Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0040
R. Wood, N. Alderman, A. Worthington
Helping brain-injured people re-adapt to society requires a system that provides individuals with opportunities to learn and apply social and functional skills in community settings. However, many types of acquired brain injury cause damage to prefrontal structures that are central to behavioural self-regulation, giving rise to complex patterns of socially challenging behaviour that can deny access to rehabilitation. Neurobehavioural rehabilitation was initially developed to address long-term problems of challenging behaviour that prevented individuals from engaging meaningfully with the rehabilitation process. However, it has evolved to promote psychosocial recovery more broadly, with the aim of changing behaviour from disabled, inappropriate, and socially handicapped to adaptive, purposeful, and ‘independent’. It is a paradigm that incorporates methods of associational learning within a structured environment that emphasizes clear feedback to raise awareness of behaviour, in a way that improves social cognition and self-regulation, to promote community independence.
{"title":"Neurobehavioural rehabilitation","authors":"R. Wood, N. Alderman, A. Worthington","doi":"10.1093/med/9780198757139.003.0040","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0040","url":null,"abstract":"Helping brain-injured people re-adapt to society requires a system that provides individuals with opportunities to learn and apply social and functional skills in community settings. However, many types of acquired brain injury cause damage to prefrontal structures that are central to behavioural self-regulation, giving rise to complex patterns of socially challenging behaviour that can deny access to rehabilitation. Neurobehavioural rehabilitation was initially developed to address long-term problems of challenging behaviour that prevented individuals from engaging meaningfully with the rehabilitation process. However, it has evolved to promote psychosocial recovery more broadly, with the aim of changing behaviour from disabled, inappropriate, and socially handicapped to adaptive, purposeful, and ‘independent’. It is a paradigm that incorporates methods of associational learning within a structured environment that emphasizes clear feedback to raise awareness of behaviour, in a way that improves social cognition and self-regulation, to promote community independence.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"104 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116801007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0020
G. Adan, S. Nightingale, C. Burness, T. Solomon
Central nervous system (CNS) infections, caused by various pathogens, can lead to a wide range of neuropsychiatric sequelae, including acute psychosis, mood disorders, and chronic dementias. Early recognition is critical as brain infections are often treatable and possible neuropsychiatric illness can be reversed if the diagnosis is timely. In addition to psychiatric symptoms, CNS infections may also present with other signs such as fever, meningism, cranial nerve deficit, and seizures. Although the presence of these additional features can often provide a clue to an underlying CNS infection, they are not always present; hence CNS infections should be considered in the differential diagnosis of psychiatric patients in certain situations. In this chapter, CNS infections that have psychiatric manifestations or have psychiatric sequelae are discussed, in particular HIV, neurosyphilis, meningitis, and encephalitis.
{"title":"Infections of the central nervous system","authors":"G. Adan, S. Nightingale, C. Burness, T. Solomon","doi":"10.1093/med/9780198757139.003.0020","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0020","url":null,"abstract":"Central nervous system (CNS) infections, caused by various pathogens, can lead to a wide range of neuropsychiatric sequelae, including acute psychosis, mood disorders, and chronic dementias. Early recognition is critical as brain infections are often treatable and possible neuropsychiatric illness can be reversed if the diagnosis is timely. In addition to psychiatric symptoms, CNS infections may also present with other signs such as fever, meningism, cranial nerve deficit, and seizures. Although the presence of these additional features can often provide a clue to an underlying CNS infection, they are not always present; hence CNS infections should be considered in the differential diagnosis of psychiatric patients in certain situations. In this chapter, CNS infections that have psychiatric manifestations or have psychiatric sequelae are discussed, in particular HIV, neurosyphilis, meningitis, and encephalitis.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124965377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1017/cbo9780511543777
M. Fink
For more than a century, catatonia has been considered a marker of the Kraepelin/Bleuler concept of schizophrenia. However, over the past half-century, it has been increasingly recognized as a separate entity, independently diagnosable and treatable. This chapter explores the diagnosis, treatment, and biological underpinnings of catatonia. Initially, it lists certain motor behaviours whose presentation might indicate catatonia, according to the Catatonia Rating Scale (CRS) such as mutism, delirium, and repetitive rhythmic acts. Through the intravenous administration of certain drugs, such as benzodiazepines, barbiturates, or gamma-aminobutyric acid (GABA) agonists, the effect on the patient’s CRS score is used to confirm the diagnosis. The treatment history of catatonia prior to the discovery of the efficacy of benzodiazepines and induced grand mal seizures (electroconvulsive therapy) is broached, such as chemically induced seizures and amobarbital. Finally, its different presentations are discussed, along with its consideration as a biological fear response.
{"title":"Catatonia","authors":"M. Fink","doi":"10.1017/cbo9780511543777","DOIUrl":"https://doi.org/10.1017/cbo9780511543777","url":null,"abstract":"For more than a century, catatonia has been considered a marker of the Kraepelin/Bleuler concept of schizophrenia. However, over the past half-century, it has been increasingly recognized as a separate entity, independently diagnosable and treatable. This chapter explores the diagnosis, treatment, and biological underpinnings of catatonia. Initially, it lists certain motor behaviours whose presentation might indicate catatonia, according to the Catatonia Rating Scale (CRS) such as mutism, delirium, and repetitive rhythmic acts. Through the intravenous administration of certain drugs, such as benzodiazepines, barbiturates, or gamma-aminobutyric acid (GABA) agonists, the effect on the patient’s CRS score is used to confirm the diagnosis. The treatment history of catatonia prior to the discovery of the efficacy of benzodiazepines and induced grand mal seizures (electroconvulsive therapy) is broached, such as chemically induced seizures and amobarbital. Finally, its different presentations are discussed, along with its consideration as a biological fear response.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131622485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0011
J. Burrell, J. Hodges, O. Piguet
Dementia presents itself in many guises, from its more common forms, such as Alzheimer’s disease (AD), vascular dementia (VaD), and dementia with Lewy bodies (DLB), to the less prevalent such as frontotemporal dementia (FTD). Although clinical diagnostic criteria for dementia, such as the DSM-5, do exist, they can be difficult to implement due to the variability of clinical features at presentation of dementia. This chapter provides an insight into the common neuropsychological profiles associated with the symptoms of various forms of dementia, along with overviews of a number of cognitive assessments, from the Mini-Mental State Examination (MMSE) to the Addenbrooke’s Cognitive Examination-III (ACE-III), along with a description of the way each tests for cognitive deficits.
痴呆症以多种形式出现，从较常见的形式，如阿尔茨海默病(AD)、血管性痴呆(VaD)和路易体痴呆(DLB)，到较不常见的形式，如额颞叶痴呆(FTD)。虽然痴呆的临床诊断标准，如DSM-5，确实存在，但由于痴呆表现时临床特征的可变性，它们可能难以实施。本章提供了与各种形式的痴呆症症状相关的常见神经心理学特征的见解，以及一些认知评估的概述，从迷你精神状态检查(MMSE)到阿登布鲁克认知检查- iii (ACE-III)，以及对每种认知缺陷测试方式的描述。
{"title":"Neuropsychological assessment of dementia","authors":"J. Burrell, J. Hodges, O. Piguet","doi":"10.1093/med/9780198757139.003.0011","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0011","url":null,"abstract":"Dementia presents itself in many guises, from its more common forms, such as Alzheimer’s disease (AD), vascular dementia (VaD), and dementia with Lewy bodies (DLB), to the less prevalent such as frontotemporal dementia (FTD). Although clinical diagnostic criteria for dementia, such as the DSM-5, do exist, they can be difficult to implement due to the variability of clinical features at presentation of dementia. This chapter provides an insight into the common neuropsychological profiles associated with the symptoms of various forms of dementia, along with overviews of a number of cognitive assessments, from the Mini-Mental State Examination (MMSE) to the Addenbrooke’s Cognitive Examination-III (ACE-III), along with a description of the way each tests for cognitive deficits.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131011234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0024
M. Edwards, Sarah R. Cope, N. Agrawal
Referred to by the ancient Greeks as ‘Hysteria’, functional neurological disorders (FNDs) are one of the most prevalent diagnoses made in neurology clinics. Nonetheless, in part, due to the uncertainty regarding the potential voluntariness of such conditions, diagnostic and treatment services for FNDs are underdeveloped by comparison to those for other causes of neurological symptoms. This chapter discusses historical approaches to the classification and approach to FNDs, before moving on to contemporary treatments for it. Various treatments are then described with regard to certain forms of FNDs, such as the effects of cognitive behavioural therapy (CBT) and psychodynamic interpersonal therapy on functional non-epileptic attacks and multidisciplinary inpatient treatment, physiotherapy, and hypnosis on functional motor disorder. Finally, the relative lack of treatment options for functional cognitive disorder (FCD) is discussed, along with the initial findings of a pilot randomized controlled trial for it.
{"title":"Functional neurological disorders","authors":"M. Edwards, Sarah R. Cope, N. Agrawal","doi":"10.1093/med/9780198757139.003.0024","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0024","url":null,"abstract":"Referred to by the ancient Greeks as ‘Hysteria’, functional neurological disorders (FNDs) are one of the most prevalent diagnoses made in neurology clinics. Nonetheless, in part, due to the uncertainty regarding the potential voluntariness of such conditions, diagnostic and treatment services for FNDs are underdeveloped by comparison to those for other causes of neurological symptoms. This chapter discusses historical approaches to the classification and approach to FNDs, before moving on to contemporary treatments for it. Various treatments are then described with regard to certain forms of FNDs, such as the effects of cognitive behavioural therapy (CBT) and psychodynamic interpersonal therapy on functional non-epileptic attacks and multidisciplinary inpatient treatment, physiotherapy, and hypnosis on functional motor disorder. Finally, the relative lack of treatment options for functional cognitive disorder (FCD) is discussed, along with the initial findings of a pilot randomized controlled trial for it.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124794871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0012
S. Bruno, N. Lahiri
To better understand the intricacies of genetic influences on neuropsychiatric disease, it is important first to have a grounding in the models of human inheritance and current diagnostic techniques. This chapter covers the fundamentals of genetic disorders, giving insights into chromosomal, single-gene, and mitochondrial disorders. Moreover, it explores the changing applications of genomic technologies, such as whole exome and whole genome sequencing, through the lens of their implications for neuropsychiatry. Clinical examples are provided to give an idea of the genetic underpinnings of Alzheimer’s disease, Parkinson’s disease, and other familiar disorders.
{"title":"Genetics of neuropsychiatric disease","authors":"S. Bruno, N. Lahiri","doi":"10.1093/med/9780198757139.003.0012","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0012","url":null,"abstract":"To better understand the intricacies of genetic influences on neuropsychiatric disease, it is important first to have a grounding in the models of human inheritance and current diagnostic techniques. This chapter covers the fundamentals of genetic disorders, giving insights into chromosomal, single-gene, and mitochondrial disorders. Moreover, it explores the changing applications of genomic technologies, such as whole exome and whole genome sequencing, through the lens of their implications for neuropsychiatry. Clinical examples are provided to give an idea of the genetic underpinnings of Alzheimer’s disease, Parkinson’s disease, and other familiar disorders.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"42 4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124971219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0006
John Hart Jr.
Knowledge of basic neuroanatomic organization is essential to understanding cognitive anatomic correlations. This chapter provides a descriptive overview of the basic neuroanatomic structures in the human brain, with a particular emphasis on the structures that are associated with cognitive and behavioural functions. These structures include the lobes of the brain (frontal, parietal, occipital, and temporal), the subcortical nuclei (basal ganglia and thalamus), the white matter, and the limbic system. A conceptual framework is presented that can be utilized to organize the anatomical locations, as well as the interconnections between regions. It is noted that neuroanatomy is not easily learnt by reading a text because it is a three-dimensional set of relationships.
{"title":"Basic neuroanatomy review","authors":"John Hart Jr.","doi":"10.1093/med/9780198757139.003.0006","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0006","url":null,"abstract":"Knowledge of basic neuroanatomic organization is essential to understanding cognitive anatomic correlations. This chapter provides a descriptive overview of the basic neuroanatomic structures in the human brain, with a particular emphasis on the structures that are associated with cognitive and behavioural functions. These structures include the lobes of the brain (frontal, parietal, occipital, and temporal), the subcortical nuclei (basal ganglia and thalamus), the white matter, and the limbic system. A conceptual framework is presented that can be utilized to organize the anatomical locations, as well as the interconnections between regions. It is noted that neuroanatomy is not easily learnt by reading a text because it is a three-dimensional set of relationships.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130241534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-01DOI: 10.1093/med/9780198757139.003.0016
N. Agrawal
Acquired brain injuries (ABIs) can be categorized as traumatic or non-traumatic brain injuries. Traumatic brain injuries (TBIs), sub-classified as either open or closed TBIs, depending on whether there is a fracture of the skull or a breach of the dura mater, are typically caused by a physical impact such as blunt trauma or a fall. Non-TBIs can be caused by cerebrovascular events, infections, or chemical factors. This chapter predominantly focuses on TBIs, exploring techniques to measure their extent, such as the Glasgow Coma Scale (GCS), and the aetiology of TBIs. Moreover, the long-term effects of TBIs are explored, such as anxiety disorders which often present themselves in their aftermath and the likelihood for TBI-induced personality change. The associated effects of non-TBIs are then examined, specifically with reference to anoxic brain injuries and those induced by drugs or alcohol.
{"title":"Brain injury","authors":"N. Agrawal","doi":"10.1093/med/9780198757139.003.0016","DOIUrl":"https://doi.org/10.1093/med/9780198757139.003.0016","url":null,"abstract":"Acquired brain injuries (ABIs) can be categorized as traumatic or non-traumatic brain injuries. Traumatic brain injuries (TBIs), sub-classified as either open or closed TBIs, depending on whether there is a fracture of the skull or a breach of the dura mater, are typically caused by a physical impact such as blunt trauma or a fall. Non-TBIs can be caused by cerebrovascular events, infections, or chemical factors. This chapter predominantly focuses on TBIs, exploring techniques to measure their extent, such as the Glasgow Coma Scale (GCS), and the aetiology of TBIs. Moreover, the long-term effects of TBIs are explored, such as anxiety disorders which often present themselves in their aftermath and the likelihood for TBI-induced personality change. The associated effects of non-TBIs are then examined, specifically with reference to anoxic brain injuries and those induced by drugs or alcohol.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"303 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114029681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-08-06DOI: 10.1176/appi.books.9781615371990.jl04
David Meagher, C. Daly, D. Adamis
Delirium is a common, complex neuropsychiatric syndrome that occurs in approximately one in five hospitalized patients. It is associated with a range of adverse healthcare outcomes that are independently predicted by the severity and duration of delirium. Typically 50% or more of cases of delirium are missed, misdiagnosed, or diagnosed late in everyday practice. However, routine systematic cognitive testing aligned to formal screening for delirium in high-risk cases can improve detection in everyday practice. The relationship between delirium and dementia is complex; dementia is a potent risk factor for delirium and 50% of delirium occurs in the context of a pre-existing dementia, but evidence also indicates that the occurrence of delirium can accelerate the course of dementia and that many cases of delirium are followed by long-term cognitive impairment. Delirium is highly preventable, with a third of cases avoidable by addressing a variety of patient, illness, and treatment factors. Treatment of incident delirium requires careful consideration of underlying causes, aggravating environmental factors, and prudent use of pharmacological strategies, with antipsychotic agents the preferred pharmacological intervention. Careful attention to post-delirium care can minimize functional loss, address any psychological sequelae, and reduce the risk of further episodes.
{"title":"Delirium","authors":"David Meagher, C. Daly, D. Adamis","doi":"10.1176/appi.books.9781615371990.jl04","DOIUrl":"https://doi.org/10.1176/appi.books.9781615371990.jl04","url":null,"abstract":"Delirium is a common, complex neuropsychiatric syndrome that occurs in approximately one in five hospitalized patients. It is associated with a range of adverse healthcare outcomes that are independently predicted by the severity and duration of delirium. Typically 50% or more of cases of delirium are missed, misdiagnosed, or diagnosed late in everyday practice. However, routine systematic cognitive testing aligned to formal screening for delirium in high-risk cases can improve detection in everyday practice. The relationship between delirium and dementia is complex; dementia is a potent risk factor for delirium and 50% of delirium occurs in the context of a pre-existing dementia, but evidence also indicates that the occurrence of delirium can accelerate the course of dementia and that many cases of delirium are followed by long-term cognitive impairment. Delirium is highly preventable, with a third of cases avoidable by addressing a variety of patient, illness, and treatment factors. Treatment of incident delirium requires careful consideration of underlying causes, aggravating environmental factors, and prudent use of pharmacological strategies, with antipsychotic agents the preferred pharmacological intervention. Careful attention to post-delirium care can minimize functional loss, address any psychological sequelae, and reduce the risk of further episodes.","PeriodicalId":205651,"journal":{"name":"Oxford Textbook of Neuropsychiatry","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129350280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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