This document discusses different types of autoimmune encephalitis. It categorizes autoimmune encephalitis as either paraneoplastic, non-paraneoplastic, or associated with vasculitis. Within non-paraneoplastic autoimmune encephalitis, several specific types are described that are associated with antibodies against receptors like NMDA, GABA, AMPA, and LGI1. Clinical features, pathogenesis, diagnosis and treatment approaches are summarized for several of these subtypes, with particular focus on anti-NMDA receptor encephalitis. Prognosis and potential neurologic sequelae are also briefly covered.
This document discusses several types of autoimmune encephalitis, including Hashimoto's encephalopathy, NMDA encephalitis, and limbic encephalitis. Hashimoto's encephalopathy is defined by the presence of thyroid peroxidase antibodies in patients with encephalitis that responds to steroids. It can cause non-specific neurological symptoms. NMDA encephalitis commonly affects young women and can cause psychiatric issues, decreased consciousness, and movement disorders. Diagnosis involves detecting NMDA receptor antibodies in CSF or serum. Limbic encephalitis involves inflammation of limbic structures and is associated with antibodies against proteins like LGI1; it typically causes memory loss, behavioral changes and seizures in older patients.
This is a brief review of autoimmune epilepsies, especially autoimmune encephalitis, SREAT, NORSE, FIRES and Rasmussen's encephalitis. A brief overview of investigations and treatment is included.
74th ICREA Colloquium "Autoimmunity meets neurodegeneration: different pathwa...ICREA
Studies during the last 10 years have revealed a new category of brain diseases in which crucial neuronal receptors are attacked by autoantibodies. As a result of this attack there is a reduction of the target synaptic proteins leading to alterations in synaptic transmission. The clinical manifestations vary according to the receptor involved, and may resemble many of the symptoms caused by neurodegenerative diseases in which specific receptors are involved, including among others Parkinson, epilepsy, chronically progressive sleep disease, or schizophrenia.
This document discusses various types of autoimmune encephalitis. It begins by providing clues that can suggest an autoimmune cause over infectious, including a subacute onset and fluctuating course. It then covers several specific autoimmune encephalitis subtypes defined by the neuronal surface antigens involved, such as anti-NMDA receptor and anti-LGI1 encephalitis. For each subtype, it discusses clinical features, investigations, and treatment approaches. The document aims to help clinicians differentiate between autoimmune and infectious causes of encephalitis.
1. The document discusses several types of synaptic autoimmune disorders including anti-NMDA receptor encephalitis, anti-AMPA receptor encephalitis, anti-GABA B encephalitis, anti-LGI1 limbic encephalitis, and anti-CASPR2 associated encephalitis.
2. These disorders are treated with immunotherapy such as steroids, intravenous immunoglobulin, and plasma exchange. If tumors are present, they are surgically removed.
3. Outcomes vary by type of disorder, but many patients recover fully or have mild deficits with treatment, though some require long-term support and rehabilitation. Relapses can occur and require continued immunotherapy.
Epileptic encephalopathies are a group of epileptic disorders that cause cognitive and behavioral impairments beyond what would be expected from seizures alone. They typically begin early in life and are characterized by frequent seizures and abnormal EEG patterns. Common types include early myoclonic encephalopathy, Ohtahara syndrome, West syndrome, Dravet syndrome, and Lennox-Gastaut syndrome. These disorders can cause developmental delays, intellectual disabilities, and in some cases early death. Treatment aims to control seizures, though many types are highly treatment resistant.
This document discusses several types of autoimmune encephalitis, including Hashimoto's encephalopathy, NMDA encephalitis, and limbic encephalitis. Hashimoto's encephalopathy is defined by the presence of thyroid peroxidase antibodies in patients with encephalitis that responds to steroids. It can cause non-specific neurological symptoms. NMDA encephalitis commonly affects young women and can cause psychiatric issues, decreased consciousness, and movement disorders. Diagnosis involves detecting NMDA receptor antibodies in CSF or serum. Limbic encephalitis involves inflammation of limbic structures and is associated with antibodies against proteins like LGI1; it typically causes memory loss, behavioral changes and seizures in older patients.
This is a brief review of autoimmune epilepsies, especially autoimmune encephalitis, SREAT, NORSE, FIRES and Rasmussen's encephalitis. A brief overview of investigations and treatment is included.
74th ICREA Colloquium "Autoimmunity meets neurodegeneration: different pathwa...ICREA
Studies during the last 10 years have revealed a new category of brain diseases in which crucial neuronal receptors are attacked by autoantibodies. As a result of this attack there is a reduction of the target synaptic proteins leading to alterations in synaptic transmission. The clinical manifestations vary according to the receptor involved, and may resemble many of the symptoms caused by neurodegenerative diseases in which specific receptors are involved, including among others Parkinson, epilepsy, chronically progressive sleep disease, or schizophrenia.
This document discusses various types of autoimmune encephalitis. It begins by providing clues that can suggest an autoimmune cause over infectious, including a subacute onset and fluctuating course. It then covers several specific autoimmune encephalitis subtypes defined by the neuronal surface antigens involved, such as anti-NMDA receptor and anti-LGI1 encephalitis. For each subtype, it discusses clinical features, investigations, and treatment approaches. The document aims to help clinicians differentiate between autoimmune and infectious causes of encephalitis.
1. The document discusses several types of synaptic autoimmune disorders including anti-NMDA receptor encephalitis, anti-AMPA receptor encephalitis, anti-GABA B encephalitis, anti-LGI1 limbic encephalitis, and anti-CASPR2 associated encephalitis.
2. These disorders are treated with immunotherapy such as steroids, intravenous immunoglobulin, and plasma exchange. If tumors are present, they are surgically removed.
3. Outcomes vary by type of disorder, but many patients recover fully or have mild deficits with treatment, though some require long-term support and rehabilitation. Relapses can occur and require continued immunotherapy.
Epileptic encephalopathies are a group of epileptic disorders that cause cognitive and behavioral impairments beyond what would be expected from seizures alone. They typically begin early in life and are characterized by frequent seizures and abnormal EEG patterns. Common types include early myoclonic encephalopathy, Ohtahara syndrome, West syndrome, Dravet syndrome, and Lennox-Gastaut syndrome. These disorders can cause developmental delays, intellectual disabilities, and in some cases early death. Treatment aims to control seizures, though many types are highly treatment resistant.
Epileptic encephalopathies are a group of epileptic disorders that cause cognitive and behavioral impairments beyond what would be expected from seizures alone. They typically begin early in life and are characterized by frequent seizures and abnormal EEG patterns. Common types include early myoclonic encephalopathy, Ohtahara syndrome, West syndrome, Dravet syndrome, and Lennox-Gastaut syndrome. These disorders can cause developmental delays, neurological deficits, and sometimes early death if not properly treated. Management involves seizure control through medications and other therapies like the ketogenic diet.
This document provides an overview of autoimmune encephalitis (AE) and discusses a case study. It begins with introducing the case of a 68-year-old female presenting with behavioral changes and seizures. Diagnostic workup showed abnormal EEG and MRI findings. Serum testing was positive for LGI1 antibodies, leading to a diagnosis of anti-LGI1 antibody encephalitis. The document then reviews AE in general, discussing pathogenesis, clinical presentation, diagnostic criteria and workup, management, and prognosis for different antibody types like anti-NMDA receptor and VGKC encephalitis. It emphasizes the importance of early recognition and treatment for potential recovery from AE.
This document discusses autoimmune encephalitis, which is caused by antibodies targeting neuronal cell surface or synaptic antigens. It can present with various neuropsychiatric symptoms and be misdiagnosed as viral encephalitis. Diagnosis is confirmed by detecting antibodies in CSF and serum, often against NMDA receptors. Treatment involves immunotherapy like steroids, IVIg, or plasma exchange. Outcomes are generally good if treated promptly, though some disorders relapse. Tumor removal may also be needed if one is present.
This document discusses autoimmune encephalitis, which occurs due to antibodies against neuronal proteins or synaptic receptors. It can comprise 5-10% of encephalitis cases. The most common type is anti-NMDAR encephalitis, which mainly affects females and presents in stages with psychiatric symptoms, decreased consciousness, and movements disorders. Diagnosis involves detecting antibodies in CSF or serum. Treatment is immunotherapy like steroids, IVIG, plasma exchange. Outcomes are generally good but some experience relapse or residual effects. It should be considered in the differential of acute encephalitis.
This document discusses autoimmune encephalitis, which occurs due to antibodies against neuronal cell proteins or synaptic receptors. It can comprise 5-10% of encephalitis cases. The most common type is anti-NMDAR encephalitis, which targets the NMDA receptor. It most often affects females under 18 and follows a predictable clinical course with psychiatric, neurological, and decreased consciousness symptoms. Diagnosis involves identifying antibodies in CSF or serum and MRI/EEG may show nonspecific abnormalities. Treatment involves immunotherapy like steroids, IVIG, plasma exchange, and rituximab. Outcomes range from full recovery to relapse or residual deficits.
This document provides an overview of epilepsy presented by Nawa Likando. It defines epilepsy as recurrent unprovoked seizures and notes its global prevalence is over 50 million people. The presentation covers the epidemiology, classification, pathophysiology, seizure types, diagnosis and management of epilepsy. It discusses focal versus generalized seizures, precipitating factors, antiepileptic drugs, surgery for refractory cases, status epilepticus, and complications of epilepsy such as sudden unexplained death. The overview addresses the definition, causes, evaluation, and treatment of this chronic neurological disorder.
Sepsis-associated encephalopathy (SE) is a brain dysfunction caused by sepsis and systemic inflammatory response syndrome. It is characterized by acute impairment of consciousness and confusion. Between 9-71% of sepsis patients develop SE. The pathophysiology involves oxidative stress, elevated pro-inflammatory cytokines, complement activation, and aromatic amino acid imbalance. Diagnosis is based on clinical assessment and EEG, while treatment focuses on managing the underlying sepsis along with supportive care. SE can cause long-term cognitive and psychiatric impairments in sepsis survivors.
The document discusses various topics related to neurology including:
1. Common neurological disorders such as headache, low back pain, and stroke.
2. Components of a neurological examination including signs, reflexes, and tests of sensory and motor function.
3. Diagnostic tools used in neurology such as CT, MRI, angiography, EEG, lumbar puncture, and PET.
4. Types of disturbances of consciousness including those caused by brainstem or cortical damage.
5. Criteria for determining brain death.
This document discusses atypical parkinsonism (AP), which accounts for 15-20% of all cases of parkinsonism. It begins by classifying AP into primary, multisystem degenerations, hereditodegenerative, and secondary types. It then focuses on the major AP syndromes - Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA), and Corticobasal Degeneration (CBD). For PSP and MSA, it provides details on clinical presentation, diagnostic criteria, investigations, pathology, and treatment approaches. The document emphasizes the importance of differentiating AP from Parkinson's disease to allow for accurate prognosis and management of patients.
Porphyrias and neurological menifestationsNeurologyKota
This document summarizes the rare metabolic disorders known as porphyrias, which result from defects in the heme biosynthesis pathway. Heme is essential for oxygen transport and energy production. The document describes the different types of porphyrias, which can be hepatic or erythropoietic in origin and inherited in autosomal dominant, recessive, or X-linked patterns. The major types that cause neurological symptoms are acute intermittent porphyria, hereditary coproporphyria, and variegate porphyria. Neurological manifestations include autonomic neuropathy, peripheral neuropathy, and encephalopathy. Treatment involves administering heme or carbohydrate precursors to reduce accumulation of toxic heme intermediates.
The document discusses recent advances in neuroimmunology, specifically regarding autoimmunity in the central nervous system. It covers how the CNS was once considered an immunologically privileged site but is now known to mount intrathecal immune responses. Several autoimmune disorders of the CNS are described, including multiple sclerosis, neuromyelitis optica spectrum disorders, and autoimmune encephalitides associated with antibodies against neuronal surface antigens. Laboratory testing for various neuronal antibodies is also summarized.
Delirium is a disturbance of consciousness and cognition characterized by acute onset and fluctuating course. It commonly occurs in the intensive care unit (ICU), with a prevalence of 32.3% among ICU patients. The three main subtypes are hypoactive, hyperactive, and mixed delirium. Potential causes of delirium include neurotransmitter imbalances, inflammation, impaired oxidative metabolism, and alterations in amino acid transport. Risk factors include older age, cognitive impairment, and medications such as benzodiazepines. Delirium is diagnosed using tools such as the Confusion Assessment Method for the ICU and managed through both nonpharmacological and pharmacological interventions.
- Antibody-mediated encephalitides are inflammatory brain diseases characterized by neuropsychiatric symptoms associated with antibodies against neuronal proteins. The estimated annual incidence is 5-8 cases per 100,000 people.
- Common forms include anti-NMDAR encephalitis, which predominantly affects young females and can cause psychiatric symptoms, seizures, and decreased consciousness. Limbic encephalitis usually affects older patients and causes confusion, behavioral changes, and memory impairment.
- Diagnosis involves detecting antibodies in CSF or serum and MRI/EEG findings. Treatment includes immunotherapy, tumor removal if applicable, and medications like steroids, IVIg, or rituximab. Outcomes can be favorable
This document summarizes recent insights into multiple system atrophy (MSA). MSA is a neurodegenerative disorder characterized by parkinsonism or cerebellar ataxia along with autonomic failure. Key points include: MSA is caused by the accumulation of alpha-synuclein protein aggregates in oligodendrogltes. Diagnostic criteria have been updated and neuroimaging may help with diagnosis. Prognosis is poor with mean survival of 7-9 years. Current treatments are only symptomatic and no disease-modifying therapies exist yet, though research into targets like alpha-synuclein aggregation are promising avenues.
auto immune encephalitis 2.pptx diagnosisaaqsa6264
This document discusses autoimmune encephalitis, which is a progressive inflammatory brain condition characterized by memory loss, altered mental status, seizures, and psychiatric symptoms associated with autoantibodies. There are several types classified by the specific autoantibodies involved, such as anti-NMDA receptor encephalitis. Diagnosis involves identifying autoantibodies in the CSF or serum. Treatment primarily consists of immunotherapy with corticosteroids, IVIG, and plasma exchange, along with tumor removal if applicable. Prognosis depends on subtype, but many patients respond well to immunotherapy.
Spirit to autoantibodies: Journey of limbic disorders from philosophy to aff...Ubaidur Rahaman
Limbic encephalitis usually presents with neuropychiatric symptomatology, often remain undiagnosed, treated as psychiatry disorders with various antipsychotic medications and die. Early diagnosis and treatment of autoimmune limbic encephalitis has good outcome, establishing these patients back into the society
This document discusses progressive supranuclear palsy (PSP). It begins by classifying PSP and outlining its diagnostic criteria and phenotypes. Key signs of PSP include early vertical supranuclear gaze palsy, postural instability with falls, and poor response to levodopa. Investigations like MRI, PET, and CSF analysis can aid in diagnosis. Pathology involves tau neurofibrillary tangles in brainstem nuclei. There is no effective treatment, only supportive and symptomatic measures. The document also briefly discusses multiple system atrophy (MSA) and corticobasal degeneration (CBD).
The debris of the ‘last major merger’ is dynamically youngSérgio Sacani
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
The cost of acquiring information by natural selectionCarl Bergstrom
This is a short talk that I gave at the Banff International Research Station workshop on Modeling and Theory in Population Biology. The idea is to try to understand how the burden of natural selection relates to the amount of information that selection puts into the genome.
It's based on the first part of this research paper:
The cost of information acquisition by natural selection
Ryan Seamus McGee, Olivia Kosterlitz, Artem Kaznatcheev, Benjamin Kerr, Carl T. Bergstrom
bioRxiv 2022.07.02.498577; doi: https://doi.org/10.1101/2022.07.02.498577
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Epileptic encephalopathies are a group of epileptic disorders that cause cognitive and behavioral impairments beyond what would be expected from seizures alone. They typically begin early in life and are characterized by frequent seizures and abnormal EEG patterns. Common types include early myoclonic encephalopathy, Ohtahara syndrome, West syndrome, Dravet syndrome, and Lennox-Gastaut syndrome. These disorders can cause developmental delays, neurological deficits, and sometimes early death if not properly treated. Management involves seizure control through medications and other therapies like the ketogenic diet.
This document provides an overview of autoimmune encephalitis (AE) and discusses a case study. It begins with introducing the case of a 68-year-old female presenting with behavioral changes and seizures. Diagnostic workup showed abnormal EEG and MRI findings. Serum testing was positive for LGI1 antibodies, leading to a diagnosis of anti-LGI1 antibody encephalitis. The document then reviews AE in general, discussing pathogenesis, clinical presentation, diagnostic criteria and workup, management, and prognosis for different antibody types like anti-NMDA receptor and VGKC encephalitis. It emphasizes the importance of early recognition and treatment for potential recovery from AE.
This document discusses autoimmune encephalitis, which is caused by antibodies targeting neuronal cell surface or synaptic antigens. It can present with various neuropsychiatric symptoms and be misdiagnosed as viral encephalitis. Diagnosis is confirmed by detecting antibodies in CSF and serum, often against NMDA receptors. Treatment involves immunotherapy like steroids, IVIg, or plasma exchange. Outcomes are generally good if treated promptly, though some disorders relapse. Tumor removal may also be needed if one is present.
This document discusses autoimmune encephalitis, which occurs due to antibodies against neuronal proteins or synaptic receptors. It can comprise 5-10% of encephalitis cases. The most common type is anti-NMDAR encephalitis, which mainly affects females and presents in stages with psychiatric symptoms, decreased consciousness, and movements disorders. Diagnosis involves detecting antibodies in CSF or serum. Treatment is immunotherapy like steroids, IVIG, plasma exchange. Outcomes are generally good but some experience relapse or residual effects. It should be considered in the differential of acute encephalitis.
This document discusses autoimmune encephalitis, which occurs due to antibodies against neuronal cell proteins or synaptic receptors. It can comprise 5-10% of encephalitis cases. The most common type is anti-NMDAR encephalitis, which targets the NMDA receptor. It most often affects females under 18 and follows a predictable clinical course with psychiatric, neurological, and decreased consciousness symptoms. Diagnosis involves identifying antibodies in CSF or serum and MRI/EEG may show nonspecific abnormalities. Treatment involves immunotherapy like steroids, IVIG, plasma exchange, and rituximab. Outcomes range from full recovery to relapse or residual deficits.
This document provides an overview of epilepsy presented by Nawa Likando. It defines epilepsy as recurrent unprovoked seizures and notes its global prevalence is over 50 million people. The presentation covers the epidemiology, classification, pathophysiology, seizure types, diagnosis and management of epilepsy. It discusses focal versus generalized seizures, precipitating factors, antiepileptic drugs, surgery for refractory cases, status epilepticus, and complications of epilepsy such as sudden unexplained death. The overview addresses the definition, causes, evaluation, and treatment of this chronic neurological disorder.
Sepsis-associated encephalopathy (SE) is a brain dysfunction caused by sepsis and systemic inflammatory response syndrome. It is characterized by acute impairment of consciousness and confusion. Between 9-71% of sepsis patients develop SE. The pathophysiology involves oxidative stress, elevated pro-inflammatory cytokines, complement activation, and aromatic amino acid imbalance. Diagnosis is based on clinical assessment and EEG, while treatment focuses on managing the underlying sepsis along with supportive care. SE can cause long-term cognitive and psychiatric impairments in sepsis survivors.
The document discusses various topics related to neurology including:
1. Common neurological disorders such as headache, low back pain, and stroke.
2. Components of a neurological examination including signs, reflexes, and tests of sensory and motor function.
3. Diagnostic tools used in neurology such as CT, MRI, angiography, EEG, lumbar puncture, and PET.
4. Types of disturbances of consciousness including those caused by brainstem or cortical damage.
5. Criteria for determining brain death.
This document discusses atypical parkinsonism (AP), which accounts for 15-20% of all cases of parkinsonism. It begins by classifying AP into primary, multisystem degenerations, hereditodegenerative, and secondary types. It then focuses on the major AP syndromes - Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA), and Corticobasal Degeneration (CBD). For PSP and MSA, it provides details on clinical presentation, diagnostic criteria, investigations, pathology, and treatment approaches. The document emphasizes the importance of differentiating AP from Parkinson's disease to allow for accurate prognosis and management of patients.
Porphyrias and neurological menifestationsNeurologyKota
This document summarizes the rare metabolic disorders known as porphyrias, which result from defects in the heme biosynthesis pathway. Heme is essential for oxygen transport and energy production. The document describes the different types of porphyrias, which can be hepatic or erythropoietic in origin and inherited in autosomal dominant, recessive, or X-linked patterns. The major types that cause neurological symptoms are acute intermittent porphyria, hereditary coproporphyria, and variegate porphyria. Neurological manifestations include autonomic neuropathy, peripheral neuropathy, and encephalopathy. Treatment involves administering heme or carbohydrate precursors to reduce accumulation of toxic heme intermediates.
The document discusses recent advances in neuroimmunology, specifically regarding autoimmunity in the central nervous system. It covers how the CNS was once considered an immunologically privileged site but is now known to mount intrathecal immune responses. Several autoimmune disorders of the CNS are described, including multiple sclerosis, neuromyelitis optica spectrum disorders, and autoimmune encephalitides associated with antibodies against neuronal surface antigens. Laboratory testing for various neuronal antibodies is also summarized.
Delirium is a disturbance of consciousness and cognition characterized by acute onset and fluctuating course. It commonly occurs in the intensive care unit (ICU), with a prevalence of 32.3% among ICU patients. The three main subtypes are hypoactive, hyperactive, and mixed delirium. Potential causes of delirium include neurotransmitter imbalances, inflammation, impaired oxidative metabolism, and alterations in amino acid transport. Risk factors include older age, cognitive impairment, and medications such as benzodiazepines. Delirium is diagnosed using tools such as the Confusion Assessment Method for the ICU and managed through both nonpharmacological and pharmacological interventions.
- Antibody-mediated encephalitides are inflammatory brain diseases characterized by neuropsychiatric symptoms associated with antibodies against neuronal proteins. The estimated annual incidence is 5-8 cases per 100,000 people.
- Common forms include anti-NMDAR encephalitis, which predominantly affects young females and can cause psychiatric symptoms, seizures, and decreased consciousness. Limbic encephalitis usually affects older patients and causes confusion, behavioral changes, and memory impairment.
- Diagnosis involves detecting antibodies in CSF or serum and MRI/EEG findings. Treatment includes immunotherapy, tumor removal if applicable, and medications like steroids, IVIg, or rituximab. Outcomes can be favorable
This document summarizes recent insights into multiple system atrophy (MSA). MSA is a neurodegenerative disorder characterized by parkinsonism or cerebellar ataxia along with autonomic failure. Key points include: MSA is caused by the accumulation of alpha-synuclein protein aggregates in oligodendrogltes. Diagnostic criteria have been updated and neuroimaging may help with diagnosis. Prognosis is poor with mean survival of 7-9 years. Current treatments are only symptomatic and no disease-modifying therapies exist yet, though research into targets like alpha-synuclein aggregation are promising avenues.
auto immune encephalitis 2.pptx diagnosisaaqsa6264
This document discusses autoimmune encephalitis, which is a progressive inflammatory brain condition characterized by memory loss, altered mental status, seizures, and psychiatric symptoms associated with autoantibodies. There are several types classified by the specific autoantibodies involved, such as anti-NMDA receptor encephalitis. Diagnosis involves identifying autoantibodies in the CSF or serum. Treatment primarily consists of immunotherapy with corticosteroids, IVIG, and plasma exchange, along with tumor removal if applicable. Prognosis depends on subtype, but many patients respond well to immunotherapy.
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Limbic encephalitis usually presents with neuropychiatric symptomatology, often remain undiagnosed, treated as psychiatry disorders with various antipsychotic medications and die. Early diagnosis and treatment of autoimmune limbic encephalitis has good outcome, establishing these patients back into the society
This document discusses progressive supranuclear palsy (PSP). It begins by classifying PSP and outlining its diagnostic criteria and phenotypes. Key signs of PSP include early vertical supranuclear gaze palsy, postural instability with falls, and poor response to levodopa. Investigations like MRI, PET, and CSF analysis can aid in diagnosis. Pathology involves tau neurofibrillary tangles in brainstem nuclei. There is no effective treatment, only supportive and symptomatic measures. The document also briefly discusses multiple system atrophy (MSA) and corticobasal degeneration (CBD).
The debris of the ‘last major merger’ is dynamically youngSérgio Sacani
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
The cost of acquiring information by natural selectionCarl Bergstrom
This is a short talk that I gave at the Banff International Research Station workshop on Modeling and Theory in Population Biology. The idea is to try to understand how the burden of natural selection relates to the amount of information that selection puts into the genome.
It's based on the first part of this research paper:
The cost of information acquisition by natural selection
Ryan Seamus McGee, Olivia Kosterlitz, Artem Kaznatcheev, Benjamin Kerr, Carl T. Bergstrom
bioRxiv 2022.07.02.498577; doi: https://doi.org/10.1101/2022.07.02.498577
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As the population is increasing and will reach about 9 billion upto 2050. Also due to climate change, it is difficult to meet the food requirement of such a large population. Facing the challenges presented by resource shortages, climate
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The pygmy halfbeak Dermogenys colletei, is known for its viviparous nature, this presents an intriguing case of relatively low fecundity, raising questions about potential compensatory reproductive strategies employed by this species. Our study delves into the examination of fecundity and the Gonadosomatic Index (GSI) in the Pygmy Halfbeak, D. colletei (Meisner, 2001), an intriguing viviparous fish indigenous to Sarawak, Borneo. We hypothesize that the Pygmy halfbeak, D. colletei, may exhibit unique reproductive adaptations to offset its low fecundity, thus enhancing its survival and fitness. To address this, we conducted a comprehensive study utilizing 28 mature female specimens of D. colletei, carefully measuring fecundity and GSI to shed light on the reproductive adaptations of this species. Our findings reveal that D. colletei indeed exhibits low fecundity, with a mean of 16.76 ± 2.01, and a mean GSI of 12.83 ± 1.27, providing crucial insights into the reproductive mechanisms at play in this species. These results underscore the existence of unique reproductive strategies in D. colletei, enabling its adaptation and persistence in Borneo's diverse aquatic ecosystems, and call for further ecological research to elucidate these mechanisms. This study lends to a better understanding of viviparous fish in Borneo and contributes to the broader field of aquatic ecology, enhancing our knowledge of species adaptations to unique ecological challenges.
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5. Vasculitis asso. encephalopathy
Primary CNS vasculitis
Secondary CNS vasculitis
• SLE
• Sjogren’s
• APLA syn
• Behcet’s
• other - PAN, WG, CSS
Uncertain etiology but responsive to immunotherapy
Neurosarcoidosis
Hypereosinophilic syndromes
6. Antibodies in AE
Antibodies
associated
with AE
Abs against
intracellular
antigens
Markers but not
pathogenic
Levels remain
high despite
improvement
Cell/ synaptic
surface Abs
Pathogenic
Levels rapidly ↓
with
immunotherapy
7. Anti-NMDA Receptor Encephalitis
Clinical features-
Age- 5–76 yrs, mean age- 23 years--- female (80-
90%)
Disease evolution – 5 phases
phase 1 or “prodromal phase,” - flu like illness
phase 2 or “psychiatric phase,” –
behavioral disturbances, psychosis, hallucinations,
agitation and paranoia;
temper tantrums or hyperactivity in children.
8. Language disintegration- echolalia, ↓verbal output
& then mutism.
phase 3 –
Alteration of sensorium (88%) and seizures (76%).
Frank dysautonomia (70%)- cardiac arrhythmias,
hypo or hyperthermia, central hypoventilation
(66%), apneic spells and BP fluctuations.
Dissociative responses to stimuli.
9. phase 4 “hyperkinetic phase”
Oro-facial dyskinesias, bruxism, lip and tongue
biting, dystonia, complex stereotyped movements,
ophisthotonus, oculogyric crises and choreiform
movements.
phase 5 “recovery phase”
gradual return of awareness & responsiveness. Some
patients are left with cognitive deficits- memory
dysfunction, frontal lobe signs, behavioral and
attention deficit disorders.
10. Anti-NMDA Receptor Encephalitis
Pathogenesis-
NMDAR - ligand-gated cation channel involved in
synaptic transmission.
two heteromers, Glu N1 and Glu N2.
NMDAR Ab binding to NMDAR --- internalization of
the receptors by the cell, decreasing the synaptic
transmission of NMDA clusters.
magnitude of changes directly proportional to the
antibody titer.
11. NMDAR abs block GABAergic neurons, leading to a
disinhibition of the excitatory pathways and ↑
extracellular glutamate.
Hence, hyperkinetic movement disorders.
Ovarian teratomas express Glu N1.
12. Diagnosis-
1. Imaging
CT brain usually normal.
MRI brain normal (50%)or may show nonspecific
abnormalities in T2 or FLAIR sequences in the mesial
TL, cerebral cortex (esp frontobasal), cerebellum, basal
ganglia.
MRI cortical-----> subcortical progression
Transient meningeal/ cortical enhancement can be seen.
Serial MRIs can show cerebral atrophy (reversible).
13.
14. 2. Lumbar puncture
Lymphocytic pleocytosis; mean count of 26 cells on presentation (5 to
200 cells).
Protein levels elevated.
Glucose often normal.
CSF IgG index elevated, indicating intrathecal ab synthesis
CSF oligoclonal bands seen in about 50%.
CSF anti-NMDAR antibodies are highly positive and titers correlate
with the disease severity.
Few patients show positive mycoplasma serology- significance unclear.
15. 3. EEG
Electrographic sz (10%)
Generalized/ frontotemporal polymorphic delta
Extreme delta brush pattern : Rhythmic delta (1–3 Hz) activity with bursts of
beta (20–30 Hz) superimposed on the delta waves - seen in 30% - relatively
specific
Some abnormal movements can be misinterpreted as seizures & have no EEG
correlate.
4. Search for ovarian teratoma.
In ~ 60% of the women, an ovarian teratoma is found by abdominal USG, CT or
MRI of pelvis.
5. Brain biopsy non-diagnostic
17. Clinical features vary depending on distributions
of the target antigens.
LGI1 protein expressed mainly in hippocampus.
CASPR2 expressed strongly in both PNS & CNS
neurons.
18. Clinical features in LGI1 related LE-
short-term memory impairment
psychiatric symptoms- personality change,
depression, anxiety, hallucinations, confusion
seizures - complex partial— temporal or classical
faciobrachial tonic seizures
myoclonus (40%)
19. Clinical features in CASPR2 related encephalitis-
psychiatric symptoms & hallucinations,
sleep dysfunction,
autonomic dysfunction,
peripheral nerve hyperexcitability (Morvan disease).
Allodynia
Neuropathic pain
21. Other investigations-
CSF- pleocytosis, lymphocytic predominance, raised
protein & oligoclonal bands.
Hyponatremia (50%)
EEG- focal or generalized epileptiform discharges or
slow wave activity.
Search for tumor (In contrast to NMDAR encephalitis,
associated tumour found in only 11%).
22. GABA- B receptor encephalitis:
Mean Age – 62 yrs, M=F
Malignancy- 50%; Majority SCLC
Presentation- LE, seizures early & prominent
Most seizures appear to have a temporal-lobe onset with
secondary generalization,
some - status epilepticus or subclinical seizures demonstrated on
EEG.
The brain MRI - abnormal in 2/3, showing unilateral or bilateral
medial temporal lobe FLAIR/T2 signal – s/o LE
CSF - lymphocytic pleocytosis.
GABAB receptor antibodies
other autoantibodies (e.g., TPO, ANA, GAD65), reflecting a
tendency to autoimmunity
23. Other less common forms
AMPA receptor encephalitis:
Typical patient- female , median age 60 yrs
Presentation- limbic encephalitis
Syndrome lacks movement disorders,
autonomic dysfunction & hypoventilation
Malignancy (70%)- lung, breast, thymus
Pathogenesis- ↓ no of receptors at synapse alter
function
24.
25.
26.
27.
28.
29. Chronic treatment-
Steroids are mainstay of maintenance Rx
Alternate day schedules are preferred
Daily Calcium + Vit D, GI ulcer prophylaxis, glucose &
BP monitoring
Steroid sparing agents – Azathioprine, MMF to
overlap with steroids for months
Duration – 2- 3 years, No RCT available
30. Other aspects of management
Symptomatic Rx
AEDs for seizures (usually requires > 1 AED in view of
refractoriness)
antipsychotics, antidepressants and medications for sleep
disorders.
Intubation & mechanical ventilation for airway protection and
hypoventilation
Movement disorders resistant to medications require sedation,
including propofol, IV benzodiazepine, NM blockade to prevent
lip and tongue injury and loss of dentition.
31. Pacemaker to prevent severe symptomatic brady/
tachyarrhythmias.
Tumor removal can improve response to
immunotherapy.
32. Serial CBC, RFT, LFT
Latent TB screening
Pregnancy test
IgA level
Mesna in Cyclophosphamide
S-methyltransferase enzyme in AZT
Pneumocystis prophylaxis with TMP-SMZ
Hepatitis screen in Rituximab
33. Prognosis
Response rate – 75 to 80% with tumor removal & immunosuppression.
Time to full recovery : 1–14 months
In NMDA-R encephalitis, Ab titres, esp CSF correlate with disease
severity.
Long term (> 1 yr) maintenance immunosuppression is required in
80%.
Recovery more favorable in patients with an underlying tumor than in
idiopathic cases.
Relapse can be associated with reappearance of 2nd teratoma. USG or
MRI of pelvis - yearly for at least 2 yrs after recovery.
34. Neurologic sequalae
Hemi/ quadriparesis
aphasia
signs of frontal lobe disturbance (apathy,
disinhibition, lack of planning and poor judgment)
sleep disturbance
35. Conclusion
AE should always be considered in evaluation of rapidly
progressive dementia esp in young patients.
Combination of psychiatric illness, hyperkinetic movement
disorders (especially oro-facial dyskinesias), dysautonomia and
central hypoventilation should arouse the suspicion of NMDAR-E.
Similarity of NMDAR-E to Japanese encephalitis is striking, so,
presumed JE cases with negative serology should be
further investigated to rule out NMDARE.
Early initiation of immunotherapy is likely to improve
outcome.
36. References
Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL. Bradley's neurology in clinical practice. Elsevier
Health Sciences; 2015 Oct 25.
FLANAGAN EP, DRUBACH DA, BOEVE BF. Autoimmune dementia and encephalopathy.
Handbook of clinical neurology. 2016 Mar 11;133:247.
Autoimmune encephalopathy. Flanagan et al., Semin Neurol, April 2011.
Immune mediated encephalopathies with an emphasis on paraneoplastic encephalopathies. Pruitt.,
Semin Neurol, April 2011.
Update on paraneoplastic & autoimmune disorders of CNS. Rosenfeld et al., Semin Neurol, March
2010.
Steroid responsive encephalopathy associated with autoimmune thyroiditis. Castillo et al., Arch
Neurol, 2006, 63, 197-202.
Clinical experience and laboratory investigations in patients with anti-NMDAR
encephalitis. Dalmau et al., Lancet Neurol 10(1):63-74, 2011.