This document discusses anti-epileptic drugs. It provides information on the classification, causes, and treatment of seizures. Some key points:
- Epilepsy is characterized by recurrent seizures and affects over 2.5 million Americans. There are many forms and the treatment aims to prevent seizures but not provide a cure.
- Seizures can be caused by factors like infection, tumors, or injury. They are classified as partial (focal) or generalized based on where they originate in the brain.
- Common anti-epileptic drugs work by modifying ion conductances like sodium channels or enhancing GABAergic inhibition. They have similar pharmacokinetic properties like oral absorption and liver metabolism.
-
In this ppt I mentioned all the imp point related to pain pathway and pain pathophysiology. refrence: essentials of interventional techniques in managing chronic pain (laxmaiah manchikanti)
This document discusses various types of seizures and antiepileptic drugs. It describes partial and generalized seizures. The main types of antiepileptic drugs are hydantoins like phenytoin, barbiturates like phenobarbital, succinimides like ethosuximide, GABA transaminase inhibitors like valproic acid, benzodiazepines like diazepam, and newer drugs like gabapentin, vigabatrin, and tiagabine. Adverse effects and uses of select antiepileptic drugs like phenytoin, phenobarbital, carbamazepine, valproic acid, and diazepam are outlined. Status epile
This document discusses antiepileptic drugs, including their mechanisms of action, uses, and side effects. It covers common antiepileptics like phenobarbital, phenytoin, carbamazepine, ethosuximide, valproic acid, diazepam, gabapentin, vigabatrin, and tiagabine. It also describes the classification and types of seizures as well as the treatment of status epilepticus.
Epilepsy results from excessive electrical activity in the brain and manifests as seizures. It is not a single disorder but rather a family of related conditions. Seizures can be focal, remaining in one area of the brain, or generalize and spread. Antiepileptic drugs work to stabilize neuronal activity and suppress seizures by mechanisms such as blocking sodium channels. Common antiepileptics include carbamazepine, phenytoin, phenobarbital, and gabapentin. Patients require lifelong treatment to control seizures and medical monitoring for therapeutic effects and adverse reactions from antiepileptic drugs.
Antiepilepticdrugs(Harbhusan Gain, Student, Dept. of Pharmacy,World Universit...University of Dhaka
The document discusses antiepileptic drugs and provides information on the history and classification of epilepsy. It defines what epilepsy is and describes different types of seizures including generalized seizures like tonic-clonic, absence and myoclonic seizures. It also covers partial or focal seizures and status epilepticus. The document discusses experimental models used to study epilepsy and potential causes. It provides a classification of antiepileptic drugs and describes mechanisms of seizure and how various drugs work, including by modifying ion conductance and increasing GABAergic transmission. Specific drugs like phenobarbital, phenytoin, ethosuximide and valproate are also covered in terms of their pharmacological properties, mechanisms of action, adverse effects
This document discusses anti-epileptic drugs. It provides information on the classification, causes, and treatment of seizures. Some key points:
- Epilepsy is characterized by recurrent seizures and affects over 2.5 million Americans. There are many forms and the treatment aims to prevent seizures but not provide a cure.
- Seizures can be caused by factors like infection, tumors, or injury. They are classified as partial (focal) or generalized based on where they originate in the brain.
- Common anti-epileptic drugs work by modifying ion conductances like sodium channels or enhancing GABAergic inhibition. They have similar pharmacokinetic properties like oral absorption and liver metabolism.
-
In this ppt I mentioned all the imp point related to pain pathway and pain pathophysiology. refrence: essentials of interventional techniques in managing chronic pain (laxmaiah manchikanti)
This document discusses various types of seizures and antiepileptic drugs. It describes partial and generalized seizures. The main types of antiepileptic drugs are hydantoins like phenytoin, barbiturates like phenobarbital, succinimides like ethosuximide, GABA transaminase inhibitors like valproic acid, benzodiazepines like diazepam, and newer drugs like gabapentin, vigabatrin, and tiagabine. Adverse effects and uses of select antiepileptic drugs like phenytoin, phenobarbital, carbamazepine, valproic acid, and diazepam are outlined. Status epile
This document discusses antiepileptic drugs, including their mechanisms of action, uses, and side effects. It covers common antiepileptics like phenobarbital, phenytoin, carbamazepine, ethosuximide, valproic acid, diazepam, gabapentin, vigabatrin, and tiagabine. It also describes the classification and types of seizures as well as the treatment of status epilepticus.
Epilepsy results from excessive electrical activity in the brain and manifests as seizures. It is not a single disorder but rather a family of related conditions. Seizures can be focal, remaining in one area of the brain, or generalize and spread. Antiepileptic drugs work to stabilize neuronal activity and suppress seizures by mechanisms such as blocking sodium channels. Common antiepileptics include carbamazepine, phenytoin, phenobarbital, and gabapentin. Patients require lifelong treatment to control seizures and medical monitoring for therapeutic effects and adverse reactions from antiepileptic drugs.
Antiepilepticdrugs(Harbhusan Gain, Student, Dept. of Pharmacy,World Universit...University of Dhaka
The document discusses antiepileptic drugs and provides information on the history and classification of epilepsy. It defines what epilepsy is and describes different types of seizures including generalized seizures like tonic-clonic, absence and myoclonic seizures. It also covers partial or focal seizures and status epilepticus. The document discusses experimental models used to study epilepsy and potential causes. It provides a classification of antiepileptic drugs and describes mechanisms of seizure and how various drugs work, including by modifying ion conductance and increasing GABAergic transmission. Specific drugs like phenobarbital, phenytoin, ethosuximide and valproate are also covered in terms of their pharmacological properties, mechanisms of action, adverse effects
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.
Trans cranial magnetic stimulation - Diagnostic & Therapeutic applicationNeurologyKota
Transcranial magnetic stimulation (TMS) is a non-invasive technique that uses electromagnetic induction to stimulate neural tissue without causing pain. TMS can have acute effects like activating neural circuits or disrupting speech, as well as prolonged effects like changing synaptic strength and modulating cortical excitability. TMS has diagnostic applications like measuring motor thresholds and central motor conduction time to evaluate motor pathways, and therapeutic applications for treating depression, Parkinson's disease, neuropathic pain, and more. Common TMS protocols include single pulse, paired pulse, and repetitive TMS with low or high frequency stimulation. TMS is generally safe but can infrequently cause minor side effects like headaches.
Neurodegenerative disorders like Alzheimer's and Parkinson's diseases result from the progressive degeneration or death of nerve cells in the brain. Alzheimer's is the most common form of dementia and slowly destroys memory and thinking skills over time. Drugs used to treat Alzheimer's include donepezil, galantamine, and rivastigmine. Parkinson's disease is caused by dopamine deficiency in the brain and its symptoms include tremors and difficulty with movement. Levodopa is commonly used to treat Parkinson's by increasing dopamine levels. Other neurodegenerative disorders discussed include ALS, Huntington's disease, and senile dementia.
This document provides an overview of antiepileptic drugs. It discusses the types and classification of epilepsy, the neurophysiology and pathophysiology of seizures, and the major mechanisms of action of various antiepileptic drugs. Specific drugs discussed in detail include phenobarbital, phenytoin, carbamazepine, ethosuximide, valproic acid, clonazepam, lamotrigine, gabapentin and their indications, mechanisms of action, pharmacokinetics, uses, and adverse effects.
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. Anticonvulsants work through various mechanisms such as enhancing GABA inhibition, blocking sodium and calcium channels, and reducing glutamate-mediated excitation.
2. Epilepsy is the second most common neurological disorder and is classified as partial or generalized seizures depending on where neural discharges start and spread.
3. Common anticonvulsants like phenobarbital, phenytoin, carbamazepine, and valproate work through different mechanisms like sodium channel blockade but can have side effects and drug interactions.
This document discusses antiepileptic drugs. It provides background on epilepsy, noting that it is characterized by recurrent seizures caused by abnormal neuronal discharge in the brain. Over 40 forms of epilepsy have been identified. Current drug therapies aim to prevent seizures but do not provide a cure. The document then discusses the classification and neuronal mechanisms of different types of seizures, as well as the cellular targets and mechanisms of action of common antiepileptic drugs, which generally aim to modulate ion channels or enhance GABAergic inhibition to suppress neuronal excitability and synchronization.
The Neurobiology of Depression (Dr Imran Waheed)Imran Waheed
A lecture delivered in the West Midlands by Dr Imran Waheed, Consultant Psychiatrist, on The Neurobiology of Depression. For further information visit www.bhampsych.com
The document summarizes information about neurodegenerative diseases. It discusses several major neurodegenerative diseases including Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, and ischemic brain damage. For each disease, it describes the etiology, signs and symptoms, pathophysiology, and pharmacotherapy options. Common causes and mechanisms like protein misfolding and aggregation, excitotoxicity, apoptosis, and oxidative stress are also summarized. The document concludes by mentioning recent updates in treatment using natural compounds and gene therapy approaches.
Hi,
This is Syed Masood Ahmed Quadri, Pharm.D
this presentation has varied range of details like,
history of disease,
signs and symptoms,
prevalence,
facts,
risk factors,
manifestations,
diagnosis,
pathology,
treatment,
and other interesting slides
hope you enjoy the read
Epilepsy is a chronic neurological disorder characterized by recurrent seizures. It affects approximately 1% of the population globally. Seizures occur due to an imbalance between excitatory and inhibitory neurotransmitters in the brain. Epilepsy is classified based on the origin of abnormal neuronal discharges as either focal or generalized seizures. Treatment involves pharmacotherapy with anti-epileptic drugs such as sodium channel blockers, calcium channel modulators, and GABA analogues to suppress seizure activity and control symptoms.
The document discusses antiepileptic drugs and the treatment of seizures. It covers the classification of seizures as either partial or generalized, describes common seizure types like tonic-clonic and absence seizures, and discusses the neuronal mechanisms involved. It also summarizes the mechanisms of action and pharmacokinetic properties of major antiepileptic drug classes, including barbiturates, hydantoins, benzodiazepines, and newer drugs. The goal of treatment is to prevent seizures with the simplest drug regimen possible.
This document provides information about antiepileptic drugs. It defines epilepsy as a disorder characterized by seizures resulting from neuronal discharges in the brain. Current drugs effectively control seizures in 70% of cases but have side effects. The document discusses the nature and types of epilepsy, including partial and generalized seizures. It explains the mechanisms of action of antiepileptic drugs, including enhancing GABA action, inhibiting sodium channels, and inhibiting calcium channels. Several major antiepileptic drugs are described, including phenytoin, carbamazepine, valproate, and ethosuximide. The document classifies antiepileptic drugs and discusses newer agents with improved side effect profiles.
This document discusses several theories of depression from a neurobiological perspective. It summarizes the monoamine hypothesis, which proposes that depression is caused by deficiencies in neurotransmitters like serotonin and norepinephrine. However, evidence for this theory is lacking. Alternative hypotheses examine abnormalities in neurotransmitter receptors and the impact of stress on factors like BDNF and brain atrophy. The document also reviews how depression affects various neuroendocrine systems and discusses symptoms in relation to specific brain circuits involved in emotional processing.
This document discusses various causes of falls, including syncope (transient loss of consciousness) and non-syncopal causes. It covers topics such as neurocardiogenic, cardiac, and neurological causes of syncope including seizures, progressive supranuclear palsy, third ventricular cysts, and more. Investigations discussed include Holter monitoring, loop recorders, tilt table testing, and imaging. Differential diagnosis and management are also covered.
Anti epileptic agents or drugs pharmacologysonalinghatmal
This document summarizes information about antiepileptic drugs used to treat epilepsy. It discusses the pathophysiology of epilepsy, how it is diagnosed, and classifications of antiepileptic drugs. It then focuses on the pharmacology of phenytoin, an antiepileptic drug, covering its mechanism of action, pharmacokinetics, uses, adverse effects and drug interactions. Phenytoin works by stabilizing neuronal membranes and modifying the body's normal response to seizures. It has a wide range of adverse effects and interacts with many other drugs by inducing or inhibiting liver enzymes.
by: Dr. Vishal Pawar, MD Pharmacology
All the recent updates regarding antiepileptics, composed into a single ppt presentation to make researching and learning easier
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.
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.
Trans cranial magnetic stimulation - Diagnostic & Therapeutic applicationNeurologyKota
Transcranial magnetic stimulation (TMS) is a non-invasive technique that uses electromagnetic induction to stimulate neural tissue without causing pain. TMS can have acute effects like activating neural circuits or disrupting speech, as well as prolonged effects like changing synaptic strength and modulating cortical excitability. TMS has diagnostic applications like measuring motor thresholds and central motor conduction time to evaluate motor pathways, and therapeutic applications for treating depression, Parkinson's disease, neuropathic pain, and more. Common TMS protocols include single pulse, paired pulse, and repetitive TMS with low or high frequency stimulation. TMS is generally safe but can infrequently cause minor side effects like headaches.
Neurodegenerative disorders like Alzheimer's and Parkinson's diseases result from the progressive degeneration or death of nerve cells in the brain. Alzheimer's is the most common form of dementia and slowly destroys memory and thinking skills over time. Drugs used to treat Alzheimer's include donepezil, galantamine, and rivastigmine. Parkinson's disease is caused by dopamine deficiency in the brain and its symptoms include tremors and difficulty with movement. Levodopa is commonly used to treat Parkinson's by increasing dopamine levels. Other neurodegenerative disorders discussed include ALS, Huntington's disease, and senile dementia.
This document provides an overview of antiepileptic drugs. It discusses the types and classification of epilepsy, the neurophysiology and pathophysiology of seizures, and the major mechanisms of action of various antiepileptic drugs. Specific drugs discussed in detail include phenobarbital, phenytoin, carbamazepine, ethosuximide, valproic acid, clonazepam, lamotrigine, gabapentin and their indications, mechanisms of action, pharmacokinetics, uses, and adverse effects.
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. Anticonvulsants work through various mechanisms such as enhancing GABA inhibition, blocking sodium and calcium channels, and reducing glutamate-mediated excitation.
2. Epilepsy is the second most common neurological disorder and is classified as partial or generalized seizures depending on where neural discharges start and spread.
3. Common anticonvulsants like phenobarbital, phenytoin, carbamazepine, and valproate work through different mechanisms like sodium channel blockade but can have side effects and drug interactions.
This document discusses antiepileptic drugs. It provides background on epilepsy, noting that it is characterized by recurrent seizures caused by abnormal neuronal discharge in the brain. Over 40 forms of epilepsy have been identified. Current drug therapies aim to prevent seizures but do not provide a cure. The document then discusses the classification and neuronal mechanisms of different types of seizures, as well as the cellular targets and mechanisms of action of common antiepileptic drugs, which generally aim to modulate ion channels or enhance GABAergic inhibition to suppress neuronal excitability and synchronization.
The Neurobiology of Depression (Dr Imran Waheed)Imran Waheed
A lecture delivered in the West Midlands by Dr Imran Waheed, Consultant Psychiatrist, on The Neurobiology of Depression. For further information visit www.bhampsych.com
The document summarizes information about neurodegenerative diseases. It discusses several major neurodegenerative diseases including Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, and ischemic brain damage. For each disease, it describes the etiology, signs and symptoms, pathophysiology, and pharmacotherapy options. Common causes and mechanisms like protein misfolding and aggregation, excitotoxicity, apoptosis, and oxidative stress are also summarized. The document concludes by mentioning recent updates in treatment using natural compounds and gene therapy approaches.
Hi,
This is Syed Masood Ahmed Quadri, Pharm.D
this presentation has varied range of details like,
history of disease,
signs and symptoms,
prevalence,
facts,
risk factors,
manifestations,
diagnosis,
pathology,
treatment,
and other interesting slides
hope you enjoy the read
Epilepsy is a chronic neurological disorder characterized by recurrent seizures. It affects approximately 1% of the population globally. Seizures occur due to an imbalance between excitatory and inhibitory neurotransmitters in the brain. Epilepsy is classified based on the origin of abnormal neuronal discharges as either focal or generalized seizures. Treatment involves pharmacotherapy with anti-epileptic drugs such as sodium channel blockers, calcium channel modulators, and GABA analogues to suppress seizure activity and control symptoms.
The document discusses antiepileptic drugs and the treatment of seizures. It covers the classification of seizures as either partial or generalized, describes common seizure types like tonic-clonic and absence seizures, and discusses the neuronal mechanisms involved. It also summarizes the mechanisms of action and pharmacokinetic properties of major antiepileptic drug classes, including barbiturates, hydantoins, benzodiazepines, and newer drugs. The goal of treatment is to prevent seizures with the simplest drug regimen possible.
This document provides information about antiepileptic drugs. It defines epilepsy as a disorder characterized by seizures resulting from neuronal discharges in the brain. Current drugs effectively control seizures in 70% of cases but have side effects. The document discusses the nature and types of epilepsy, including partial and generalized seizures. It explains the mechanisms of action of antiepileptic drugs, including enhancing GABA action, inhibiting sodium channels, and inhibiting calcium channels. Several major antiepileptic drugs are described, including phenytoin, carbamazepine, valproate, and ethosuximide. The document classifies antiepileptic drugs and discusses newer agents with improved side effect profiles.
This document discusses several theories of depression from a neurobiological perspective. It summarizes the monoamine hypothesis, which proposes that depression is caused by deficiencies in neurotransmitters like serotonin and norepinephrine. However, evidence for this theory is lacking. Alternative hypotheses examine abnormalities in neurotransmitter receptors and the impact of stress on factors like BDNF and brain atrophy. The document also reviews how depression affects various neuroendocrine systems and discusses symptoms in relation to specific brain circuits involved in emotional processing.
This document discusses various causes of falls, including syncope (transient loss of consciousness) and non-syncopal causes. It covers topics such as neurocardiogenic, cardiac, and neurological causes of syncope including seizures, progressive supranuclear palsy, third ventricular cysts, and more. Investigations discussed include Holter monitoring, loop recorders, tilt table testing, and imaging. Differential diagnosis and management are also covered.
Anti epileptic agents or drugs pharmacologysonalinghatmal
This document summarizes information about antiepileptic drugs used to treat epilepsy. It discusses the pathophysiology of epilepsy, how it is diagnosed, and classifications of antiepileptic drugs. It then focuses on the pharmacology of phenytoin, an antiepileptic drug, covering its mechanism of action, pharmacokinetics, uses, adverse effects and drug interactions. Phenytoin works by stabilizing neuronal membranes and modifying the body's normal response to seizures. It has a wide range of adverse effects and interacts with many other drugs by inducing or inhibiting liver enzymes.
by: Dr. Vishal Pawar, MD Pharmacology
All the recent updates regarding antiepileptics, composed into a single ppt presentation to make researching and learning easier
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.
Epilepsy is a chronic neurological condition characterized by recurrent seizures. The document discusses the epidemiology, pathophysiology, classification, symptoms, risk factors, diagnosis, and treatment of epilepsy. It also outlines the pharmacist's role in managing epilepsy, including educating patients, ensuring proper adherence and monitoring, and adjusting drug therapy as needed. A case study is then presented of an 11-year old patient experiencing frequent seizures who is prescribed multiple antiepileptic drugs.
Journal presentation on essential tremorEjaj Ahmed
1) Essential tremor is a syndrome of isolated tremor of the upper limbs that has been present for at least 3 years, with or without tremor in other locations like the head or voice.
2) Propranolol and primidone are first-line pharmacological treatments that can reduce tremor severity by 55-60% through effects on the cortico-ponto-cerebellar-thalamic circuit implicated in essential tremor pathophysiology.
3) When medications are ineffective, neurostimulation techniques like deep brain stimulation targeting the thalamus or focused ultrasound thalamotomy can provide relief of tremors, though effectiveness may diminish over time and risks include ataxia, dys
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.
1. Status epilepticus (SE) is a medical emergency defined as a seizure lasting more than 5 minutes or recurrent seizures without regaining consciousness. SE can be convulsive or non-convulsive.
2. The annual incidence of SE is estimated to be between 9,000-14,000 new cases per year in the UK. Mortality is about 20-30% and is higher in the elderly.
3. SE is initially treated with benzodiazepines like lorazepam or diazepam. If seizures continue, second line drugs like fosphenytoin or phenytoin are used. For refractory SE, anesthetic drugs under ICU care may be required
Epilepsy: Diagnostics, Medications, Myths and Factsabdul waheed
The document discusses epilepsy, a chronic brain disorder characterized by recurrent seizures. It provides details on the types of seizures, experimental models used to study epilepsy, antiepileptic drugs and their mechanisms of action, diagnostic tools, myths and facts about epilepsy, and references. Epilepsy affects people of all ages worldwide and imbalances in neurotransmitters like glutamate and GABA are believed to underlie seizure mechanisms.
Antiepileptic drugs : Dr Rahul Kunkulol's Power point preparationsRahul Kunkulol
This document discusses epilepsy and anti-epileptic drugs. It defines epilepsy as a chronic neurological disorder characterized by recurrent seizures. It notes that more than 40 forms of epilepsy have been identified. While drugs can prevent seizures, there is no cure currently available. Common causes of seizures are listed. The different types of seizures are classified and described. Finally, several commonly used anti-epileptic drugs are outlined, including their mechanisms of action and side effect profiles.
- 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.
A 31-year-old male presented with a fever for one week and seizures and altered sensorium for three days. He experienced generalized tonic-clonic seizures that were initially uncontrolled. Imaging showed findings suggestive of viral or autoimmune encephalitis. Refractory status epilepticus was diagnosed and treated with high doses of multiple antiepileptic drugs, including lacosamide, which eventually controlled the seizures. Status epilepticus is defined as a seizure that persists for a sufficient length of time or is repeated frequently enough that recovery between attacks does not occur. The pathophysiology involves reductions in inhibitory GABA receptors and increases in excitatory glutamate receptors over time.
Epilepsy is a chronic neurological disorder characterized by recurrent seizures originating from abnormal neuronal discharge in the brain. It affects people of all ages globally. Seizures occur when there is sudden excessive signaling between brain cells. Epilepsy has various etiologies and can be difficult to diagnose, requiring ruling out other conditions and use of EEG or MRI to identify abnormal electrical activity or structural lesions. While 70% of epilepsy can be treated effectively, many in developing areas do not receive needed treatment. Common anti-epileptic drugs work by enhancing GABA inhibition, blocking sodium or calcium channels, or inhibiting glutamate, with phenytoin a first-line treatment for generalized and partial seizures as well as status epilepticus.
The document defines epilepsy as a group of disorders characterized by chronic recurrent seizures caused by abnormalities in brain electrical activity. It provides definitions for several epilepsy-related terms and seizure types. It also summarizes epidemiological data on incidence and prevalence of epilepsy worldwide. Classification systems for seizures, antiepileptic drugs, and treatment principles and approaches for status epilepticus are outlined.
Post-traumatic epilepsy (PTE) is defined as recurrent seizures occurring after traumatic brain injury (TBI). TBI accounts for 10-20% of epilepsy cases. Risk factors for early PTE include GCS <10, intracranial hematoma, and seizures within 24 hours of injury. Risk factors for late PTE include penetrating injury, intracranial hematoma, early PTE, and age over 35. Temporal lobes are the most common localization. Standard anticonvulsants are used to treat established PTE but prophylaxis is ineffective at preventing late PTE. Surgery may be considered for refractory late PTE if the seizure focus is well-localized.
This document discusses convulsive status epilepticus (CSE). It notes that the worldwide incidence of CSE is highest in children and the elderly, with mortality rates ranging from 10.5-28% and neurological sequelae occurring in 11-16% of patients. The most common causes of CSE are listed as low anti-epileptic drug levels, stroke, alcohol withdrawal, anoxic brain injury, and metabolic disturbances. The document provides details on the definition, types, risk factors, complications, management, and treatment of CSE.
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.
The document provides information on the pharmacology of antiepileptic drugs (AEDs). It discusses the basic mechanisms of seizures and epilepsy, including abnormal neuronal excitation and synchronization. It then covers the epidemiology and classification of seizure types. The mechanisms by which epilepsy develops, both acquired and genetic, are described. Finally, the document outlines the cellular targets of AEDs and examples of drugs that act on GABA, sodium channels, calcium channels and other targets to reduce neuronal excitability and seizures.
Epilepsy is caused by excessive neuronal discharge in the brain and can cause seizures and abnormal neurological symptoms depending on the site of origin. Seizures are generally classified as partial or generalized based on whether neuronal activity is localized or spreads widely. Anti-seizure medications work by various mechanisms like enhancing GABA inhibition, blocking sodium or calcium channels, and interfering with glutamate transmission to suppress seizure activity. Treatment choice depends on seizure type, patient factors, and drug characteristics and side effects.
Similar to Status epilepticus sign and symptoms, etiology ,pathogenesis , diagnostic tests and treatment protocol (20)
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...Leonel Morgado
Current descriptions of immersive learning cases are often difficult or impossible to compare. This is due to a myriad of different options on what details to include, which aspects are relevant, and on the descriptive approaches employed. Also, these aspects often combine very specific details with more general guidelines or indicate intents and rationales without clarifying their implementation. In this paper we provide a method to describe immersive learning cases that is structured to enable comparisons, yet flexible enough to allow researchers and practitioners to decide which aspects to include. This method leverages a taxonomy that classifies educational aspects at three levels (uses, practices, and strategies) and then utilizes two frameworks, the Immersive Learning Brain and the Immersion Cube, to enable a structured description and interpretation of immersive learning cases. The method is then demonstrated on a published immersive learning case on training for wind turbine maintenance using virtual reality. Applying the method results in a structured artifact, the Immersive Learning Case Sheet, that tags the case with its proximal uses, practices, and strategies, and refines the free text case description to ensure that matching details are included. This contribution is thus a case description method in support of future comparative research of immersive learning cases. We then discuss how the resulting description and interpretation can be leveraged to change immersion learning cases, by enriching them (considering low-effort changes or additions) or innovating (exploring more challenging avenues of transformation). The method holds significant promise to support better-grounded research in immersive learning.
PPT on Direct Seeded Rice presented at the three-day 'Training and Validation Workshop on Modules of Climate Smart Agriculture (CSA) Technologies in South Asia' workshop on April 22, 2024.
Sexuality - Issues, Attitude and Behaviour - Applied Social Psychology - Psyc...PsychoTech 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!
Authoring a personal GPT for your research and practice: How we created the Q...Leonel Morgado
Thematic analysis in qualitative research is a time-consuming and systematic task, typically done using teams. Team members must ground their activities on common understandings of the major concepts underlying the thematic analysis, and define criteria for its development. However, conceptual misunderstandings, equivocations, and lack of adherence to criteria are challenges to the quality and speed of this process. Given the distributed and uncertain nature of this process, we wondered if the tasks in thematic analysis could be supported by readily available artificial intelligence chatbots. Our early efforts point to potential benefits: not just saving time in the coding process but better adherence to criteria and grounding, by increasing triangulation between humans and artificial intelligence. This tutorial will provide a description and demonstration of the process we followed, as two academic researchers, to develop a custom ChatGPT to assist with qualitative coding in the thematic data analysis process of immersive learning accounts in a survey of the academic literature: QUAL-E Immersive Learning Thematic Analysis Helper. In the hands-on time, participants will try out QUAL-E and develop their ideas for their own qualitative coding ChatGPT. Participants that have the paid ChatGPT Plus subscription can create a draft of their assistants. The organizers will provide course materials and slide deck that participants will be able to utilize to continue development of their custom GPT. The paid subscription to ChatGPT Plus is not required to participate in this workshop, just for trying out personal GPTs during it.
Immersive Learning That Works: Research Grounding and Paths ForwardLeonel Morgado
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
(June 12, 2024) Webinar: Development of PET theranostics targeting the molecu...Scintica Instrumentation
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The binding of cosmological structures by massless topological defectsSérgio Sacani
Assuming spherical symmetry and weak field, it is shown that if one solves the Poisson equation or the Einstein field
equations sourced by a topological defect, i.e. a singularity of a very specific form, the result is a localized gravitational
field capable of driving flat rotation (i.e. Keplerian circular orbits at a constant speed for all radii) of test masses on a thin
spherical shell without any underlying mass. Moreover, a large-scale structure which exploits this solution by assembling
concentrically a number of such topological defects can establish a flat stellar or galactic rotation curve, and can also deflect
light in the same manner as an equipotential (isothermal) sphere. Thus, the need for dark matter or modified gravity theory is
mitigated, at least in part.
2. CONTENTS
STATUS EPILEPTICUS
1: Introduction of Status Epilepticus
2: Sign and symptoms
3: Etiology
4: Pathogenesis
5: EEG pattern & interpretation
6: Diagnostic tests and their interpretation
7: Detailed Treatment protocols for management of status epilepticus (Describe each drug
in detail)
8: Protocols for prevention of episodes of status epilepticus
9: Role of clinical pharmacists in management of status epilepticus
10: Role of pharmacist to prevent the episodes of status epilepticus
3. INTRODUCTION
Status epilepticus (SE) is a medical emergency associatedwith significant morbidity,it is a
common neurologic disorder , (SE) one of the a life threatening condition .
In that requires emergency care mostly consisting of parentral administration of a fast
acting agents like Benzodiazepine, over slower acting agents such as phenytoin,
fosphenytoin,divalproex and levetiracetam.
Status epilepticus usually three types includes Focal seizure , myoclonic seizure,
generalized tonic–clonic seizure (GTCS) , generalized tonic clonic seizure is a common
types of status epilepticus .
Status epilecpticus:
Continuous seizures or repetitive discrete seizures with impaired or harm consciousness ,
( seizures more then 5 minutes in duration ).
OR
Continuous seizures activity lasting for more then five minutes without returning to
normal .
Classified in
Convulsive status epilepticus. This type occurs with convulsions. It may be more likely to
lead to long-term injury. Convulsions may involve jerking motions, grunting sounds,
drooling, and rapid eye movements.
Nonconvulsive status epilepticus. People with this type may appear confused or look like
they're daydreaming. They may be unable to speak. They may also behave in an irrational
way.
If repetitive seizure s consciousness is not regained between.
most frequently status epilepticus due to anticonvulsant withdrawal ,metabolic disorder ,
drug toxicity central nerves systeminfection ,tumor, head trauma et cetera .
4. CLINICAL FEATURES
increase sympathetic activity
Hyperthermia( rise body temperature ) >98.6F*.
Tachycardia (rise heart rate ) >100 per min.
Hypertension (rise blood pressure )>140/90mmHg.
SYMPTOMS OF STATUS EPILEPTICUS
Muscle spasms( contraction in muscle)
Falling (moving from a higher to a lower level, typically rapidly and without control)
Confusion
Unusual noises
Loss of bowel or bladder control
Clenched teeth (Clenching is simply holding the teethtogether and tightening the jaw
muscles.)
Irregular breathing
Strange behavior
Trouble speaking.
ETIOLOGY
*Low level of automated external defibrillator (AED)
An automated external defibrillator (AED) is a portable electronic device that
automatically diagnoses the life-threatening cardiac arrhythmias of ventricular fibrillation
(VF) and pulseless ventricular tachycardia, and is able to treat them through defibrillation.
*Stroke
*Alcohol withdrawal
*Anoxic brain injury and remote brain injury
5. *Metabolic disturbance
*infections ( viral or bacterial exp.. Meningitis)
*Brain neoplasms (Brain tumors )
*idiopathic ( UNKNOWN CAUSE OF DISEAS ) disease or condition which arises
spontaneously or for which the cause is unknow.
in children, the main cause of status epilepticus is an infection with a fever.
PATHOGENESIS
Mechanism of status epilepticus
Clinical and experimental studies have appear that Status epilepticus progress through
an initiation phase to a maintenance phase.
In the initiation phase the Activate stimuli give rise to discrete seizures that tend to abate
as soon as the stimulus is removed.
In the subsequent maintenance phase discrete seizures combine together into a continuum,
with activate stimuli no longer required to sustain a train of seizures.
The intensity and duration of the stimulation has a direct influence on the transition from
the initiation phase to the maintenance phase.
A variety of signaling molecules such as GABA-A (γ-aminobutyric acid) antagonists,
glutamate agonists, cholinergic (muscarinic) agonists, tachykinins, galanin antagonists, and
opiate k antagonists have been found to be involved in the initiation phase.
In contrast to this, much less is known about the maintenance phase. In fact only a limited
number of molecules have been found that block the maintenance phase (e.g., NMDA and
Ampa (N-methyl-D aspartate) antagonists, substance P antagonist, galanin, and
dynorphin)
The adaptation of a single seizure to Status epilepticus depends on several factors.
In experimental electrogenic Status epilepticus , at least 30 min of stimulation is required to
produce self-sustained SEtus epilepticus .
6. The limbic system is clearly at increased risk for injury during Status epilepticus and, due
to its nature and connections with the rest of the brain, it may play a crucial role in
generating seizures, it has prevents excitatory stimulation from spreading through the
hippocampus until a point of maximal dentate activation is reached.
Once this point is increase, excitatory inputs can spread through the hippocampus and
may then propagate to involve widespread neocortical areas.
It is likely that ineffective recruitment of inhibitory neurons, together with excessive
neuronal excitation, plays a role in the initiation and propagation of the electrical
disturbance occurring in Status epilepticus .
GABA is the major inhibitory neurotransmitter in the CNS, It is releasedfrom GABAgic
neurons and binds to several types of GABA receptors such as , GABA-A (GABA type A),
GABA-B, and GABA-C receptors.
GABA receptors are macromolecular proteins that form a chloride ion channel complex
and contain specific binding sites for GABA and a number of allosteric ( modified the
shape of protein) regulators. including barbiturates, benzodiazepines, and a number of
anesthetic agents.
GABA receptor–mediated inhibition may be responsible for the normal termination of a
seizure.
the activation of the NMDA receptor by the excitatory neurotransmitter glutamate may be
required for the propagation of seizure activity.
The activation of NMDA receptors results in enhance or increase the levels of intracellular
calcium, which may responsible for the nerve cell injury seenin patients with Status
epilepticus .
This phenomenon has important clinical suggestion . Benzodiazepine-like drugs, which
potentiate GABAergic inhibition, have an important role in the early initiation phase of
Status epileptics but they may prove ineffective in the advanced stages of SE.when NMDA
antagonists have the potential to be beneficial. Prolonged epileptiform bursting results in a
reduction of GABA-mediated synaptic inhibition.
*Reversible post-translational modification of proteins (Protein phosphorylation )
In early stage of millisecond or second ,Ions channels opening and closing
neurotransmitter release .
*Receptor trafficking
Second stage of second minutes Reduce the level inhibitory Gama amino butyric
acid (GABAA) neurotransmitter and beta2 and gama subunit effects to reduce the
GABAergic activity in the cell effected in the seizures discharge .
7. Increase in excitatory N-methyl-D-aspartate receptor (NMDA receptor) and α-
amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor AMPA receptor .
*Neuropeptide Expression
In third stage of minutes hours At this stage increase the level of excitatory
substances p.
Alteration in neuropeptide expression in status epilepticus
Hippocampus
It is a type of brain which control the loss of memory .
Example (in hippocampus decrease in inhibitory piptides, dynorphin
,Galanin,somatostatin and neuropeptide Y. and increase in proconvulsant
tachykinins ,substance P ( is an undecapeptide (a peptide composed of a chain of 11
amino acid residues) member of the tachykinin neuropeptide family.
It is a neuropeptide, acting as a neurotransmitter and as a neuromodulator.and
neurokinin B (Neurokinin B belongs in the family of tachykinin peptides.
Neurokinin B is implicated in a variety of human functions and pathways such as
the secretion of gonadotropin-releasing hormone. Additionally, NKB is associated
with pregnancy in females and maturation in young adults
Insufficient renewal inhibitory neuropeptide Y.
Genetic and epigenetic modification
Gene expression
at the fourth stage of days weeks Gene expression is the process by which
information from a gene is used in the synthesis of a functional gene product. These
products are often proteins, but in non-protein-coding genes such as transfer RNA
or small nuclear RNA genes, the product is a functional RNA.
Gene methylation
Process in which CH3yl groups added to DNA molecules, it can alter the activity of
a DNA segments without changing the sequence .
Tuning or regulation microRNA.
8. ELECTROENCEPHALOGRAM (EEG) INTERPRETATION
Below terms to express (EEG) patterns in status epileptics :
POSITION: generalized (including bilateral synchronous patterns )lateralized,
bilateral free multifocal .
NAME OF THE PATTERNS : periodic discharge rhythmic delta activity or spike
and wave ,sharp and wave pulse sub type.
MORPHOLOGY : sharpness numbers of phases like (triphasic morphology)
absolute and relative amplitude ,polarity .
TIME RELATED FEATURES OR CHARACTERISTIC:
prevalence ,frequency ,duration daily patterns duration and index onset
(sudden verses gradual ), and dynamics(evolving, fluctuating or static or rest)
MODULATION : stimulus induced vs, spontaneous.
EFFCT OF INTERVENTION : medication on Electroencephalogram (EEG)
STANDARD OR CARITERIA FOR NON-CONVULSIVE SEIZURES
Some patterns lasting at least 10 seconds satisfying any one of the following criteria.
Primary: a) focal spikes , sharp waves, spike and wave or sharp and slow wave
complexes or repetitive generalized at greater -3 per second .
b) repetitive generalized or focal spikes , sharp waves, spike and wave or sharp
and slow wave complexes at less then 3 per second and secondary criterion.
c) Sequential rhythmic periodic or quasi periodic wave at greater – 1per second and
unequivocal evolution in frequency morphology or position .
.
Secondary: a) significant improvement in clinical state or appearance of
previously absent normal EEG patterns such as posterior dominant rhythm
temporally coupled to acute administration of a fast acting automated external
defibrillator (AED).
9. b) Resolution of the epileptiform discharges , leaving diffuses slowing without
clinical improvement and without appearance of previously absent normal EEG
patterns , would not Satisfy the secondary criterion .
DIAGNOSTIC TESTS AND THEIR INTERPRETATION IN (SE)
The diagnostic examination should be done one the patient is stabilized and appropriate
pharmacotherapy for Status epileptics is initiated .
DIAGNOSTIC THRASH (OUT) OR WORKUP ALL PATIENTS
Monitor vital signs ABC
get intravenous access
Head CT Scan (Computerized Tomography)appropriate for most cases )
Laboratory Blood glucose ,
renal function tests
, test for electrolytes
,AED level ,
Continuous EEG (cEEG)monitoring .
Examination based on clinical presentation
Brain MRT(Magnetic resonance imaging)
Lumber puncture , Toxicology panel ( examples isoniazid (TCAs) Theophylline
cocaine sympathomimetic organophosphates, cyclosporine )
10. DETAILED TREATMENT PROTOCOLS FOR MANAGMENTS OF STATUS
EPILEPTICUS (EXPLAIN EACH DRUG IN DETAILS)
The first line of therapy in status epileptics are Benzodiazepines
MOA: mechanism of action
These drugs bind to the gamma-aminobutyric acid (GABA)-A receptors, increasing
channel opening central ion channels at the receptor, result influx of chloride conductance
and neuronal hyper polarization, leading to enhanced inhibitory neurotransmission and
antiepileptic action
Lorazepam (Intravenous (IV) and Intranasal (IN)
Lorazepam can be administered either intravenously or intranasally, although to date most
evidence in the treatment of Status epileptics refers to its IV use.
Although it has a longer initial duration of action than diazepam, lorazepam administered
intravenously is usually preferred as initial treatment of early Status epileptics , because it
is less lipid-soluble and consequently does not undergo the rapid redistribution into
peripheral tissues seenwith diazepam. lorazepam long therapeutic half life anti seizures
effects 6 to 12 hours , 2mg dose uptoa max dose of 8mg in total .
Dose 0,1-0.5mg/kg iv upto 4-6mg over 1-2 minutes
If Status epileptics persists repeat every 5 to 10 minutes
Diazepam (IV, Rectal) Diazepam is a highly lipophilic benzodiazepine, which rapidly
enters into the brain but subsequently is rapidly redistributed into peripheral tissues.
The pharmacokinetic property of Diazepam is responsible for its fast anticonvulsant effect
in spite of its longer elimination half-life.
Diazepam can be administered either intravenously or rectally, with demonstrated
significantly higher efficacy over placebo in terms of controlling acute repetitive convulsive
seizures in adults and children for both methods of administration.
Dose -10mg iv push over 30-60 seconds
Repeat after 10-15 mins upto 40mg (5mg/min)
11. Repeat after2-4 hours (max 100mg/day)
Bolus dose should be given undiluted from at rate not exceeding 2-5mg per minutes
Midazolam (IV, Intramuscular (IM), Intranasal, Buccal)
Midazolam is a benzodiazepine with the advantage of multiple routes of administration,
due to its water solubility.
At physiologic pH the ring structure of midazolam closes and it becomes highly lipophilic,
crossing the blood-brain barrier rapidly midazolam administered intravenously was found
to be similar in terms of seizure recurrence to IV diazepam or IV lorazepam in a pediatric
non-randomized, controlled trial, with no significant differences in mean duration to
clinical seizure cessation.
Dose 10mg intramuscularly
Common ADRS They include drowsiness, dizziness, and decreased alertness and
concentration. Lack of coordination may result in falls and injuries, in particular, in the
elderly.
Second stage Phenytoin and Fosphentoin
MOA
These antiepileptic drug blockade the voltage gated sodium channels by selectively binding
to the channels in the inactive state and showing recovery ,it is effective for treatments of
focal and generalized tonic clonic seizures and status epilepticus .
Phenytoin: extravasations purple glow syndrome .
Dose 20mg per kG body weight .
Fosphentoin: prodrug more water soluble non irritating .
12. 20mg prt kG body weight .
Barbiturates
Phenobarbital (IV, IM)
MOA
These drugs potentiate GABA action on chloride entry into the neuron by prolonging the
duration of the chloride channel openings , addition barbiturates blockade excitatory
glutamate receptor ,these molecular action lead to decreased neuronal activity .
In a randomized, controlled trial on CSE, IV phenobarbital was at least as effective as a
combination of diazepam and phenytoin.
The central depressive effect of phenobarbital, especially following the use of
benzodiazepines, limits its clinical utility, when alternatives are available. However, over
the years wide experience has been gained in adults and children, as well as in the
newborn. These drug produce respiratory and CNS depression .
Dose 20mg per kg, 100mg per minute
Common ADRS Dizziness.Drowsiness.Fatigue.Nausea.Tremor.Rash.Weight gain.
Valproic Acid (IV)
MOA
This drug is a also anticonvulsant effect has been attributed to the blockade of voltage-
gated sodium channels and increased brain levels of gamma-aminobutyric acid (GABA).
Dose 20-40mg per kg continuous infusion 1-5 mg per kg per hours
13. Levetiracetam (IV)
Levetiracetam is an efficacious and well tolerated drug with a broad spectrum of efficacy
against all seizure types and a low potential for interactions due to minimal hepatic
metabolism and low plasma protein binding.
The safety profile of levetiracetam is advantageous, with a very low rate of adverse effects
reported (most often somnolence and sedation, and rarely agitation and
thrombocytopenia)( is a condition in which you have a low blood platelet count)
MOA
Levetiracetam exhibit anticonvulsant activity it binds and modulate synaptic vesicle
glycoprotein 2A (SV2A) in the brain .
(SV2A) is a protein expressedin neurons and endocrine cells and involved in the regulation
of neurotransmitter release)
Dose 30-60mg per kg
Lacosamide (IV)
This is anticonvulsant drug which decrease the irregular electrical activities in brain.
It generally used bolus dose 400 mg, followed by a daily dose of 200–400 mg.
MOA
There are multiple mechanism of action of locosamide , it affects voltage gated sodium
channels resulting in stabilization of hyper-excitable neuronal membranes and inhibition
of repetitive neuronal shooting.
Dose bolus dose was 200-400mg over 3-5 minutes
Maintenance dose 100mg (BD) twice a day.
Common ADRS sedation Dizziness.Drowsiness.Fatigue.Nausea.Tremor.Rash.Weight gain.
14. OTHER AGENTS USED IN STATUS EPILEPTICUS
Propofol , iv
Propofol is an anesthetic agent, acting as an N-methyl-D-aspartate (NMDA) antagonist in
vitro, with a shorter duration of action and lower tendency to accumulate in the body than
barbiturates.
It may cause hypotension, but reduces intracranial pressure and brain metabolic
requirements, no difference was found between the drugs with respect to control of seizure
activity .
MOA
These anesthetic drug which increasing GABA-mediated inhibatory tone in the CNS,
It reduce the rate of dissociation of the GABA from the receptor, thereby increasing the
duration of the GABA-activated,opening of the chloride channel with resulting hyper
polarization accurse in cell membranes.
Dose intravenous loading dose of 3mg per kg although 3-5mg per kg .1-2mg per kg load iv.
Infusion 1-15mgper kg per hours .
Ketamine (IV infusion)
Ketamine has a strong antagonistic effect on the NMDA-glutamate receptor. It has a half-
life of 2–3 h and is extensively metabolized by the hepatic cytochrome P450 pathway to its
active metabolite, norketamine.
MOA
It is a antagonist for the NMDA receptors and inhabit the excitatory signals that are
found in nerve cells. These receptors are involved in processing central nervous system
input.
Ketamine blocks this sensory input. This action is what accounts for most of the effects
seenfrom ketamine.
Dose 1.5-4.mg per kg in iv load and 2.75.5mg per kg/hours .
Common ADRS
High blood pressure (hypertension) Increased cardiac output
Increased intracranial pressure Fast or slow heart rate Involuntary eye movement.
15. Protocols for prevention of episodes of status epilepticus
Treatment should begin immediately with a benzodiazepine. Use lorazepam 0.1 mg/kg IV
or midazolam 0.2 mg/kg IM.
Avoid giving midazolam IV because this is more likely to cause respiratory arrest and force
endotracheal intubation upon a patient who might not have required it.
Guidelines for the treatment of status epilepticus Treatment should begin immediately
with a benzodiazepine. Use lorazepam 0.1 mg/kg IV or midazolam 0.2 mg/kg IM.
Avoid giving midazolam IV because this is more likely to cause respiratory arrest and force
endotracheal intubation upon a patient who might not have required it.
Immediately after an appropriate dose of benzodiazepine is given, obtain medications
necessary to support the patient if they develop respiratory failure or hypotension. This
involves preparing medications for endotracheal intubation .
Refractory status epilepticus Refractory status epilepticus is treated with general
anesthesia and mechanical ventilation.
If a patient have epilepsy, taking your medicines as directed may help him prevent status
epilepticus. If patient had status epilepticus, patient may need to begin taking seizure
medicines or change medicines patients already taking. Avoiding other causes of this
condition, such as alcohol abuse or low blood sugar, may also help prevent it.
The healthcare provider will want to end the seizure as quickly as possible and treat any
underlying problems that are causing it. you may receive oxygen, have blood tests, and an
intravenous (IV) line. you may be given glucose (sugar) if low blood sugar may be causing
the seizure.
Status epilepticus has many causes. Some can be prevented such as low blood glucose or
alcohol and drug abuse.
Individuals who have epilepsy must take their medicine as directed.
A seizure that lasts more than 5 minutes, or having more than 1 within a 5 minute period is
an emergency that requires immediate medical care.
healthcare providers suggest to give protocol as use anti-seizure medication for prevents
the problem, including.
Diazepam,Lorazepam ,Phenytoin ,Fosphenytoin ,Phenobarbital ,Valproate ,Levetiracetam
,Lacosamide ,Propofol , Ketamine.gabapenten also.
16. Role of clinical pharmacists in management of status epilepticus
analyzed the effectiveness of clinical pharmacists in improving medical records and patient
with status epilepticus .compliance with outpatient drug regimens.
Records of patients followed up in a SE and were reviewed and compared with their
pharmacy files.
Records were evaluated for completeness and accuracy of drugs ordered by the clinic
physician.
Compliance was estimated by examining drug refills.
This review was performed before (control group) the introduction of a clinical pharmacist
into the clinics.
A six-month analysis demonstrates that the pharmacist significantly improved drug
documentation,
decreased the duplication of prescriptions, and improved compliance of prescribed drugs.
The study suggests that the pharmacist improves documentation of drug therapy and
estimated patient compliance .
the decrease in duplicate prescriptions could prevent the risk of overdose and does reduce
drug costs.
Our review indicates that pharmacists are involved in the following clinical activities for the
cprevention of patient with status epileptic :
A ) Therapeutic drug monitoring
b ) medication review
c) pharmacotherapeutic d ) pharmaceutical counseling,
f) systematic measurement and evaluation of health results from the drug treatment.
17. Role of pharmacist to prevent the episodes of status epilepticus
Status epilepticus is a chronic disorder that continues to be a huge economic burden.
Although newer AEDs aim to increase treatment success and decrease the risk for adverse
effects, there is still a strong need for improving patient outcomes.
Pharmacists can play a significant role in optimizing therapy for patients with SE.
1: Patient counseling on the potential adverse effects of AEDs is important.
2: Patients and family members should be educated on expectedCNS and cognitive side
effects, potential skin reactions, and the risk for suicidal behavior
3: Patient education should also address the importance of medication adherence.
4: Patient medication profiles should be reviewed for possible drug interactions,
and dosage adjustments or alternative agents should be recommended if necessary.
5: Additionally pharmacists can advise clinicians on appropriate therapeutic drug
monitoring..
Its treatment is complex and may involve the use of antiepileptic drugs (AEDs), a special
diet, immunotherapy, and neurostimulation.
pharmacists are important health professionals in counseling and monitoring patients with
status epileptics, because they are easily accessible and know about pharmacotherapy,
health education, and management of chronic diseases .
pharmacist can detect the emergence of health problems and can help prevent the
progression of comorbidities.
pharmacists evaluated medication use, identified therapeutic problems, and proposed
changes in prescriptions to a health team, when the pharmacotherapy was not appropriate.
Thus, pharmacists performed pharmaceutical counseling and pharmacotherapeutic
follow-up, as well as systematic measurement and development of results.
pharmacists provided guidance to ensure the adequacy of the pharmacotherapy through
therapeutic drug monitoring.