1) Epilepsy is defined as two or more unprovoked seizures occurring more than 24 hours apart or one unprovoked seizure with a high risk of further seizures in the next 10 years.
2) GABA, glutamate, and other neurotransmitters play a role in epileptogenesis. During seizures, GABAergic inhibition is compromised while glutamatergic excitation increases.
3) Many factors can cause seizures including vascular, metabolic, infectious, autoimmune, genetic, and drug-induced causes by altering excitatory and inhibitory neurotransmission in the brain.
Epileptogenesis is the process by which the brain becomes epileptic. It occurs in three phases - an initial injury, a latent period of neuronal changes, and chronic epilepsy. During the latent period, various molecular pathways are dysregulated, including mTOR and REST, and neuronal circuits like the dentate gate and temporoammonic pathway are altered. These changes involve loss of inhibitory interneurons and abnormal sprouting, leading to recurrent seizures. Understanding epileptogenesis may help develop new treatments targeting the latent period to prevent epilepsy.
Epileptogenesis is the process by which normal brain tissue is transformed into tissue capable of generating spontaneous recurrent seizures. It involves multiple mechanisms including genetic and acquired factors. The hippocampus is particularly susceptible to epileptogenesis due to its circuitry. Status epilepticus animal models are commonly used to study the process. Epileptogenesis occurs in acute, subacute, and chronic stages. Acute changes include increased expression of immediate early genes and post-translational modifications of proteins. Subacute changes involve neuronal death, alterations in neurotrophic factors and inflammation. Chronic changes include mossy fiber sprouting and neurotransmission alterations.
Neurotransmitters are chemical messengers that transmit signals between neurons. The document discusses the history and criteria for classifying a substance as a neurotransmitter. Neurotransmitters are classified based on their chemical nature as amino acids, amines, or others. They are also classified based on their function as either excitatory or inhibitory. The document describes examples from each group and where they are secreted in the body. It further explains the processes of transport, release, inactivation, and reuptake of neurotransmitters at the synapse.
Neurotransmitters ne-ach-histamine by dr.rujul modiRujul Modi
1. The document discusses several neurotransmitters including norepinephrine, epinephrine, acetylcholine, and histamine. It describes their synthesis pathways and where they are produced in the body.
2. Details are provided on the receptors for each neurotransmitter, including subtypes. The roles of the different neurotransmitters are discussed.
3. Information is presented on drugs that target various parts of the neurotransmitter pathways, and the conditions they are used to treat such as depression, Alzheimer's disease, and hypertension.
This document provides an overview of basic neurochemistry. It discusses the organization of the nervous system including the central nervous system made up of the brain and spinal cord, and the peripheral nervous system. It describes the basic neuron structure and function including dendrites, axons, myelin sheaths, and synapses. It explains action potentials and neurotransmission involving neurotransmitters such as serotonin, dopamine, GABA, and acetylcholine. It also summarizes receptors, fate of neurotransmitters, and factors involved in neuropharmacology.
This document outlines synaptic functions and neurotransmission. It discusses the basic functions of synapses, types of synapses including chemical and electrical synapses. The mechanisms of neurotransmission are explained including the roles of neurotransmitters, receptors, and ion channels. Over 50 known neurotransmitters are summarized including small molecule transmitters like acetylcholine, amines, amino acids and neuropeptides.
Epileptogenesis is the process by which the brain becomes epileptic. It occurs in three phases - an initial injury, a latent period of neuronal changes, and chronic epilepsy. During the latent period, various molecular pathways are dysregulated, including mTOR and REST, and neuronal circuits like the dentate gate and temporoammonic pathway are altered. These changes involve loss of inhibitory interneurons and abnormal sprouting, leading to recurrent seizures. Understanding epileptogenesis may help develop new treatments targeting the latent period to prevent epilepsy.
Epileptogenesis is the process by which normal brain tissue is transformed into tissue capable of generating spontaneous recurrent seizures. It involves multiple mechanisms including genetic and acquired factors. The hippocampus is particularly susceptible to epileptogenesis due to its circuitry. Status epilepticus animal models are commonly used to study the process. Epileptogenesis occurs in acute, subacute, and chronic stages. Acute changes include increased expression of immediate early genes and post-translational modifications of proteins. Subacute changes involve neuronal death, alterations in neurotrophic factors and inflammation. Chronic changes include mossy fiber sprouting and neurotransmission alterations.
Neurotransmitters are chemical messengers that transmit signals between neurons. The document discusses the history and criteria for classifying a substance as a neurotransmitter. Neurotransmitters are classified based on their chemical nature as amino acids, amines, or others. They are also classified based on their function as either excitatory or inhibitory. The document describes examples from each group and where they are secreted in the body. It further explains the processes of transport, release, inactivation, and reuptake of neurotransmitters at the synapse.
Neurotransmitters ne-ach-histamine by dr.rujul modiRujul Modi
1. The document discusses several neurotransmitters including norepinephrine, epinephrine, acetylcholine, and histamine. It describes their synthesis pathways and where they are produced in the body.
2. Details are provided on the receptors for each neurotransmitter, including subtypes. The roles of the different neurotransmitters are discussed.
3. Information is presented on drugs that target various parts of the neurotransmitter pathways, and the conditions they are used to treat such as depression, Alzheimer's disease, and hypertension.
This document provides an overview of basic neurochemistry. It discusses the organization of the nervous system including the central nervous system made up of the brain and spinal cord, and the peripheral nervous system. It describes the basic neuron structure and function including dendrites, axons, myelin sheaths, and synapses. It explains action potentials and neurotransmission involving neurotransmitters such as serotonin, dopamine, GABA, and acetylcholine. It also summarizes receptors, fate of neurotransmitters, and factors involved in neuropharmacology.
This document outlines synaptic functions and neurotransmission. It discusses the basic functions of synapses, types of synapses including chemical and electrical synapses. The mechanisms of neurotransmission are explained including the roles of neurotransmitters, receptors, and ion channels. Over 50 known neurotransmitters are summarized including small molecule transmitters like acetylcholine, amines, amino acids and neuropeptides.
Neurotransmission, Neuropsychiatry, and Neuropharmacology 2013 dfsmithdfsmith
Neurotransmission, Neuropsychiatry, and Neuropharmacology 2013 Postgraduate Course at Aarhus University includes historical information on Masters of Neuropsychopharmacology
Neurotransmitters are chemical messengers that transmit signals between neurons. They are synthesized in the presynaptic neuron, stored in vesicles, released into the synaptic cleft upon an action potential, and bind to receptors on the postsynaptic neuron. Common neurotransmitters include acetylcholine, dopamine, GABA, glutamate, and serotonin. Neurotransmitters are involved in communication between neurons and play a role in diseases when their function is impaired.
Neurohumoral transmission in ans final fully1cl frahulsharma3589
1) Neurohumoral transmission involves the release of neurotransmitters from nerve terminals that activate specialized receptors on target cells, eliciting physiological responses.
2) Key events in neurohumoral transmission include axonal conduction, neurotransmitter release, receptor activation, post-junctional signal propagation, and neurotransmitter destruction.
3) The autonomic nervous system relies on neurohumoral transmission, using acetylcholine at parasympathetic nerve endings and norepinephrine at most sympathetic nerve endings.
The document discusses neurotransmitters and their roles in the nervous system. It outlines the criteria for classifying a molecule as a neurotransmitter, identifies major types of neurotransmitters including amino acids, amines, and peptides. It describes the mechanism of neurotransmitter release and action, and discusses clinical disorders that can arise from disruptions in neurotransmitter metabolism such as Parkinson's disease, schizophrenia, and addiction.
Neurohumoral transmission involve release from a nerve terminal of a neurotransmitter that react with specialized receptors area on the enervated cell.
The document discusses neurohumoral transmission and the peripheral nervous system. It describes how the autonomic nervous system controls visceral functions through two neurons, while the somatic nervous system controls voluntary movement through a single neuron. The key types of neurotransmission are described, including the roles of neurotransmitters like acetylcholine and adrenaline. The processes of neurotransmission, including synthesis, storage, release and termination of neurotransmitters, are summarized.
Lecture 6 from a college level neuropharmacology course taught in the spring 2012 semester by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University. Includes neurotransmitter release, reuptake, and inactivation
Various neurotransmitters, mechanism of action and their physiological functions are explained and is useful for ug and pg students of medicine, neurology, psychiatry branches.
This document discusses neurohumoral transmission and the criteria for identifying neurotransmitters. It describes several major neurotransmitters like acetylcholine, adrenaline, norepinephrine, dopamine, serotonin, and others. It explains the principles of chemical transmission including Dale's principle and denervation supersensitivity. The document provides details about the synthesis, storage, release and termination of various neurotransmitters including acetylcholine, adrenaline, serotonin, ATP and others. It also discusses cotransmission and neuromodulation in neurotransmission.
Autonomic Nervous Sytem and neurohumoral transmission-Dr.Jibachha Sah,M.V.Sc,...Dr. Jibachha Sah
The document provides an introduction to the autonomic nervous system and neurohumoral transmission. It discusses that the autonomic nervous system controls involuntary functions and is divided into the sympathetic and parasympathetic divisions. The sympathetic division is associated with the fight or flight response while the parasympathetic promotes rest and digestion. Neurotransmission in the autonomic nervous system involves the release of acetylcholine at neuromuscular junctions and the release of acetylcholine or norepinephrine at effector cells, depending on if the transmission is parasympathetic or sympathetic. Receptors on effector cells are nicotinic, muscarinic, alpha-adrenergic, or beta-adrenergic depending on the neurotransmit
This document provides an overview of neuropharmacology and neurotransmission. It defines neuropharmacology and describes the two main branches. It explains what neurotransmission is and how it works, describing the role of neurons, neurotransmitters, and the mechanism of neurotransmission. It discusses different types of neurons, neurotransmitters like acetylcholine and dopamine, and conditions they are involved in like Alzheimer's and Parkinson's disease. The document also provides interesting facts about neurons and neurotransmitters. It concludes with a recent discovery about how endocannabinoids travel in the brain to reach receptors.
THIS REFER BY THE ESSENTIALS OF MEDICAL PHYSIOLOGY BOOK (SIX EDITION)
HELLO!
I AM MEET DESAI.
STUDENT OF A PHYSIOTHERAPY.
THIS IS MY COLLEGE PROJECT . I'M SHARING TO STUDENT LIKE ME..
THIS AVAILABLE MY LINK LIKE..https://www.linkedin.com/in/meet-desai-18296b178
THANK YOU SO MACH .TO SEE
1. Neurotransmitters are chemicals that transmit signals from one neuron to another across synapses. They are synthesized in the presynaptic neuron and released into the synaptic cleft upon electrical stimulation.
2. There are different types of chemical signaling in the body including neurotransmitters which act locally between neurons, neurohormones which travel through the blood, and hormones secreted by endocrine glands.
3. Neurotransmitters bind to receptor proteins on the postsynaptic neuron, causing changes in membrane potential or opening ion channels that influence neuronal excitability. There is diversity in the neurotransmitters used between the central and peripheral nervous systems.
Monoamine neurotransmitters include catecholamines like dopamine, norepinephrine, and epinephrine as well as indoleamines like serotonin. They are produced in different areas of the body and brain and act through a variety of receptors. They are packaged into vesicles and released at synapses before being recycled or broken down. Deficiencies or imbalances of these neurotransmitters can lead to disorders like Parkinson's disease which results from loss of dopamine-producing neurons in the substantia nigra.
Basic science of sleep by dr. rujul modiRujul Modi
The document provides an overview of the basic science of sleep. It discusses the stages of sleep including REM and NREM sleep. It describes the neurobiology and physiology of sleep, including the structures and neurotransmitters involved in regulating sleep and wakefulness. The document also discusses how sleep is organized in cycles and how it changes with age. It provides definitions of sleep and covers topics like the functions of sleep and its assessment.
1) Neurotransmitters are chemicals that transmit signals between neurons in the brain and body, allowing communication throughout the nervous system. They can affect mood, sleep, concentration and other functions.
2) Neurotransmitters are synthesized in neurons and stored in vesicles, then released into the synaptic cleft and bind to receptors on the postsynaptic neuron. This may cause excitation or inhibition of the postsynaptic neuron.
3) Common neurotransmitters include glutamate, GABA, dopamine, serotonin, acetylcholine, and norepinephrine. They have different functions and are broken down or reabsorbed after signaling to terminate their effects.
This document provides an overview of the basic mechanisms of epilepsy. It begins with definitions of seizures and epilepsy. It then discusses the histology of the cerebral cortex and key neurotransmitters like GABA and glutamate. Genetic factors that can contribute to epilepsy, like mutations in sodium channels, are reviewed. The role of neuroinflammation in the development and persistence of seizures is also examined. The conclusion emphasizes that epilepsy arises from disturbances in the excitation-inhibition balance in the brain due to various causes, and this involves multiple biological factors interacting in a self-reinforcing manner.
Epileptogenesis is the process by which a brain network that was previously normal is functionally altered toward increased seizure susceptibility, thus having an enhanced probability to generate spontaneous recurrent seizures (SRSs). The process of epileptogenesis occurs in 3 phases: the occurrence of a precipitating injury; a 'latent' period of epileptogenesis and chronic, established epilepsy. Structural and molecular changes associated with epileptogenesis include selective neuronal loss,axonal and dendritic reorganisation, neurogenesis, altered expression of neurotransmitters, and changes at glial architecture. Antiepileptogenesis can be complete or partial. Complete prevention aborts the development of epilepsy while partial prevention can delay the development of epilepsy or reduce its severity. Targeting signaling pathways that alter the expression of genes involved in epileptogenesis may provide novel therapeutic approaches for preventing epileptogenesis. The mTOR and REST pathways are exciting new potential targets for intervention in the epileptogenic process.
Neurotransmission, Neuropsychiatry, and Neuropharmacology 2013 dfsmithdfsmith
Neurotransmission, Neuropsychiatry, and Neuropharmacology 2013 Postgraduate Course at Aarhus University includes historical information on Masters of Neuropsychopharmacology
Neurotransmitters are chemical messengers that transmit signals between neurons. They are synthesized in the presynaptic neuron, stored in vesicles, released into the synaptic cleft upon an action potential, and bind to receptors on the postsynaptic neuron. Common neurotransmitters include acetylcholine, dopamine, GABA, glutamate, and serotonin. Neurotransmitters are involved in communication between neurons and play a role in diseases when their function is impaired.
Neurohumoral transmission in ans final fully1cl frahulsharma3589
1) Neurohumoral transmission involves the release of neurotransmitters from nerve terminals that activate specialized receptors on target cells, eliciting physiological responses.
2) Key events in neurohumoral transmission include axonal conduction, neurotransmitter release, receptor activation, post-junctional signal propagation, and neurotransmitter destruction.
3) The autonomic nervous system relies on neurohumoral transmission, using acetylcholine at parasympathetic nerve endings and norepinephrine at most sympathetic nerve endings.
The document discusses neurotransmitters and their roles in the nervous system. It outlines the criteria for classifying a molecule as a neurotransmitter, identifies major types of neurotransmitters including amino acids, amines, and peptides. It describes the mechanism of neurotransmitter release and action, and discusses clinical disorders that can arise from disruptions in neurotransmitter metabolism such as Parkinson's disease, schizophrenia, and addiction.
Neurohumoral transmission involve release from a nerve terminal of a neurotransmitter that react with specialized receptors area on the enervated cell.
The document discusses neurohumoral transmission and the peripheral nervous system. It describes how the autonomic nervous system controls visceral functions through two neurons, while the somatic nervous system controls voluntary movement through a single neuron. The key types of neurotransmission are described, including the roles of neurotransmitters like acetylcholine and adrenaline. The processes of neurotransmission, including synthesis, storage, release and termination of neurotransmitters, are summarized.
Lecture 6 from a college level neuropharmacology course taught in the spring 2012 semester by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University. Includes neurotransmitter release, reuptake, and inactivation
Various neurotransmitters, mechanism of action and their physiological functions are explained and is useful for ug and pg students of medicine, neurology, psychiatry branches.
This document discusses neurohumoral transmission and the criteria for identifying neurotransmitters. It describes several major neurotransmitters like acetylcholine, adrenaline, norepinephrine, dopamine, serotonin, and others. It explains the principles of chemical transmission including Dale's principle and denervation supersensitivity. The document provides details about the synthesis, storage, release and termination of various neurotransmitters including acetylcholine, adrenaline, serotonin, ATP and others. It also discusses cotransmission and neuromodulation in neurotransmission.
Autonomic Nervous Sytem and neurohumoral transmission-Dr.Jibachha Sah,M.V.Sc,...Dr. Jibachha Sah
The document provides an introduction to the autonomic nervous system and neurohumoral transmission. It discusses that the autonomic nervous system controls involuntary functions and is divided into the sympathetic and parasympathetic divisions. The sympathetic division is associated with the fight or flight response while the parasympathetic promotes rest and digestion. Neurotransmission in the autonomic nervous system involves the release of acetylcholine at neuromuscular junctions and the release of acetylcholine or norepinephrine at effector cells, depending on if the transmission is parasympathetic or sympathetic. Receptors on effector cells are nicotinic, muscarinic, alpha-adrenergic, or beta-adrenergic depending on the neurotransmit
This document provides an overview of neuropharmacology and neurotransmission. It defines neuropharmacology and describes the two main branches. It explains what neurotransmission is and how it works, describing the role of neurons, neurotransmitters, and the mechanism of neurotransmission. It discusses different types of neurons, neurotransmitters like acetylcholine and dopamine, and conditions they are involved in like Alzheimer's and Parkinson's disease. The document also provides interesting facts about neurons and neurotransmitters. It concludes with a recent discovery about how endocannabinoids travel in the brain to reach receptors.
THIS REFER BY THE ESSENTIALS OF MEDICAL PHYSIOLOGY BOOK (SIX EDITION)
HELLO!
I AM MEET DESAI.
STUDENT OF A PHYSIOTHERAPY.
THIS IS MY COLLEGE PROJECT . I'M SHARING TO STUDENT LIKE ME..
THIS AVAILABLE MY LINK LIKE..https://www.linkedin.com/in/meet-desai-18296b178
THANK YOU SO MACH .TO SEE
1. Neurotransmitters are chemicals that transmit signals from one neuron to another across synapses. They are synthesized in the presynaptic neuron and released into the synaptic cleft upon electrical stimulation.
2. There are different types of chemical signaling in the body including neurotransmitters which act locally between neurons, neurohormones which travel through the blood, and hormones secreted by endocrine glands.
3. Neurotransmitters bind to receptor proteins on the postsynaptic neuron, causing changes in membrane potential or opening ion channels that influence neuronal excitability. There is diversity in the neurotransmitters used between the central and peripheral nervous systems.
Monoamine neurotransmitters include catecholamines like dopamine, norepinephrine, and epinephrine as well as indoleamines like serotonin. They are produced in different areas of the body and brain and act through a variety of receptors. They are packaged into vesicles and released at synapses before being recycled or broken down. Deficiencies or imbalances of these neurotransmitters can lead to disorders like Parkinson's disease which results from loss of dopamine-producing neurons in the substantia nigra.
Basic science of sleep by dr. rujul modiRujul Modi
The document provides an overview of the basic science of sleep. It discusses the stages of sleep including REM and NREM sleep. It describes the neurobiology and physiology of sleep, including the structures and neurotransmitters involved in regulating sleep and wakefulness. The document also discusses how sleep is organized in cycles and how it changes with age. It provides definitions of sleep and covers topics like the functions of sleep and its assessment.
1) Neurotransmitters are chemicals that transmit signals between neurons in the brain and body, allowing communication throughout the nervous system. They can affect mood, sleep, concentration and other functions.
2) Neurotransmitters are synthesized in neurons and stored in vesicles, then released into the synaptic cleft and bind to receptors on the postsynaptic neuron. This may cause excitation or inhibition of the postsynaptic neuron.
3) Common neurotransmitters include glutamate, GABA, dopamine, serotonin, acetylcholine, and norepinephrine. They have different functions and are broken down or reabsorbed after signaling to terminate their effects.
This document provides an overview of the basic mechanisms of epilepsy. It begins with definitions of seizures and epilepsy. It then discusses the histology of the cerebral cortex and key neurotransmitters like GABA and glutamate. Genetic factors that can contribute to epilepsy, like mutations in sodium channels, are reviewed. The role of neuroinflammation in the development and persistence of seizures is also examined. The conclusion emphasizes that epilepsy arises from disturbances in the excitation-inhibition balance in the brain due to various causes, and this involves multiple biological factors interacting in a self-reinforcing manner.
Epileptogenesis is the process by which a brain network that was previously normal is functionally altered toward increased seizure susceptibility, thus having an enhanced probability to generate spontaneous recurrent seizures (SRSs). The process of epileptogenesis occurs in 3 phases: the occurrence of a precipitating injury; a 'latent' period of epileptogenesis and chronic, established epilepsy. Structural and molecular changes associated with epileptogenesis include selective neuronal loss,axonal and dendritic reorganisation, neurogenesis, altered expression of neurotransmitters, and changes at glial architecture. Antiepileptogenesis can be complete or partial. Complete prevention aborts the development of epilepsy while partial prevention can delay the development of epilepsy or reduce its severity. Targeting signaling pathways that alter the expression of genes involved in epileptogenesis may provide novel therapeutic approaches for preventing epileptogenesis. The mTOR and REST pathways are exciting new potential targets for intervention in the epileptogenic process.
- Epilepsy is a chronic neurological disorder characterized by recurrent seizures. It affects approximately 1% of the population worldwide. While medications can control seizures for many, there is no cure currently.
- Anti-epileptic drugs work by various mechanisms such as enhancing GABA inhibition, blocking sodium or calcium channels, or reducing glutamate excitation in the brain. Common drug classes include hydantoins, barbiturates, benzodiazepines, and succinimides.
- Choosing an anti-epileptic drug depends on seizure type, epilepsy syndrome, side effect profile, interactions with other medications, and cost. While monotherapy is preferred, multiple drugs may be needed to control seizures in some cases.
EPILEPSY CLASSIFICATION, PATHOENESIS, AND MANAGEMENT.pdfAdamu Mohammad
The document summarizes key aspects of epilepsy classifications, pathogenesis, and management. It describes:
1. The ILAE's 2017 classification system which focuses on seizures, epilepsies, and epilepsy syndromes, introducing new terminology like focal impaired awareness and focal to bilateral tonic-clonic.
2. Factors in epilepsy pathogenesis including neurotransmission pathways, molecular/genetic mechanisms, neurogenesis/rewiring, and inflammation. Epileptogenesis involves increased neuronal excitability.
3. Epilepsy categories of idiopathic, acquired, and cryptogenic based on identifiable brain lesions, and management considers seizure type, age of onset, family history, and test results.
The document discusses epilepsy, including its definition, causes, classification of seizures, and treatment. Epilepsy is defined as a group of disorders that cause recurrent, unprovoked seizures. Seizures are caused by abnormal electrical discharges in the brain and can have various causes including genetic defects, brain injuries, tumors, or lack of sleep. Seizures are classified as either partial/focal or generalized depending on where they originate and spread in the brain. Treatment involves anticonvulsant drugs which work by various mechanisms to prevent neuronal overexcitation as well as surgical removal of epileptic brain regions.
Hyper-excitable neurons lead to excessive excitability in surrounding neurons, causing seizures (hyper-synchronization). This occurs due to an imbalance of excitatory vs inhibitory neurotransmitters - glutamate activation and lowered calcium channel thresholds increase neuronal excitation, while reduced GABA inhibition decreases the inhibitory surround. This disruption of the normal depolarization-afterhyperpolarization cycle in neurons results in a continuous firing state and seizure focus.
This document provides information about epilepsy and seizures. It begins with a brief history of epilepsy, noting that ancient cultures believed it was caused by supernatural forces. It was not until the 19th century that epilepsy began to be viewed as a medical condition. The document then discusses the physiology and causes of seizures, classifying them as partial or generalized seizures. Partial seizures can be simple, involving isolated symptoms, or complex, involving impaired awareness. The pathophysiology involves abnormal electrical firing in groups of neurons in the brain. In summary, the document covers the history, types, causes and neurological mechanisms of epilepsy and seizures.
Hippocrates first suggested epilepsy was a brain disorder in 400 BC. It is defined as brief episodes of loss of consciousness due to abnormal brain neuron firing. Seizures can be focal or generalized. Common seizure types include generalized tonic-clonic, absence, myoclonic, complex partial, and simple partial. Antiepileptic drugs work by modifying ion conductances like sodium channels, increasing GABA effects, or blocking glutamate receptors. Common antiepileptic drugs include phenytoin, carbamazepine, valproic acid, ethosuximide, and phenobarbital. Adverse effects and drug interactions must be monitored with long-term antiepileptic treatment.
1) Electroconvulsive therapy (ECT) involves delivering electricity to the brain to induce a seizure. It is a standard psychiatric treatment used to improve abnormal mental states.
2) ECT was developed in the 1930s-1940s as an alternative to inducing seizures through chemicals. It gained acceptance after Italian scientists successfully applied electricity to a patient's scalp in 1938.
3) The exact mechanisms of how ECT works are unclear but theories involve effects on neurotransmitter systems, neuroendocrine functions, anticonvulsant properties, and psychological factors. Modern ECT aims to optimize safety and efficacy.
- Seizures are caused by abnormal excessive neuronal excitation and synchronization in the brain. Epilepsy is a tendency toward recurrent seizures. Antiepileptic drugs (AEDs) work by decreasing neuronal excitability through various mechanisms like enhancing GABA inhibition, blocking sodium and calcium channels, and modulating glutamate.
- Common AED targets include GABA receptors, sodium channels, and calcium channels. Older AEDs like phenytoin, carbamazepine, and phenobarbital are effective but have more side effects due to sedation. Newer AEDs have fewer side effects. AEDs can interact through metabolic pathways and altering drug levels. Proper AED selection
The document summarizes key aspects of the endocrine system and hormone signaling. It describes two main coordinating systems - the endocrine system which secretes hormones to regulate slower processes like growth and metabolism, and the nervous system which uses fast electrical signals. Hormones are classified by their range and effects. The endocrine system uses hormones to coordinate processes in the body and maintain homeostasis via feedback loops, such as insulin and glucagon regulating blood glucose levels. Disorders like diabetes occur when these regulatory processes are disrupted.
Epilepsy is caused by excessive and synchronous discharge of cerebral neurons resulting in seizures. Seizures can be detected by EEG and categorized by origin, etiology, clinical presentation, and electrophysiology. They are broadly classified as partial or generalized. Anti-epileptic drugs work by enhancing GABA, inhibiting sodium channels, inhibiting calcium channels, or blocking glutamate receptors. Phenytoin is a first-line treatment for tonic-clonic, simple partial, and complex partial seizures as well as status epilepticus. It has many potential adverse effects and drug interactions that require monitoring.
1. Septic encephalopathy is an acute brain dysfunction that can occur in patients with sepsis and is characterized by impaired consciousness including coma.
2. The pathophysiology is multifactorial but is thought to involve the action of inflammatory mediators and free radicals on the brain resulting from systemic inflammation.
3. Septic encephalopathy is associated with worse prognosis and higher mortality in sepsis patients. The severity of encephalopathy correlates with mortality.
Epilepsy is a disorder characterized by recurrent seizures that involve abnormal neuronal activity in the brain. It is caused by an imbalance between excitatory and inhibitory neurotransmitters like glutamate and GABA. Anti-seizure drugs work by enhancing GABA activity, blocking sodium and calcium channels, or modulating glutamate activity. Treatment depends on the type of seizures, which can be focal, generalized tonic-clonic, absence or myoclonic. Adverse effects include skin rashes, weight changes, fatigue and cognitive issues. Novel approaches include targeted drug delivery and electrical brain stimulation to prevent seizures.
This document summarizes various in vitro and in vivo models used for anti-epileptic drug screening. The in vitro models described include tests measuring effects on GABA and glutamate receptors, transporters, and uptake/release. The in vivo models involve inducing seizures chemically or through focal lesions in rodents and examining effects of test compounds. Several genetic and transgenic animal models of epilepsy are also mentioned. The document provides details on procedures and evaluation methods for key screening tests involving GABA uptake/release in hippocampal slices and electroshock induction in mice.
This document discusses various mechanisms of cell death, specifically necrosis and apoptosis. It describes the roles of caspases, cytochrome c, Bcl-2 family members, and other factors in apoptotic signaling pathways. It then discusses evidence of apoptosis in different neurodegenerative diseases like Alzheimer's, Parkinson's, Huntington's, and ALS. Various potential therapeutic targets and strategies aimed at inhibiting apoptosis are also outlined.
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
3. An seizure is a transient occurrence of signs and/or
symptoms due to abnormal excessive or synchronous
neuronal activity in the brain.
A person is considered to have epilepsy if they meet any
of the following conditions:(As per ILAE)
1. At least two unprovoked (or reflex) seizures occurring
greater than 24 hours apart.
2. One unprovoked (or reflex) seizure and a probability of
further seizures similar to the general recurrence risk (at
least 60%) after two unprovoked seizures, occurring
over the next 10 years.
4. Babylonians-presence of
demons
Greeks and romans-
curse of gods
Hippocrates offered
epilepsy as a disease
Electrical hypothesis was
discovered by hans berger
when he invented the EEG
John Jackson (father of
epilepsy)-“occasional
sudden,excessive,rapid and
local discharge of gray matter”
5. The process of the brain
acquiring an initial insult and
secondarily undergoing a
series of epileptic events until
the first observable seizure
occurs.
Sloviter & Bumanglag
(2012) have proposed a
secondary term “epileptic
maturation” to describe the all
encompassing processes that
happen after epileptogenesis
and that influence the
secondary changes in the
clinical phenotype.
7. It consists of mainly 2 receptors:
GABA A
GABA B
8. Location of GABA A receptors-
• Synaptic receptors -gamma
subunits(mostly post synaptic)
• perisynaptic /extra synaptic -
deltas sub units responsible
for phasic and tonic inhibition.
During status epileptics, there is
increased neuronal hyper
excitability and inhibitory
GABAergic synaptic transmission
becomes compromised
• Miniature inhibitory post-
synaptic currents (mIPSCs) are
reduced
• Number of active GABAA
receptors per dentate granule
cell is also decreased.
9. Short term(during SE)
• In vitro-large
decrease in GABA-
gated chloride
currents.
• In vivo-rapid
reduction in the
number of
physiologically
active GABA
receptors.
10. Changes in latency period-
1.Minutes to hours –
Activation of plasma
membrane receptors result in
changes in the intracellular
signal transduction pathways
involved in the maintenance of
vital cellular functions.
2. Hours to days-
Long term changes in gene
expression result from the
combined effects of repeated
seizures, seizure-induced cell
death, and subsequent
neuronal reorganization
11. 2 types of receptors:
GABA B 1
GABA B2
Types:
Slow - downstream
Ca2+/K+ channels upon
binding with its
endogenous ligand,
GABA.
Long term- Ligand
activation of GABAB
receptors initiates G
protein–dependent cell
signaling pathways.
12. Presynaptic receptors prevent
neurotransmitter release
• Down-regulating the activity of
voltage-sensitive Ca 2+-channels
• Direct inhibition of the release
machinery.
Auto receptors inhibit the release of
GABA, whereas hetero receptors inhibit
the release of glutamate and several
other neurotransmitters.
Postsynaptic receptors induce sIPSCs by
activating Kir3-type K+-channels, which
hyperpolarizes the membrane, favors
voltage-sensitive block of NMDA
receptors and shunts excitatory
currents
Dendritic receptors inhibit back
propagating action potentials through
activation of K+-channels.
13. Two types of receptors:
1.Ionotropic
NMDA
AMPA
Kainate
2.Metabotropic(8)
Group1
Group2
Group3
14. 1.NMDA-
An increase in glutamate excitatory transmission in the
hippocampus.
Increase in the pool of ready-release glutamate at the mossy fiber-
pyramidal cell synapse in the CA3 as well as in DG.
Number of NMDA receptors present in neuronal cell membranes
appears to increase.
2.AMPA:
• Ca2+ influx into neurons causing excitotoxicity and cell death.
• Synaptic changes due to alterations in second messenger signaling
15. 3.KAINATE:
Causes slow EPSP’s to promote epileptogenesis.
4. METABOTROPIC RECEPTORS:
Group I- epileptogenic in nature when bound by glutamate.
Group II- promote antiepileptogenic effects when bound by
glutamate
5.Several morphological changes in the hippocampus occur during
epileptogenesis associated with glutamate dysregulation:
Hippocampal sclerosis, shrinkage, and reactive gliosis
Neuronal loss in hilar mossy cells, interneurons, and pyramidal
neurons of the CA3 and CA1 are also observed in the granule cell
layer
16. Receptor Mechanism of action
NMDA Glutamate and Glycine
mediated
AMPA Influx of Na+,Ca+ and
efflux of K+
KAINATE Slow EPSP’s
Group I(1,5) Phospholipase C (PLPC),
protein kinase C (PKC)
Group II(2,3) Inhibits c-amp formation,
directly activates K+
channels and inhibits
voltage sensitive
Ca2+ channels
Group III(4,6,7,8) Inhibits neuro-transmitter
release
17. Promote epileptogenesis such as a decrease in
GABAergic interneurons (which could cause an in
increase in glutamate neurotransmission)
A decrease in membrane expressed GABAB receptors
(which could also cause an increase in glutamate
neurotransmission)
18. Ach causes increased seizure activity by
acting on following brain parts:
Piriform cortex>amydala>hippocampus>
thalamus >cortical areas &striatum
Specific areas:
Piriform cortex-(substantia nigra & area
tempestas)
19. MECHANISM-
Cytotoxic activity seen in hippocampus and
cortical neurons
Disruption of polymerization of microtubules
Altered sensitivity to glutamate excitotoxicity
Decrease in expression of synaptic proteins.
Area tempestas-hyperactivity in hippocampus
Direct cholinergic input/indirect to ento-
rhinal cortex.
20. Dopamine
receptors
Location in brain
D1 CP, nucleus
accumbens ,
substantia nigra
D2 CP, nac, SN pars
compacta
D3 Limbic system
D4 Frontal cortex,
amygdala, SN,
hippocampus
D5 Entorhinal cortex,
SNR, and
hippocampus
(dentate gyrus)
21. Receptor Action
D1 type(D1,D5)(PRO-
CONVULSANT)
increases cAMP levels and
protein kinase A (PKA) activity via
the stimulation of adenylyl
cyclase (AC)
D2 type(ANTI-CONVULSANT)
(D2,D3,D4)
inhibit AC activity,antogonises D1
action(c-amp dependent)
Activation of glycogen synthase
kinase 3β(c-amp independent)
22.
23. Serotonin has a
protective mechanism
against epilepsy.
Main mechanism:
Hyperpolarization of
glutamatergic neurons by 5-
HT1A receptors(K+
conductance)
Depolarization of
GABAergic neurons by 5-
HT2C receptors.
24.
25.
26.
27.
28. Considered to have
protective role in
epilepsy.
Highest affinity for a2
adrenergic receptors.
Established role in the
control of limbic seizures
by increasing
noradrenaline levels in
structures that are
critically involved in the
generation of limbic
seizures, such as the
hippocampus.
35. Various mechanism seen are:
A particular body system has been sufficiently
impaired to produce a lowering of the seizure
threshold and the induction of “reactive seizures.
A state of cortical neuronal instability, such as a
(stroke with infarction, hemorrhage, embolus)
Encephalopathy
36.
37. Study of inheritance of heritable changes in
gene expression that occur with no
modifications to the DNA sequence.
Different types:
DNA methylation
histone modification
action of non-coding RNA
42. Drug Mechanism
Anti-infective
Peniciilin and related drugs Inhibits GABA binding to GABAA
receptor(allosteric modulation)
Blocks GABAA chloride channel
Fluoroquinolones Inhibit GABA binding to GABAA receptor
Isoniazid Inhibits pyridoxine kinase, resulting in
decreased GABA synthesis(formation of IPH)
Bromocriptine,pergolide Blocks dopaminergic transmission
Metronidazole Leads to accumulation of hydroxy- and 1-
acetic acid metabolite
TCA Inhibition of serotonin uptake in the cleft
Phenothiazine Dopamine blocking property
MOA –A inhibitor Produces serotergic activation(alpha-motor
neuron excitability)
Selective serotonin reuptake
Inhibitor
Decreases GABA transmission in the
hippocampus
Phenothiazines Antagonizes postsynaptic, mesolimbic
dopamine receptors in the brain
43. Local anesthetics Antagonizes Na1 channels
Meperidine Leads to accumulation of normeperidine
metabolite
Tramadol Inhibits monoamine uptake
Theophylline Antagonizes anticonvulsant effects of brain
adenosine
Calcineurin Down regulates GABAA receptor activation
Brain-stem stimulants
Pentetrazol
Picro-toxin
GABA excitation and inhibits GABA
inhibition respectively
Spinal stimulants
strychnine
Blocks inhibitory action of glycine at post
synaptic receptor
General anesthesia
Enflurane
etomidate
Increased excitability in limbic system
Disinhibit ion of sub-cortical activity
Local anaesthesia+epinephrine Ischemia in spinal cord(transient epilepsy)
Radio contrast dye(gadolinium) Direct action on cerebral cortex
47. The PRES has been described
after the intake of
immunosuppressants such as
tacrolimus, Cyclosporine.
It is characterized by capillary-leak
syndrome in the brain caused by
changes affecting the vascular
endothelium.
Clinical symptoms are headache,
vomiting, confusion, seizures,
cortical blindness and other visual
symptoms.
48. Drug Effect
Variant methionine synthetase,
modified effect of methotrexate
On homocysteine metabolism
Methotrexate encephalopathy
Human thymidylate synthetase gene 5- fluorouracil-associated
hyperammonemic encephalopathy
49. Benzodiazepine- in association with LENNOX
GASTAUT Syndrome or WEST Syndrome
Valproate/carbamazepine induced
encephalopathy(accumulation of CBZ
epoxide) esp. in children
Vigabatrin-increased GABA in brain
50.
51. Use in animal experimental model
PENICILLIN MODEL
PENTYLENTETRAZOL MODEL
BICUCULLINE MODEL
KAINIC ACID MODEL
52. 1.Marco I. Gonzáleza, Amy Brooks-Kayala; Altered GABAA receptor expression during epileptogenesis; Neuroscience Letters497 (2011) 218–
222
2. Amy R. Brooks-Kayal, M.D.; Regulation of GABAA Receptor Gene Expression and Epilepsy; Jasper's Basic Mechanisms of the Epilepsies
3. Mauro DiNuzzoa, Silvia Mangiab; REVIEW Physiological bases of the K+and the glutamate/GABA hypotheses of epilepsy; Epilepsy Research
;1st April(2014)
4. Seth R. Batten; GLUTAMATE DYSREGULATION AND HIPPOCAMPAL DYSFUNCTION IN EPILEPTOGENESIS; University of Kentucky, Theses and
Dissertations--Medical Sciences Medical Sciences,2013.
5. YuriBozzi, EmilianaBorrelli; The role of dopamine signaling in epileptogenesis; Frontiers in Cellular Neuroscience; September 2013 |
Volume7 | Article 157
6. Carl J. Vaughan, MD, MRCPI and Norman Delanty, MB, FRCPI; Pathophysiology of Acute Symptomatic Seizures; Seizures: Medical Causes
and Management;
7. Niels Hansen; Drug-Induced Encephalopathy; Miscellanea on Encephalopathies – A Second Look; 25, April, 2012
8. L. Pulido Fontesa, P. Quesada Jimeneza, M. Mendioroz Iriarte ; Epigenetics and epilepsy; NEUROLOGÍA; 2015;30(2):111—118
9. Rocio Sanchez-Carpintero;Genetic causes of epilepsy; THE NEUROLOGIST; DECEMBER 2007
10. PRATIBHA SINGHI; Infectious causes of seizures and epilepsy in the developing world; Developmental Medicine & Child Neurology 2011,
53: 600–609
11.Dennis o brien; Toxic and Metabolic Causes of Seizures; Clinical Techniques m Small Animal Practice, Vol 13, No 3 (August), 1998: pp 159-
166
12. Todd H Ahern, Martin A Javors, Douglas A Eagles, Jared Martillotti, Heather A Mitchell, Larry Cameron Liles and David Weinshenker; The
Effects of Chronic Norepinephrine Transporter Inactivation on Seizure Susceptibility in Mice; Neuropsychopharmacology (2006) 31, 730–738
13. Gyorgy Bagdy, Valeria Kecskemeti; Serotonin and epilepsy; Journal of Neurochemistry, 2007, 100, 857–873
14. LEONARDO COCITO, M.D., EMILIO FAVALE, M.D.; Epileptic Seizures in Cerebral Arterial Occlusive Disease; Stroke, Vol 13, No 2,1982
15. ROBRECHT RAEDT;VNS, noradrenaline and seizure suppression|; Journal of Neurochemistry, 2011; International Society for
Neurochemistry, J. Neurochem. (2011) 117, 461–469