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Lancet (London, England) Jul 2016Schizophrenia is a complex, heterogeneous behavioural and cognitive syndrome that seems to originate from disruption of brain development caused by genetic or... (Review)
Review
Schizophrenia is a complex, heterogeneous behavioural and cognitive syndrome that seems to originate from disruption of brain development caused by genetic or environmental factors, or both. Dysfunction of dopaminergic neurotransmission contributes to the genesis of psychotic symptoms, but evidence also points to a widespread and variable involvement of other brain areas and circuits. Disturbances of synaptic function might underlie abnormalities of neuronal connectivity that possibly involves interneurons, but the precise nature, location, and timing of these events are uncertain. At present, treatment mainly consists of antipsychotic drugs combined with psychological therapies, social support, and rehabilitation, but a pressing need for more effective treatments and delivery of services exists. Advances in genomics, epidemiology, and neuroscience have led to great progress in understanding the disorder, and the opportunities for further scientific breakthrough are numerous--but so are the challenges.
Topics: Antipsychotic Agents; Brain; Cognition Disorders; Environmental Exposure; Humans; Psychotherapy; Schizophrenia; Schizophrenic Psychology; Social Support; Social Work
PubMed: 26777917
DOI: 10.1016/S0140-6736(15)01121-6 -
Dialogues in Clinical Neuroscience Sep 2019In this targeted review, we summarize current knowledge on substance-use disorder (SUD)-related cognitive deficits, the link between these deficits and clinical... (Review)
Review
In this targeted review, we summarize current knowledge on substance-use disorder (SUD)-related cognitive deficits, the link between these deficits and clinical outcomes, and the cognitive training, remediation, and pharmacological approaches that have the potential to rescue cognition. We conclude that: (i) people with SUDs have moderate deficits in memory, attention, executive functions, and decision-making (including reward expectancy, valuation, and learning); (ii) deficits in higher-order executive functions and decision-making are significant predictors of relapse; (iii) cognitive training programs targeting reward-related appetitive biases, cognitive remediation strategies targeting goal-based decision-making, and pharmacotherapies targeting memory, attention, and impulsivity have potential to rescue SUD-related cognitive deficits. We suggest avenues for future research, including developing brief, clinically oriented harmonized cognitive testing suites to improve individualized prediction of treatment outcomes; computational modeling that can achieve deep phenotyping of cognitive subtypes likely to respond to different interventions; and phenotype-targeted cognitive, pharmacological, and combined interventions. We conclude with a tentative model of neuroscience-informed precision medicine. .
Topics: Behavior, Addictive; Central Nervous System Stimulants; Cognition; Cognition Disorders; Cognitive Behavioral Therapy; Humans; Substance-Related Disorders
PubMed: 31749652
DOI: 10.31887/DCNS.2019.21.3/gdom -
Continuum (Minneapolis, Minn.) Apr 2016This article provides an overview of the clinical features, neuropathologic findings, diagnostic criteria, and management of dementia with Lewy bodies (DLB) and... (Review)
Review
PURPOSE OF REVIEW
This article provides an overview of the clinical features, neuropathologic findings, diagnostic criteria, and management of dementia with Lewy bodies (DLB) and Parkinson disease dementia (PDD), together known as the Lewy body dementias.
RECENT FINDINGS
DLB and PDD are common, clinically similar syndromes that share characteristic neuropathologic changes, including deposition of α-synuclein in Lewy bodies and neurites and loss of tegmental dopamine cell populations and basal forebrain cholinergic populations, often with a variable degree of coexisting Alzheimer pathology. The clinical constellations of DLB and PDD include progressive cognitive impairment associated with parkinsonism, visual hallucinations, and fluctuations of attention and wakefulness. Current clinical diagnostic criteria emphasize these features and also weigh evidence for dopamine cell loss measured with single-photon emission computed tomography (SPECT) imaging and for rapid eye movement (REM) sleep behavior disorder, a risk factor for the synucleinopathies. The timing of dementia relative to parkinsonism is the major clinical distinction between DLB and PDD, with dementia arising in the setting of well-established idiopathic Parkinson disease (after at least 1 year of motor symptoms) denoting PDD, while earlier cognitive impairment relative to parkinsonism denotes DLB. The distinction between these syndromes continues to be an active research question. Treatment for these illnesses remains symptomatic and relies on both pharmacologic and nonpharmacologic strategies.
SUMMARY
DLB and PDD are important and common dementia syndromes that overlap in their clinical features, neuropathology, and management. They are believed to exist on a spectrum of Lewy body disease, and some controversy persists in their differentiation. Given the need to optimize cognition, extrapyramidal function, and psychiatric health, management can be complex and should be systematic.
Topics: Autonomic Nervous System Diseases; Cognition Disorders; Disease Management; Humans; Lewy Body Disease; Mental Disorders; Parkinson Disease; REM Sleep Behavior Disorder
PubMed: 27042903
DOI: 10.1212/CON.0000000000000309 -
Orphanet Journal of Rare Diseases Dec 2010Huntington disease (HD) is a rare neurodegenerative disorder of the central nervous system characterized by unwanted choreatic movements, behavioral and psychiatric... (Review)
Review
Huntington disease (HD) is a rare neurodegenerative disorder of the central nervous system characterized by unwanted choreatic movements, behavioral and psychiatric disturbances and dementia. Prevalence in the Caucasian population is estimated at 1/10,000-1/20,000. Mean age at onset of symptoms is 30-50 years. In some cases symptoms start before the age of 20 years with behavior disturbances and learning difficulties at school (Juvenile Huntington's disease; JHD). The classic sign is chorea that gradually spreads to all muscles. All psychomotor processes become severely retarded. Patients experience psychiatric symptoms and cognitive decline. HD is an autosomal dominant inherited disease caused by an elongated CAG repeat (36 repeats or more) on the short arm of chromosome 4p16.3 in the Huntingtine gene. The longer the CAG repeat, the earlier the onset of disease. In cases of JHD the repeat often exceeds 55. Diagnosis is based on clinical symptoms and signs in an individual with a parent with proven HD, and is confirmed by DNA determination. Pre-manifest diagnosis should only be performed by multidisciplinary teams in healthy at-risk adult individuals who want to know whether they carry the mutation or not. Differential diagnoses include other causes of chorea including general internal disorders or iatrogenic disorders. Phenocopies (clinically diagnosed cases of HD without the genetic mutation) are observed. Prenatal diagnosis is possible by chorionic villus sampling or amniocentesis. Preimplantation diagnosis with in vitro fertilization is offered in several countries. There is no cure. Management should be multidisciplinary and is based on treating symptoms with a view to improving quality of life. Chorea is treated with dopamine receptor blocking or depleting agents. Medication and non-medical care for depression and aggressive behavior may be required. The progression of the disease leads to a complete dependency in daily life, which results in patients requiring full-time care, and finally death. The most common cause of death is pneumonia, followed by suicide.
Topics: Adolescent; Adult; Age of Onset; Aged; Child; Child, Preschool; Chorea; Cognition Disorders; Humans; Huntington Disease; Mental Disorders; Middle Aged; Young Adult
PubMed: 21171977
DOI: 10.1186/1750-1172-5-40 -
Annual Review of Clinical Psychology 2010Cognitive theories of depression posit that people's thoughts, inferences, attitudes, and interpretations, and the way in which they attend to and recall information,... (Review)
Review
Cognitive theories of depression posit that people's thoughts, inferences, attitudes, and interpretations, and the way in which they attend to and recall information, can increase their risk for depression. Three mechanisms have been implicated in the relation between biased cognitive processing and the dysregulation of emotion in depression: inhibitory processes and deficits in working memory, ruminative responses to negative mood states and negative life events, and the inability to use positive and rewarding stimuli to regulate negative mood. In this review, we present a contemporary characterization of depressive cognition and discuss how different cognitive processes are related not only to each other, but also to emotion dysregulation, the hallmark feature of depression. We conclude that depression is characterized by increased elaboration of negative information, by difficulties disengaging from negative material, and by deficits in cognitive control when processing negative information. We discuss treatment implications of these conclusions and argue that the study of cognitive aspects of depression must be broadened by investigating neural and genetic factors that are related to cognitive dysfunction in this disorder. Such integrative investigations should help us gain a more comprehensive understanding of how cognitive and biological factors interact to affect the onset, maintenance, and course of depression.
Topics: Cognition Disorders; Depressive Disorder, Major; Humans; Life Change Events; Mental Processes; Neuropsychological Tests; Prevalence; Psychological Theory; Severity of Illness Index
PubMed: 20192795
DOI: 10.1146/annurev.clinpsy.121208.131305 -
Brain : a Journal of Neurology Oct 2020An increasing proportion of cognitive difficulties are recognized to have a functional cause, the chief clinical indicator of which is internal inconsistency. When these... (Review)
Review
An increasing proportion of cognitive difficulties are recognized to have a functional cause, the chief clinical indicator of which is internal inconsistency. When these symptoms are impairing or distressing, and not better explained by other disorders, this can be conceptualized as a cognitive variant of functional neurological disorder, termed functional cognitive disorder (FCD). FCD is likely very common in clinical practice but may be under-diagnosed. Clinicians in many settings make liberal use of the descriptive term mild cognitive impairment (MCI) for those with cognitive difficulties not impairing enough to qualify as dementia. However, MCI is an aetiology-neutral description, which therefore includes patients with a wide range of underlying causes. Consequently, a proportion of MCI cases are due to non-neurodegenerative processes, including FCD. Indeed, significant numbers of patients diagnosed with MCI do not 'convert' to dementia. The lack of diagnostic specificity for MCI 'non-progressors' is a weakness inherent in framing MCI primarily within a deterministic neurodegenerative pathway. It is recognized that depression, anxiety and behavioural changes can represent a prodrome to neurodegeneration; empirical data are required to explore whether the same might hold for subsets of individuals with FCD. Clinicians and researchers can improve study efficacy and patient outcomes by viewing MCI as a descriptive term with a wide differential diagnosis, including potentially reversible components such as FCD. We present a preliminary definition of functional neurological disorder-cognitive subtype, explain its position in relation to other cognitive diagnoses and emerging biomarkers, highlight clinical features that can lead to positive diagnosis (as opposed to a diagnosis of exclusion), and red flags that should prompt consideration of alternative diagnoses. In the research setting, positive identifiers of FCD will enhance our recognition of individuals who are not in a neurodegenerative prodrome, while greater use of this diagnosis in clinical practice will facilitate personalized interventions.
Topics: Cognition Disorders; Cognitive Dysfunction; Dementia; Diagnosis, Differential; Disease Progression; Humans
PubMed: 32791521
DOI: 10.1093/brain/awaa224 -
British Journal of Pharmacology Oct 2011Developing reliable, predictive animal models for complex psychiatric disorders, such as schizophrenia, is essential to increase our understanding of the neurobiological... (Review)
Review
Developing reliable, predictive animal models for complex psychiatric disorders, such as schizophrenia, is essential to increase our understanding of the neurobiological basis of the disorder and for the development of novel drugs with improved therapeutic efficacy. All available animal models of schizophrenia fit into four different induction categories: developmental, drug-induced, lesion or genetic manipulation, and the best characterized examples of each type are reviewed herein. Most rodent models have behavioural phenotype changes that resemble 'positive-like' symptoms of schizophrenia, probably reflecting altered mesolimbic dopamine function, but fewer models also show altered social interaction, and learning and memory impairment, analogous to negative and cognitive symptoms of schizophrenia respectively. The negative and cognitive impairments in schizophrenia are resistant to treatment with current antipsychotics, even after remission of the psychosis, which limits their therapeutic efficacy. The MATRICS initiative developed a consensus on the core cognitive deficits of schizophrenic patients, and recommended a standardized test battery to evaluate them. More recently, work has begun to identify specific rodent behavioural tasks with translational relevance to specific cognitive domains affected in schizophrenia, and where available this review focuses on reporting the effect of current and potential antipsychotics on these tasks. The review also highlights the need to develop more comprehensive animal models that more adequately replicate deficits in negative and cognitive symptoms. Increasing information on the neurochemical and structural CNS changes accompanying each model will also help assess treatments that prevent the development of schizophrenia rather than treating the symptoms, another pivotal change required to enable new more effective therapeutic strategies to be developed.
Topics: Amphetamine; Animals; Antipsychotic Agents; Cognition Disorders; Disease Models, Animal; Female; Humans; Male; Mice; Models, Genetic; Models, Neurological; Neuropsychological Tests; Rats; Schizophrenia
PubMed: 21449915
DOI: 10.1111/j.1476-5381.2011.01386.x -
European Review For Medical and... Jun 2015Parkinsons Disease (PD) is a neurodegenerative disorder of the dopaminergic neurons in the substantia nigra. Much of the scientific literature on the Parkinson's disease... (Review)
Review
Parkinsons Disease (PD) is a neurodegenerative disorder of the dopaminergic neurons in the substantia nigra. Much of the scientific literature on the Parkinson's disease has been focused on the evaluation and management of motor conditions in PD. Much less stress has been laid on evaluating and managing the cognitive disturbances found comorbidly in this condition. Studies have suggested that the cognitive dysfunction observed in PD can range anywhere from individual cognitive deficits to the clinical picture of minimal cognitive impairment to as much as a full-blown dementia like clinical picture. Perhaps because of this poor understanding, the treatments for this comorbidity have not been able to be adequately developed. Right now, only rivastigmine is the approved drug of choice for treatment of dementia associated with PD. In this review we aim at elaborating the individual cognitive deficits associated with PD instead of focusing on full-blown dementia. Our aim at focusing on individual symptoms is important because these symptoms should be evaluated even at the most beginning stages of PD rather than waiting for the patient to report for the symptoms. Therefore, we will aim at elaborating the prevalence, symptomatology and implications for treatment for these cognitive dysfunctions individually. Because covering all the domains of cognitive dysfunctions are not possible here, we will focus on three cognitive impairments which are most commonly observed in the PD patients. These are the (1) Executive function deficits (2) Memory deficits and (3) visuospatial deficits. We will, finally, have an overview of the condition of minimal cognitive deficits observed in PD.
Topics: Cognition; Cognition Disorders; Dementia; Humans; Neurodegenerative Diseases; Parkinson Disease
PubMed: 26166654
DOI: No ID Found -
British Journal of Anaesthesia Nov 2018Cognitive change affecting patients after anaesthesia and surgery has been recognised for more than 100 yr. Research into cognitive change after anaesthesia and surgery... (Review)
Review
Cognitive change affecting patients after anaesthesia and surgery has been recognised for more than 100 yr. Research into cognitive change after anaesthesia and surgery accelerated in the 1980s when multiple studies utilised detailed neuropsychological testing for assessment of cognitive change after cardiac surgery. This body of work consistently documented decline in cognitive function in elderly patients after anaesthesia and surgery, and cognitive changes have been identified up to 7.5 yr afterwards. Importantly, other studies have identified that the incidence of cognitive change is similar after non-cardiac surgery. Other than the inclusion of non-surgical control groups to calculate postoperative cognitive dysfunction, research into these cognitive changes in the perioperative period has been undertaken in isolation from cognitive studies in the general population. The aim of this work is to develop similar terminology to that used in cognitive classifications of the general population for use in investigations of cognitive changes after anaesthesia and surgery. A multispecialty working group followed a modified Delphi procedure with no prespecified number of rounds comprised of three face-to-face meetings followed by online editing of draft versions. Two major classification guidelines [Diagnostic and Statistical Manual for Mental Disorders, fifth edition (DSM-5) and National Institute for Aging and the Alzheimer Association (NIA-AA)] are used outside of anaesthesia and surgery, and may be useful for inclusion of biomarkers in research. For clinical purposes, it is recommended to use the DSM-5 nomenclature. The working group recommends that 'perioperative neurocognitive disorders' be used as an overarching term for cognitive impairment identified in the preoperative or postoperative period. This includes cognitive decline diagnosed before operation (described as neurocognitive disorder); any form of acute event (postoperative delirium) and cognitive decline diagnosed up to 30 days after the procedure (delayed neurocognitive recovery) and up to 12 months (postoperative neurocognitive disorder).
Topics: Anesthesia; Cognition Disorders; Diagnostic and Statistical Manual of Mental Disorders; Emergence Delirium; Humans; Incidence; Neuropsychological Tests; Postoperative Complications; Preexisting Condition Coverage; Research Design; Terminology as Topic
PubMed: 30336844
DOI: 10.1016/j.bja.2017.11.087 -
The Journal of Clinical Psychiatry Jul 2015Research into the neuroanatomy and physiology of cognition is a growing field with applications for the treatment of major depressive disorder. The most common cognitive... (Review)
Review
Research into the neuroanatomy and physiology of cognition is a growing field with applications for the treatment of major depressive disorder. The most common cognitive impairments in people with depression are related to executive function, memory, attention, and processing speed along with negative bias. Based on data from improved imaging technology, many cognitive functions once assumed to be localized in specific areas of the brain are now thought to result from deficits in 3 key networks (the central executive network, the salience network, and the default mode network) and their interactions with each other and other brain areas. New discoveries in the connections and functions of brain networks and regions may provide novel treatment targets for cognitive symptoms in major depressive disorder.
Topics: Cognition Disorders; Depressive Disorder, Major; Executive Function; Humans; Nerve Net
PubMed: 26231020
DOI: 10.4088/JCP.13086tx3c