Frontotemporal Dementia: An Overview
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The document describes frontotemporal lobar degeneration (FTLD), which includes frontotemporal dementia, primary progressive aphasia, and semantic dementia, and characterizes the clinical features and treatment approaches for each. Case examples are presented to illustrate the diverse presentations of FTLD.
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The Frontotemporal Dementias
This document provides an overview of frontotemporal dementia (FTD) including its causes, clinical presentation, diagnosis, and management options. It discusses that FTD is caused by protein misfolding and accumulation in the brain. There are three main clinical variants - behavioral variant FTD, semantic dementia, and progressive nonfluent aphasia. Diagnosis involves ruling out other causes and may include brain imaging. Treatment focuses on managing symptoms but medications have limited effectiveness. Caregiver burden can be high due to patient behaviors, so support groups are recommended.
Frontotemporal dementia: Neural circuits, genetics and neuropathology
This document discusses frontotemporal dementia (FTD), including its subtypes, genetics, neuropathology, and clinical presentation. FTD is characterized by degeneration of the frontal and temporal lobes. The main subtypes are behavioral variant FTD, semantic dementia, and progressive nonfluent aphasia. Genetic factors like mutations in the MAPT and PGRN genes contribute to FTD. Neuropathologically, FTD involves tauopathies or TDP-43 proteinopathies. Imaging shows atrophy typically in the frontal and temporal regions depending on the subtype.
Frontotemporal dementia 2018
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Frontotemporal dementia - current concepts
Frontotemporal dementia (FTD) is an early-onset form of dementia characterized by progressive deterioration of behavior and language abilities due to degeneration of the frontal and temporal lobes. There are three main variants of FTD - behavioral variant FTD (bvFTD), semantic variant primary progressive aphasia (svPPA), and nonfluent/agrammatic variant PPA (nfvPPA). FTD is highly heritable and can be caused by mutations in MAPT, GRN, and C9orf72 genes. Diagnosis involves clinical evaluation, neuropsychological testing demonstrating executive dysfunction and relative sparing of memory, and neuroimaging showing frontal and temporal lobe atrophy.
Frontotemporal dementia
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Temporal lobe and its role in psychiatry
The temporal lobe is involved in processing sensory input, memory formation, language comprehension, and emotional processing. It contains structures like the hippocampus and amygdala that are important for memory and emotional associations. Disorders of the temporal lobe can cause problems like epilepsy, memory deficits, language issues like aphasia, and behavioral changes. Temporal lobe epilepsy is a common type of seizure originating in structures of the anteromedial temporal lobe. Bilateral damage to the amygdala and inferior temporal cortex can cause Klüver-Bucy syndrome characterized by changes in behavior and cognition. The temporal lobe also plays a key role in conditions like Alzheimer's disease, frontotemporal dementia, and traumatic brain injury.
Dementia
The world’s population is ageing rapidly, and with it is coming to a significant increase in the number of
older people with dementia. This increase presents major challenges for the provision of healthcare
generally and for dementia care in particular, for as more people have dementia, there will be more
people exhibiting behavioural and psychological symptoms of dementia (BPSD).
BPSD exact a high price from both the patient and the caregiver in terms of the distress and disability
they cause if left untreated. BPSD is recognisable, understandable and treatable. The recognition and
appropriate management of BPSD are important factors in improving our care of dementia patients
and their caregivers,
Approach to dementia
This document outlines an approach to diagnosing and evaluating dementia. It discusses the subtypes of mild cognitive impairment and dementia, the importance of a detailed patient history and neurological exam, and diagnostic criteria. Investigations may include cognitive testing, brain imaging, and lab tests to identify reversible causes or distinguish between dementia subtypes like Alzheimer's disease or Lewy body dementia. Follow up is important to monitor progression. The take home message is that dementia causes significant impairment, so a thorough history and early diagnosis are crucial.
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Frontotemporal dementia 2018
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Frontotemporal dementia - current concepts
Frontotemporal dementia (FTD) is an early-onset form of dementia characterized by progressive deterioration of behavior and language abilities due to degeneration of the frontal and temporal lobes. There are three main variants of FTD - behavioral variant FTD (bvFTD), semantic variant primary progressive aphasia (svPPA), and nonfluent/agrammatic variant PPA (nfvPPA). FTD is highly heritable and can be caused by mutations in MAPT, GRN, and C9orf72 genes. Diagnosis involves clinical evaluation, neuropsychological testing demonstrating executive dysfunction and relative sparing of memory, and neuroimaging showing frontal and temporal lobe atrophy.
Frontotemporal dementia
Frontotemporal dementia is an early-onset form of dementia that typically affects people between 50-60 years old. It is caused by the progressive loss of brain cells in the frontal and temporal lobes of the brain. Inherited genetic mutations may play a role in some cases. There are several clinical variants of frontotemporal dementia characterized by different behavioral or language symptoms, including behavioral variant FTD, semantic dementia, progressive nonfluent aphasia, logopenic aphasia, corticobasal syndrome, and progressive supranuclear palsy.
Temporal lobe and its role in psychiatry
The temporal lobe is involved in processing sensory input, memory formation, language comprehension, and emotional processing. It contains structures like the hippocampus and amygdala that are important for memory and emotional associations. Disorders of the temporal lobe can cause problems like epilepsy, memory deficits, language issues like aphasia, and behavioral changes. Temporal lobe epilepsy is a common type of seizure originating in structures of the anteromedial temporal lobe. Bilateral damage to the amygdala and inferior temporal cortex can cause Klüver-Bucy syndrome characterized by changes in behavior and cognition. The temporal lobe also plays a key role in conditions like Alzheimer's disease, frontotemporal dementia, and traumatic brain injury.
Dementia
The world’s population is ageing rapidly, and with it is coming to a significant increase in the number of
older people with dementia. This increase presents major challenges for the provision of healthcare
generally and for dementia care in particular, for as more people have dementia, there will be more
people exhibiting behavioural and psychological symptoms of dementia (BPSD).
BPSD exact a high price from both the patient and the caregiver in terms of the distress and disability
they cause if left untreated. BPSD is recognisable, understandable and treatable. The recognition and
appropriate management of BPSD are important factors in improving our care of dementia patients
and their caregivers,
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This document outlines an approach to diagnosing and evaluating dementia. It discusses the subtypes of mild cognitive impairment and dementia, the importance of a detailed patient history and neurological exam, and diagnostic criteria. Investigations may include cognitive testing, brain imaging, and lab tests to identify reversible causes or distinguish between dementia subtypes like Alzheimer's disease or Lewy body dementia. Follow up is important to monitor progression. The take home message is that dementia causes significant impairment, so a thorough history and early diagnosis are crucial.
Frontotemporal dementia
Frontotemporal dementia (FTD) is the second most common early-onset dementia. There are several variants of FTD including behavioral variant FTD and primary progressive aphasias like semantic dementia and progressive nonfluent aphasia. Genetic causes include mutations in MAPT, GRN, and C9ORF72 genes. Neuroimaging shows characteristic patterns of frontal and temporal lobe atrophy depending on the variant. Biomarkers like increased blood GFAP levels may help with diagnosis. Currently, there are no approved disease-modifying treatments, but some medications may help treat symptoms. Research focuses on new targets like gene therapy to potentially slow progression in the future.
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This document provides information about dementia, including:
1. Dementia is characterized by progressive deterioration of intellect, behavior, and personality due to diffuse brain disease, especially affecting the cortex and hippocampus. Memory impairment is required for diagnosis.
2. Symptoms include memory loss, abnormal behavior, intellectual decline, mood changes, and difficulty with daily tasks. Insight is initially retained but lost over time.
3. Causes of dementia include Alzheimer's disease (60% of cases), cerebrovascular disease, neurodegenerative diseases, infections, head injuries, and tumors. Dementia must be distinguished from delirium and depression.
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This document provides information about dementia, including:
1. Dementia is characterized by progressive deterioration of intellect, behavior, and personality due to diffuse brain disease, especially affecting the cortex and hippocampus. Memory impairment is required for diagnosis.
2. Symptoms include memory loss, abnormal behavior, intellectual decline, mood changes, and difficulty with daily tasks. Insight is initially retained but lost over time.
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Frontal Lobe Syndromes [2014]
- The document discusses executive functions which are mental processes that control and coordinate other cognitive processes. Damage to the prefrontal cortex can cause frontal lobe syndromes characterized by difficulties with tasks like planning, problem solving, and behavioral control.
- Specific executive functions discussed include switching attention, response inhibition, sequencing tasks, and monitoring multiple activities simultaneously. Tests used to assess executive functions are also described.
- Symptoms of two common frontal lobe syndromes - orbitofrontal and frontal convexity - are outlined. The document also discusses how executive dysfunction can affect personality, behavior, and social skills.
Mild Cognitive Imparement
This document discusses mild cognitive impairment (MCI), including its history, clinical presentations, investigations, treatment and prognosis. MCI is defined as a decline in cognitive abilities beyond normal aging but not significant enough to interfere with daily life. People with MCI are at higher risk of progressing to dementia. While no treatments have proven effective, lifestyle factors like exercise may help. Predictors of progression to dementia include severity of memory impairment, brain volume changes on MRI, and ApoE genotype. Monitoring is important as many people with MCI will convert to Alzheimer's disease within 6 years. MCI represents an important clinical entity as it may be a precursor to dementia.
Lewy Body Dementia
This document discusses Lewy body dementia, including its clinical features such as visual hallucinations and parkinsonism. It describes two types of Lewy body dementia: diffuse Lewy body disease, which presents at an early age with widespread Lewy body formation and rapid progression, and Lewy body variant of Alzheimer's disease, which presents later in life with mild parkinsonism and global cognitive impairment. The diagnosis, medications used to treat it such as cholinesterase inhibitors and antiparkinson drugs, and behavioral management strategies are also outlined.
EEG Maturation - Serial evolution of changes from Birth to Old Age
This presentation discusses in detail the evolution of the EEG patterns in the human brain, as the brain develops and matures. The sequence of changes as well as the shifting patterns coinciding with Myelination are discussed.
Approach to Dementia
1. Dementia is a growing problem worldwide, affecting over 47 million people in 2015 and projected to increase significantly by 2050 as populations age.
2. Dementia involves the deterioration of cognitive abilities such as memory, judgment, and problem solving that impair daily living. It can be caused by neurodegenerative, vascular, or other medical conditions.
3. Assessing dementia involves evaluating memory impairment, ruling out other causes like depression, and using screening tools such as the MMSE alongside medical exams and tests to determine severity and guide further evaluation.
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Christian Haas Webinar July 2014
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Vascular Dementia Final
Vascular dementia is caused by problems in the supply of blood to the brain, often due to conditions like strokes or mini-strokes. It is characterized by stepwise cognitive decline following vascular events and symptoms that overlap with Alzheimer's disease, though it often occurs at a younger age. Risk factors include age, history of strokes, high blood pressure, diabetes, smoking, and atrial fibrillation. Treatment focuses on controlling vascular risk factors and symptoms.
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Alzheimer's disease is a chronic, progressive brain disorder that causes loss of memory and cognitive abilities. It is the most common form of dementia. Changes in the brain include accumulation of amyloid plaques and neurofibrillary tangles that disrupt communication between neurons. Symptoms start with short-term memory loss and progress to include problems with language, visual processing, motor skills, reasoning, and personality changes. Diagnosis involves ruling out other conditions through tests like CT or MRI scans and neuropsychological evaluations. Currently, cholinesterase inhibitors are the only approved treatment for cognitive symptoms, while antipsychotics may help behavioral issues.
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PSYCHIATRIC MANIFESTATIONS OF PARKINSONISM.pptx
Parkinson's disease is associated with various psychiatric manifestations that can affect up to 90% of patients. These include cognitive disturbances like dementia, depression in 40-50% of patients, anxiety in about 40%, and behavioral issues. Depression can predate motor symptoms and increases mortality risk. Mania or hypomania may occur due to dopaminergic medications. Compulsive behaviors are associated with dopamine replacement therapy. Apathy is also common and linked to cognitive and executive dysfunction. Accurate diagnosis and treatment of psychiatric conditions in Parkinson's patients is important for quality of life.
Psychiatric manifestations of Parkinson's Disease
Parkinson's disease is associated with various psychiatric manifestations that can affect up to 90% of patients. These include cognitive disturbances like dementia, depression in 40-50% of patients, anxiety in about 40%, and behavioral issues. Depression can predate motor symptoms and increases mortality risk. Mania or hypomania may occur due to dopaminergic medications. Compulsive behaviors are associated with dopamine replacement therapy. Apathy is also common and linked to cognitive and executive dysfunction. Accurate diagnosis and treatment of psychiatric conditions in Parkinson's patients is important for quality of life.
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3. The presentation covered diagnostic approaches including history, cognitive assessment, exams, and biomarkers. Biomarkers like CSF proteins and neuroimaging can help predict conversion from MCI to dementia.
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A presentation for undergraduate Education on ADHD. for more, and for original PPTXs, visit:
https://psych.thinkific.com
My question bank:
https://psych.thinkific.com/courses/Psychiatry-question-bank-for-MRCPsych
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Frontotemporal Dementia: An Overview
- 1. Frontotemporal Dementia An Overview October 13, 2012 Brian S. Appleby, M.D. Staff, Lou Ruvo Center for Brain Health, Cleveland Clinic
- 2. Disclosures • Co-PI, memantine for frontotemporal dementia, Forest Pharmaceuticals
- 3. Objectives • Describe the illnesses within the frontotemporal lobar degeneration (FTLD) spectrum • Characterize the common types of FTLD • Illustrate case examples of FTLD
- 4. Frontotemporal Lobar Degeneration Semantic PPA dementia PSP AGD FTD FTD-MND CBD FUS NIFID HSD IBMPFD
- 5. Papageorgiou S, et al. Alzheimer Dis Assoc Disord, 2009 AD FTLD
- 6. Survival Time Garcin B, Neurology 2009
- 7. Appleby BS, Dementi Geriatr Cog Disord 2008
- 8. CJD FTD SD PPA AD CBD ZBI=Zarit Burden Interview Johns Hopkins FTD/YOD Clinic
- 9. Hemispheric Asymmetry (MRI and PET)
- 10. Frontotemporal dementia (55%) Primary progressive aphasia Semantic dementia (25%) (20%)
- 11. Frontotemporal Dementia • Mean age of onset: 55-65 years-of-age • Male>Female • Prominent frontal lobe symptoms - Disinhibition - Poor insight/judgment - Loss of social graces - Perseverative behaviors - Apathy
- 12. Primary Progressive Aphasia • Progressive non-fluent aphasia • Decreased speech output • Speech apraxia • Changes in grammar use • Neuropathology is often progressive supranuclear palsy or corticobasal degeneration Josephs KA, Brain 2006
- 13. Semantic Dementia Animal Bird
- 14. Treatment
- 15. Cholinesterase Inhibitors Irwin D, Am J Alzheimers Dis Other Disord 2010
- 16. Memantine • Increases brain FDG-PET metabolism in FTD and SD (Chow 2011, 2012) • No improvement in behavior/cognition (Diehl-Schmid 2008, Vercelletto 2011) • Transient improvement in neuropsych symptoms in FTD and PPA (Swanberg 2007, Boxer 2009) • Currently in multisite RCT
- 17. Antipsychotics • Often used because of behavioral symptoms • Mounting evidence of hypersensitivity to EPS in FTD (Mendez 2001, Pijnenburg 2003, Czarnecki 2008) • Think of overlap of FTLD with “Parkinson’s-Plus” disorders
- 18. Benzodiazepines “Do you really want to give a disinhibiting medication to a demented person with no frontal lobes?”
- 19. Antidepressants • Loss of serotonergic neurons->replete with serotonergic drugs • Trazodone (Lebert 2004) • SSRIs (Swartz 1997, Moretti 2003, Herrmann 2011) • Paroxetine: no effect, worsened cognition (Deakin 2004)
- 20. Non-Pharmacological Interventions • Environment (locked behavioral dementia unit) • Caregiver support (FTD support groups) • SSDI Compassionate Allowances • Elder care lawyer involvement early • Driving (different concerns) • Travel letters
- 21. Case #1 • 58 y.o. AAM attorney with h/o dyslexia with a 2 yr h/o cognitive decline and personality change • Distracted, poor concentration, low mood, fatigued • Only reads comic books and watches cartoons, often the same ones repeatedly
- 22. Exam General: Asked to leave room several times to walk around. Buccal stereotypies (i.e., blowing) Speech: Sparse, poverty of content Affect: Flat, no brightening MMSE: 19/30 Brain MRI: Mild generalized atrophy
- 23. Further Work-up
- 24. Case #2 • 60 y.o. WM with no past neuropsych hx • Initial complaint is stuttering/stammering • Phonemic paraphrasic errors on exam • MoCA=28/30 • “f”=2 words, “animals”=18 • At next visit, has complaints of poor concentration and distractibility
- 25. Case #3 • 60 y.o. WF with h/o rheumatic fever, GERD, vit D def, osteopenia, and liver/brain hemangiomas • 1 yr h/o progressive strabismus with diplopia (repaired with return 1 mo later), parkinsonism, dysarthria, and short-term amnesia, fatigue, anxiety, panic attacks
- 26. Exam Speech: hypophonic, sparse, dysarthric Thought Process: bradyphrenic Affect: stable, flat without brightening MMSE: 7/30 UPDRS II: 43 Neuro: vertical gaze impairment, choppy saccades, hypomimia, axial rigidity
- 27. Case #4 • 50 y.o. female from Spain with 4 yr h/o gradual executive dysfxn, short-term amnesia, progressive non-fluent aphasia, parkinsonism, and myoclonus • Paces frequently, apathetic, crying when frustrated, seen responding to internal stimuli, and sometimes thinks others are stealing from her
- 28. Exam Gait: slow, shuffling, leans to left Speech: Effortful, paraphrasic errors MMSE: 5/30 3MS: 17/100 Clock: 1/5 UPDRS II: 44 •Myoclonus with speech and action •Left-sided neglect, finger agnosia
- 29. Exam Pentagons Clock
Editor's Notes
- EOD<65