Abstract: Bening Rolandic Epilepsy 3 1.Abstract Benign rolandic epilepsy or Bening epilepsy of childhood with centro-temporal spikes (BECT) is the most widely recognized epilepsy disorder in the pediatric age group, with a beginning between age 3 and 13 years. The average introduction is a fractional seizure with parasthesias and tonic or clonic action of the lower face related with drooling and dysarthria. Seizures regularly happen around evening time and may turn out to be generalized. They are typically rare and may not require antiepileptic medicates in any case, whenever treated, they will in general be effectively controlled. Youngsters with BECT are neurologically and psychologically normal. The EEG shows trademark high-voltage sharp waves in the centro-temporal districts, which are enacted with sleepiness and rest. Right now, BECT is effectively perceived. Be that as it may, atypical cases are normal and the meaning of BECT can get obscured. Albeit further examinations are not required in cases with common clinical and EEG discoveries and typical neurologic assessments, neuro-imaging studies might be required in atypical cases to preclude other pathology. The long-term. medical and psychosocial forecast of BECT is magnificent, with basically all children entering long- term remission by mid-adolescene.
EEG in idiopathic generalised epilepsiesNeurologyKota
This document provides information on idiopathic generalized epilepsies (IGE), which are a group of epilepsy disorders characterized by generalized bilateral spike-wave complexes on EEG. It describes the main seizure types seen in IGE including absence seizures, myoclonic seizures, and generalized tonic-clonic seizures. It also discusses several specific IGE syndromes like childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy. For each syndrome it provides details on clinical presentation, EEG features, treatment approaches, and prognosis.
This document provides an overview of various epilepsy syndromes classified by onset in the brain and cause of seizures. It describes several generalized and focal epilepsy syndromes including childhood absence epilepsy, juvenile myoclonic epilepsy, benign epilepsy with centrotemporal spikes, Panayiotopoulos syndrome, autosomal dominant nocturnal frontal lobe epilepsy, Doose's syndrome, Dravet's syndrome, infantile spasms/West syndrome, Lennox-Gastaut syndrome, and Ohtahara syndrome. For each syndrome, it covers key characteristics, EEG findings, treatment approaches, and typical prognosis.
1) Disorders of consciousness range from mild impairment to coma and include conditions like confusion, delirium, vegetative state, and brain death.
2) The pathophysiology of consciousness involves the ascending reticular activating system and connections between the brainstem and cortex. Loss of consciousness can result from disruption of these systems.
3) Etiologies of impaired consciousness and coma include infectious or inflammatory causes, structural abnormalities, and metabolic/toxic derangements. Common causes in children are infections, trauma, seizures, and metabolic disorders.
This document provides a summary of age dependent epileptic syndromes and focuses on primary generalized epilepsy and benign Rolandic epilepsy. It discusses the key characteristics of each condition including typical age of onset, common seizure types and EEG patterns. The summary concludes that these conditions are age determined and often seen in childhood, with seizures typically remitting by late adolescence.
This document provides an overview of evaluating the etiology of seizures. It discusses the initial evaluation steps, including distinguishing epileptic from non-epileptic events. It reviews diagnostic investigations like imaging, EEG, and bloodwork. Common structural etiologies and epilepsy syndromes are described. The document emphasizes performing a thorough history, physical exam, and targeted workup to identify underlying causes and guide treatment and prognosis.
Temporal lobe epilepsy (TLE) is characterized by recurrent seizures originating from the temporal lobe. Hippocampal sclerosis, involving cell loss in the hippocampus, is the most common pathological finding in TLE. Auras occur in about 80% of temporal lobe seizures and can involve somatosensory, special sensory, autonic, or psychic symptoms. Diagnostic workup involves brain imaging like MRI and PET, as well as EEG to identify abnormalities in the temporal lobe.
Temporal lobe epilepsy is one of the most common forms of epilepsy. It can be caused by hippocampal sclerosis or lesions in the temporal lobe. Hippocampal sclerosis involves neuronal loss and gliosis in the hippocampus and is the most common pathological finding in temporal lobe epilepsy patients. Interictal EEG findings like temporal intermittent rhythmic delta activity and temporal sharp waves help lateralize the seizure focus. Video EEG monitoring helps capture seizures and interictal discharges. Treatment involves antiepileptic drugs and potentially resective surgery for drug-resistant cases.
EEG in idiopathic generalised epilepsiesNeurologyKota
This document provides information on idiopathic generalized epilepsies (IGE), which are a group of epilepsy disorders characterized by generalized bilateral spike-wave complexes on EEG. It describes the main seizure types seen in IGE including absence seizures, myoclonic seizures, and generalized tonic-clonic seizures. It also discusses several specific IGE syndromes like childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy. For each syndrome it provides details on clinical presentation, EEG features, treatment approaches, and prognosis.
This document provides an overview of various epilepsy syndromes classified by onset in the brain and cause of seizures. It describes several generalized and focal epilepsy syndromes including childhood absence epilepsy, juvenile myoclonic epilepsy, benign epilepsy with centrotemporal spikes, Panayiotopoulos syndrome, autosomal dominant nocturnal frontal lobe epilepsy, Doose's syndrome, Dravet's syndrome, infantile spasms/West syndrome, Lennox-Gastaut syndrome, and Ohtahara syndrome. For each syndrome, it covers key characteristics, EEG findings, treatment approaches, and typical prognosis.
1) Disorders of consciousness range from mild impairment to coma and include conditions like confusion, delirium, vegetative state, and brain death.
2) The pathophysiology of consciousness involves the ascending reticular activating system and connections between the brainstem and cortex. Loss of consciousness can result from disruption of these systems.
3) Etiologies of impaired consciousness and coma include infectious or inflammatory causes, structural abnormalities, and metabolic/toxic derangements. Common causes in children are infections, trauma, seizures, and metabolic disorders.
This document provides a summary of age dependent epileptic syndromes and focuses on primary generalized epilepsy and benign Rolandic epilepsy. It discusses the key characteristics of each condition including typical age of onset, common seizure types and EEG patterns. The summary concludes that these conditions are age determined and often seen in childhood, with seizures typically remitting by late adolescence.
This document provides an overview of evaluating the etiology of seizures. It discusses the initial evaluation steps, including distinguishing epileptic from non-epileptic events. It reviews diagnostic investigations like imaging, EEG, and bloodwork. Common structural etiologies and epilepsy syndromes are described. The document emphasizes performing a thorough history, physical exam, and targeted workup to identify underlying causes and guide treatment and prognosis.
Temporal lobe epilepsy (TLE) is characterized by recurrent seizures originating from the temporal lobe. Hippocampal sclerosis, involving cell loss in the hippocampus, is the most common pathological finding in TLE. Auras occur in about 80% of temporal lobe seizures and can involve somatosensory, special sensory, autonic, or psychic symptoms. Diagnostic workup involves brain imaging like MRI and PET, as well as EEG to identify abnormalities in the temporal lobe.
Temporal lobe epilepsy is one of the most common forms of epilepsy. It can be caused by hippocampal sclerosis or lesions in the temporal lobe. Hippocampal sclerosis involves neuronal loss and gliosis in the hippocampus and is the most common pathological finding in temporal lobe epilepsy patients. Interictal EEG findings like temporal intermittent rhythmic delta activity and temporal sharp waves help lateralize the seizure focus. Video EEG monitoring helps capture seizures and interictal discharges. Treatment involves antiepileptic drugs and potentially resective surgery for drug-resistant cases.
Disorders of consciousness can affect perception, attention, thinking, and orientation. There are three main types: dream-like changes where consciousness is lowered and hallucinations may occur; depressed consciousness where awareness is reduced; and restricted consciousness where awareness is narrowed to a few ideas. Specific disorders include delirium, characterized by cognitive impairment and fluctuating consciousness; confusion involving disorientation; and twilight states where consciousness is briefly interrupted. Qualitative changes in consciousness are important to understand for clinical and legal purposes.
Disorders of consciousness include coma, vegetative state, minimally conscious state, and locked-in syndrome. Coma is characterized by unarousable unresponsiveness, while the vegetative state involves spontaneous eye opening without purposeful responses. The minimally conscious state involves limited but meaningful responses. Locked-in syndrome involves quadriplegia with preserved consciousness. Evaluation of coma involves stabilization, history, exam including Glasgow Coma Scale, and testing of cranial nerves and motor/sensory function. Brain death criteria require demonstrating lack of brainstem and cortical function over an observation period.
Caring for patients who experience hallucinationsReenaDevgan
Hallucinations are sensory perceptions experienced without an external stimulus. They can affect any of the five senses and have various causes including neurological conditions, medications, drugs, and mental illnesses. Common types are auditory and visual hallucinations. The nurse's role is to assess the patient's needs, ensure safety, monitor for withdrawn behavior, and report any new problems while showing compassion. Guidelines recommend pharmacological and psychological interventions for managing conditions associated with hallucinations.
This document discusses seizure semiology and how symptoms can help localize seizure onset zones. It outlines various ictal symptoms including sensory phenomena, psychic manifestations, head and limb movements, eye movements, dystonic posturing, automatisms, behavioral changes, and autonomic symptoms. Each symptom is described and associated brain regions are provided to help lateralize or localize seizure onset. Diagnostic protocols for epilepsy rely on detailed analysis of clinical semiology through video-EEG monitoring combined with neuroimaging and other assessments.
This document summarizes different types of generalized epilepsies based on their EEG patterns and clinical presentations. It discusses primary generalized epilepsies, which have no identifiable cause and normal brain imaging. It also discusses more serious secondary generalized epilepsies, which are caused by diffuse brain injury and often associated with developmental delays. Specific syndromes like Lennox-Gastaut syndrome and West syndrome are examined in detail based on their characteristic EEG patterns including slow spike wave discharges, hypsarrhythmia, and independent multifocal spike discharges.
Epilepsy is defined as two or more unprovoked seizures and is caused by underlying brain dysfunction. It is a common neurological disease with varying prevalence worldwide. The causes of epilepsy are often unknown, though common causes in developed countries include cerebrovascular disease, tumors, alcohol use, and head trauma. Epilepsy results from an imbalance between excitation and inhibition in the brain, which can be caused by structural abnormalities. Diagnosis is based on eyewitness accounts of seizures, which can include generalized convulsions or localized symptoms. Investigations help characterize seizures and guide management.
This document discusses different types of brain waves seen on EEGs, including alpha, beta, theta, and delta waves. It then summarizes several common epilepsy syndromes such as benign centrotemporal lobe epilepsy of childhood, juvenile myoclonic epilepsy, autosomal dominant nocturnal frontal lobe epilepsy, Lennox-Gastaut syndrome, childhood absence epilepsy, and others. It provides examples of EEG findings associated with these conditions, such as Rolandic spikes, generalized spike and wave discharges, and hypsarrhythmic patterns.
The document summarizes a seminar on spinal cord syndromes presented by Teka Degefa. It discusses the anatomy of the spinal cord and outlines common spinal cord syndromes including complete spinal cord transection, ventral cord syndrome, Brown-Séquard syndrome, central spinal cord lesions, posterior and lateral column diseases, anterior horn cell syndromes, combined anterior horn cell and pyramidal tract disease, conus medullaris syndrome, and cauda equina syndrome. Objectives of the seminar were to discuss spinal cord anatomy, differentiate common syndromes, and learn how to evaluate patients with spinal lesions.
There are two main types of seizures - partial and generalized. Partial seizures originate in one area of the brain while generalized seizures affect the whole brain. Some specific childhood epilepsies discussed include benign Rolandic epilepsy, Rasmussen's syndrome, childhood absence epilepsy, myoclonic epilepsies, Lennox-Gastaut syndrome, West syndrome (infantile spasms), and Landau-Kleffner syndrome. Many childhood epilepsies have genetic components and vary in their symptoms, treatment response, and long-term prognosis.
Epilepsy syndromes can be categorized based on age of onset from neonates to childhood. Syndromes include self-limited, developmental and epileptic encephalopathies, and genetic generalized epilepsies. Syndromes are defined by seizure type, EEG findings, development, and treatment response/prognosis. Examples provided include benign familial neonatal epilepsy, Dravet syndrome, childhood absence epilepsy, Lennox-Gastaut syndrome, and Landau-Kleffner syndrome.
This document provides an overview of the approach to evaluating and diagnosing hypotonia in infants. It discusses the distinction between central and peripheral causes of hypotonia based on clinical features. The key steps in evaluation include obtaining a detailed history, performing a thorough physical exam to assess tone and weakness, and selecting initial investigations like CK levels and brain imaging. The most common etiologies of central hypotonia are hypoxic-ischemic injury and intraventricular hemorrhage in preterms. Common peripheral causes are spinal muscular atrophy and congenital myopathies. The goal of diagnosis is to identify life-threatening conditions, provide prognostic information, and guide further testing and management.
SISCOM may help differentiate PNES from epileptic seizures by showing changes in brain perfusion during seizures in epileptic seizures but not PNES. However, its diagnostic accuracy is limited and normal findings do not rule out epileptic seizures. Overall, EEG monitoring remains the gold standard for differentiating the two.
Alteration of consciousness can result from diminished alertness due to widespread brain abnormalities or reduced activity of the reticular activating system. Confusion is characterized by impaired attention/concentration and disorientation, while delirium involves additional symptoms like agitation, hallucinations, and convulsions. Levels of consciousness range from alert to comatose. Confusion can be caused by medical/surgical diseases, infections, drugs, or nervous system disorders and is evaluated through history, exam focusing on attentiveness/orientation, and controlling underlying illnesses. The Glasgow Coma Scale assesses eye, motor, and verbal responses to determine coma depth.
Approach to disturbance of consciousnessOsama Ragab
This document provides an overview of consciousness and approaches to disturbances of consciousness such as coma. It defines key terms like coma, stupor, and delirium. Coma can be caused by structural brain insults, metabolic derangements, infections, drugs or toxins. The clinical approach involves stabilizing vital functions, assessing severity using scales like Glasgow Coma Scale, and evaluating for immediate life-threatening causes through diagnostic tests and empirical treatment when needed to prevent further brain damage. A thorough neurological exam evaluates factors like consciousness level, pupil size and reactivity, ocular motility, motor responses and more to localize the cause. Distinguishing features between toxic/metabolic vs. structural comas are discussed.
This document discusses epileptic encephalopathies, which are a group of heterogeneous brain disorders occurring during brain development where epileptiform activity contributes to cognitive and behavioral regression beyond the underlying pathology. It defines and classifies several early-onset epileptic encephalopathy syndromes according to age of onset such as Ohtahara syndrome, early myoclonic encephalopathy, West syndrome, Dravet syndrome, Lennox-Gastaut syndrome, and myoclonic-astatic epilepsy. It provides details on clinical presentation, EEG features, causes, and treatment approaches for each condition.
This document discusses epilepsy and seizures. It defines seizures and epilepsy, describes different types of seizures including partial and generalized seizures. Common causes of epilepsy including strokes, brain injuries, tumors are mentioned. Management of seizures focuses on preventing injuries, identifying and removing seizure triggers, and treating with anti-seizure medications to control seizures. Nursing care revolves around safety during seizures, airway management, education, and supporting patients' psychosocial needs.
This document provides information on genetic epilepsy and juvenile myoclonic epilepsy. It defines epilepsy and describes its various classifications including idiopathic, symptomatic and cryptogenic epilepsy. Juvenile myoclonic epilepsy is discussed in detail, including its genetics, clinical manifestations such as myoclonic jerks and absence seizures, diagnosis through EEG findings, and treatment options involving anti-seizure medications. Circumstances for genetic testing in epilepsy cases are outlined.
This document discusses coma and disorders of consciousness. It defines coma as a state of unresponsiveness and unconsciousness, and notes that coma can be a medical emergency requiring intervention. The document outlines different levels of arousal from alert to coma and describes conditions like encephalopathy, locked-in syndrome, and persistent vegetative state. Causes of impaired consciousness discussed include alcohol, epilepsy, intoxication, trauma, infection, stroke, and hypoxia-ischemia. The Glasgow Coma Scale for assessing coma is also summarized.
Dizziness is a common complaint in older adults that increases in prevalence with age. It is a nonspecific term used to describe various sensations including vertigo, lightheadedness, and imbalance. Dizziness can be caused by disturbances in various body systems including the vestibular system, visual pathways, proprioceptive fibers, and brain. Common causes include benign positional vertigo, orthostatic hypotension, cerebrovascular disease, and medication side effects. A thorough history and physical exam is needed to evaluate dizziness due to its subjective nature and multiple potential causes.
This document discusses several epilepsy syndromes categorized by age of onset:
- Neonatal onset syndromes include benign neonatal seizures and early infantile epileptic encephalopathy.
- Infantile onset syndromes include Dravet syndrome, West syndrome, and myoclonic epilepsy in infancy.
- Childhood syndromes include Panayiotopoulos syndrome, Lennox-Gastaut syndrome, and benign epilepsy with centrotemporal spikes.
- Later onset syndromes extending into adolescence and adulthood include juvenile absence epilepsy and juvenile myoclonic epilepsy.
Dravet syndrome is a rare and severe form of epilepsy that begins in infancy. It is characterized by frequent febrile seizures in the first year of life followed by other types of seizures and developmental delays. Genetic testing reveals mutations in the SCN1A gene in many patients. Treatment involves medications like valproate and benzodiazepines as well as a ketogenic diet, but seizures often remain difficult to control. The prognosis includes permanent neurological and cognitive impairments.
Disorders of consciousness can affect perception, attention, thinking, and orientation. There are three main types: dream-like changes where consciousness is lowered and hallucinations may occur; depressed consciousness where awareness is reduced; and restricted consciousness where awareness is narrowed to a few ideas. Specific disorders include delirium, characterized by cognitive impairment and fluctuating consciousness; confusion involving disorientation; and twilight states where consciousness is briefly interrupted. Qualitative changes in consciousness are important to understand for clinical and legal purposes.
Disorders of consciousness include coma, vegetative state, minimally conscious state, and locked-in syndrome. Coma is characterized by unarousable unresponsiveness, while the vegetative state involves spontaneous eye opening without purposeful responses. The minimally conscious state involves limited but meaningful responses. Locked-in syndrome involves quadriplegia with preserved consciousness. Evaluation of coma involves stabilization, history, exam including Glasgow Coma Scale, and testing of cranial nerves and motor/sensory function. Brain death criteria require demonstrating lack of brainstem and cortical function over an observation period.
Caring for patients who experience hallucinationsReenaDevgan
Hallucinations are sensory perceptions experienced without an external stimulus. They can affect any of the five senses and have various causes including neurological conditions, medications, drugs, and mental illnesses. Common types are auditory and visual hallucinations. The nurse's role is to assess the patient's needs, ensure safety, monitor for withdrawn behavior, and report any new problems while showing compassion. Guidelines recommend pharmacological and psychological interventions for managing conditions associated with hallucinations.
This document discusses seizure semiology and how symptoms can help localize seizure onset zones. It outlines various ictal symptoms including sensory phenomena, psychic manifestations, head and limb movements, eye movements, dystonic posturing, automatisms, behavioral changes, and autonomic symptoms. Each symptom is described and associated brain regions are provided to help lateralize or localize seizure onset. Diagnostic protocols for epilepsy rely on detailed analysis of clinical semiology through video-EEG monitoring combined with neuroimaging and other assessments.
This document summarizes different types of generalized epilepsies based on their EEG patterns and clinical presentations. It discusses primary generalized epilepsies, which have no identifiable cause and normal brain imaging. It also discusses more serious secondary generalized epilepsies, which are caused by diffuse brain injury and often associated with developmental delays. Specific syndromes like Lennox-Gastaut syndrome and West syndrome are examined in detail based on their characteristic EEG patterns including slow spike wave discharges, hypsarrhythmia, and independent multifocal spike discharges.
Epilepsy is defined as two or more unprovoked seizures and is caused by underlying brain dysfunction. It is a common neurological disease with varying prevalence worldwide. The causes of epilepsy are often unknown, though common causes in developed countries include cerebrovascular disease, tumors, alcohol use, and head trauma. Epilepsy results from an imbalance between excitation and inhibition in the brain, which can be caused by structural abnormalities. Diagnosis is based on eyewitness accounts of seizures, which can include generalized convulsions or localized symptoms. Investigations help characterize seizures and guide management.
This document discusses different types of brain waves seen on EEGs, including alpha, beta, theta, and delta waves. It then summarizes several common epilepsy syndromes such as benign centrotemporal lobe epilepsy of childhood, juvenile myoclonic epilepsy, autosomal dominant nocturnal frontal lobe epilepsy, Lennox-Gastaut syndrome, childhood absence epilepsy, and others. It provides examples of EEG findings associated with these conditions, such as Rolandic spikes, generalized spike and wave discharges, and hypsarrhythmic patterns.
The document summarizes a seminar on spinal cord syndromes presented by Teka Degefa. It discusses the anatomy of the spinal cord and outlines common spinal cord syndromes including complete spinal cord transection, ventral cord syndrome, Brown-Séquard syndrome, central spinal cord lesions, posterior and lateral column diseases, anterior horn cell syndromes, combined anterior horn cell and pyramidal tract disease, conus medullaris syndrome, and cauda equina syndrome. Objectives of the seminar were to discuss spinal cord anatomy, differentiate common syndromes, and learn how to evaluate patients with spinal lesions.
There are two main types of seizures - partial and generalized. Partial seizures originate in one area of the brain while generalized seizures affect the whole brain. Some specific childhood epilepsies discussed include benign Rolandic epilepsy, Rasmussen's syndrome, childhood absence epilepsy, myoclonic epilepsies, Lennox-Gastaut syndrome, West syndrome (infantile spasms), and Landau-Kleffner syndrome. Many childhood epilepsies have genetic components and vary in their symptoms, treatment response, and long-term prognosis.
Epilepsy syndromes can be categorized based on age of onset from neonates to childhood. Syndromes include self-limited, developmental and epileptic encephalopathies, and genetic generalized epilepsies. Syndromes are defined by seizure type, EEG findings, development, and treatment response/prognosis. Examples provided include benign familial neonatal epilepsy, Dravet syndrome, childhood absence epilepsy, Lennox-Gastaut syndrome, and Landau-Kleffner syndrome.
This document provides an overview of the approach to evaluating and diagnosing hypotonia in infants. It discusses the distinction between central and peripheral causes of hypotonia based on clinical features. The key steps in evaluation include obtaining a detailed history, performing a thorough physical exam to assess tone and weakness, and selecting initial investigations like CK levels and brain imaging. The most common etiologies of central hypotonia are hypoxic-ischemic injury and intraventricular hemorrhage in preterms. Common peripheral causes are spinal muscular atrophy and congenital myopathies. The goal of diagnosis is to identify life-threatening conditions, provide prognostic information, and guide further testing and management.
SISCOM may help differentiate PNES from epileptic seizures by showing changes in brain perfusion during seizures in epileptic seizures but not PNES. However, its diagnostic accuracy is limited and normal findings do not rule out epileptic seizures. Overall, EEG monitoring remains the gold standard for differentiating the two.
Alteration of consciousness can result from diminished alertness due to widespread brain abnormalities or reduced activity of the reticular activating system. Confusion is characterized by impaired attention/concentration and disorientation, while delirium involves additional symptoms like agitation, hallucinations, and convulsions. Levels of consciousness range from alert to comatose. Confusion can be caused by medical/surgical diseases, infections, drugs, or nervous system disorders and is evaluated through history, exam focusing on attentiveness/orientation, and controlling underlying illnesses. The Glasgow Coma Scale assesses eye, motor, and verbal responses to determine coma depth.
Approach to disturbance of consciousnessOsama Ragab
This document provides an overview of consciousness and approaches to disturbances of consciousness such as coma. It defines key terms like coma, stupor, and delirium. Coma can be caused by structural brain insults, metabolic derangements, infections, drugs or toxins. The clinical approach involves stabilizing vital functions, assessing severity using scales like Glasgow Coma Scale, and evaluating for immediate life-threatening causes through diagnostic tests and empirical treatment when needed to prevent further brain damage. A thorough neurological exam evaluates factors like consciousness level, pupil size and reactivity, ocular motility, motor responses and more to localize the cause. Distinguishing features between toxic/metabolic vs. structural comas are discussed.
This document discusses epileptic encephalopathies, which are a group of heterogeneous brain disorders occurring during brain development where epileptiform activity contributes to cognitive and behavioral regression beyond the underlying pathology. It defines and classifies several early-onset epileptic encephalopathy syndromes according to age of onset such as Ohtahara syndrome, early myoclonic encephalopathy, West syndrome, Dravet syndrome, Lennox-Gastaut syndrome, and myoclonic-astatic epilepsy. It provides details on clinical presentation, EEG features, causes, and treatment approaches for each condition.
This document discusses epilepsy and seizures. It defines seizures and epilepsy, describes different types of seizures including partial and generalized seizures. Common causes of epilepsy including strokes, brain injuries, tumors are mentioned. Management of seizures focuses on preventing injuries, identifying and removing seizure triggers, and treating with anti-seizure medications to control seizures. Nursing care revolves around safety during seizures, airway management, education, and supporting patients' psychosocial needs.
This document provides information on genetic epilepsy and juvenile myoclonic epilepsy. It defines epilepsy and describes its various classifications including idiopathic, symptomatic and cryptogenic epilepsy. Juvenile myoclonic epilepsy is discussed in detail, including its genetics, clinical manifestations such as myoclonic jerks and absence seizures, diagnosis through EEG findings, and treatment options involving anti-seizure medications. Circumstances for genetic testing in epilepsy cases are outlined.
This document discusses coma and disorders of consciousness. It defines coma as a state of unresponsiveness and unconsciousness, and notes that coma can be a medical emergency requiring intervention. The document outlines different levels of arousal from alert to coma and describes conditions like encephalopathy, locked-in syndrome, and persistent vegetative state. Causes of impaired consciousness discussed include alcohol, epilepsy, intoxication, trauma, infection, stroke, and hypoxia-ischemia. The Glasgow Coma Scale for assessing coma is also summarized.
Dizziness is a common complaint in older adults that increases in prevalence with age. It is a nonspecific term used to describe various sensations including vertigo, lightheadedness, and imbalance. Dizziness can be caused by disturbances in various body systems including the vestibular system, visual pathways, proprioceptive fibers, and brain. Common causes include benign positional vertigo, orthostatic hypotension, cerebrovascular disease, and medication side effects. A thorough history and physical exam is needed to evaluate dizziness due to its subjective nature and multiple potential causes.
This document discusses several epilepsy syndromes categorized by age of onset:
- Neonatal onset syndromes include benign neonatal seizures and early infantile epileptic encephalopathy.
- Infantile onset syndromes include Dravet syndrome, West syndrome, and myoclonic epilepsy in infancy.
- Childhood syndromes include Panayiotopoulos syndrome, Lennox-Gastaut syndrome, and benign epilepsy with centrotemporal spikes.
- Later onset syndromes extending into adolescence and adulthood include juvenile absence epilepsy and juvenile myoclonic epilepsy.
Dravet syndrome is a rare and severe form of epilepsy that begins in infancy. It is characterized by frequent febrile seizures in the first year of life followed by other types of seizures and developmental delays. Genetic testing reveals mutations in the SCN1A gene in many patients. Treatment involves medications like valproate and benzodiazepines as well as a ketogenic diet, but seizures often remain difficult to control. The prognosis includes permanent neurological and cognitive impairments.
Epilepsy is a chronic neurological disorder characterized by recurrent seizures. Around 50 million people worldwide have epilepsy, with nearly 90% living in developing regions. Epilepsy can often be controlled with anti-epileptic drug treatment, though many in developing areas lack access to treatment. Seizures have various clinical manifestations depending on their location and spread in the brain. Diagnosis is based on the characteristics of seizures, though tests like EEG and MRI can provide additional information. Treatment involves lifestyle management of seizures and long-term use of anti-epileptic drugs to control seizures, with slow titration and withdrawal of drugs to avoid adverse effects.
Dr Nivedita Bajaj - Basic Facts About Childhood EpilepsyNiveditabajaj
The basics Epilepsy by Dr Nivedita Bajaj , She is a Consultant Paediatrician working within NHS, currently employed by East and North Herts NHS Trust. Dr Bajaj has extensive experience in assessment and management of a wide range of neurodevelopmental conditions and neurodiabilities. She leads clinical autism service in her trust.
Visit - https://drniveditabajaj.blogspot.co.uk/
For more - https://www.nhs.uk/profiles/consultant/6068845
Read More - https://about.me/drniveditabajaj
Overview of neonatal epilepsy syndromes.pptxphilipolielo1
This document provides an overview of several neonatal epilepsy syndromes:
1) Self-limited neonatal epilepsy is characterized by focal tonic seizures in the first weeks that resolve by 6 months, caused by genes KCNQ2 and KCNQ3.
2) Early infantile developmental and epileptic encephalopathy includes Ohtahara syndrome and early myoclonic encephalopathy, presenting with severe, intractable seizures in the first months associated with developmental impairment.
3) Pyridoxine-dependent and pyridoxamine 5'-phosphate oxidase deficiency developmental and epileptic encephalopathy cause seizures beginning prenatally or at birth responsive to pyridoxine/pyridoxamine
This document provides an overview of epilepsy, including its epidemiology, classification, causes, pathophysiology, investigations, management, and social considerations. Some key points:
- Epilepsy affects approximately 5% of children and less than 1% have epilepsy. The incidence is highest in pre-school years. Causes include genetic factors, injuries, infections, tumors, and other structural brain abnormalities.
- Seizures are classified based on their origin in the brain as generalized or localized/partial. Generalized seizures involve both sides of the brain while partial seizures originate in one area.
- Management involves drug therapy with anti-epileptic medications as first-line treatment, as well as lifestyle modifications and
This document discusses various types of seizures that can occur in children. It describes how seizures may be localized to one part of the body or widespread. Seizures in newborns and toddlers can present differently. Characteristics of seizures include abrupt onset, brief duration, altered mental status and postictal state. Causes of seizures in children include infections, developmental problems, head trauma and unknown causes. The most common type is febrile seizures associated with fever. Other causes, treatments, and types like tonic, clonic, absence and myoclonic seizures are outlined as well. Status epilepticus and its management are also discussed.
Dr. Shamanthakamani Narendran provides an overview of epilepsy, including its definition, classification, causes, diagnosis, treatment, and management. Epilepsy is a chronic neurological condition characterized by recurrent seizures and affects approximately 50 million people worldwide. It is usually controlled through medication, though not cured. The causes can be genetic, due to injury or illness, or idiopathic. Treatment involves medication to prevent or reduce seizures, and in some cases surgery may be an option.
This document provides an overview of epilepsy including:
- Epilepsy is a chronic neurological condition characterized by recurrent seizures and affects around 50 million people worldwide.
- Seizures have various classifications based on factors like location in the brain, observable manifestations, underlying medical conditions, and triggers.
- Epilepsy is typically diagnosed and managed through medication but may also involve lifestyle changes, surgery, dietary therapies, or vagus nerve stimulation in some cases.
- The causes can be genetic, due to brain injury or infection, and in some cases the cause is unknown. Proper response in an emergency involves preventing injury and calling for help for prolonged seizures.
It contains description and salient points to diagnose various epileptic encephalopathies seen during infancy such as early myoclonic encephalopathies, Otahara syndrome, Dravet syndrome, West syndrome.
This document discusses various epileptic syndromes categorized by age of onset - infantile, childhood, adolescent. Key syndromes described in detail include West syndrome, Dravet syndrome, GEFS+, Panayiotopoulos syndrome, Benign epilepsy with centrotemporal spikes, Electrical status epilepticus in slow sleep, Myoclonic-atonic epilepsy, Lennox-Gastaut syndrome. For each syndrome, the document outlines clinical features, investigations such as common EEG findings and genetic causes, treatment approaches, and typical prognosis.
This document discusses various epileptic syndromes categorized by age of onset - infantile, childhood, adolescent. Key syndromes described in detail include West syndrome, Dravet syndrome, GEFS+, Panayiotopoulos syndrome, Benign epilepsy with centrotemporal spikes, Electrical status epilepticus in slow sleep, Myoclonic-atonic epilepsy, Lennox-Gastaut syndrome. For each syndrome, the document outlines clinical features, investigations such as common EEG findings and genetic causes, treatment approaches, and typical prognosis.
This CME presentation on epilepsy provided an overview of the disorder, including definitions, epidemiology, pathophysiology, classification, diagnosis, and management. Some key points included:
- Epilepsy is one of the most common neurological disorders worldwide, affecting over 50 million people.
- It is characterized by recurrent seizures that can be focal or generalized.
- Evaluation involves a detailed history, physical exam, EEG, and neuroimaging to determine the underlying cause and guide treatment.
- Management consists of pharmacotherapy with antiepileptic drugs as first-line treatment. For refractory cases, surgical options like resection or vagus nerve stimulation may be considered.
The document discusses convulsive disorders in children, including febrile seizures and epilepsy. It defines febrile seizures as seizures precipitated by fever between 6 months and 6 years of age. Epilepsy is defined as recurring seizures that can be classified as partial or generalized. Diagnostic procedures and treatment principles for seizures are also outlined.
Temporal lobe epilepsy is characterized by seizures originating in the temporal lobe. It is the most common localization-related epilepsy, accounting for around 60% of such cases. Mesial temporal lobe epilepsy is the most frequent form, often caused by hippocampal sclerosis. Auras are common and can include epigastric sensations, cephalic sensations, anxiety, hallucinations and more. Automatisms like lip smacking or gesturing often occur during seizures. Around 60% of temporal lobe epilepsy patients respond well to antiepileptic drug treatment, while the remaining 40% have drug-resistant epilepsy and may require surgery.
This document discusses mesial temporal sclerosis, a common cause of temporal lobe epilepsy. It presents a case of a 23-year old woman with intractable seizures beginning with an odd smell and staring spells. Mesial temporal lobe epilepsy often begins in late adolescence/early adulthood and can be caused by hippocampal sclerosis or other lesions. Clinical features include auras and seizures characterized by automatisms or dystonic posturing localized to the affected temporal lobe. EEGs show interictal temporal spikes maximum over the affected side while ictal patterns involve rhythmic activity spreading within and between temporal lobes. MRI is used to identify hippocampal sclerosis or other lesions as the cause of seizures.
This document discusses neonatal seizures, including their causes, types, diagnosis, treatment and prognosis. Some key points:
- Neonatal seizures are caused by metabolic disturbances, toxins, structural abnormalities or infections. They present differently than in older children or adults due to incomplete brain development in newborns.
- There are several recognized seizure types in newborns, including focal, multifocal, tonic, myoclonic and subtle seizures. EEG is used to classify seizures as clinical-EEG correlated, clinical-EEG uncorrelated or electrical-only seizures.
- Common etiologies of neonatal seizures include hypoxic ischemic encephalopathy, intracranial hemorrhage, and various metabolic
Guillain-Barré syndrome is an autoimmune disorder that causes inflammation of the nerves. It is often triggered by a bacterial or viral infection. The main symptoms are progressive weakness in the legs and arms, loss of reflexes, and ascending paralysis. Diagnosis involves examining CSF, nerve conduction tests, and ruling out other causes. Treatment for severe cases includes IVIG or plasmapheresis. Most patients recover fully, but some have long-term weakness or paralysis if respiratory muscles are affected.
Similar to Neurology: Bening Rolandic Epilepsy (20)
Comparing the Coronavirus pandemic in New Zealand and Iraq: A Preventive Medi...Vedica Sethi
The first cases of COVID-19 pandemic were identified in people with pneumonia in Wuhan, China, in late December 2019. It is first and foremost the most publicized pandemic, which has taken the lives of many people. It has thrown everyone into doubt and has created a collective moment of contemplation about the future. The clinical enlistment organization MedWorld of New Zealand offered for resigned and low maintenance specialists to help endeavors by the health care division and Government to battle the spread of COVID-19, in New Zealand. ( ) Starting in April, more than 20,000 tests have been done in Iraq in general (counting the Kurdistan Region), with 1202 of them turning out positive. Of those tests, half of the,m were finished by the Kurdish Ministry of Health, which implies that the other tests were finished by the Iraqi Ministry of Health. ( ) While KRG populace has been tried, just 0.05% of the remainder of the nation has been tried, along these lines featuring the conceivable difference between absolute positive case numbers between locales. Iraq is considered "particularly powerless against the plague due to being desolated" – by war and United Nations sanctions, and by partisan clash in the course of recent decades.
This paper primarily focuses on analyzing the accessible information through research papers, peer- reviewed and non-peer reviewed to understand the pandemic affecting two different countries like New Zealand- a developed country and Iraq- a developing country.
HEALTH INSURANCE PROVIDED BY GOVERNMENT VS PRIVATE SECTOR IN INDIAVedica Sethi
Healthcare is significant for each individual on the planet, on account of this each nation should focus on wellbeing, because of increment pace of sickness and ailments.
In India medical coverage part is an undiscovered market, still it has crying needs. There is colossal potential for this part. The medical coverage suppliers are not satisfying this interest. After 1999 the privatization of protection area, the protection segment has developed in past decade. By and by there are 25 medical coverage suppliers, in that four are with open area and twenty one private medical coverage suppliers. The piece of the overall industry of open segment is 60 rates while the rest with other private players.
This paper inspects the present status of medical coverage in India, advancement in health care coverage area and difficulties looked by it. It additionally investigates the job of both open and private medical coverage players to arrive at most extreme inclusion in health care coverage.
The document summarizes key aspects of CRISPR genome editing technology. It describes how CRISPR uses Cas9 and guide RNA to precisely target and edit DNA sequences. It provides a brief history of CRISPR discovery and outlines its components and mechanism of action. The document also discusses several medical applications of CRISPR including treating Duchenne muscular dystrophy, beta-thalassemia, and testing for viruses. It concludes that CRISPR is a flexible and accurate gene editing tool being explored for various applications in agriculture, biotechnology, and medicine.
Coronavirus: medical management in a developed country that is china versus a...Vedica Sethi
The systemic review has focused on to compare the available treatment options applied by China and India to manage the current pandemic situation, in their respective countries.
Australia vs India: Health care insuranceVedica Sethi
Health care insurance: A Comparative overview.
The retrospective review focuses on the timeline of Healthcare systems and development of Healthcare Insurance policies of India and Australia. The review also includes
the consensus and impact of Healthcare legislature in India and Australia and offers a
comparison to the development in the BRICS countries.
Abstract: Uremia is a clinical manifestation of chronic kidney failure (CKD) and is defined as the elevation of urea levels in plasma associated to fluid, electrolytes and hormonal imbalances and metabolic abnormalities. Uremia even though arises from CKD, it can also occur with Acute Kidney injury (AKI). The terms uremia was first coined by Piorry which translates to urine in blood. Also, Uremia and uremic syndrome have been used interchangeably for a long time. Comparatively, Azotemia is also uremia but the only difference is that the urea elevation in azotemia is not high enough to have manifesting signs or symptoms. Thus, Uremia is pathological and symptomatic manifestations of severe azotemia.
Urea itself has direct and indirect toxic effects on our body; parathyroid hormone (PTH), beta2 microglobulin, polyamines, advanced glycosylation end products, and other middle molecules, are thought to contribute to the clinical syndrome. Patient’s symptoms range from mild bleeds to severe congestive heart failure. If left untreated complications include seizure, coma, cardiac arrest, and death. He most severe is cardiac arrest secondary to electrolyte abnormalities such as hyperkalemia, metabolic acidosis, or hypocalcemia. The patients, who are diabetic, tend to develop severe hypoglycemic reactions if the medications are not adjusted for creatinine clearance. Renal failure and renal osteodystrophy may cause early onset osteoporosis or formation of adynamic bone which predisposes the patient to fractures on mild trauma. Also medications the patient was previously on can lead to unwanted side effects due to impaired clearance e.g. Digoxin toxicity secondary to renal failure, increased sensitivity to narcotics.
Key Words: Uremia, Uremic syndrome, Chronic kidney failure, azotemia, beta 2 microglobulins, congestive heart failure, electrolyte abnormalities, hyperkalemia, hyocalcemia, metabolic acidosis, creatinine, osteodystrophy
Postexposure prophylaxis after needle sticks injuryVedica Sethi
Needle stick injury is defined as penetration of skin by a needle or other sharp object that has been in contact with blood products, tissue or any other body fluids before exposure. Even though the effect is negligible, it predisposes the patient to occupational exposure of human immunodeficiency virus (HIV), hepatitis B virus (HVB), and hepatitis C Virus (HVC). ( ) The most common population to be affected is health care workers and lab personnel. The occupational exposure of such viruses is not only transmission via needle stick injury but also via contamination of mucous membranes e.g. eyes, blood or body fluids, even though needle stick injuries make up the majority of all percutaneous exposure cases. Other occupations with increased risk of needle stick injury are tattoo artists, agriculture workers, law enforcement workers, and laborers. ( )
Recognizing the occupational hazard posed by needle stick injury and the long term effect it could have on a health care worker is the most important need, with developing interventions to minimize it.
Abstract Lung Abscess is a liquefactive necrosis of the lung tissue and arrangement of cavitation (in excess of 2 cm) containing necrotic debris and liquid brought about by parenchymal infection. It very well may be brought about by yearning, which may happen during changed cognizance and it for the most part causes a discharge filled depression. In addition, liquor addiction is the most widely recognized condition inclining to lung abscesses. Lung abscess is viewed as essential (60%) when it comes about because of existing lung parenchymal process and is named auxiliary when it entangles another procedure, e.g., vascular emboli or follows rupture of extrapulmonary abscess into lung. There are a few imaging strategies which can distinguish the material inside the thorax, for example, electronic tomography (CT) output of the thorax and ultrasound of the thorax. Broad Spectrum anti-biotics to cover blended vegetation is the pillar of treatment. Pneumonic physiotherapy and postural drainage are additionally significant. Surgeries are required in specific patients for pneumonic resection Keywords: Lung abscess, anti-bodies, video-assissted thoracoscopic medical procedure (VATS), thoracoscopy
Abstract Transplant- associated Thrombotic Microangiopathy (TA- TMA) is a hematopoietic disorder that leads to inflammatory and thrombotic changes of microvasculature with associated hemolytic anemia, thrombocytopenia and organ failure i.e. acute renal failure. This syndrome is visualized more commonly in allogeneic hematopoietic stem cell transplants (HSCTs) compared to autologous transplant. TA- TMA offers a diagnostic challenge as it can’t be categorized in the two most recognized TMA’s i.e. Atypical Hemolytic Uremic Syndrome (aHUS) or Thrombotic Thrombocytopenic Purpura (TTP). Despite the fact, that the patient receiving the transplant might face complications associated with the transplant i.e. infection, graft-versus-host disease (GVHD) , and disseminated intravascular coagulation (DIC), as well as the side effects of immunosuppressive drugs, all of which can be misdiagnosed as TMA. Since, the pathophysiology of this syndrome is not understood; management of the syndrome is suboptimal with a high mortality rate. A recent study of TA-TMA patients has identified the patients diagnosed with TA-TMA lack suppression of ADAMTS13 which is a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 1 and do not have a complete response to plasma exchange, thus indicating characteristics a TTP-like disorder is not involved. Recent advances in the treatment of aHUS may offer a therapeutic option in the aHUS-like TMAs associated with HSCTs, which still faces the difficulties associated with the diagnosis and treatment of TA-TMA. Keywords: Transplant- associated Thrombotic Microangiopathy (TA- TMA), hematopoetic, hemolytic anemia, thrombocytopenia, acutre renal failure, Atypical Hemolytic Uremic Syndrome (aHUS), Thrombotic Thrombocytopenic Purpura (TTP), graft-versus-host disease (GVHD) , disseminated intravascular coagulation (DIC)
Cardiology: Treatment of Heart FailureVedica Sethi
Abstract Heart Failure (HF) is the most widely recognized cardiovascular disorder behind medical clinic affirmation for individuals more established than 60 years old. Hardly any regions in medication have advanced as surprisingly as HF treatment in the course of recent decades. Be that as it may, progress has been reliable just for ceaseless HF with diminished discharge part. In intensely decompensated HF and HF with safeguarded discharge part, none of the medications tried to date have been conclusively demonstrated to improve endurance. Deferring or forestalling HF has gotten progressively significant in patients who are inclined to HF. The anticipation of declining interminable HF and hospitalisations for intense decompensation is likewise critical. The target of this paper is to give a compact and down to earth rundown of the accessible medication medicines for HF. The most ideal proof based medication treatment (counting inhibitors of the renin–angiotensin– aldosterone framework and β blockers) is helpful just when ideally actualized. Notwithstanding, usage may be testing. To accept that ailment the executives projects can be useful in giving a multidisciplinary, comprehensive way to deal with the conveyance of ideal clinical consideration. Keywords; heart failure, multidisciplinary approach, Beat-blocker, RAAS framework
Surgical vs Conservative Management of Colonic DiverticulitisVedica Sethi
The document summarizes the treatment options for colonic diverticulitis, including conservative, medical, and surgical approaches. Conservative treatment involves antibiotics, bed rest, and fluid diets for uncomplicated cases. Medical management uses antibiotics both as outpatient treatment for mild cases or inpatient IV antibiotics for severe cases. Surgical options include resection of the affected colon either with or without anastomosis, with laparoscopic procedures becoming more common due to lower complication rates. While guidelines favor initially conservative approaches, optimal treatment remains complex and individualized based on each patient's presentation and risk factors.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
DECLARATION OF HELSINKI - History and principlesanaghabharat01
This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
Co-Chairs, Val J. Lowe, MD, and Cyrus A. Raji, MD, PhD, prepared useful Practice Aids pertaining to Alzheimer’s disease for this CME/AAPA activity titled “Alzheimer’s Disease Case Conference: Gearing Up for the Expanding Role of Neuroradiology in Diagnosis and Treatment.” For the full presentation, downloadable Practice Aids, and complete CME/AAPA information, and to apply for credit, please visit us at https://bit.ly/3PvVY25. CME/AAPA credit will be available until June 28, 2025.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
low birth weight presentation. Low birth weight (LBW) infant is defined as the one whose birth weight is less than 2500g irrespective of their gestational age. Premature birth and low birth weight(LBW) is still a serious problem in newborn. Causing high morbidity and mortality rate worldwide. The nursing care provide to low birth weight babies is crucial in promoting their overall health and development. Through careful assessment, diagnosis,, planning, and evaluation plays a vital role in ensuring these vulnerable infants receive the specialize care they need. In India every third of the infant weight less than 2500g.
Birth period, socioeconomical status, nutritional and intrauterine environment are the factors influencing low birth weight
Summer is a time for fun in the sun, but the heat and humidity can also wreak havoc on your skin. From itchy rashes to unwanted pigmentation, several skin conditions become more prevalent during these warmer months.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. Bening Rolandic Epilepsy
2
Table of Contents:
1. Abstract
2. What is Benign Rolandic epilepsy?
3. Signs and symptoms
4. Causes
5. Diagnosis
6. Differential Diagnosis
7. Treatment
8. Prognosis
9. Epidemiology
10. References
3. Bening Rolandic Epilepsy
3
1.Abstract
Benign rolandic epilepsy or Bening epilepsy of childhood with centro-temporal spikes
(BECT) is the most widely recognized epilepsy disorder in the pediatric age group, with
a beginning between age 3 and 13 years. The average introduction is a fractional
seizure with parasthesias and tonic or clonic action of the lower face related with
drooling and dysarthria. Seizures regularly happen around evening time and may turn
out to be generalized. They are typically rare and may not require antiepileptic
medicates in any case, whenever treated, they will in general be effectively controlled.
Youngsters with BECT are neurologically and psychologically normal. The EEG shows
trademark high-voltage sharp waves in the centro-temporal districts, which are
enacted with sleepiness and rest. Right now, BECT is effectively perceived. Be that as it
may, atypical cases are normal and the meaning of BECT can get obscured. Albeit
further examinations are not required in cases with common clinical and EEG
discoveries and typical neurologic assessments, neuro-imaging studies might be
required in atypical cases to preclude other pathology. The long-term. medical and
psychosocial forecast of BECT is magnificent, with basically all children entering long-
term remission by mid-adolescene.
Key Words: Centrotemporal-Benign rolandic epilepsy of childhood.
4. Bening Rolandic Epilepsy
4
2. What is Bening Rolandic Epilepsy?
The primary instance of bening rolandic epilepsy (BECT) was depicted by
Martinus Rulandus [1] in the 16th century, the particular electrographic and
clinical highlights have just been perceived during the previous 40 years.
Gastaut [2] gave the underlying depiction of the electrographic includes in
1952, and perceived that these "pre-rolandic" spikes were inconsequential to
central pathology. Gibbs [3], in 1954 remarked that Rolandic epilepsy might be
seen without clinical seizures. In 1958, Nayrac and Beaussart [4] depicted the
clinical indications of Rolandic epilepsy with centro-temporal spikes (BECT), in
view of their investigation of 21 cases. Good prognosis for this epileptic
disorder, contrasted with the poor result in psychomotor epilepsy, was
perceived early.
In spite of the fact that BECT is effortlessly perceived in its pure structure,
atypical features are normal. In cases that are marginally atypical, the analysis
can in any case be acknowledged. In any case, when major or a few minor
atypical highlights are available, the meaning of BECT can turn out to be very
doubtful. The finding is frequently made reflectively, simply after these cases
are followed for quite a long while until abatement happens. [5][6]
As mentioned, Bening Rolandic epilepsy or bening epilepsy of childhood with
centro-temporal spikes (BCECTS) is the most well-known epilepsy disorder in
childhood. Most youngsters will grow out of the disorder (it begins around the
age of 3–13 with a top around 8–9 years and stops around age 14–18),
subsequently the mark considerate. The seizures, in some cases alluded to as
sylvian seizures, start around the focal sulcus of the brain, also called as the
1 van Huffelen, “A Tribute to Martinus Rulandus. A 16th-Century Description of Benign Focal
Epilepsy of Childhood.”
2 Gibbs and Gibbs, “Good Prognosis of Mid-Temporal Epilepsy.”
3 Lombroso, “Sylvian Seizures and Midtemporal Spike Foci in Children.”
4 Panayiotopoulos, A Clinical Guide to Epileptic Syndromes and Their Treatment.
5 Lombroso, “Sylvian Seizures and Midtemporal Spike Foci in Children.”
6 Gibbs and Gibbs, “Good Prognosis of Mid-Temporal Epilepsy.”
5. Bening Rolandic Epilepsy
5
centro-temporal region, situated around the Rolandic gap, is named after after
Luigi Rolando.[7]
3. Signs and Symptoms
The cardinal highlights of Rolandic epilepsy are rare, frequently solitary, central
seizures comprising of:
a. unilateral facial sensorimotor symptoms (30% of patients)
b. oropharyngolaryngeal manifestations (53% of patients)
c. speech arrest (40% of patients), and
d. hypersalivation (30% of patients) [8][9][10][11][12][13][14][15]
1. Hemifacial sensorimotor seizures:
localised in the lower lip or spread to the ipsilateral hand.
Motor signs are abrupt, nonstop or explosions of clonic compressions,
normally enduring from a couple of moments to a moment.
Ipsilateral tonic deviation of the mouth
Hemifacial tactile side effects comprise of ipsilateral numbness.
Hemifacial seizures are often associated with an inability to speak and
hypersalivation.
Negative myoclonus can be observed in some cases, as an interruption
of tonic muscular activity
2. Oropharyngolaryngeal ictal manifestations
unilateral sensorimotor symptoms inside the mouth Numbness, and more
commonly paraesthesias (tingling, prickling, freezing), are usually diffuse
on one side or, exceptionally, may be highly localised even to one tooth.
7 “Childhood Epilepsy with Centro-Temporal Spikes | Epilepsy Action.”
8 “Rolandic Epilepsy.”
9 Beaussart, “Benign Epilepsy of Children with Rolandic (Centro-Temporal) Paroxysmal Foci A
Clinical Entity. Study of 221 Cases.”
10 Beaussart.
11 Lerman and Kivity, “Benign Focal Epilepsy of Childhood.”
12 Panayiotopoulos, Benign Childhood Partial Seizures and Related Epileptic Syndromes.
13 Roger, Epileptic Syndromes in Infancy, Childhood and Adolescence.
14 Roger.
15 Panayiotopoulos et al., “Benign Childhood Focal Epilepsies.”
6. Bening Rolandic Epilepsy
6
Motor oropharyngolaryngeal symptoms produce strange sounds, such as
death rattle, gargling, grunting and guttural sounds, and combinations:
3. Arrest of speech is a form of anarthria; The child can't articulate a
solitary coherent word and endeavors to speak with motions or gestures.
4. Hypersalivation, is frequently connected with hemifacial seizures,
oro-pharyngo-laryngeal manifestations and discourse capture.
5. Syncope-like epileptic seizures may occur, probably as a concurrent
symptom of Panayiotopoulos syndrome.
6. Consciousness and recollection are fully retained in more than half
(58%) of Rolandic seizures. In the remainder (42%), consciousness
becomes impaired during the ictal progress and in one third there is no
rmemory of ictal events.
7. Progression to hemiconvulsions or generalised tonic-clonic
seizures Movement to hemiconvulsions or summed up tonic-clonic
seizures happens in around half of youngsters and hemiconvulsions
might be trailed by postictal Todd's hemiparesis.
8. Duration and circadian distribution: Rolandic seizures are typically
concise, going on for 1–3 minutes. Seventy five percent of seizures
happen during non-quick eye development rest, fundamentally at rest
beginning or not long before arousing.
9. Status epilepticus:
Although rare, focal motor status or hemiconvulsive status
epilepticus is more likely to occur than secondarily generalised
convulsive status epilepticus, which is exceptional.[16][17]
Opercular status epilepticus might be incited via
carbamazepine or lamotrigine. by carbamazepine or
lamotrigine.
The state lasts for hours to months and consists of ongoing
unilateral or bilateral contractions of the mouth, tongue or
eyelids, positive or negative subtle perioral or other
16 Deonna, Ziegler, and Despland, “Combined Myoclonic-Astatic And.”
17 “Atypical Evolutions of Benign Localization‐Related Epilepsies in Children: Are They
Predictable? - Fejerman - 2000 - Epilepsia - Wiley Online Library.”
7. Bening Rolandic Epilepsy
7
myoclonus, dysarthria, speech arrest, difficulties in
swallowing, buccofacial apraxia and hypersalivation.
These are often associated with continuous spikes and
waves on an EEG during NREM sleep.
10. Other seizure types: Despite noticeable hypersalivation,
central seizures with essentially autonomic signs (autonomic
seizures) are not viewed as a major aspect of the center clinical
disorder of Rolandic epilepsy. Notwithstanding, a few kids may
give autonomous autonomic seizures or seizures with blended
Rolandic-autonomic signs incorporating emesis as in
Panayiotopoulos disorder. [18][19]
11. Atypical forms: Rolandic epilepsy may present with atypical
manifestations such early age at onset, developmental delay or
learning difficulties at inclusion, other seizure types, atypical EEG
abnormalities.[20][21][22] These children usually have normal
intelligence and development.[23] Learning can remain unimpaired
while a child is afflicted with Rolandic epilepsy.
18 Caraballo, Cersósimo, and Fejerman, “Panayiotopoulos Syndrome.”
19 Specchio et al., “Panayiotopoulos Syndrome.”
20 “Benign Rolandic Epilepsy: Atypical Features Are Very Common - Elaine C. Wirrell, Peter R.
Camfield, Kevin E. Gordon, Joseph M. Dooley, Carol S. Camfield, 1995.”
21 “Atypical Presentations of Benign Childhood Epilepsy With Centrotemporal Spikes: A Review -
Uri Kramer, 2008.”
22 “Benign Rolandic Epilepsy: Atypical Features Are Very Common - Elaine C. Wirrell, Peter R.
Camfield, Kevin E. Gordon, Joseph M. Dooley, Carol S. Camfield, 1995.”
23 Wirrell, “Benign Epilepsy of Childhood With Centrotemporal Spikes.”
8. Bening Rolandic Epilepsy
8
4. Causes
Genetic factors:
Benign epilepsy with centrotemporal spikes is thought to be a genetic disorder.
An autosomal dominant inheritance with age dependency and variable
penetrance has been reported, although not all studies support this theory.
[24][25]
Linkage considers have highlighted a potential weakness district on
chromosome 15q14, in the region of the alpha-7 subunit of the acetylcholine
receptor. [26] Most studies show a slight male predominance.[27] Because of the
benign course and and age-explicit event, it is thought to speak to an innate
weakness of brain development.
An association with ELP4 has been identified. [28]
5. Diagnosis
The diagnosis can be confirmed when the characteristic centrotemporal
spikes are seen on electroencephalography (EEG). [29]
Usage ofsleep-EEG
Technically, the label "benign" can only be confirmed if the child's
development improvement keeps on being normal during development.
Neuroimaging, usually with an MRI scan, is just prompted for cases with
atypical findings on clinical assessment or EEG.
24 Bali et al., “Autosomal Dominant Inheritance of Centrotemporal Sharp Waves in Rolandic
Epilepsy Families.”
25 “The Genetics of Rolandic Epilepsy - PubMed.”
26 Neubauer et al., “Centrotemporal Spikes in Families with Rolandic Epilepsy.”
27 Chahine and Mikati, “Benign Pediatric Localization-Related Epilepsies.”
28 “Centrotemporal Sharp Wave EEG Trait in Rolandic Epilepsy Maps to Elongator Protein
Complex 4 (ELP4).”
29 Stephani, “Typical Semiology of Benign Childhood Epilepsy with Centrotemporal Spikes
(BCECTS).”
9. Bening Rolandic Epilepsy
9
6. Differential Diagnosis
Centrotemporal spikes without seizures
Centrotemporal spikes with a cerebral lesion
Temporal lobe epilepsy
Panayiotopoulos syndrome
Landau-Kleffner syndrome [30]
7. Treatment
Often in benign rolandic epilepsy, no treatment is required or suggested. Seizures
in benign rolandic epilepsy are usually mild, inconsistent, and infrequent. Virtually
all children outgrow the condition.
Anti-epileptic medications:
Carbamazepine (most frequently used first-line drug)
Valproate
Phenytoin
Gabapentin
Levetiracetam or Keppra
Sultiameas [31]
Treatment has shown to decrease tonic- clonic seizures, yet facial
twitching continues. Sleep- time dosing is prompted by few.
Treatment can be short and medications can in all likelihood be
suspended following two years without seizures and with typical EEG
discoveries. [32]
30 “Rolandic Epilepsy.”
31 Chahine and Mikati, “Benign Pediatric Localization-Related Epilepsies.”
32 Panayiotopoulos, Benign Childhood Partial Seizures and Related Epileptic Syndromes.
10. Bening Rolandic Epilepsy
10
8. Prognosis
The prognosis for Rolandic seizures is invariably excellent, with probably less
than 2% risk of developing absence seizures and less often GTCS in adult
life. Remission normally happens inside 2–4 years from beginning and before
the age of 16 years. [33][34][35][36] These might be more severe in children with
beginning of seizures before 8 years old, high pace of event and multifocal EEG
spikes. [37][38]
9. Epidemiology
The period of beginning extents from 1 to 14 years with 75% beginning
between 7–10 years. There is a 1.5 male power, pervasiveness is around 15% in
kids matured 1–15 years with non-febrile seizures and frequency is 10–
20/100,000 of kids matured 0–15 years. [39][40][41][42][43]
33 Goldberg-Stern et al., “Neuropsychological Aspects of Benign Childhood Epilepsy with
Centrotemporal Spikes.”
34 Neri et al., “Neuropsychological Assessment of Children with Rolandic Epilepsy.”
35 Callenbach et al., “Long Term Outcome of Benign Childhood Epilepsy with Centrotemporal
Spikes.”
36 Danielsson and Petermann, “Cognitive Deficits in Children with Benign Rolandic Epilepsy of
Childhood or Rolandic Discharges.”
37 Piccinelli et al., “Academic Performance in Children with Rolandic Epilepsy.”
38 Bulgheroni et al., “Verbal Dichotic Listening Performance and Its Relationship with EEG
Features in Benign Childhood Epilepsy with Centrotemporal Spikes.”
39 Sidenvall, Forsgren, and Heijbel, “Prevalence and Characteristics of Epilepsy in Children in
Northern Sweden.”
40 Astradsson et al., “Rolandic Epilepsy.”
41 Bouma et al., “The Course of Benign Partial Epilepsy of Childhood with Centrotemporal
Spikes.”
42 Sidenvall, Forsgren, and Heijbel, “Prevalence and Characteristics of Epilepsy in Children in
Northern Sweden.”
43 Berg et al., “Newly Diagnosed Epilepsy in Children.”
11. Bening Rolandic Epilepsy
11
10.References
1. Huffelen, A. C. van. “A Tribute to Martinus Rulandus. A 16th-Century Description of Benign
Focal Epilepsy of Childhood.” Archives of Neurology 46, no. 4 (April 1989): 445–47.
https://doi.org/10.1001/archneur.1989.00520400105027.
2. Gibbs, Erna L., and Frederic A. Gibbs. “Good Prognosis of Mid-Temporal Epilepsy.” Epilepsia
1, no. 1–5 (1959): 448–53. https://doi.org/10.1111/j.1528-1157.1959.tb04279.x.
3. Lombroso, Cesare T. “Sylvian Seizures and Midtemporal Spike Foci in Children.” Archives of
Neurology 17, no. 1 (July 1, 1967): 52–59.
https://doi.org/10.1001/archneur.1967.00470250056005.
4. Panayiotopoulos, C. P. A Clinical Guide to Epileptic Syndromes and Their Treatment. Springer
Science & Business Media, 2010.
5. Lombroso, Cesare T. “Sylvian Seizures and Midtemporal Spike Foci in Children.”
Archives of Neurology 17, no. 1 (July 1, 1967): 52–59.
https://doi.org/10.1001/archneur.1967.00470250056005.
6. Gibbs, Erna L., and Frederic A. Gibbs. “Good Prognosis of Mid-Temporal Epilepsy.” Epilepsia
1, no. 1–5 (1959): 448–53. https://doi.org/10.1111/j.1528-1157.1959.tb04279.x
7. “Childhood Epilepsy with Centro-Temporal Spikes | Epilepsy Action.” Accessed April 9, 2020.
https://www.epilepsy.org.uk/info/syndromes/benign-rolandic-epilepsy.
8. Rolandic Epilepsy.” In Wikipedia, February 19, 2020.
9. Beaussart, Marc. “Benign Epilepsy of Children with Rolandic (Centro-Temporal) Paroxysmal
Foci A Clinical Entity. Study of 221 Cases.” Epilepsia 13, no. 6 (1972): 795–811.
https://doi.org/10.1111/j.1528-1157.1972.tb05164.x.10
10. Beaussart, Marc. “Benign Epilepsy of Children with Rolandic (Centro-Temporal) Paroxysmal
Foci A Clinical Entity. Study of 221 Cases.” Epilepsia 13, no. 6 (1972): 795–811.
https://doi.org/10.1111/j.1528-1157.1972.tb05164.x.
11. Lerman, Pinchas, and Sara Kivity. “Benign Focal Epilepsy of Childhood: A Follow-Up Study of
100 Recovered Patients.” Archives of Neurology 32, no. 4 (April 1, 1975): 261–64.
https://doi.org/10.1001/archneur.1975.00490460077010.
12. Panayiotopoulos, Chrysostomos P. Benign Childhood Partial Seizures and Related Epileptic
Syndromes. John Libbey Eurotext, 1999.
13. Roger, Joseph. Epileptic Syndromes in Infancy, Childhood and Adolescence. John Libbey
Eurotext, 2005.
14. Roger, Joseph. Epileptic Syndromes in Infancy, Childhood and Adolescence. John Libbey
Eurotext, 2005.
12. Bening Rolandic Epilepsy
12
15. Panayiotopoulos, Chrysostomos P., Michael Michael, Sue Sanders, Thalia Valeta, and Michael
Koutroumanidis. “Benign Childhood Focal Epilepsies: Assessment of Established and
Newly Recognized Syndromes.” Brain 131, no. 9 (September 1, 2008): 2264–86.
https://doi.org/10.1093/brain/awn162.
16. Deonna, Th, A.-L. Ziegler, and P. A. Despland. “Combined Myoclonic-Astatic And.”
Neuropediatrics 17, no. 03 (August 1986): 144–51. https://doi.org/10.1055/s-2008-
1052516.
17. “Atypical Evolutions of Benign Localization‐Related Epilepsies in Children: Are They
Predictable? - Fejerman - 2000 - Epilepsia - Wiley Online Library.” Accessed April 9,
2020. https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1528-1157.2000.tb00177.x.
18. Caraballo, Roberto, Ricardo Cersósimo, and Natalio Fejerman. “Panayiotopoulos Syndrome:
A Prospective Study of 192 Patients.” Epilepsia 48, no. 6 (2007): 1054–61.
https://doi.org/10.1111/j.1528-1167.2007.01085.x.
19. Specchio, Nicola, Marina Trivisano, Vincenzo Di Ciommo, Simona Cappelletti, Giovanni
Masciarelli, Josiv Volkov, Lucia Fusco, and Federico Vigevano. “Panayiotopoulos
Syndrome: A Clinical, EEG, and Neuropsychological Study of 93 Consecutive Patients.”
Epilepsia 51, no. 10 (2010): 2098–2107. https://doi.org/10.1111/j.1528-
1167.2010.02639.x.
20. “Benign Rolandic Epilepsy: Atypical Features Are Very Common - Elaine C. Wirrell, Peter R.
Camfield, Kevin E. Gordon, Joseph M. Dooley, Carol S. Camfield, 1995.” Accessed April 9, 2020.
21. “Atypical Presentations of Benign Childhood Epilepsy With Centrotemporal Spikes: A Review
- Uri Kramer, 2008.” Accessed April 9, 2020.
https://journals.sagepub.com/doi/10.1177/0883073808316363.
22. “Benign Rolandic Epilepsy: Atypical Features Are Very Common - Elaine C. Wirrell, Peter R.
Camfield, Kevin E. Gordon, Joseph M. Dooley, Carol S. Camfield, 1995.” Accessed April 9, 2020.
23. Wirrell, Elaine C. “Benign Epilepsy of Childhood With Centrotemporal Spikes.” Epilepsia 39,
no. s4 (1998): S32–41. https://doi.org/10.1111/j.1528-1157.1998.tb05123.x.
24. Bali, Bhavna, Lewis L. Kull, Lisa J. Strug, Tara Clarke, Peregrine L. Murphy, Cigdem I. Akman,
David A. Greenberg, and Deb K. Pal. “Autosomal Dominant Inheritance of
Centrotemporal Sharp Waves in Rolandic Epilepsy Families.” Epilepsia 48, no. 12
(December 2007): 2266–72. https://doi.org/10.1111/j.1528-1167.2007.01221.x.
25. “The Genetics of Rolandic Epilepsy - PubMed.” Accessed April 9, 2020.
https://pubmed.ncbi.nlm.nih.gov/11231229/.
26. Neubauer, B. A., B. Fiedler, B. Himmelein, F. Kämpfer, U. Lässker, G. Schwabe, I. Spanier, et
al. “Centrotemporal Spikes in Families with Rolandic Epilepsy: Linkage to Chromosome
15q14.” Neurology 51, no. 6 (December 1998): 1608–12.
https://doi.org/10.1212/wnl.51.6.1608.
13. Bening Rolandic Epilepsy
13
27. Chahine, Lama M., and Mohamad A. Mikati. “Benign Pediatric Localization-Related
Epilepsies.” Epileptic Disorders 8, no. 4 (December 1, 2006): 243–58.
https://doi.org/10.1684/epd.2006.0036.
28. “Centrotemporal Sharp Wave EEG Trait in Rolandic Epilepsy Maps to Elongator Protein
Complex 4 (ELP4).” Accessed April 9, 2020.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729813/.
29. Stephani, U. “Typical Semiology of Benign Childhood Epilepsy with Centrotemporal Spikes
(BCECTS).” Epileptic Disorders: International Epilepsy Journal with Videotape 2 Suppl 1
(2000): S3-4.
30. “Rolandic Epilepsy.” In Wikipedia, February 19, 2020.
https://en.wikipedia.org/w/index.php?title=Rolandic_epilepsy&oldid=941653936
31. Chahine, Lama M., and Mohamad A. Mikati. “Benign Pediatric Localization-Related
Epilepsies.” Epileptic Disorders 8, no. 4 (December 1, 2006): 243–58.
https://doi.org/10.1684/epd.2006.0036.
32. Panayiotopoulos, Chrysostomos P. Benign Childhood Partial Seizures and Related Epileptic
Syndromes. John Libbey Eurotext, 1999.
33. Goldberg-Stern, H., O. M. Gonen, M. Sadeh, S. Kivity, A. Shuper, and D. Inbar.
“Neuropsychological Aspects of Benign Childhood Epilepsy with Centrotemporal Spikes.”
Seizure 19, no. 1 (January 2010): 12–16.
https://doi.org/10.1016/j.seizure.2009.10.004.
34. Neri, Marina L., Catarina A. Guimarães, Ecila P. Oliveira, Marcos H. Duran, Livia L. Medeiros,
Maria Augusta Montenegro, Mirela Boscariol, and Marilisa M. Guerreiro. “Neuropsychological
Assessment of Children with Rolandic Epilepsy: Executive Functions.” Epilepsy & Behavior: E&B
24, no. 4 (August 2012): 403–7. https://doi.org/10.1016/j.yebeh.2012.04.131.
35. Callenbach, Petra M. C., Paul A. D. Bouma, Ada T. Geerts, Willem Frans M. Arts, Hans
Stroink, Els A. J. Peeters, Cees A. van Donselaar, A. C. Boudewijn Peters, and Oebele F.
Brouwer. “Long Term Outcome of Benign Childhood Epilepsy with Centrotemporal
Spikes: Dutch Study of Epilepsy in Childhood.” Seizure 19, no. 8 (October 2010): 501–6.
https://doi.org/10.1016/j.seizure.2010.07.007.
36. Danielsson, Julia, and Franz Petermann. “Cognitive Deficits in Children with Benign Rolandic
Epilepsy of Childhood or Rolandic Discharges: A Study of Children between 4 and 7
Years of Age with and without Seizures Compared with Healthy Controls.” Epilepsy &
Behavior: E&B 16, no. 4 (December 2009): 646–51.
https://doi.org/10.1016/j.yebeh.2009.08.012.
37. Piccinelli, P., R. Borgatti, A. Aldini, D. Bindelli, M. Ferri, S. Perna, G. Pitillo, C. Termine, F.
Zambonin, and U. Balottin. “Academic Performance in Children with Rolandic Epilepsy.”
Developmental Medicine and Child Neurology 50, no. 5 (May 2008): 353–56.
https://doi.org/10.1111/j.1469-8749.2007.02040.x.
14. Bening Rolandic Epilepsy
14
38. Bulgheroni, Sara, Silvana Franceschetti, Chiara Vago, Arianna Usilla, Chiara Pantaleoni,
Stefano D’Arrigo, and Daria Riva. “Verbal Dichotic Listening Performance and Its
Relationship with EEG Features in Benign Childhood Epilepsy with Centrotemporal
Spikes.” Epilepsy Research 79, no. 1 (March 2008): 31–38.
https://doi.org/10.1016/j.eplepsyres.2007.12.016.
39. Epilepsy in Children in Northern Sweden.” Seizure 5, no. 2 (June 1996): 139–46.
https://doi.org/10.1016/s1059-1311(96)80108-7.
40. Astradsson, A., E. Olafsson, P. Ludvigsson, H. Björgvinsson, and W. A. Hauser. “Rolandic
Epilepsy: An Incidence Study in Iceland.” Epilepsia 39, no. 8 (August 1998): 884–86.
https://doi.org/10.1111/j.1528-1157.1998.tb01185.x.
41. Bouma, P. A., A. C. Bovenkerk, R. G. Westendorp, and O. F. Brouwer. “The Course of Benign
Partial Epilepsy of Childhood with Centrotemporal Spikes: A Meta-Analysis.” Neurology 48, no.
2 (February 1997): 430–37. https://doi.org/10.1212/wnl.48.2.430.
42. Sidenvall, R., L. Forsgren, and J. Heijbel. “Prevalence and Characteristics of Epilepsy in
Children in Northern Sweden.” Seizure 5, no. 2 (June 1996): 139–46.
https://doi.org/10.1016/s1059-1311(96)80108-7.
43. Berg, A. T., S. Shinnar, S. R. Levy, and F. M. Testa. “Newly Diagnosed Epilepsy in Children:
Presentation at Diagnosis.” Epilepsia 40, no. 4 (April 1999): 445–52.
https://doi.org/10.1111/j.1528-1157.1999.tb00739.x.