec 1;11(4):210-4.Domain-specific versus generalized cognitive screening in acute strokeDemeyere N, Riddoch MJ, Slavkova ED, Jones K, Reckless I, Mathieson P, et al. Domain-specific versus generalized cognitive screening in acute stroke. J Neurol (2016) 263:306–15.ScienceDirectKapasi A, Schneider JA. Vascular contributions to cognitive impairment, clinical Alzheimer's disease, and dementia in older persons. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease. 2016 May 1;1862(5):878-86Trajectory of Cognitive Decline After Incident StrokeLevine DA, Galecki AT, Langa KM, Unverzagt FW, Kabeto MU, Giordani B, Wadley VG. Trajectory of cognitive decline after incident stroke. JAMA 2015 Jul 7;314(1):41-51.Post‐stroke cognitive impairment is common even after successful clinical recoveryJokinen H, Melkas S, Ylikoski R, Pohjasvaara T, Kaste M, Erkinjuntti T, Hietanen M. Post‐stroke cognitive impairment is common even after successful clinical recovery. European Journal of Neurology. 2015 Sep;22(9):1288-94.Diagnostic criteria for vascular cognitive disorders: a VASCOG statementSachdev P, Kalaria R, O'Brien J, et al. Diagnostic criteria for vascular cognitive disorders: a VASCOG statement. Alzheimer Dis Assoc Disord. 2015;28:206–18https://s3.amazonaws.com/academia.edu.documents/42982662/Underestimation_of_cognitive_impairments20160223-14304-1tp1wv.pdf?AWSAccessKeyId=AKIAIWOWYYGZ2Y53UL3A&Expires=1552353397&Signature=V8yclxqU%2BoKcwr7cqQdKocep0K8%3D&response-content-disposition=inline%3B%20filename%3DUnderestimation_of_cognitive_impairments.pdfChan E, Khan S, Oliver R, Gill SK, Werring DJ, Cipolotti L. Underestimation of cognitive impairments by the Montreal Cognitive Assessment (MoCA) in an acute stroke unit population. Journal of the neurological sciences. 2014 Aug 15;343(1-2):176-9.Delirium in Acute StrokeShi Q, Presutti R, Selchen D, Saposnik G. Delirium in acute stroke: a systematic review and meta‐analysis. Stroke. 2012; 43:645–649.Incidence and Prognosis of Transient Neurological AttacksBos MJ, van Rijn MJ, Witteman JC, Hofman A, Koudstaal PJ, Breteler MM. Incidence and prognosis of transient neurological attacks. JAMA 2007 Dec 26;298(24):2877-85.