The document presents revised criteria for diagnosing Alzheimer's disease (AD) dementia put forth by a workgroup convened by the National Institute on Aging and the Alzheimer's Association. The summary is:
1. The workgroup updated the 1984 NINCDS-ADRDA criteria for AD dementia to incorporate advances in understanding of AD pathology and clinical presentation, as well as biomarkers.
2. The revised criteria distinguish between all-cause dementia, probable AD dementia based on clinical criteria alone, and probable or possible AD dementia when biomarkers are also considered.
3. Probable AD dementia requires a gradual onset of cognitive decline in one of several domains including memory, language, visuospatial skills or executive function.
Toward defining the preclinical stages of Alzheimer's diseaseDario Yac
1) The document discusses recommendations from a workgroup on defining the preclinical stages of Alzheimer's disease.
2) It proposes a conceptual framework that defines Alzheimer's disease as encompassing the underlying pathophysiological process (AD-P) rather than just the clinical stages of the disease.
3) The framework suggests there is a long asymptomatic period during which the pathological process is progressing, and individuals may be at increased risk for future cognitive impairment even if symptoms have not emerged yet.
Evolution of the diagnostic criteria for degenerative and cognitive disordersDario Yac
The diagnostic criteria for Alzheimer's disease have evolved over the past 25 years to incorporate biomarkers and define the disease from preclinical to dementia stages. Recent criteria proposed by the National Institute on Aging and Alzheimer's Association aim to provide a unified framework accounting for biomarkers to support clinical diagnosis. While biomarkers show Alzheimer's pathology may precede symptoms, the criteria caution about their validation and relationship to symptom onset is still unclear. The diagnostic process first determines if a patient meets criteria for dementia by showing impairments in memory and at least one other cognitive domain significantly impacting functioning.
Introduction to Revised Criteria for the Diagnosis of Alzheimer’s DiseaseDario Yac
This document introduces revised criteria for diagnosing Alzheimer's disease from the National Institute on Aging and the Alzheimer's Association. It discusses advances in understanding AD since the original 1984 criteria. The revised criteria distinguish between AD pathophysiological processes and clinical symptoms. Biomarkers of amyloid and neuronal degeneration are incorporated formally. The criteria are intended to better account for the gradual progression of cognitive impairment in AD and differences from other dementias.
This document proposes revising the diagnostic criteria for Alzheimer's disease (AD) to better capture the earliest stages of the disease before full dementia. The current NINCDS-ADRDA criteria have low specificity for differentiating AD from other dementias. New biomarkers from neuroimaging and cerebrospinal fluid now enable more definitive identification of AD pathology. The proposed revisions center on early episodic memory impairment and require at least one abnormal biomarker. Revised criteria are needed to reliably identify AD at its earliest stages to better test emerging disease-modifying therapies aimed at preventing progression to dementia.
The diagnosis of mild cognitive impairment due to Alzheimer’s disease:Dario Yac
The document provides recommendations from a workgroup on criteria for mild cognitive impairment (MCI) due to Alzheimer's disease (AD). It outlines two sets of criteria:
1. Core clinical criteria for MCI diagnosis that do not require biomarkers and can be used in any clinical setting. This includes evidence of cognitive decline from the patient or informant and impairment in one or more cognitive domains with preserved functional abilities.
2. Clinical research criteria for use in research settings that incorporate biomarkers based on imaging and cerebrospinal fluid measures. This criteria has four levels of certainty depending on biomarker findings.
Considerable further research is needed to validate the biomarker-based criteria and standardize biomarkers before they can be used
This document lists 53 publications by Dr. Nelleen Baboolal, including:
1) Peer-reviewed journal articles on topics like dementia research in Trinidad and Tobago, emotional intelligence, and biomarkers for Alzheimer's disease.
2) Book chapters on mental health issues in the Caribbean region and risk factors for Alzheimer's disease.
3) Conference presentations and papers on quantifying EEG waves and determining diagnostic methods for mental illnesses.
4) A dissertation on special educational needs in children.
5) Non-peer reviewed articles in regional medical journals.
6) Other publications such as lecture notes and an educational video.
1) Generalized Anxiety Disorder (GAD) is highly prevalent, affecting approximately 2% of the population annually, yet it often goes undiagnosed.
2) GAD frequently presents with medically unexplained symptoms like insomnia or pain rather than anxiety itself, making it challenging to diagnose. It also commonly co-occurs with other psychiatric or medical conditions.
3) While GAD has a substantial personal and economic burden, primary care physicians correctly diagnose it in only about one-third of cases. Better physician education is needed to improve recognition and management of GAD.
This research article reviews recent studies on Barrett's esophagus with epithelial changes indefinite for dysplasia (BE IND). The studies show that BE IND carries a significant risk of prevalent advanced neoplasia, ranging from 1.9-15% within one year. The risk of progression to advanced neoplasia for BE IND is 0.43-1.2 cases per 100 person-years. Several factors may help stratify this risk, including length of Barrett's esophagus, multifocality of IND, abnormal p53 expression, inflammation, and abnormal DNA content. However, additional large prospective studies are needed to better understand how to manage patients with a diagnosis of BE IND.
Toward defining the preclinical stages of Alzheimer's diseaseDario Yac
1) The document discusses recommendations from a workgroup on defining the preclinical stages of Alzheimer's disease.
2) It proposes a conceptual framework that defines Alzheimer's disease as encompassing the underlying pathophysiological process (AD-P) rather than just the clinical stages of the disease.
3) The framework suggests there is a long asymptomatic period during which the pathological process is progressing, and individuals may be at increased risk for future cognitive impairment even if symptoms have not emerged yet.
Evolution of the diagnostic criteria for degenerative and cognitive disordersDario Yac
The diagnostic criteria for Alzheimer's disease have evolved over the past 25 years to incorporate biomarkers and define the disease from preclinical to dementia stages. Recent criteria proposed by the National Institute on Aging and Alzheimer's Association aim to provide a unified framework accounting for biomarkers to support clinical diagnosis. While biomarkers show Alzheimer's pathology may precede symptoms, the criteria caution about their validation and relationship to symptom onset is still unclear. The diagnostic process first determines if a patient meets criteria for dementia by showing impairments in memory and at least one other cognitive domain significantly impacting functioning.
Introduction to Revised Criteria for the Diagnosis of Alzheimer’s DiseaseDario Yac
This document introduces revised criteria for diagnosing Alzheimer's disease from the National Institute on Aging and the Alzheimer's Association. It discusses advances in understanding AD since the original 1984 criteria. The revised criteria distinguish between AD pathophysiological processes and clinical symptoms. Biomarkers of amyloid and neuronal degeneration are incorporated formally. The criteria are intended to better account for the gradual progression of cognitive impairment in AD and differences from other dementias.
This document proposes revising the diagnostic criteria for Alzheimer's disease (AD) to better capture the earliest stages of the disease before full dementia. The current NINCDS-ADRDA criteria have low specificity for differentiating AD from other dementias. New biomarkers from neuroimaging and cerebrospinal fluid now enable more definitive identification of AD pathology. The proposed revisions center on early episodic memory impairment and require at least one abnormal biomarker. Revised criteria are needed to reliably identify AD at its earliest stages to better test emerging disease-modifying therapies aimed at preventing progression to dementia.
The diagnosis of mild cognitive impairment due to Alzheimer’s disease:Dario Yac
The document provides recommendations from a workgroup on criteria for mild cognitive impairment (MCI) due to Alzheimer's disease (AD). It outlines two sets of criteria:
1. Core clinical criteria for MCI diagnosis that do not require biomarkers and can be used in any clinical setting. This includes evidence of cognitive decline from the patient or informant and impairment in one or more cognitive domains with preserved functional abilities.
2. Clinical research criteria for use in research settings that incorporate biomarkers based on imaging and cerebrospinal fluid measures. This criteria has four levels of certainty depending on biomarker findings.
Considerable further research is needed to validate the biomarker-based criteria and standardize biomarkers before they can be used
This document lists 53 publications by Dr. Nelleen Baboolal, including:
1) Peer-reviewed journal articles on topics like dementia research in Trinidad and Tobago, emotional intelligence, and biomarkers for Alzheimer's disease.
2) Book chapters on mental health issues in the Caribbean region and risk factors for Alzheimer's disease.
3) Conference presentations and papers on quantifying EEG waves and determining diagnostic methods for mental illnesses.
4) A dissertation on special educational needs in children.
5) Non-peer reviewed articles in regional medical journals.
6) Other publications such as lecture notes and an educational video.
1) Generalized Anxiety Disorder (GAD) is highly prevalent, affecting approximately 2% of the population annually, yet it often goes undiagnosed.
2) GAD frequently presents with medically unexplained symptoms like insomnia or pain rather than anxiety itself, making it challenging to diagnose. It also commonly co-occurs with other psychiatric or medical conditions.
3) While GAD has a substantial personal and economic burden, primary care physicians correctly diagnose it in only about one-third of cases. Better physician education is needed to improve recognition and management of GAD.
This research article reviews recent studies on Barrett's esophagus with epithelial changes indefinite for dysplasia (BE IND). The studies show that BE IND carries a significant risk of prevalent advanced neoplasia, ranging from 1.9-15% within one year. The risk of progression to advanced neoplasia for BE IND is 0.43-1.2 cases per 100 person-years. Several factors may help stratify this risk, including length of Barrett's esophagus, multifocality of IND, abnormal p53 expression, inflammation, and abnormal DNA content. However, additional large prospective studies are needed to better understand how to manage patients with a diagnosis of BE IND.
This document contains abstracts from research, innovations, and clinical vignettes presented at the 2011 Hospital Medicine annual meeting. The abstracts are divided into sections for research, innovations, and clinical vignettes. Some of the abstracts presented include evaluations of HIV screening practices, the safety of arthrocentesis for patients on warfarin therapy, incidence of venous thromboembolism in homebound patients, and an assessment of pain in patients undergoing bone marrow biopsies. The abstracts cover a wide range of topics in hospital medicine and include results from studies, innovations, and case reports.
Transitional Care for Pediatric Patients with Neuromuscular Diseases: A Healt...HTAi Bilbao 2012
Transitional Care for Pediatric Patients with Neuromuscular Diseases: A Health Technology Assessment
Jackie Tran, MD
University of Medicine and Dentistry of New Jersey, USA
HTAi 9th Annual Meeting, Bilbao
Integrated Care for a Patient Centered System
25 June, 2012
This document discusses biomarkers for epileptogenesis and the challenges in developing clinically useful biomarkers to predict epilepsy risk, progression, and treatment response. It notes that while many potential biomarkers have been identified in preclinical studies, none have translated to clinical use. Some key challenges include the long timescales between injury and seizures, heterogeneity of epilepsy types and patients, and a focus on retrospective studies in refractory epilepsy patients rather than prospective validation. The document argues that combinatorial biomarkers analyzing multiple mechanisms may be more promising than single biomarkers, and that biomarkers should be validated as direct measures of patient outcomes rather than relying solely on seizure occurrence.
The document provides an overview of the Canadian Consensus Document on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). It summarizes the development of the consensus document, which was spearheaded by the National ME/FM Action Network of Canada in response to the need for a clinical case definition and guidelines for diagnosis and treatment of ME/CFS. An expert panel of 11 clinicians and researchers with experience treating over 20,000 ME/CFS patients was selected to develop the consensus document. The panel held a funded workshop to reach consensus on a clinical case definition, diagnostic guidelines, and treatment guidelines for medical practitioners dealing with ME/CFS patients.
This document summarizes research on non-specific low back pain. It discusses the epidemiology, including the high lifetime prevalence and risk of recurrence. While mechanical factors may not play a major role, genetic factors are important. Clinical imaging should only be used restrictively for diagnosis, as many imaging findings are common in asymptomatic individuals. Treatments have unclear mechanisms and low effect sizes; self-management is generally recommended over surgery or overtreatment.
To describe the frequency, type, and clinical course
of hearing loss in Wegener’s granulomatosis and assess hearing
loss as an indicator of disease activity.
Neurosarcoidosis is a rare condition where sarcoidosis affects the nervous system. It can be difficult to diagnose as it often presents with non-specific neurological symptoms. Diagnosis requires a combination of CSF analysis, MRI imaging showing characteristic abnormalities, and biopsy evidence of granulomas. A multidisciplinary team approach is needed to manage this complex condition.
This document provides an overview and summary of a presentation on assessing pain, sedation, and delirium in intensive care unit patients. It discusses:
- The importance of using validated scales like the Richmond Agitation-Sedation Scale (RASS) and Sedation-Agitation Scale (SAS) to accurately assess sedation levels in patients receiving sedatives.
- The challenges of assessing delirium given confounding factors like a patient's sedation level, wakefulness, and other psychiatric diagnoses. Scales like the Confusion Assessment Method for the ICU (CAM-ICU) are used but their accuracy depends on a patient's sedation.
- How pharmacokinetic factors like drug-
FACTORES ASOCIADOS A LA FALTA DE ESPERANZAKaierleiki
This study examined the prevalence and factors associated with hopelessness in a population sample of 1,722 adults in Finland. The researchers found that 11% of subjects reported at least moderate hopelessness. Factors independently associated with higher odds of hopelessness included poor financial situation, poor subjective health, and reduced working ability. Subjects who were dissatisfied with life, depressed, had alexithymia (difficulty identifying and describing emotions), or suicidal ideation also had significantly higher odds of moderate or severe hopelessness. The study demonstrated a moderately high prevalence of hopelessness in the general population and identified important indicators of low subjective well-being that healthcare providers should be aware of.
This document provides guidelines from the 2012 American College of Rheumatology for the management of gout, focusing on non-pharmacologic and pharmacologic approaches to hyperuricemia. It recommends patient education as a core treatment, and xanthine oxidase inhibitors such as allopurinol or febuxostat as first-line urate-lowering therapy. The target serum urate level is less than 6 mg/dl and often less than 5 mg/dl. It also addresses treatment of chronic tophaceous gouty arthritis and the use of pegloticase for severe refractory gout.
Neurocysticercosis the notorious vanishing ring enhancing lesion ijar feb 2015Sachin Adukia
This document summarizes a study of 25 patients presenting with ring enhancing lesions (RELs) on MRI brain scans. The study aimed to evaluate clinical features and diagnoses of RELs and treatment outcomes. Of the 25 patients, 8 (32%) were diagnosed with neurocysticercosis based on clinical features, investigations and MRI findings. All 8 neurocysticercosis patients presented with seizures and most with headache. Lesions were typically solitary and less than 10mm. Treatment with albendazole, anti-convulsants and steroids resulted in complete resolution in 6 patients (75%) and regression/calcification in the remaining 2, demonstrating neurocysticercosis has an excellent prognosis with appropriate treatment.
- An acute gouty arthritis attack should be treated with pharmacologic therapy initiated within 24 hours of onset. Established urate-lowering therapy should be continued without interruption during an attack.
- Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or oral colchicine are appropriate first-line options for treating acute gout. Certain combinations can be used for severe or refractory attacks.
- Pharmacologic anti-inflammatory prophylaxis is recommended for all gout patients starting urate-lowering therapy and should continue if gout disease activity persists or serum urate target is unmet. Oral colchicine is an appropriate first-line option
el mundo desarrollado tiene un mayor indice de epilepsia, Nuevos conocimientos sobre las causas y consecuencias de la epilepsia en los países en desarrollo ofrecen oportunidad para la prevención y / o tratamiento mejorado, que se complementan con las directrices publicadas recientemente epilepsia cuidado para su uso en este entorno
The document discusses PTSD and emergence delirium in veterans undergoing surgery, defining the conditions, reviewing evidence on risk factors and treatments, and proposing strategies for preoperative evaluation, intraoperative care, and postoperative management to prevent emergence delirium in high-risk patients and improve outcomes. It also examines the pathophysiology of how general anesthesia and PTSD may interact to increase risks of delirium and outlines areas for further research and dissemination of guidelines.
This document is a curriculum vitae for Dr. Marwan Sabbagh. It lists his current positions, which include directorships at research institutes and professorships. It then outlines his extensive previous professional experience in academic medicine and clinical research spanning over 25 years. The CV provides details of his education, honors, memberships, and publications. It presents Dr. Sabbagh as a highly accomplished neurologist and leader in Alzheimer's disease and dementia research.
23 September 2010 - National Council for Palliative Care / National End of Life Care Programme / the neurological alliance 15 February 2013 - National End of Life Care Programme / Whole Systems Partnership
This document aims to set out an EoLC framework for implementation that speciï¬cally meets the needs of those with neurological conditions.
It covers:
Strategic context
End of life care tools
End of life care in neurological disease
Communication and advance care planning
Co-ordination and multidisciplinary approach to care
Management of physical symptoms
Holistic care - psychosocial and spiritual aspects
Care at the end of life
Carers
Workforce, education and training
Commissioning health and social care services
International classification of headache disorders changes in ichd2Prashant Makhija
1. The document discusses the International Classification of Headache Disorders (ICHD), which provides a standardized system for classifying headaches to facilitate communication between professionals, research, and treatment guidelines.
2. The ICHD has evolved over time through various editions, with the current ICHD-II published in 2004. ICHD-III is expected in 2013 and will include revisions based on new research findings.
3. While the ICHD has advanced the field, it also has limitations like being too detailed for clinical practice and not considering other important diagnostic factors. ICHD-III aims to address some of these issues.
Long-term cognitive impairment after critical illness (CIACI) is frequently reported in up to 66% of patients three months after intensive care hospitalization. The condition has overlapping neurological changes with stroke, traumatic brain injury, and neurodegenerative disorders. Risk factors for CIACI include depression, biomarkers for Alzheimer's disease, delirium duration during hospitalization, and exposure to certain drugs. Current strategies to prevent or treat CIACI focus on reducing delirium and agitation, as well as physical and cognitive rehabilitation. Neurotrophic factors may play a role in neurogenesis, blood-brain barrier integrity, and neuronal repair, suggesting they could be a potential target for novel CIACI treatments.
Gavin Giovannoni - Brain health: why time matters in MSMS Trust
1) The document discusses the importance of early intervention in multiple sclerosis (MS) to maximize long-term brain health and prevent disability progression over time.
2) It promotes a strategy of treating MS patients aggressively early on to minimize clinical relapses, focal lesions detected by MRI, and underlying brain atrophy.
3) The goal is to create an initiative called MS Brain Health that encourages adopting a therapeutic approach aiming to optimize brain health for all people living with MS through their lifetime.
This document summarizes the treatment of Alzheimer's disease and related dementias. It discusses the history and neuropathology of Alzheimer's disease, prevalence and treatment rates, disease progression, clinical diagnosis, differential diagnosis, approved drug therapies including cholinesterase inhibitors, guidelines for treatment, and links between vascular risk factors and the pathology of Alzheimer's disease. Management includes education, safety measures, medications, and screening for behaviors, depression, and driving ability.
This document provides an overview of different types of dementia, including the key features and areas of the brain affected. It discusses cortical dementias like Alzheimer's disease and frontotemporal dementia, characterized by deterioration of the cerebral cortex. Subcortical dementias like Parkinson's and Huntington's disease involve basal ganglia and related structures. Mixed dementias include vascular dementia and Lewy body dementia. The prevalence of dementia is increasing in India along with the aging population. Psychologists can help with family support, assessment, rehabilitation and managing emotional changes with dementia patients.
This document contains abstracts from research, innovations, and clinical vignettes presented at the 2011 Hospital Medicine annual meeting. The abstracts are divided into sections for research, innovations, and clinical vignettes. Some of the abstracts presented include evaluations of HIV screening practices, the safety of arthrocentesis for patients on warfarin therapy, incidence of venous thromboembolism in homebound patients, and an assessment of pain in patients undergoing bone marrow biopsies. The abstracts cover a wide range of topics in hospital medicine and include results from studies, innovations, and case reports.
Transitional Care for Pediatric Patients with Neuromuscular Diseases: A Healt...HTAi Bilbao 2012
Transitional Care for Pediatric Patients with Neuromuscular Diseases: A Health Technology Assessment
Jackie Tran, MD
University of Medicine and Dentistry of New Jersey, USA
HTAi 9th Annual Meeting, Bilbao
Integrated Care for a Patient Centered System
25 June, 2012
This document discusses biomarkers for epileptogenesis and the challenges in developing clinically useful biomarkers to predict epilepsy risk, progression, and treatment response. It notes that while many potential biomarkers have been identified in preclinical studies, none have translated to clinical use. Some key challenges include the long timescales between injury and seizures, heterogeneity of epilepsy types and patients, and a focus on retrospective studies in refractory epilepsy patients rather than prospective validation. The document argues that combinatorial biomarkers analyzing multiple mechanisms may be more promising than single biomarkers, and that biomarkers should be validated as direct measures of patient outcomes rather than relying solely on seizure occurrence.
The document provides an overview of the Canadian Consensus Document on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). It summarizes the development of the consensus document, which was spearheaded by the National ME/FM Action Network of Canada in response to the need for a clinical case definition and guidelines for diagnosis and treatment of ME/CFS. An expert panel of 11 clinicians and researchers with experience treating over 20,000 ME/CFS patients was selected to develop the consensus document. The panel held a funded workshop to reach consensus on a clinical case definition, diagnostic guidelines, and treatment guidelines for medical practitioners dealing with ME/CFS patients.
This document summarizes research on non-specific low back pain. It discusses the epidemiology, including the high lifetime prevalence and risk of recurrence. While mechanical factors may not play a major role, genetic factors are important. Clinical imaging should only be used restrictively for diagnosis, as many imaging findings are common in asymptomatic individuals. Treatments have unclear mechanisms and low effect sizes; self-management is generally recommended over surgery or overtreatment.
To describe the frequency, type, and clinical course
of hearing loss in Wegener’s granulomatosis and assess hearing
loss as an indicator of disease activity.
Neurosarcoidosis is a rare condition where sarcoidosis affects the nervous system. It can be difficult to diagnose as it often presents with non-specific neurological symptoms. Diagnosis requires a combination of CSF analysis, MRI imaging showing characteristic abnormalities, and biopsy evidence of granulomas. A multidisciplinary team approach is needed to manage this complex condition.
This document provides an overview and summary of a presentation on assessing pain, sedation, and delirium in intensive care unit patients. It discusses:
- The importance of using validated scales like the Richmond Agitation-Sedation Scale (RASS) and Sedation-Agitation Scale (SAS) to accurately assess sedation levels in patients receiving sedatives.
- The challenges of assessing delirium given confounding factors like a patient's sedation level, wakefulness, and other psychiatric diagnoses. Scales like the Confusion Assessment Method for the ICU (CAM-ICU) are used but their accuracy depends on a patient's sedation.
- How pharmacokinetic factors like drug-
FACTORES ASOCIADOS A LA FALTA DE ESPERANZAKaierleiki
This study examined the prevalence and factors associated with hopelessness in a population sample of 1,722 adults in Finland. The researchers found that 11% of subjects reported at least moderate hopelessness. Factors independently associated with higher odds of hopelessness included poor financial situation, poor subjective health, and reduced working ability. Subjects who were dissatisfied with life, depressed, had alexithymia (difficulty identifying and describing emotions), or suicidal ideation also had significantly higher odds of moderate or severe hopelessness. The study demonstrated a moderately high prevalence of hopelessness in the general population and identified important indicators of low subjective well-being that healthcare providers should be aware of.
This document provides guidelines from the 2012 American College of Rheumatology for the management of gout, focusing on non-pharmacologic and pharmacologic approaches to hyperuricemia. It recommends patient education as a core treatment, and xanthine oxidase inhibitors such as allopurinol or febuxostat as first-line urate-lowering therapy. The target serum urate level is less than 6 mg/dl and often less than 5 mg/dl. It also addresses treatment of chronic tophaceous gouty arthritis and the use of pegloticase for severe refractory gout.
Neurocysticercosis the notorious vanishing ring enhancing lesion ijar feb 2015Sachin Adukia
This document summarizes a study of 25 patients presenting with ring enhancing lesions (RELs) on MRI brain scans. The study aimed to evaluate clinical features and diagnoses of RELs and treatment outcomes. Of the 25 patients, 8 (32%) were diagnosed with neurocysticercosis based on clinical features, investigations and MRI findings. All 8 neurocysticercosis patients presented with seizures and most with headache. Lesions were typically solitary and less than 10mm. Treatment with albendazole, anti-convulsants and steroids resulted in complete resolution in 6 patients (75%) and regression/calcification in the remaining 2, demonstrating neurocysticercosis has an excellent prognosis with appropriate treatment.
- An acute gouty arthritis attack should be treated with pharmacologic therapy initiated within 24 hours of onset. Established urate-lowering therapy should be continued without interruption during an attack.
- Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or oral colchicine are appropriate first-line options for treating acute gout. Certain combinations can be used for severe or refractory attacks.
- Pharmacologic anti-inflammatory prophylaxis is recommended for all gout patients starting urate-lowering therapy and should continue if gout disease activity persists or serum urate target is unmet. Oral colchicine is an appropriate first-line option
el mundo desarrollado tiene un mayor indice de epilepsia, Nuevos conocimientos sobre las causas y consecuencias de la epilepsia en los países en desarrollo ofrecen oportunidad para la prevención y / o tratamiento mejorado, que se complementan con las directrices publicadas recientemente epilepsia cuidado para su uso en este entorno
The document discusses PTSD and emergence delirium in veterans undergoing surgery, defining the conditions, reviewing evidence on risk factors and treatments, and proposing strategies for preoperative evaluation, intraoperative care, and postoperative management to prevent emergence delirium in high-risk patients and improve outcomes. It also examines the pathophysiology of how general anesthesia and PTSD may interact to increase risks of delirium and outlines areas for further research and dissemination of guidelines.
This document is a curriculum vitae for Dr. Marwan Sabbagh. It lists his current positions, which include directorships at research institutes and professorships. It then outlines his extensive previous professional experience in academic medicine and clinical research spanning over 25 years. The CV provides details of his education, honors, memberships, and publications. It presents Dr. Sabbagh as a highly accomplished neurologist and leader in Alzheimer's disease and dementia research.
23 September 2010 - National Council for Palliative Care / National End of Life Care Programme / the neurological alliance 15 February 2013 - National End of Life Care Programme / Whole Systems Partnership
This document aims to set out an EoLC framework for implementation that speciï¬cally meets the needs of those with neurological conditions.
It covers:
Strategic context
End of life care tools
End of life care in neurological disease
Communication and advance care planning
Co-ordination and multidisciplinary approach to care
Management of physical symptoms
Holistic care - psychosocial and spiritual aspects
Care at the end of life
Carers
Workforce, education and training
Commissioning health and social care services
International classification of headache disorders changes in ichd2Prashant Makhija
1. The document discusses the International Classification of Headache Disorders (ICHD), which provides a standardized system for classifying headaches to facilitate communication between professionals, research, and treatment guidelines.
2. The ICHD has evolved over time through various editions, with the current ICHD-II published in 2004. ICHD-III is expected in 2013 and will include revisions based on new research findings.
3. While the ICHD has advanced the field, it also has limitations like being too detailed for clinical practice and not considering other important diagnostic factors. ICHD-III aims to address some of these issues.
Long-term cognitive impairment after critical illness (CIACI) is frequently reported in up to 66% of patients three months after intensive care hospitalization. The condition has overlapping neurological changes with stroke, traumatic brain injury, and neurodegenerative disorders. Risk factors for CIACI include depression, biomarkers for Alzheimer's disease, delirium duration during hospitalization, and exposure to certain drugs. Current strategies to prevent or treat CIACI focus on reducing delirium and agitation, as well as physical and cognitive rehabilitation. Neurotrophic factors may play a role in neurogenesis, blood-brain barrier integrity, and neuronal repair, suggesting they could be a potential target for novel CIACI treatments.
Gavin Giovannoni - Brain health: why time matters in MSMS Trust
1) The document discusses the importance of early intervention in multiple sclerosis (MS) to maximize long-term brain health and prevent disability progression over time.
2) It promotes a strategy of treating MS patients aggressively early on to minimize clinical relapses, focal lesions detected by MRI, and underlying brain atrophy.
3) The goal is to create an initiative called MS Brain Health that encourages adopting a therapeutic approach aiming to optimize brain health for all people living with MS through their lifetime.
This document summarizes the treatment of Alzheimer's disease and related dementias. It discusses the history and neuropathology of Alzheimer's disease, prevalence and treatment rates, disease progression, clinical diagnosis, differential diagnosis, approved drug therapies including cholinesterase inhibitors, guidelines for treatment, and links between vascular risk factors and the pathology of Alzheimer's disease. Management includes education, safety measures, medications, and screening for behaviors, depression, and driving ability.
This document provides an overview of different types of dementia, including the key features and areas of the brain affected. It discusses cortical dementias like Alzheimer's disease and frontotemporal dementia, characterized by deterioration of the cerebral cortex. Subcortical dementias like Parkinson's and Huntington's disease involve basal ganglia and related structures. Mixed dementias include vascular dementia and Lewy body dementia. The prevalence of dementia is increasing in India along with the aging population. Psychologists can help with family support, assessment, rehabilitation and managing emotional changes with dementia patients.
This document discusses the structure and function of nervous tissue. It describes the different cell types found in the central and peripheral nervous systems, including neurons, astrocytes, oligodendrocytes, microglia, and Schwann cells. It explains how the blood-brain barrier restricts transport of molecules to the brain and discusses specific transport mechanisms for glucose, amino acids, lipids, proteins, and other compounds. The document also covers topics like axonal transport, myelination, astrocyte functions, and metabolism of ammonia and glutamate in the brain.
El documento habla sobre el olvido en el envejecimiento y cómo no siempre es patológico. Resume que el envejecimiento no implica deterioro, sino cambio y adaptación. Además, la plasticidad neuronal permite compensar la acumulación de años a través de mecanismos como la remielinización y la ramificación axonal. Recomienda no preocuparse sino ocuparse cuidando la salud a través de una dieta sana, ejercicio, evitar hábitos tóxicos y mantener la actividad intelectual con entrenamiento cognitivo de
El documento resume los tipos de olvidos normales y patológicos. Los olvidos benignos son olvidos de detalles poco importantes y son parte del envejecimiento normal, mientras que los olvidos patológicos involucran detalles más significativos y son motivo de preocupación para la familia, requiriendo una evaluación médica.
Presentation delivered by Dr. Carol Manning at the live webinar hosted by AlzPossible at www.alzpossible.org on the 17th of March, 2014.
www.alzpossible.org
Este documento discute la estimulación cognitiva en adultos mayores desde la perspectiva de la terapia ocupacional. Explica que la estimulación cognitiva permite que los pacientes alcancen su máximo rendimiento intelectual para mejorar su calidad de vida. También describe los componentes de la cognición como la memoria, razonamiento y orientación. Finalmente, enfatiza la importancia de seleccionar actividades que se correspondan con la capacidad cognitiva funcional del paciente para lograr un óptimo desempeño.
The document discusses dementia, amnesia, and delirium. It defines dementia as a global impairment of cognitive function affecting memory, visuospatial skills, language, concentration and attention. The most common causes of dementia are Alzheimer's disease and cerebral vascular disease. Delirium is distinguished from dementia by its acute onset, fluctuating course, and clouded consciousness.
An overview of dementia gives an introduction to epidemiology, causes, clinical features, investigations, diagnosis, and management of dementia. Also a short description of related topics like difference between cortical and sub cortical dementia, psuedo dementia, mild cognitive impairment and reversible causes of dementia is also included.
Dementia is an acquired persistent and progressive impairment in intellectual function, with compromise of memory and at least one other cognitive domain. The key features of dementia include progressive decline in intellectual functions over months to years, loss of short term memory and at least one other cognitive deficit, no disturbance of consciousness, deficits severe enough to cause impairment in daily functioning, and not being in a state of delirium. Dementia can be categorized into reversible or partially reversible dementias and nonreversible dementias. Nonreversible dementias include Alzheimer's disease, vascular dementia, dementia with Lewy bodies, and frontotemporal dementias. Treatment involves acetylcholinesterase inhibitors, memantine, managing behavioral problems non-
1. Dementia is defined as a progressive impairment of cognitive functions occurring in clear consciousness. The most common causes are Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, and vascular dementia.
2. Neuroimaging and neuropathological findings help characterize different dementias. Alzheimer's disease shows hippocampal and temporal lobe atrophy on MRI and beta-amyloid plaques and neurofibrillary tangles microscopically. Frontotemporal dementia presents with frontal and anterior temporal lobe atrophy.
3. Treatment involves pharmacological interventions like cholinesterase inhibitors and memantine for Alzheimer's, as well as non-pharmacological approaches like cognitive stimulation, environmental modifications, and
Delirium, Dementia, and Amnestic Disordersguestd889da58
This document provides information on delirium and dementia:
- Delirium is characterized by a rapid deterioration in higher cognitive functions, fluctuating mental status, and symptoms that last hours to days. Common causes include age over 60, drug or alcohol use, and prior brain injuries.
- Dementia involves impaired social or occupational functioning and impaired memory plus deficits in other cognitive domains. It is not the same as Alzheimer's disease but can be caused by conditions like Alzheimer's.
- Symptoms of dementia include disrupted sleep, wandering, and aggressive behavior in some patients. The prevalence of dementia increases significantly with age.
Alzheimer's disease is a progressive brain disorder that causes memory loss and cognitive decline. It was first described by Alois Alzheimer in 1906 after examining brain tissue from a deceased patient. The disease results from the buildup of beta-amyloid plaques and tau protein tangles in the brain, which damage and kill neurons. Risk factors include age, family history, and genetic factors. There is no cure for Alzheimer's, but medications and caregiving can temporarily ease symptoms.
Hypothetical model of dynamic biomarkers of the alzheimer pathological cascadeCarolinaRamrez60
The document presents a hypothetical model of biomarkers for Alzheimer's disease progression. It proposes that:
1) Abnormal amyloid beta processing occurs first, before symptoms, which is detected by reduced CSF Aβ42 and increased amyloid PET tracer retention.
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The document provides revised guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Key changes from the 1997 criteria include: 1) separating the clinical diagnosis of AD from the neuropathological assessment of AD brain changes, 2) emphasizing the assessment of co-existing brain pathologies that may contribute to cognitive impairment, and 3) providing updated guidance on the neuropathological assessment of AD changes, Lewy body disease, vascular brain injury, and hippocampal sclerosis.
The document provides revised guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Key changes from the 1997 criteria include: 1) separating the clinical diagnosis of AD from the neuropathological assessment of AD changes, 2) emphasizing the assessment of co-existing brain pathologies that may contribute to cognitive impairment, and 3) providing updated guidance on the neuropathological changes of AD and other common diseases seen in aging and dementia.
This document summarizes research on adding nuances to Alzheimer's disease models by accounting for risk modifiers like Apolipoprotein E (APOE) ε4 and cognitive reserve. Studies found APOE ε4 is associated with earlier age of onset and affects biomarkers like amyloid load, neuronal injury, and brain atrophy. Cognitive reserve was not correlated with biomarkers but may influence the relationship between biomarkers and cognition. Future work aims to longitudinally map disease progression accounting for individual risk modifiers and apply models to patient care.
1. The document discusses recommendations from a workgroup on defining the preclinical stages of Alzheimer's disease.
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This document describes a study conducted at a neurogenetics clinic in Argentina that aimed to assess the diagnostic yield of evaluating patients with suspected genetic neurological disorders. The study included 387 patients seen between 2008-2014. Overall, a genetic diagnosis was made in 27.4% of patients. When only considering patients that underwent genetic testing, the diagnostic yield was 45%. For the 140 patients evaluated for progressive ataxia, a genetic cause was identified in 23.5% of patients and 57.5% of patients with a positive family history. The most common causes of ataxia identified were spinocerebellar ataxia types 2, 3 and Friedreich ataxia. This study demonstrates that specialized evaluation can provide a
The document summarizes current research efforts in the prevention and treatment of Alzheimer's disease and related dementias. Key points include: 1) New biomarkers like PET amyloid and tau imaging help diagnose AD earlier; 2) A new A/T/N framework conceptualizes AD as a continuum from preclinical to symptomatic stages; 3) Conditions like LATE can resemble AD but lack amyloid/tau; and 4) Treatments focus on modifying disease progression through therapies targeting amyloid and tau before symptoms arise.
Status of ADRD Research 10-27-2020.pptxssuser65002f
The document summarizes current research efforts in the prevention and treatment of Alzheimer's disease and related dementias. Key points include: 1) New biomarkers like PET amyloid and tau imaging help diagnose AD earlier; 2) A new A/T/N framework conceptualizes AD as a continuum from preclinical to symptomatic stages; 3) Conditions like LATE can resemble AD but lack amyloid/tau; and 4) Treatments focus on modifying disease progression through therapies targeting amyloid and tau before symptoms arise.
A Brief Cognitive Assessment For Use With Schizophrenia Patients In Community...Sarah Marie
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This study examines changes in dendritic branching and spines in the frontal, temporal, and parietal cortex from individuals diagnosed as non-cognitively impaired (NCI), with mild cognitive impairment (MCI), or with Alzheimer's disease (AD). Brain tissue was analyzed using the Golgi impregnation method to quantify dendritic branching and spines. Results showed each cortical region had distinct patterns of dendritic changes from NCI to MCI to AD. The temporal cortex saw a 20% loss of branching in MCI and a further 5% loss in AD. The parietal cortex had a mild 4% loss in MCI and a 10% loss in AD. In contrast, the frontal cortex showed a
This study assessed cognitive function, cortisol levels, and symptoms severity in 30 schizophrenia patients and 30 healthy controls. Schizophrenia patients performed significantly worse on cognitive tests and had higher cortisol levels. Cortisol levels did not correlate with symptoms severity or cognitive performance. The study suggests cognitive impairment is a core feature of schizophrenia and cortisol may be elevated, but the small sample size limits generalizability. Larger studies are needed to clarify relationships between cortisol, symptoms, and cognition.
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EIS technology : bioimpedance application in selective serotonin reuptakeES-Teck India
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2. McKhann et al. Page 2
the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis.
We also retained the term possible AD dementia, but redefined it in a manner more focused than
before. Bio-marker evidence was also integrated into the diagnostic formulations for probable and
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possible AD dementia for use in research settings. The core clinical criteria for AD dementia will
continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is
expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much
work lies ahead for validating the biomarker diagnosis of AD dementia.
Keywords
Alzheimer’s disease; Dementia; Diagnosis; Magnetic resonance brain imaging; Position emission
tomography; Cerebrospinal fluid
1. Introduction
In the fall of 1983, a group was convened by the National Institute of Neurological and
Communicative Disorders and Stroke (NINCDS) and the Alzheimer’s Disease and Related
Disorders Association (ADRDA) to establish criteria and to describe the clinical diagnosis
of Alzheimer’s disease (AD). The group addressed issues of medical history, clinical
examination, neuropsychological testing, and laboratory assessments and then produced a
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report, which was published in July 1984 [1]. The criteria in this report, commonly referred
to as the NINCDS-ADRDA criteria, have been quite successful, surviving for over 27 years.
These criteria have been reliable for the diagnosis of probable AD, and across more than a
dozen clinical pathological studies have had a sensitivity of 81% and specificity of 70% [2],
They have been widely used in clinical trials and clinical research.
However, now 27 years later, these criteria require revision. Therefore, the National Institute
on Aging and the Alzheimer’s Association charged a workgroup with the task of revising
the 1984 criteria for AD dementia. Details of the charge to the workgroup are described in
the Introduction that accompanies this article [3]. The characterization of the preclinical [4]
and mild cognitive impairment (MCI) [5] phases of the AD pathophysiological processes is
described in the companion articles.
Our knowledge of the clinical manifestations and biology of AD has increased vastly. The
features of the original criteria that required revision include the following:
1. The fact that the histological pathology of AD (or surrogates for this pathology)
may be found across a broad clinical spectrum (including individuals who are
cognitively normal, those with MCI, and those with dementia) [6,7]. Therefore,
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throughout this article, we use the term AD patho-physiological process to
encompass the antemortem biological changes that precede the postmortem neu-
ropathological diagnosis of AD as well as the neuropathological substrate. AD
dementia refers to the clinical syndrome that arises as a consequence of the AD
pathophysiological process.
2. Lack of acknowledgment of distinguishing features of other dementing conditions
that occur in a similarly aged population, which were not completely recognized
decades ago. For example, Dementia with Lewy bodies [8], vascular dementia [9],
behavior variant frontotemporal dementia [10–12], and primary progressive aphasia
[13] have been characterized extensively.
3. No inclusion of results of magnetic resonance imaging, positron emission
tomography (PET) imaging, and cerebrospinal fluid (CSF) assays (that we will
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3. McKhann et al. Page 3
refer to subsequently as biomarkers) in decision-making. Initial efforts to
incorporate biomarkers into the diagnosis of AD dementia and MCI [14] need to be
coupled with a more comprehensive approach to the diagnostic process.
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4. The implication that memory impairment is always the primary cognitive deficit in
all patients with AD dementia. Experience has shown that there are several
nonamnestic presentations of the pathophysiological process of AD, the most
common ones being the syndrome of posterior cortical atrophy [15] and the
syndrome of logopenic-primary progressive aphasia [16].
5. Lack of information about genetics of AD. Mutations in three genes—amyloid
precursor protein, presenilin 1, and presenilin 2—cause an early onset, autosomal
dominantly inherited AD [17].
6. Proposed age cutoffs for the diagnosis of AD dementia. Work over the past decades
has established that AD dementia in those aged <40 years, although rare, does not
differ in its pathophysiology from older persons [18]. AD dementia in persons aged
>90 years is also part of that same spectrum as that of younger persons, even
though clinical–pathological correlations are attenuated [19].
7. Extreme heterogeneity of the “Possible” AD dementia category, including a group
of patients who would now be diagnosed as “Mild cognitive impairment (MCI).”
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The objective of our committee was to focus on the criteria for AD dementia, that is,
dementia secondary to the pathophysiology of AD. It was our intention to first review the
NINDS–ADRDA criteria and then to update them, incorporating more modern innovations
in clinical, imaging, and laboratory assessment. We will first propose (1) Criteria for all-
cause dementia and then, (2) Criteria for dementia caused by AD. We set ourselves the goal
of ensuring that the revised criteria would be flexible enough to be used by both general
healthcare providers without access to neuropsychological testing, advanced imaging, and
CSF measures, as well as specialized investigators involved in research or in clinical trial
studies who would have these measures available.
2. Criteria for all-cause dementia: Core clinical criteria
In this section, we outline core clinical criteria to be used in all clinical settings. Because
there are many causes of dementia, we will first outline the criteria for all-cause dementia.
The diagnosis of dementia is intended to encompass the spectrum of severity, ranging from
the mildest to the most severe stages of dementia. The methodology for staging of dementia
severity was beyond the charge of the workgroup. Dementia is diagnosed when there are
cognitive or behavioral (neuropsychiatric) symptoms that:
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1. Interfere with the ability to function at work or at usual activities; and
2. Represent a decline from previous levels of functioning and performing; and
3. Are not explained by delirium or major psychiatric disorder;
4. Cognitive impairment is detected and diagnosed through a combination of (1)
history-taking from the patient and a knowledgeable informant and (2) an objective
cognitive assessment, either a “bedside” mental status examination or
neuropsychological testing. Neuropsychological testing should be performed when
the routine history and bedside mental status examination cannot provide a
confident diagnosis.
5. The cognitive or behavioral impairment involves a minimum of two of the
following domains:
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a. Impaired ability to acquire and remember new information—symptoms
include: repetitive questions or conversations, misplacing personal
belongings, forgetting events or appointments, getting lost on a familiar
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route.
b. Impaired reasoning and handling of complex tasks, poor judgment—
symptoms include: poor understanding of safety risks, inability to manage
finances, poor decision-making ability, inability to plan complex or
sequential activities.
c. Impaired visuospatial abilities—symptoms include: inability to recognize
faces or common objects or to find objects in direct view despite good
acuity, inability to operate simple implements, or orient clothing to the
body.
d. Impaired language functions (speaking, reading, writing)—symptoms
include: difficulty thinking of common words while speaking, hesitations;
speech, spelling, and writing errors.
e. Changes in personality, behavior, or comportment—symptoms include:
uncharacteristic mood fluctuations such as agitation, impaired motivation,
initiative, apathy, loss of drive, social withdrawal, decreased interest in
previous activities, loss of empathy, compulsive or obsessive behaviors,
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socially unacceptable behaviors.
The differentiation of dementia from MCI (see companion article [5] on the diagnosis of
MCI) rests on the determination of whether or not there is significant interference in the
ability to function at work or in usual daily activities. This is inherently a clinical judgment
made by a skilled clinician on the basis of the individual circumstances of the patient and the
description of daily affairs of the patient obtained from the patient and from a
knowledgeable informant.
3. Proposed classification criteria for AD dementia
We propose the following terminology for classifying individuals with dementia caused by
AD: (1) Probable AD dementia, (2) Possible AD dementia, and (3) Probable or possible AD
dementia with evidence of the AD pathophysiological process. The first two are intended for
use in all clinical settings. The third is currently intended for research purposes.
4. Probable AD dementia: Core clinical criteria
4.1. Probable AD dementia is diagnosed when the patient
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1. Meets criteria for dementia described earlier in the text, and in addition, has the
following characteristics:
A. Insidious onset. Symptoms have a gradual onset over months to years, not
sudden over hours or days;
B. Clear-cut history of worsening of cognition by report or observation; and
C. The initial and most prominent cognitive deficits are evident on history
and examination in one of the following categories.
a. Amnestic presentation: It is the most common syndromic
presentation of AD dementia. The deficits should include
impairment in learning and recall of recently learned
information. There should also be evidence of cognitive
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5. McKhann et al. Page 5
dysfunction in at least one other cognitive domain, as
defined earlier in the text.
b. Nonamnestic presentations:
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• Language presentation: The most
prominent deficits are in word-finding, but
deficits in other cognitive domains should
be present.
• Visuospatial presentation: The most
prominent deficits are in spatial cognition,
including object agnosia, impaired face
recognition, simultanagnosia, and alexia.
Deficits in other cognitive domains should
be present.
• Executive dysfunction: The most
prominent deficits are impaired reasoning,
judgment, and problem solving. Deficits in
other cognitive domains should be present.
D. The diagnosis of probable AD dementia should not be applied when there
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is evidence of (a) substantial concomitant cerebrovascular disease, defined
by a history of a stroke temporally related to the onset or worsening of
cognitive impairment; or the presence of multiple or extensive infarcts or
severe white matter hyperintensity burden; or (b) core features of
Dementia with Lewy bodies other than dementia itself; or (c) prominent
features of behavioral variant frontotemporal dementia; or (d) prominent
features of semantic variant primary progressive aphasia or nonfluent/
agrammatic variant primary progressive aphasia; or (e) evidence for
another concurrent, active neurological disease, or a non-neurological
medical comorbidity or use of medication that could have a substantial
effect on cognition.
Note: All patients who met criteria for “probable AD” by the 1984 NINCDS–ADRDA
criteria [1] would meet the current criteria for probable AD dementia mentioned in the
present article.
4.2. Probable AD dementia with increased level of certainty
4.2.1. Probable AD dementia with documented decline—In persons who meet the
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core clinical criteria for probable AD dementia, documented cognitive decline increases the
certainty that the condition represents an active, evolving pathologic process, but it does not
specifically increase the certainty that the process is that of AD pathophysiology.
Probable AD dementia with documented decline is defined as follows: evidence of
progressive cognitive decline on subsequent evaluations based on information from
informants and cognitive testing in the context of either formal neuropsychological
evaluation or standardized mental status examinations.
4.2.2. Probable AD dementia in a carrier of a causative AD genetic mutation—
In persons who meet the core clinical criteria for probable AD dementia, evidence of a
causative genetic mutation (in APP, PSEN1, or PSEN2), increases the certainty that the
condition is caused by AD pathology. The workgroup noted that carriage of the ε4 allele of
the apolipoprotein E gene was not sufficiently specific [20] to be considered in this category.
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6. McKhann et al. Page 6
5. Possible AD dementia: Core clinical criteria
A diagnosis of possible AD dementia should be made in either of the circumstances
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mentioned in the following paragraphs.
5.1. Atypical course
Atypical course meets the core clinical criteria in terms of the nature of the cognitive deficits
for AD dementia, but either has a sudden onset of cognitive impairment or demonstrates
insufficient historical detail or objective cognitive documentation of progressive decline,
Or
5.2. Etiologically mixed presentation
Etiologically mixed presentation meets all core clinical criteria for AD dementia but has
evidence of (a) concomitant cerebrovascular disease, defined by a history of stroke
temporally related to the onset or worsening of cognitive impairment; or the presence of
multiple or extensive infarcts or severe white matter hyperintensity burden; or (b) features of
Dementia with Lewy bodies other than the dementia itself; or (c) evidence for another
neurological disease or a non-neurological medical comorbidity or medication use that could
have a substantial effect on cognition
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Note: A diagnosis of “possible AD” by the 1984 NINCDS-ADRDA criteria [1] would not
necessarily meet the current criteria for possible AD dementia. Such a patient would need to
be re-evaluated.
6. Probable AD dementia with evidence of the AD pathophysiological
process
The rationale for including biomarkers for the pathophysiological process of AD in the
diagnostic criteria is summarized in the Introduction to this series of articles [3], The major
AD biomarkers that have been widely investigated at this time (see [21] for review) may be
broken into two classes based on the biology which they measure. Biomarkers of brain
amyloid-beta (Aβ) protein deposition are low CSF Aβ42 and positive PET amyloid imaging
[22,23]. The second category is that of biomarkers of downstream neuronal degeneration or
injury. The three major bio-markers in this category are elevated CSF tau, both total tau and
phosphorylated tau (p-tau); decreased 18fluorodeoxyglucose (FDG) uptake on PET in
temporo–parietal cortex; and disproportionate atrophy on structural magnetic resonance
imaging in me-dial, basal, and lateral temporal lobe, and medial parietal cortex. Total tau
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and p-tau are treated equivalently in this study, although p-tau may have more specificity for
AD than other dementing diseases.
In persons who meet the core clinical Criteria for probable AD dementia biomarker evidence
may increase the certainty that the basis of the clinical dementia syndrome is the AD
pathophysiological process. However, we do not advocate the use of AD biomarker tests
for routine diagnostic purposes at the present time. There are several reasons for this
limitation: (1) the core clinical criteria provide very good diagnostic accuracy and utility in
most patients; (2) more research needs to be done to ensure that criteria that include the use
of biomarkers have been appropriately designed, (3) there is limited standardization of
biomarkers from one locale to another, and (4) access to biomarkers is limited to varying
degrees in community settings. Presently, the use of biomarkers to enhance certainty of AD
pathophysiological process may be useful in three circumstances: investigational studies,
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7. McKhann et al. Page 7
clinical trials, and as optional clinical tools for use where available and when deemed
appropriate by the clinician.
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Biomarker test results can fall into three categories–clearly positive, clearly negative, and
indeterminate. We envision that application of biomarkers for the AD pathophysiological
process would operate as outlined in the Table 1.
7. Possible AD dementia with evidence of the AD pathophysiological
process
This category is for persons who meet clinical criteria for a non-AD dementia but who have
either biomarker evidence of AD pathophysiological process, or meet the neuropathological
criteria for AD. Examples would include persons who meet clinical criteria for dementia
with Lewy bodies or for a subtype of frontotemporal lobar degeneration, but who have a
positive AD biomarker study or at autopsy are found to meet pathological criteria for AD. In
the biomarker table, we indicate that both categories of biomarkers must be positive for an
individual who presents clinically with a non-AD phenotype to meet criteria for possible
AD. This is a conservative approach that may change as more information is gained
concerning the long-term outcomes of different combinations of biomarker findings. A
diagnosis of possible AD dementia with evidence of AD pathophysiological process does
not preclude the possibility that a second pathophysiological condition is also present.
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8. Considerations related to the incorporation of biomarkers into AD
dementia criteria
As described in the two companion articles on the preclinical [4] and MCI [5] phases of the
AD pathophysiological process, AD dementia is part of a continuum of clinical and
biological phenomena. AD dementia is fundamentally a clinical diagnosis. To make a
diagnosis of AD dementia with biomarker support, the core clinical diagnosis of AD
dementia must first be satisfied.
According to their nature, CSF biomarkers rely on a quantitative interpretation in
comparison with normative standards. Imaging biomarkers can be interpreted in both a
qualitative or quantitative manner. In many cases, biomarker results will be clearly normal
or abnormal. In these cases, a qualitative interpretation of a biomarker test will
unequivocally identify “positive” findings that imply the presence of the underlying AD
pathophysiological process, or negative findings that unequivocally imply absence of an AD
pathophysiological process. However, in some cases, ambiguous or indeterminate results
will be obtained. This is inevitable given that all biomarkers are continuous measures, and
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the diagnostic labels of “positive” or “negative” require that cutoff values be applied to
continuous biological phenomena. Although sophisticated quantitative and objective image
analysis methods do exist, at present, accepted standards for quantitative analysis of AD
imaging tests are lacking. Standard clinical practice in diagnostic imaging is qualitative in
nature. Therefore, quantification of imaging biomarkers must rely on local laboratory
specific standards. The same holds true for CSF biomarkers, although standardization efforts
are more advanced for CSF biomarkers than for the imaging tests. Quantitative analytic
techniques are, and will continue to be in evolution for some time. Therefore, practical use
of biomarkers must follow best-practice guidelines within laboratory-specific contexts, until
standardization has been fully accomplished.
A sequence of events has been described with Aβ pathophysiological processes becoming
abnormal first and downstream neuronal injury biomarkers becoming abnormal later [6,7],
This might imply a hierarchical ranking of Aβ biomarkers over downstream neuronal injury
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8. McKhann et al. Page 8
biomarkers for diagnostic purposes. However, at this time, the reliability of such a
hierarchical scheme has not been sufficiently well established for use in AD dementia.
Given the number of different AD biomarkers, it is inevitable that different combinations of
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test results can occur. For example, individual cases might be encountered with a positive
Aβ and negative neuronal injury biomarker, or a positive FDG PET and negative tau
measure, and so on. At present, the data are insufficient to recommend a scheme that
arbitrates among all different biomarker combinations. Further studies are needed to
prioritize biomarkers and to determine their value and validity in practice and research
settings.
9. Pathophysiologically proved AD dementia
The diagnosis of pathophysiologically proved AD dementia would apply if the patient meets
the clinical and cognitive criteria for AD dementia outlined earlier in the text, and the
neuropathological examination, using widely accepted criteria [24], demonstrates the
presence of the AD pathology.
10. Dementia unlikely to be due to AD
1. Does not meet clinical criteria for AD dementia.
2. a. Regardless of meeting clinical criteria for probable or possible AD
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dementia, there is sufficient evidence for an alternative diagnosis such as
HIV dementia, dementia of Huntington’s disease, or others that rarely, if
ever, overlap with AD.
b. Regardless of meeting clinical criteria for possible AD dementia, both Aβ
and neuronal injury biomarkers are negative (see section 6, earlier in the
text).
Acknowledgments
The authors acknowledge the assistance of Dr. Cerise Elliott at the National Institute on Aging.
Guy McKhann serves on a Data Safety Monitoring Board for Merck. David Knopman serves on a Data Safety
Monitoring Board for Lilly Pharmaceuticals and is an investigator for clinical trials sponsored by Elan
Pharmaceuticals, Forest Pharmaceuticals, and Baxter Healthcare; he is deputy editor of Neurology and receives
compensation for editorial activities. Howard Chertkow serves as a consultant to Pfizer Canada, Lundbeck Canada,
Janssen Ortho, Novartis Canada, and Bristol Myers Squibb; he receives a research grant from Pfizer Canada.
Bradley Hyman serves as a consultant to EMD Serrano, Janssen, Takeda, BMS, Neurophage, Pfizer, Quanterix,
foldrx, Elan, and Link, and receives funding from the NIH, the Alzheimer’s Association, and Fidelity Biosciences.
Clifford Jack serves as a consultant for Eli Lilly, Eisai, and Élan; he is an investigator in clinical trials sponsored by
NIH-PA Author Manuscript
Baxter and Pfizer Inc., and owns stock in Johnson and Johnson. Claudia Kawas serves on a Data Safety Monitoring
Board for Lilly Pharmaceuticals, Elan Pharmaceuticals, and Lundbeck; she is an investigator in a trial sponsored by
Avid Radiopharmaceuticals. William Klunk serves as a consultant to GE Healthcare and receives research grants
from the same; he also receives royalties from GE Healthcare for PiB PET technology and owns stock or options in
Neuroptix, a company seeking to commercialize detection of amyloid in the eye. Walter Koroshetz are employees
of the U.S. Government and report no conflicts. Jennifer Manly reports no conflicts of interests. Richard Mayeux
serves on scientific advisory board of Psycho-Genics. Richard Mohs is a full-time employee of Eli Lilly and
Company and holds stock in Lilly. Avid Radiopharmaceuticals is a wholly owned subsidiary of Eli Lilly and Co.
John Morris serves as a consultant to Astra Zeneca, Bristol-Myers Squibb, Eisai, Janssen, Genetic, Eli Lilly, Merck,
Novartis, Otsuka, Pfizer, and Schering Plough. University College London receives payment for Martin Rossor
serving on the Safety Monitoring Committees for Janssen and Servier trials in AD. Philip Scheltens serves as a
consultant to Pfizer Pharmaceuticals, Genetech, Danone Research, Lundbeck Pharmaceuticals, GE Healthcare,
Roche, and Novartis; he also serves on a speakers bureau for Lundbeck Pharmaceuticals. Maria Carrillo and Bill
Thies are employees of the Alzheimer’s Association and reports no conflicts. Sandra Weintraub reports no conflicts
of interest and Creighton Phelps.
Alzheimers Dement. Author manuscript; available in PMC 2012 March 25.
9. McKhann et al. Page 9
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Table 1
AD dementia criteria incorporating biomarkers
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Biomarker
probability of AD Neuronal injury (CSF tau, FDG-
Diagnostic category etiology Aβ (PET or CSF) PET, structural MRI)
Probable AD dementia
Based on clinical criteria Uninformative Unavailable, conflicting, or Unavailable, conflicting, or
indeterminate indeterminate
With three levels of evidence of AD Intermediate Unavailable or indeterminate Positive
pathophysiological process Intermediate Positive Unavailable or indeterminate
High Positive Positive
Possible AD dementia (atypical
clinical presentation)
Based on clinical criteria Uninformative Unavailable, conflicting, or Unavailable, conflicting, or
indeterminate indeterminate
With evidence of AD High but does not Positive Positive
pathophysiological process rule out second
etiology
Dementia-unlikely due to AD Lowest Negative Negative
Abbreviations: AD, Alzheimer’s disease; Aβ, amyloid-beta; PET, positron emission tomography; CSF, cerebrospinal fluid;
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FDG, 18fluorodeoxyglucose; MRI, magnetic resonance imaging.
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Alzheimers Dement. Author manuscript; available in PMC 2012 March 25.