Síndrome Post Polio. Actualización, Dr. Jaime López-Ventura. II Jornadas sobre los Efectos Tardíos de la Polio y Síndrome Postpolio. Hospital de Antequera. Asociación AMAPyP. Málaga, 25-10-2017
A guideline for discontinuing antiepileptic drugs in seizure-free patients – ...Dr. Rafael Higashi
The document discusses guidelines for discontinuing antiepileptic drug (AED) treatment in patients who have been seizure-free. It summarizes studies that identified factors associated with risk of seizure recurrence after stopping AEDs. For patients who are seizure-free for 2-5 years, have had only partial or generalized seizures, have a normal neurological exam and IQ, and a normalized EEG with treatment, the risk of recurrence is about 69% for children and 61% for adults. The guidelines recommend considering discontinuing AEDs for patients meeting these criteria. Future research is still needed to better predict individual patient risks.
Estatus Epiléptico por Dr. Cristian Carpio Bazán - CMP CR XXV Amazonas (28/04...Cristian Carpio Bazan
Tema "Estatus Epiléptico" por Dr. Cristian Carpio Bazán en Curso de Emergencias Neurológicas en Tiempos de Pandemia organizado por el Colegio Médico del Perú - Consejo Regional XXV Amazonas - Consejo Directivo - Decano Dr. Richard Flores Malpartida (28 de Abril del 2021)
This document provides an overview of peripheral neuropathy, including:
1. It describes the anatomy of peripheral nerves and different types of peripheral neuropathies such as mononeuropathy, mononeuropathy multiplex, polyneuropathy, polyradiculopathy, and plexopathy.
2. It outlines the various clinical presentations of peripheral neuropathy including sensory, motor, and autonomic symptoms as well as patterns of nerve fiber involvement.
3. It discusses the etiology, clinical course, investigations and management of different peripheral neuropathies.
Multiple sclerosis (MS) is a chronic disease that affects the central nervous system by demyelinating neurons. It most commonly affects people between 20-40 years of age and women more than men. The cause is unknown but is thought to involve an autoimmune reaction triggered by a viral infection. Symptoms vary depending on the areas of the brain and spinal cord that are affected and can include problems with mobility, sensation, vision, and bladder or bowel function. Diagnosis involves neurological exams, MRI scans to detect lesions, and ruling out other possibilities. Treatment focuses on managing relapses, reducing disease progression, and alleviating symptoms, using medications, physical therapy, and lifestyle changes. Nursing care centers around addressing issues like impaired mobility
This document summarizes key events in neuromuscular transmission and discusses different types of neuromuscular blocking drugs used in surgery. It describes how non-depolarizing drugs like tubocurarine work competitively at nicotinic receptors to block acetylcholine, while depolarizing drugs like succinylcholine mimic acetylcholine's action. The document also discusses cholinesterase inhibitors and their use in treating myasthenia gravis by inhibiting breakdown of acetylcholine in the neuromuscular junction.
This document describes a case of Miller Fisher syndrome in a 24-year-old female patient presenting with gait instability, facial weakness, eye movement abnormalities, limb numbness, and dysphagia. Electrodiagnostic testing showed normal nerve conduction but abnormal sensory Ia afferent conduction, supporting a diagnosis of Miller Fisher syndrome. Key findings included hypotonia, areflexia, loss of the H-reflex, and decreased sensory evoked potentials attributed to increased intracranial pressure. The multiple cranial neuropathies with normal MRI and abnormal afferent conduction established a diagnosis of Miller Fisher syndrome associated with benign intracranial hypertension.
A 50-year-old female presented with postural instability, frequent falling, and vertical gaze palsy. MRI showed selective atrophy of the midbrain, known as the "hummingbird sign", along with other findings consistent with progressive supranuclear palsy (PSP). PSP is characterized by degeneration of midbrain cells involved in eye movements and balance control, causing symptoms like vertical gaze palsy and falling. The cause is unknown but may involve tau protein aggregation in the brain. The diagnosis is clinical based on symptoms and MRI findings of midbrain atrophy.
This document summarizes several neurological conditions including Bell's palsy, trigeminal neuralgia, post-herpetic neuralgia, parkinsonism, and others. For each condition, it discusses epidemiology, risk factors, signs and symptoms, diagnostic workup, and treatment options. The document is intended to provide an overview of these neuralgias and palsies for medical students and physicians.
A guideline for discontinuing antiepileptic drugs in seizure-free patients – ...Dr. Rafael Higashi
The document discusses guidelines for discontinuing antiepileptic drug (AED) treatment in patients who have been seizure-free. It summarizes studies that identified factors associated with risk of seizure recurrence after stopping AEDs. For patients who are seizure-free for 2-5 years, have had only partial or generalized seizures, have a normal neurological exam and IQ, and a normalized EEG with treatment, the risk of recurrence is about 69% for children and 61% for adults. The guidelines recommend considering discontinuing AEDs for patients meeting these criteria. Future research is still needed to better predict individual patient risks.
Estatus Epiléptico por Dr. Cristian Carpio Bazán - CMP CR XXV Amazonas (28/04...Cristian Carpio Bazan
Tema "Estatus Epiléptico" por Dr. Cristian Carpio Bazán en Curso de Emergencias Neurológicas en Tiempos de Pandemia organizado por el Colegio Médico del Perú - Consejo Regional XXV Amazonas - Consejo Directivo - Decano Dr. Richard Flores Malpartida (28 de Abril del 2021)
This document provides an overview of peripheral neuropathy, including:
1. It describes the anatomy of peripheral nerves and different types of peripheral neuropathies such as mononeuropathy, mononeuropathy multiplex, polyneuropathy, polyradiculopathy, and plexopathy.
2. It outlines the various clinical presentations of peripheral neuropathy including sensory, motor, and autonomic symptoms as well as patterns of nerve fiber involvement.
3. It discusses the etiology, clinical course, investigations and management of different peripheral neuropathies.
Multiple sclerosis (MS) is a chronic disease that affects the central nervous system by demyelinating neurons. It most commonly affects people between 20-40 years of age and women more than men. The cause is unknown but is thought to involve an autoimmune reaction triggered by a viral infection. Symptoms vary depending on the areas of the brain and spinal cord that are affected and can include problems with mobility, sensation, vision, and bladder or bowel function. Diagnosis involves neurological exams, MRI scans to detect lesions, and ruling out other possibilities. Treatment focuses on managing relapses, reducing disease progression, and alleviating symptoms, using medications, physical therapy, and lifestyle changes. Nursing care centers around addressing issues like impaired mobility
This document summarizes key events in neuromuscular transmission and discusses different types of neuromuscular blocking drugs used in surgery. It describes how non-depolarizing drugs like tubocurarine work competitively at nicotinic receptors to block acetylcholine, while depolarizing drugs like succinylcholine mimic acetylcholine's action. The document also discusses cholinesterase inhibitors and their use in treating myasthenia gravis by inhibiting breakdown of acetylcholine in the neuromuscular junction.
This document describes a case of Miller Fisher syndrome in a 24-year-old female patient presenting with gait instability, facial weakness, eye movement abnormalities, limb numbness, and dysphagia. Electrodiagnostic testing showed normal nerve conduction but abnormal sensory Ia afferent conduction, supporting a diagnosis of Miller Fisher syndrome. Key findings included hypotonia, areflexia, loss of the H-reflex, and decreased sensory evoked potentials attributed to increased intracranial pressure. The multiple cranial neuropathies with normal MRI and abnormal afferent conduction established a diagnosis of Miller Fisher syndrome associated with benign intracranial hypertension.
A 50-year-old female presented with postural instability, frequent falling, and vertical gaze palsy. MRI showed selective atrophy of the midbrain, known as the "hummingbird sign", along with other findings consistent with progressive supranuclear palsy (PSP). PSP is characterized by degeneration of midbrain cells involved in eye movements and balance control, causing symptoms like vertical gaze palsy and falling. The cause is unknown but may involve tau protein aggregation in the brain. The diagnosis is clinical based on symptoms and MRI findings of midbrain atrophy.
This document summarizes several neurological conditions including Bell's palsy, trigeminal neuralgia, post-herpetic neuralgia, parkinsonism, and others. For each condition, it discusses epidemiology, risk factors, signs and symptoms, diagnostic workup, and treatment options. The document is intended to provide an overview of these neuralgias and palsies for medical students and physicians.
This document provides an overview of multiple sclerosis (MS), including its epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment. Some key points:
1. MS typically affects people between the ages of 15-45 and is more common in women. It has a variable geographic distribution and prevalence of around 0.1% in the US.
2. The pathophysiology involves chronic inflammation and demyelination in the central nervous system resulting in neurological deficits. MRI is an important tool for diagnosis and monitoring disease progression.
3. Clinical symptoms can include visual disturbances, motor and sensory problems, fatigue, and cognitive issues. Relapsing-remitting is the most common disease course.
Peripheral neuropathies are common neurological disorders caused by dysfunction of peripheral nerves. A systematic diagnostic approach involving detailed history, physical exam, electrodiagnostic studies, and possibly additional testing is recommended to determine the nature and location of nerve lesions. Diagnostic tests should not be ordered without understanding their significance. Biopsy may be needed in some cases to confirm diagnoses like vasculitis or amyloidosis. Treatment involves managing underlying causes, IVIG or immunomodulators for rapidly progressive neuropathies, and symptomatic treatments like antidepressants, antiepileptics, and topical agents.
This document provides an overview of several neurologic disorders, including:
- Multiple sclerosis, which causes fatigue, vision issues, weakness and more. Treatment focuses on retaining function and limiting disability.
- Myasthenia gravis, an autoimmune disorder causing severe muscle weakness. Medications aim to improve symptoms.
- Guillain-Barré syndrome, an acute inflammatory disorder causing ascending paralysis. Supportive care and monitoring of respiratory function are priorities.
- Parkinson's disease, characterized by tremors and rigidity. Medications may provide relief but symptoms gradually worsen over time.
- Huntington's disease, an inherited disorder causing chorea and dementia. No cure exists, and
This document provides an overview of peripheral neuropathy including:
1. It describes a typical case of diabetic peripheral neuropathy presenting with leg weakness, numb feet, and pain.
2. It asks questions to help classify the neuropathy including type of nerve fibers involved and diagnostic approach.
3. It outlines the lesson which will define neuropathy, discuss anatomy/physiology, classification, clinical features, investigations and management.
This document provides an overview of peripheral neuropathy, including types of nerves and symptoms, common causes, classification, evaluation, and diagnostic testing. It discusses systemic disorders, toxic and hereditary causes, and drugs that can cause neuropathy. Sensory, motor, and autonomic symptoms are described. Evaluation involves assessing for features like asymmetry, acute onset, or autonomic involvement. Electrodiagnostics and biopsies can provide clues to determine if neuropathy is mononeuropathy, mononeuritis multiplex, or polyneuropathy, and the pattern of involvement can indicate certain disorders.
This document discusses neuropathy and provides an approach to evaluating patients presenting with neuropathy symptoms. It defines neuropathy as a functional disturbance or pathological change in the peripheral nervous system. The document then covers types of neuropathies, history taking, physical examination, investigations such as electrodiagnostic testing and nerve biopsy, and how to differentiate various conditions that can present as neuropathy, including leprosy, vitamin B12 deficiency, diabetes mellitus, and hypothyroidism.
Parkinson's disease is a progressive neurodegenerative disorder that affects movement. It is characterized by tremors, rigidity, bradykinesia, and postural instability. The disease results from degeneration of dopaminergic neurons in the substantia nigra, leading to dopamine depletion in the striatum. Common treatments include levodopa and dopamine agonists to supplement the loss of dopamine, though long term use can cause motor complications. Surgical and rehabilitation therapies may also be used to manage motor symptoms of Parkinson's disease.
Guillain-Barre syndrome; the murderer enemySamir Mounir
This document provides information about Guillain-Barré syndrome (GBS), including:
1. GBS is an acute immune-mediated polyneuropathy that affects the peripheral nervous system and can be life-threatening. It has several subtypes with different clinical features.
2. The cause is unknown but is thought to involve molecular mimicry between microbial antigens and peripheral nerve antigens, triggering an autoimmune response.
3. Treatment involves supportive care to address symptoms like weakness, respiratory issues, and pain. Immunotherapy with IVIG or plasmapheresis within 2 weeks of onset can improve outcomes.
This document discusses progressive myoclonic epilepsy (PME), a group of rare genetic neurological disorders characterized by myoclonus and epileptic seizures with progressive neurological decline. It describes several specific forms of PME, including neuronal ceroid lipofuscinoses (NCLs), Lafora body disease, Unverricht-Lundborg disease, and myoclonic epilepsy with ragged-red fibers. For each, it covers clinical features, genetics, investigations such as EEG and MRI findings, pathology, treatment approaches, and prognosis. The document provides a detailed review and comparison of these progressive myoclonic epilepsy syndromes.
Guillain-Barré syndrome is an acute polyneuropathic disorder that causes muscle weakness, loss of reflexes, and numbness in the limbs and face. It occurs when the immune system mistakenly attacks the peripheral nervous system. The symptoms can range from mild tingling to total paralysis. The disorder is usually triggered by a bacterial or viral infection. Treatment focuses on speeding recovery through measures like plasmapheresis, IVIG, respiratory therapy, and monitoring for complications like respiratory failure or paralysis. Nurses help manage symptoms, provide education, and address problems with mobility, swallowing, and sensation that arise due to the disease process.
Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy characterized by acute onset of peripheral and cranial nerve dysfunction and progressive muscle weakness. It is caused by an autoimmune reaction directed against peripheral nerves, often preceded by a viral infection. Clinically, GBS presents with rapidly progressive symmetric weakness, loss of tendon reflexes, and sensory symptoms like paresthesia. Electrodiagnostic studies are diagnostic in most cases and show features of demyelination like prolonged latencies and conduction block. Treatment involves supportive care and immunotherapy.
Progressive supranuclear palsy and multiple system atrophySooraj Patil
This document provides an overview of Progressive Supranuclear Palsy (PSP) and Multiple System Atrophy (MSA). It defines PSP and MSA as neurodegenerative diseases characterized by selective neuronal dysfunction and loss associated with pathologically altered proteins. The document discusses the pathophysiology, clinical features, subtypes, diagnostic criteria and investigations for PSP and MSA. Key points include that PSP is the second most common cause of parkinsonism after IPD, and involves characteristic tau protein deposits in the brain. Clinical features of PSP include early falls, vertical gaze palsy, speech and swallowing problems, and frontal cognitive deficits. The MDS criteria aim to improve diagnosis of early and variant
This document summarizes a case study of a 14-year-old girl presenting with progressive muscle weakness over 10 days. Her examination showed diminished and symmetric muscle strength, loss of vibratory sense, absent reflexes, and impaired handling of secretions. Investigations including lumbar puncture, MRI, and bloodwork were normal. The diagnosis was Guillain-Barré syndrome based on the clinical presentation and findings.
Progressive supranuclear palsy (PSP) is a neurodegenerative disorder characterized by tau protein aggregation that causes loss of brainstem and basal ganglia structures. It presents with gait impairment, bradykinesia, frontal dementia, and vertical supranuclear gaze palsy. Diagnosis is based on clinical features and MRI showing midbrain atrophy. There is no cure, and treatment focuses on managing symptoms, with levodopa and coenzyme Q10 potentially helping rigidity and bradykinesia.
- Multiple sclerosis (MS) is a neurological disease involving damage to the protective myelin sheath surrounding the nerves in the central nervous system. It presents with a variety of symptoms such as vision problems, tingling/numbness, muscle weakness, balance issues, and fatigue.
- There are several types of MS defined by patterns of relapse and progression of symptoms. Management involves medications to reduce inflammation and manage relapses as well as physiotherapy focusing on exercises, balance training, managing fatigue, and compensatory strategies to improve function and quality of life.
This document discusses various types and causes of neuropathies, including focal (mononeuropathy), multifocal (mononeuropathy multiplex), and generalized (polyneuropathy) neuropathies. Common causes include entrapment neuropathies, diabetes, vitamin deficiencies, toxins/drugs, and systemic diseases. Specific conditions discussed include Bell's palsy, trigeminal neuralgia, and hemifacial spasm. Diagnostic testing and management strategies are also outlined.
Spirit to autoantibodies: Journey of limbic disorders from philosophy to aff...Ubaidur Rahaman
Limbic encephalitis usually presents with neuropychiatric symptomatology, often remain undiagnosed, treated as psychiatry disorders with various antipsychotic medications and die. Early diagnosis and treatment of autoimmune limbic encephalitis has good outcome, establishing these patients back into the society
A 40-year-old legally blind female presented with bilateral lower extremity weakness and inability to walk. She has a history of similar episodes since age 16 diagnosed as a demyelinating disorder. Her current presentation is her worst episode yet with more rapid progression of symptoms and new bowel incontinence. Imaging showed a T6 spinal cord lesion. Laboratory tests confirmed high aquaporin-4 antibody levels consistent with Neuromyelitis Optica Spectrum Disorder. The neurologist recommended additional treatments like Rituximab or plasma exchange but the patient wished to try steroids first.
Guillain-Barré Syndrome (GBS) is an autoimmune disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and possible paralysis. It is usually preceded by a bacterial or viral infection. Symptoms include progressive muscle weakness starting in the legs and ascending over time. Diagnosis involves neurological exams, nerve conduction studies, and spinal fluid analysis. Treatment focuses on rehabilitation and managing symptoms, as there is no cure. Recovery can take several months but most patients do regain function over time.
This document discusses post-encephalitic psychiatric sequelae. Encephalitis is an inflammation of the brain that can be caused by viruses or bacteria. While some cases result in full recovery, others can lead to transient or persisting psychiatric symptoms. These post-encephalitic symptoms present in a variety of ways and can include conditions like organic personality disorder, post-encephalitic syndrome, and post-concussional syndrome. Specific viruses and infections like herpes simplex virus, Epstein-Barr virus, Japanese encephalitis, and influenza have all been linked to post-encephalitic psychiatric manifestations.
After watching this lecture, learners will be able to:
Describe the various etiologies of non-traumatic paralysis
Illustrate the neuro exam for the paralyzed patient
Recognize the signs and symptoms of acute peripheral neuropathies
Explain the treatment of acute peripheral neuropathies
This document provides an overview of multiple sclerosis (MS), including its epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment. Some key points:
1. MS typically affects people between the ages of 15-45 and is more common in women. It has a variable geographic distribution and prevalence of around 0.1% in the US.
2. The pathophysiology involves chronic inflammation and demyelination in the central nervous system resulting in neurological deficits. MRI is an important tool for diagnosis and monitoring disease progression.
3. Clinical symptoms can include visual disturbances, motor and sensory problems, fatigue, and cognitive issues. Relapsing-remitting is the most common disease course.
Peripheral neuropathies are common neurological disorders caused by dysfunction of peripheral nerves. A systematic diagnostic approach involving detailed history, physical exam, electrodiagnostic studies, and possibly additional testing is recommended to determine the nature and location of nerve lesions. Diagnostic tests should not be ordered without understanding their significance. Biopsy may be needed in some cases to confirm diagnoses like vasculitis or amyloidosis. Treatment involves managing underlying causes, IVIG or immunomodulators for rapidly progressive neuropathies, and symptomatic treatments like antidepressants, antiepileptics, and topical agents.
This document provides an overview of several neurologic disorders, including:
- Multiple sclerosis, which causes fatigue, vision issues, weakness and more. Treatment focuses on retaining function and limiting disability.
- Myasthenia gravis, an autoimmune disorder causing severe muscle weakness. Medications aim to improve symptoms.
- Guillain-Barré syndrome, an acute inflammatory disorder causing ascending paralysis. Supportive care and monitoring of respiratory function are priorities.
- Parkinson's disease, characterized by tremors and rigidity. Medications may provide relief but symptoms gradually worsen over time.
- Huntington's disease, an inherited disorder causing chorea and dementia. No cure exists, and
This document provides an overview of peripheral neuropathy including:
1. It describes a typical case of diabetic peripheral neuropathy presenting with leg weakness, numb feet, and pain.
2. It asks questions to help classify the neuropathy including type of nerve fibers involved and diagnostic approach.
3. It outlines the lesson which will define neuropathy, discuss anatomy/physiology, classification, clinical features, investigations and management.
This document provides an overview of peripheral neuropathy, including types of nerves and symptoms, common causes, classification, evaluation, and diagnostic testing. It discusses systemic disorders, toxic and hereditary causes, and drugs that can cause neuropathy. Sensory, motor, and autonomic symptoms are described. Evaluation involves assessing for features like asymmetry, acute onset, or autonomic involvement. Electrodiagnostics and biopsies can provide clues to determine if neuropathy is mononeuropathy, mononeuritis multiplex, or polyneuropathy, and the pattern of involvement can indicate certain disorders.
This document discusses neuropathy and provides an approach to evaluating patients presenting with neuropathy symptoms. It defines neuropathy as a functional disturbance or pathological change in the peripheral nervous system. The document then covers types of neuropathies, history taking, physical examination, investigations such as electrodiagnostic testing and nerve biopsy, and how to differentiate various conditions that can present as neuropathy, including leprosy, vitamin B12 deficiency, diabetes mellitus, and hypothyroidism.
Parkinson's disease is a progressive neurodegenerative disorder that affects movement. It is characterized by tremors, rigidity, bradykinesia, and postural instability. The disease results from degeneration of dopaminergic neurons in the substantia nigra, leading to dopamine depletion in the striatum. Common treatments include levodopa and dopamine agonists to supplement the loss of dopamine, though long term use can cause motor complications. Surgical and rehabilitation therapies may also be used to manage motor symptoms of Parkinson's disease.
Guillain-Barre syndrome; the murderer enemySamir Mounir
This document provides information about Guillain-Barré syndrome (GBS), including:
1. GBS is an acute immune-mediated polyneuropathy that affects the peripheral nervous system and can be life-threatening. It has several subtypes with different clinical features.
2. The cause is unknown but is thought to involve molecular mimicry between microbial antigens and peripheral nerve antigens, triggering an autoimmune response.
3. Treatment involves supportive care to address symptoms like weakness, respiratory issues, and pain. Immunotherapy with IVIG or plasmapheresis within 2 weeks of onset can improve outcomes.
This document discusses progressive myoclonic epilepsy (PME), a group of rare genetic neurological disorders characterized by myoclonus and epileptic seizures with progressive neurological decline. It describes several specific forms of PME, including neuronal ceroid lipofuscinoses (NCLs), Lafora body disease, Unverricht-Lundborg disease, and myoclonic epilepsy with ragged-red fibers. For each, it covers clinical features, genetics, investigations such as EEG and MRI findings, pathology, treatment approaches, and prognosis. The document provides a detailed review and comparison of these progressive myoclonic epilepsy syndromes.
Guillain-Barré syndrome is an acute polyneuropathic disorder that causes muscle weakness, loss of reflexes, and numbness in the limbs and face. It occurs when the immune system mistakenly attacks the peripheral nervous system. The symptoms can range from mild tingling to total paralysis. The disorder is usually triggered by a bacterial or viral infection. Treatment focuses on speeding recovery through measures like plasmapheresis, IVIG, respiratory therapy, and monitoring for complications like respiratory failure or paralysis. Nurses help manage symptoms, provide education, and address problems with mobility, swallowing, and sensation that arise due to the disease process.
Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy characterized by acute onset of peripheral and cranial nerve dysfunction and progressive muscle weakness. It is caused by an autoimmune reaction directed against peripheral nerves, often preceded by a viral infection. Clinically, GBS presents with rapidly progressive symmetric weakness, loss of tendon reflexes, and sensory symptoms like paresthesia. Electrodiagnostic studies are diagnostic in most cases and show features of demyelination like prolonged latencies and conduction block. Treatment involves supportive care and immunotherapy.
Progressive supranuclear palsy and multiple system atrophySooraj Patil
This document provides an overview of Progressive Supranuclear Palsy (PSP) and Multiple System Atrophy (MSA). It defines PSP and MSA as neurodegenerative diseases characterized by selective neuronal dysfunction and loss associated with pathologically altered proteins. The document discusses the pathophysiology, clinical features, subtypes, diagnostic criteria and investigations for PSP and MSA. Key points include that PSP is the second most common cause of parkinsonism after IPD, and involves characteristic tau protein deposits in the brain. Clinical features of PSP include early falls, vertical gaze palsy, speech and swallowing problems, and frontal cognitive deficits. The MDS criteria aim to improve diagnosis of early and variant
This document summarizes a case study of a 14-year-old girl presenting with progressive muscle weakness over 10 days. Her examination showed diminished and symmetric muscle strength, loss of vibratory sense, absent reflexes, and impaired handling of secretions. Investigations including lumbar puncture, MRI, and bloodwork were normal. The diagnosis was Guillain-Barré syndrome based on the clinical presentation and findings.
Progressive supranuclear palsy (PSP) is a neurodegenerative disorder characterized by tau protein aggregation that causes loss of brainstem and basal ganglia structures. It presents with gait impairment, bradykinesia, frontal dementia, and vertical supranuclear gaze palsy. Diagnosis is based on clinical features and MRI showing midbrain atrophy. There is no cure, and treatment focuses on managing symptoms, with levodopa and coenzyme Q10 potentially helping rigidity and bradykinesia.
- Multiple sclerosis (MS) is a neurological disease involving damage to the protective myelin sheath surrounding the nerves in the central nervous system. It presents with a variety of symptoms such as vision problems, tingling/numbness, muscle weakness, balance issues, and fatigue.
- There are several types of MS defined by patterns of relapse and progression of symptoms. Management involves medications to reduce inflammation and manage relapses as well as physiotherapy focusing on exercises, balance training, managing fatigue, and compensatory strategies to improve function and quality of life.
This document discusses various types and causes of neuropathies, including focal (mononeuropathy), multifocal (mononeuropathy multiplex), and generalized (polyneuropathy) neuropathies. Common causes include entrapment neuropathies, diabetes, vitamin deficiencies, toxins/drugs, and systemic diseases. Specific conditions discussed include Bell's palsy, trigeminal neuralgia, and hemifacial spasm. Diagnostic testing and management strategies are also outlined.
Spirit to autoantibodies: Journey of limbic disorders from philosophy to aff...Ubaidur Rahaman
Limbic encephalitis usually presents with neuropychiatric symptomatology, often remain undiagnosed, treated as psychiatry disorders with various antipsychotic medications and die. Early diagnosis and treatment of autoimmune limbic encephalitis has good outcome, establishing these patients back into the society
A 40-year-old legally blind female presented with bilateral lower extremity weakness and inability to walk. She has a history of similar episodes since age 16 diagnosed as a demyelinating disorder. Her current presentation is her worst episode yet with more rapid progression of symptoms and new bowel incontinence. Imaging showed a T6 spinal cord lesion. Laboratory tests confirmed high aquaporin-4 antibody levels consistent with Neuromyelitis Optica Spectrum Disorder. The neurologist recommended additional treatments like Rituximab or plasma exchange but the patient wished to try steroids first.
Guillain-Barré Syndrome (GBS) is an autoimmune disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and possible paralysis. It is usually preceded by a bacterial or viral infection. Symptoms include progressive muscle weakness starting in the legs and ascending over time. Diagnosis involves neurological exams, nerve conduction studies, and spinal fluid analysis. Treatment focuses on rehabilitation and managing symptoms, as there is no cure. Recovery can take several months but most patients do regain function over time.
This document discusses post-encephalitic psychiatric sequelae. Encephalitis is an inflammation of the brain that can be caused by viruses or bacteria. While some cases result in full recovery, others can lead to transient or persisting psychiatric symptoms. These post-encephalitic symptoms present in a variety of ways and can include conditions like organic personality disorder, post-encephalitic syndrome, and post-concussional syndrome. Specific viruses and infections like herpes simplex virus, Epstein-Barr virus, Japanese encephalitis, and influenza have all been linked to post-encephalitic psychiatric manifestations.
After watching this lecture, learners will be able to:
Describe the various etiologies of non-traumatic paralysis
Illustrate the neuro exam for the paralyzed patient
Recognize the signs and symptoms of acute peripheral neuropathies
Explain the treatment of acute peripheral neuropathies
Acute onset infection
Monophasic immune mediated polyneuropathy
Rapid progressive motor paralysis
Affects people of all ages and is not hereditary
Post infectious disease
It can follow by systemic infections
Auto immune in nature
OTHER TERMS
Acute inflammatory demyelinating poly radiculopathy (AIDP)
Acute idiopathic poly radiculo neuritis
Acute idiopathic neuritis
French polio
Landry Guillain Barre Syndrome
TYPES - Acute inflammatory demyelinating poly radiculo neuropathy (AIDP)
Acute Motor Axonal neuropathy(AMDN)
Acute Motor &Sensory Axonal neuropathy(AMSAN)
Miller Fisher Syndrome(MFS)
Polyneuritis Cranialis
CLINICAL MANIFESTATIONS
Paresthesia is frequent followed by paralysis in the extremities
Hypotonia
Areflexia Autonomic dysfunctions include orthostatic hypotension
Hypertension
Abnormal vagal responses
Bowel and bladder dysfunction
Facial flushing
Diaphoresis
Syndrome of inappropriate anti diuretic hormoneProgression of Guillain barre syndrome
include lower brain stem that involves the
Facial Nerve
Abducens Nerve
Oculo Motor Nerve
Hypoglossal Nerve
Trigeminal Nerve
Vagus Nerve
Pain Is a common symptom and It becomes worse at Night.
TREATMENT
On set to two weeks: Plasma pheresis (40-50 ml/kg four times a week
After two weeks: intravenous administration of high dose immunoglobulin (Sandoglobulin)
Beyond three weeks: plasma exchange and immunoglobulin therapies
Chest Physiotherapy
Artificial ventilation-Maintain Gas Exchange
COMPLICATIONS
Cardiac arrhythmias
Respiratory failures
Dys autonomia
Pneumonia
Adult Respiratory Distress Syndrome
Septicemia
Death
Poliomyelitis, also known as polio, is caused by a virus that attacks the nerve cells of the brain and spinal cord. It was first recorded in the late 1700s and caused epidemics in the late 1800s. While most infections result in no symptoms, it can cause paralysis in rare cases by destroying motor neurons. The poliovirus is transmitted through oral and fecal routes. Symptoms range from fever and vomiting to aseptic meningitis. Paralysis was feared during outbreaks in the early 20th century before vaccinations were developed. The polio vaccine introduced in 1955 eradicated the disease in most developed nations.
Guillain-Barré syndrome with Physiotherapeautic managementsSAGAR KUMAR GOUDA
GBS, also known as Guillain-Barre syndrome, is an acute immune-mediated polyneuropathy that results in demyelination of peripheral nerves. It typically presents with ascending paralysis, though some patients experience descending paralysis or a Miller-Fisher variant characterized by ophthalmoplegia. Physiotherapy management aims to prevent complications through techniques like chest physiotherapy, range of motion exercises, positioning, and addressing pain and weakness. Treatment includes supportive care, plasmapheresis, IVIG, and focusing on recovery of motor and sensory function.
This document discusses poliomyelitis (polio) and post-polio syndrome (PPS). It describes how polio is caused by poliovirus, spreads through the fecal-oral route, and can cause acute flaccid paralysis. It outlines the pathogenesis, clinical manifestations including monophasic or biphasic illness, and methods for diagnosis of polio. It then discusses PPS, which involves new muscle weakness or fatigue in polio survivors decades later, and the role of electrophysiological testing in evaluating PPS.
Multiple sclerosis is an autoimmune disease that destroys the myelin sheath protecting nerve fibers in the central nervous system. It causes symptoms like visual problems, motor dysfunction, fatigue, and mood changes. Diagnosis involves MRI and lumbar puncture. Nursing care focuses on promoting mobility, preventing injuries, managing symptoms, and strengthening coping.
Guillain-Barré syndrome is an autoimmune disorder where the body's immune system attacks the peripheral nervous system, causing muscle weakness and sometimes paralysis. It is usually triggered by a viral or bacterial infection. Nursing care includes maintaining respiratory function, enhancing physical mobility, providing adequate nutrition, and managing complications.
Alzheimer's disease is a progressive brain disorder causing cognitive decline. Sympt
1) Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy that is a common cause of acute flaccid paralysis.
2) It is caused by an autoimmune attack against peripheral nerves following a viral or bacterial infection. Campylobacter jejuni is a frequent trigger that shares antigens with human nerves.
3) Clinical features include ascending limb weakness, diminished reflexes, and possible involvement of cranial nerves and respiratory muscles. Diagnosis involves CSF analysis showing elevated proteins with normal cell count and electrophysiology showing demyelination.
This document provides information about poliomyelitis (polio). It defines polio as a viral illness caused by poliovirus that can lead to paralysis. There are 3 types of poliovirus. Polio spreads through the gastrointestinal tract and sometimes to the central nervous system. Most polio infections are asymptomatic, but some cause abortive or nonparalytic illness. Rarely, it causes paralytic polio. Treatment involves supportive care, while vaccines can prevent the disease.
The document describes a case of poliomyelitis in a 13-year-old patient who wanted to be a dancer. Within two weeks, they lost coordination and 20 pounds and became paralyzed, turning their passion into pain. Poliomyelitis is a highly infectious viral disease that destroys motor neurons and damages the brain and spinal cord, causing muscle weakness and paralysis. It is classified based on symptoms, and while most cases are asymptomatic or mild, some can result in paralysis affecting the legs, breathing, or both.
AN-MSN II 09.6.2020AN-GUILLAIN BARRE SYNDROME.pptxPrakash554699
This document discusses Guillain-Barré syndrome (GBS), an acute immune-mediated polyneuropathy that results in rapid progressive motor paralysis. GBS is characterized by acute onset muscle weakness that spreads throughout the body. It is caused by an autoimmune response triggered by bacterial or viral infections. Diagnosis involves neurological exams, cerebrospinal fluid analysis, electromyography, and nerve conduction studies. Treatment aims to prevent complications through respiratory support, physical therapy, intravenous immunoglobulins, and plasma exchange. Nursing care focuses on monitoring respiratory function, range of motion exercises, and managing symptoms like pain and impaired communication.
Peripheral neuropathy in systemic disease childrenNeurologyKota
This document discusses peripheral neuropathies that can occur in children due to systemic diseases. It notes that the overall prevalence of peripheral neuropathies is estimated to be 2-4% in children, with around 20-50% of cases remaining undiagnosed. It then lists and describes 12 systemic diseases that can be associated with peripheral neuropathies in children, including liver diseases, endocrinopathies, renal failure, amyloidosis, and connective tissue disorders. The document concludes by discussing some specific neuropathies in more detail, such as those related to diabetes, thyroid disease, amyloidosis, vasculitis, and critical illness.
SSPE, dr. amit vatkar, pediatric neurologistDr Amit Vatkar
Subacute sclerosing pan encephalitis (SSPE) also known as Dawson Disease, Dawson encephalitis, and measles encephalitis is a rare and chronic form of progressive brain inflammation caused by a persistent infection with measles virus.
In this presentaion i will a case a sspe and give u some information regarding daignosis and treatment
I. The peripheral nervous system carries signals between the central nervous system and the rest of the body. It has three main components - cranial, spinal, and autonomic. There are three main types of nerve fibers - A, B, and C - which differ in diameter, myelination, and function.
II. Peripheral neuropathies can be acquired through systemic diseases, trauma, infections, or inherited genetically. Common acquired neuropathies include diabetic neuropathy, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and alcoholic neuropathy. Inherited forms include Charcot-Marie-Tooth disease and hereditary liability to pressure palsies.
Seizures are episodes of abnormal brain activity resulting from excessive neuronal discharge. Epilepsy is characterized by recurrent seizures and is caused by various factors like brain tumors, genetic predisposition, trauma and infections. Seizures can be classified as partial or generalized based on the area of brain involved. Diagnostic tests include EEG, MRI and blood tests. Treatment involves medications, surgery, vagus nerve stimulation or lifestyle modifications. Nursing care focuses on safety during seizures and education about managing the condition.
Delayed recovery from anesthesia can have multiple contributing factors and causes. It is important to consider potential drug interactions, metabolic abnormalities, and organic causes that may cause prolonged unconsciousness and have serious health implications. Signs and symptoms of metabolic issues may not present normally in an anesthetized patient. The Glasgow Coma Scale provides an objective measure of conscious state regardless of cause.
Paralysis is the most devastating effect of poliovirus infection. While most polio infections are subclinical, universal vaccination and improved sanitation have led to the eradication of polio in most countries except Nigeria, Afghanistan and Pakistan. Poliovirus is transmitted via the fecal-oral route and infects the gastrointestinal tract before spreading to the central nervous system in some cases, where it can cause paralysis. Diagnosis involves isolating the virus from stool samples. Treatment is supportive only, while prevention relies on vaccination strategies promoted by the WHO.
Similar to Síndrome Post Polio, Dr. Jaime López-Ventura (20)
Exposición de resultados de la 2ª fase del estudio "Índice de fatiga en pacientes con Síndrome Postpolio (G-14), Prof. Dr. Antonio Cuesta-Vargas. Facultad Ciencias de la Salud. UMA
Este documento proporciona información sobre el Síndrome Post-Polio (SPP). Explica que el SPP afecta a sobrevivientes de la poliomielitis años después de haberse recuperado inicialmente de la enfermedad, causando una pérdida progresiva de fuerza y resistencia muscular. Describe los principales síntomas del SPP como fatiga, dolor, debilidad y problemas respiratorios. Finalmente, recomienda ejercicios suaves, estiramientos, natación y fisioterapia acuática para mejorar
Dr. Salazar Agulló, J.A. Médico jubilado. Vocal Investigación AMAPyP.
Dra. Muñoz Cobos, F. MF. CS. El Palo- Málaga.
Comunicación presentada en el II Congreso Nacional de la Medicina (COM Málaga)
Dr. Salazar Agulló, J.A. Médico jubilado. Vocal de investigación de AMAPyP.
Dr. Cuesta-Vargas, A. Cátedra Fisioterapia y Discapacidad. UMA.
DRA. Muñoz Cobos, F. MF. CS. El Palo -Málaga
Comunicación oral premiada en el II Congreso Nacional de la Medicina (Málaga, 4 y 5 abril 2019)
El individuo con poliomielitis en fase tardía. Visión ortopédica, Dr. José Carlos Montosa. II Jornadas sobre Efectos Tardíos de la Polio y Síndrome Postpolio. Hospital de Antequera. Asociación AMAPyP. Málaga, 25-10-2017
"Medidas físicas y ortésicas en pacientes con secuelas de poliomielitis", Dra. Susana Gimeno Cerezo. II Jornadas sobre los Efectos Tardíos de la Polio y Síndrome Postpolio. Hospital de Antequera. Asociación AMAPyP. Málaga, 25-10-2017
Ponencia de la Dra. Concha Pérez en la Jornada científica sobre la Poliomiemlitis, organizada por la UGC. Aparato Locomotor. Hospital U. Virgen de la Victoria de Málaga.
Málaga, 20-10-2017
Ponencia de la Dra. Belén Castro en la Jornada científica sobre la Poliomiemlitis, organizada por la UGC. Aparato Locomotor. Hospital U. Virgen de la Victoria de Málaga.
Málaga, 20-10-2017
Presentación, a cargo de la Asociación AMAPyP, en la Jornada científica: Mesa redonda en torno a la Poliomielitis, organizada por UGC. Aparato Locomotor del Hospital U. Virgen de la Victoria de Málaga (20-10-2017)
Presentación del libro "Sueños en la mirada", a beneficio de la investigación del Síndrome Postpolio (SPP) y otros efectos tardíos de la polio. 22-06-2017, en el Colegio de Médicos de Málaga. Más información: http://www.amapyp.com/suentildeos-en-la-mirada.html
El documento discute cómo la inteligencia emocional y la resiliencia pueden ayudar a mejorar la calidad de vida de los pacientes con síndrome post-polio. La inteligencia emocional se refiere a la habilidad de reconocer y regular las propias emociones y las de los demás, mientras que la resiliencia es la capacidad de sobreponerse a los problemas. El documento argumenta que desarrollar estas habilidades a través de intervenciones psicológicas puede ayudar a los pacientes a enfrentar mejor los síntomas f
Taller de Autocuidados y Tratamiento Rehabilitador (1ª sesión: 15 de mayo de 2014)
Dra. Marina Tirado Reyes, UGC. Medicina Física y de Rehabiliatción
Hospital Regional Universitario de Málaga (Hospital Civil)
Taller para personas afectadas por la polio.
UGC. Medicina Física y Rehabilitación del Hospital Regional de Málaga (H. Civil). Asociación Malagueña de Afectados Polio y Postpolio "AMAPyP".
Mesa redonda. Intervención de AMAPyP.
VIII Comisión de Participación Ciudadana de los Hospitales Universitarios Regional de Málaga y Virgen de la Victoria.
Málaga, 24 de abril de 2014
More from AMAPyP Asoc. Malague. de Afect. Polio y Postpol (20)
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.
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Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
1. SINDROME POST POLIO
ISMAEL LÓPEZ-VENTURA JIMENO
Especialista en Neurología, Especialista en Medicina Interna
AGS. Norte de Málaga
2. POSTPOLIO:ALGUNOS DATOS
PUEDEY SUELE APARECER
MUCHOS AÑOS DESPUÉS
DEL DIAGNÓSTICO
PUEDE APARECER TRAS
UNA SITUACIÓN DE
ESTRÉS, UNA CAIDA, UN
INGRESO HOSPITALARIO..
10. POSTPOLIOTEORIA
AUTOINMUNE
J Neuroinfl ammation. 2012; 9: 167.
Published online 2012 Jul 9. doi: 10.1186/1742-2094-9-167
PMCID: PMC3464723
Intravenous immunoglobulin treatment of the post-polio syndrome: sustained effects on quality of life variables and
cytokine expression after one year follow up
Henrik Gonzalez,1 Mohsen Khademi,2 Kristian Borg,1 and Tomas Olsson2
1Division of Rehabilitation Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, blg 39, fl 3, S-
192 88, Stockholm, Sweden
2Neuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
Corresponding author.
Henrik Gonzalez: moc.ailet@selaznog.kirneh; Mohsen Khademi: es.ik@imedahK.neshoM; Kristian Borg: es.ik@groB.naitsirK;
Tomas Olsson: es.ik@nosslO.samoT
14. POSTPOLIOTRATAMIENTO
TRATAMIENTO DEL DOLOR:AINES, PARACETAMOL
EJERCICIO MODERADO CON PAUSAS, DEJAR DE FUMAR
TRATAMIENTO DE APNEA DEL SUEÑO
VACUNAS DE LA GRIPEY DEL NEUMOCOCO
NUEVOS TRATAMIENTO COMO IGIV??