Mononeuritis multiplex is a peripheral neuropathy involving damage to two or more noncontiguous nerves. It can be caused by various systemic conditions like diabetes, vasculitis, infections, and rheumatological disorders. The document discusses the clinical presentation, diagnostic evaluation, management, and treatment of mononeuritis multiplex.
This document summarizes the revisions made to the McDonald criteria for diagnosing multiple sclerosis over time. The 2017 revisions aimed to simplify and clarify the 2010 criteria to facilitate earlier diagnosis when MS is likely but not definitively diagnosed. Key changes include allowing symptomatic and asymptomatic lesions to demonstrate dissemination in space and time, and cortical/juxtacortical lesions to fulfill MRI criteria. CSF oligoclonal bands alone can now establish a diagnosis. The revisions were motivated by new data on diagnostic accuracy in diverse populations and distinguishing MS from similar conditions.
This document discusses various causes of non-compressive myelopathy, including infectious, inflammatory, vascular, metabolic, degenerative, and physical agent causes. It covers specific conditions such as transverse myelitis, multiple sclerosis, spinal infarction, vascular malformations, vitamin B12 deficiency, and radiation myelopathy. Treatment approaches are mentioned for some conditions.
Approach to different Demyelinating disorders in the Paediatric age-group. Namely- acute disseminated encephalomyelitis, paediatric multiple sclerosis, neuromyelitis optica. Approach, MRI features, differences, clinical features
This document provides an overview of white matter diseases. It discusses:
1. Primary demyelinating diseases like multiple sclerosis and neuromyelitis optica which are characterized by loss of myelin.
2. Secondary demyelination caused by known etiologies like infections, metabolic disorders, or vascular issues which result in destruction of both axons and myelin.
3. Dysmyelinating/hypomyelinating leukodystrophies which involve defective or incomplete myelin formation, including some common causes like metachromatic leukodystrophy.
4. The clinical approach involves considering features like onset, progression, family history, involvement of other organs, and patterns
Mononeuritis multiplex is a peripheral neuropathy involving damage to two or more noncontiguous nerves. It can be caused by various systemic conditions like diabetes, vasculitis, infections, and rheumatological disorders. The document discusses the clinical presentation, diagnostic evaluation, management, and treatment of mononeuritis multiplex.
This document summarizes the revisions made to the McDonald criteria for diagnosing multiple sclerosis over time. The 2017 revisions aimed to simplify and clarify the 2010 criteria to facilitate earlier diagnosis when MS is likely but not definitively diagnosed. Key changes include allowing symptomatic and asymptomatic lesions to demonstrate dissemination in space and time, and cortical/juxtacortical lesions to fulfill MRI criteria. CSF oligoclonal bands alone can now establish a diagnosis. The revisions were motivated by new data on diagnostic accuracy in diverse populations and distinguishing MS from similar conditions.
This document discusses various causes of non-compressive myelopathy, including infectious, inflammatory, vascular, metabolic, degenerative, and physical agent causes. It covers specific conditions such as transverse myelitis, multiple sclerosis, spinal infarction, vascular malformations, vitamin B12 deficiency, and radiation myelopathy. Treatment approaches are mentioned for some conditions.
Approach to different Demyelinating disorders in the Paediatric age-group. Namely- acute disseminated encephalomyelitis, paediatric multiple sclerosis, neuromyelitis optica. Approach, MRI features, differences, clinical features
This document provides an overview of white matter diseases. It discusses:
1. Primary demyelinating diseases like multiple sclerosis and neuromyelitis optica which are characterized by loss of myelin.
2. Secondary demyelination caused by known etiologies like infections, metabolic disorders, or vascular issues which result in destruction of both axons and myelin.
3. Dysmyelinating/hypomyelinating leukodystrophies which involve defective or incomplete myelin formation, including some common causes like metachromatic leukodystrophy.
4. The clinical approach involves considering features like onset, progression, family history, involvement of other organs, and patterns
This document provides information on diagnosing and classifying vasculitic neuropathies. It discusses:
1) The International Chapel Hill Consensus Conference classification of vasculitis which categorizes them based on the size of blood vessels involved.
2) Diagnostic criteria for pathologically definite, probable, and possible vasculitic neuropathy based on nerve biopsy findings.
3) Clinical patterns of neuropathic involvement in vasculitic neuropathies including multiple mononeuropathies, overlapping mononeuropathies, and distal symmetric neuropathies.
This document summarizes neurological manifestations of human immunodeficiency virus (HIV). It discusses how HIV can affect both the central nervous system and peripheral nervous system. Some key points:
- Up to 50% of HIV patients experience clinically apparent neurological disease. Common manifestations involve the brain, meninges, spinal cord, peripheral nerves, and muscles.
- Direct effects of HIV include infection of cells like macrophages, monocytes, microglia, and possibly astrocytes. Indirect effects include opportunistic infections and neoplasms.
- Common CNS manifestations include HIV encephalopathy/dementia, space-occupying lesions, encephalitis, and stroke-like syndromes. Common peripheral
1) Normal pressure hydrocephalus (NPH) is characterized by abnormal gait, urinary incontinence, and dementia. It is most common in the elderly and can be caused by conditions like subarachnoid hemorrhage.
2) Diagnosis involves evaluating symptoms, imaging tests showing disproportionate ventricle enlargement, and tests like lumbar puncture to check CSF pressure and flow.
3) Treatment usually involves surgically placing a CSF shunt if symptoms improve with temporary drainage, with benefits seen in 50-61% of cases but also a high risk of complications.
This document provides an overview of leukodystrophies and discusses their clinical presentation and neuroimaging features. It begins with definitions of leukodystrophies and outlines their age of onset. Common clinical features are then described, including neurological, non-neurological, ophthalmological, and radiological findings. A stepwise approach to the neuroimaging of leukodystrophies is presented, focusing on patterns of white matter involvement that can help differentiate genetic from acquired causes.
This document provides information about acute disseminated encephalomyelitis (ADEM). It defines ADEM as a demyelinating disease of the central nervous system that typically presents as a monophasic disorder with encephalopathy and multifocal neurological symptoms. The document discusses the pathogenesis, clinical features, diagnosis, differential diagnosis and treatment of ADEM. It states that ADEM is usually treated initially with high-dose intravenous corticosteroids over 3-5 days.
This document provides an overview of approaches to diagnosing leukodystrophies. It begins by defining leukodystrophies and differentiating them from other white matter disorders. Clinical features that suggest a leukodystrophy are described. A 3-step MRI approach is outlined involving identifying symmetric white matter involvement, patterns of involvement, and distinctive features. Common leukodystrophies in adults are discussed in detail including clinical presentation, genetics, imaging findings, and diagnostic testing. The document emphasizes a systematic approach to diagnosis utilizing clinical features, imaging, and ancillary tests.
Demyelinating and inflammatory diseasesShivam Batra
Demyelinating diseases involve disruption of myelin in the central and peripheral nervous systems. Multiple sclerosis (MS) is an autoimmune demyelinating disease characterized by inflammatory demyelinating lesions throughout the white matter. MRI is useful for diagnosing MS by demonstrating dissemination of lesions in space and time. Typical MS lesions on MRI appear as oval or linear hyperintensities on T2/FLAIR images surrounding medullary veins and involving the periventricular white matter, corpus callosum, brainstem, and cortical gray matter.
1) Neurological signs that indicate dysfunction in a different area of the brain than would be expected given the location of pathology are known as false localizing signs.
2) False localizing signs can occur due to compression of brain structures distant from the site of a lesion, such as cranial nerve palsies resulting from compression against the skull base.
3) Dysfunction of motor or sensory pathways can also produce false localizing signs, like contralateral hemiparesis from transtentorial herniation compressing the cerebral peduncle.
The document discusses the importance of carefully considering alternative diagnoses to multiple sclerosis (MS) when evaluating patients. Common causes of MS misdiagnosis include nonspecific white matter abnormalities on brain MRI and vague neurological symptoms. Other disorders like neuromyelitis optica spectrum disorders, acute disseminated encephalomyelitis, and inherited disorders can mimic MS clinically and radiologically. A thorough evaluation of demographic, clinical, laboratory, and imaging factors is necessary to avoid misdiagnosis, as an MS diagnosis has significant implications for treatment.
Vitamin B12 deficiency is a common cause of nutritional myelopathy. It presents as slowly progressive myelopathy involving the posterior and lateral spinal cord. Peripheral neuropathy and neuropsychiatric manifestations may also occur. Diagnosis is based on low vitamin B12 levels and elevated methylmalonic acid and homocysteine levels. Treatment involves lifelong parenteral vitamin B12 replacement therapy. Neurological symptoms may improve over months following treatment. Nitrous oxide exposure can also cause vitamin B12 deficient myelopathy, especially in individuals with underlying B12 deficiency.
This document discusses the anatomy, landmarks, measurements, common anomalies, syndromes, and injuries of the craniovertebral junction. It begins with a brief description of the craniovertebral junction's development and components. It then outlines several key anatomical landmarks and measurements used to evaluate the region on imaging. The remainder of the document details various congenital anomalies, developmental abnormalities, syndromes, and acquired conditions that can affect the craniovertebral junction.
Parkinson plus syndrome refers to atypical Parkinsonism syndromes that are more challenging to diagnose than Parkinson's disease due to overlapping symptoms. The document discusses several Parkinson plus syndromes including progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB). It provides details on the epidemiology, clinical features, investigations, treatments, and prognosis of each condition. PSP is characterized by early falls and vertical gaze palsy. CBD presents with asymmetric rigidity and dystonia. MSA involves parkinsonism, cerebellar ataxia, and autonomic dysfunction. DLB involves early
Multiple sclerosis is a chronic disease characterized by inflammation, demyelination, and gliosis in the central nervous system. It affects around 5 million people worldwide. The cause is unknown but involves genetic and environmental factors. Symptoms vary widely and can include sensory disturbances, motor symptoms, visual problems, ataxia, and cognitive impairment. Diagnosis involves demonstrating dissemination of lesions in the CNS over time via MRI imaging or evoked potentials testing, and sometimes analysis of cerebrospinal fluid. There are several disease courses including relapsing-remitting MS, primary progressive MS, and secondary progressive MS. Management aims to reduce inflammation and disability progression.
The document discusses acute disseminated encephalomyelitis (ADEM), a rare inflammatory disease of the central nervous system. ADEM is typically triggered by an environmental stimulus in genetically susceptible individuals. It most commonly affects children between 5-8 years old, with symptoms developing within 2 weeks of a viral or bacterial infection in approximately 50-75% of cases. Diagnosis is based on clinical presentation and MRI findings showing multifocal brain inflammation. Treatment involves high-dose corticosteroids, with plasma exchange or IVIG recommended for non-responders. Most children recover fully, but some have residual symptoms like headaches or behavioral issues.
1. The document discusses various causes of myelopathy including infectious, autoimmune, demyelinating, paraneoplastic, metabolic, toxic, and vascular etiologies.
2. Clinical features, imaging, cerebrospinal fluid analysis and differential diagnosis for different types of myelopathies are provided with key distinguishing factors between compressive vs non-compressive, inflammatory vs non-inflammatory myelopathies.
3. Specific conditions like acute transverse myelitis, neuromyelitis optica, HIV myelopathy, syphilitic myelopathy, and acute disseminated encephalomyelitis are summarized in detail.
Multiple system atrophy is a rare, fatal neurodegenerative disease characterized by parkinsonian or cerebellar features and autonomic dysfunction. It is caused by the accumulation of alpha-synuclein protein in oligodendrocytes throughout the brain and spinal cord. There are no disease-modifying treatments available, so management focuses on alleviating motor symptoms and addressing problems related to autonomic failure and other non-motor issues.
1) Cerebral venous thrombosis (CVT) is an uncommon form of stroke caused by thrombosis of cerebral veins and dural sinuses. It presents with highly variable clinical features including headache, seizures, focal neurological deficits, and altered mental status.
2) Risk factors for CVT include inherited and acquired thrombophilias, pregnancy, oral contraceptive use, and various systemic diseases. Diagnosis is made using neuroimaging techniques like MRI, MRV, and CT venography.
3) Treatment involves anticoagulation with heparin or warfarin for 3-12 months depending on risk factors. Outcomes are generally good with around 80% of patients making a complete or near-complete recovery, but mortality
The craniovertebral junction (CVJ) refers to the occiput, atlas, axis, and supporting ligaments. It is a transition zone between the mobile cranium and spinal column. The CVJ encloses important neural and vascular structures.
Anatomically, the CVJ includes bony structures like the occiput, atlas, and axis along with their articulations and connecting ligaments. It also has muscles, neural elements like the medulla and lower cranial nerves, lymphatics, arteries and veins. Congenital anomalies of the CVJ can occur due to malformations during embryological development.
Radiological evaluation of the CVJ involves measurements and angles on X
Metachromatic leukodystrophy is a rare lysosomal storage disorder caused by a deficiency of the enzyme arylsulfatase A. This leads to a buildup of sulfatide in the body's cells. It is inherited in an autosomal recessive pattern and causes demyelination in the nervous system. Clinical presentations vary by age of onset, but common symptoms include cognitive and behavioral issues. Hematopoietic stem cell transplantation is the primary treatment option.
Motor neuron disease - Etiology, Pathogenesis, Clinical Features, Classificat...Chetan Ganteppanavar
This document discusses motor neuron diseases, including amyotrophic lateral sclerosis (ALS). It provides details on the classification, symptoms, signs, diagnosis, prognosis, and management of ALS and related conditions. Key points include that ALS is characterized by the degeneration of both upper and lower motor neurons, leading to muscle weakness, atrophy, and fasciculations. Diagnosis involves finding signs of both upper and lower motor neuron involvement. Prognosis is typically worse if onset is bulbar or simultaneous in multiple limbs. Treatment focuses on managing symptoms while no treatments have been proven to slow disease progression.
The document discusses the history and key developments in understanding multiple sclerosis from its initial description in 1868 to recent advances in 2001. It covers landmark events such as the discovery of myelin in 1878 and oligoclonal bands in spinal fluid in 1948. The epidemiology, immunopathogenesis, clinical course, diagnosis, and management of multiple sclerosis are also summarized.
Multiple sclerosis (MS) is a demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged.This damage disrupts the ability of parts of the nervous system to communicate, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems
This document provides information on diagnosing and classifying vasculitic neuropathies. It discusses:
1) The International Chapel Hill Consensus Conference classification of vasculitis which categorizes them based on the size of blood vessels involved.
2) Diagnostic criteria for pathologically definite, probable, and possible vasculitic neuropathy based on nerve biopsy findings.
3) Clinical patterns of neuropathic involvement in vasculitic neuropathies including multiple mononeuropathies, overlapping mononeuropathies, and distal symmetric neuropathies.
This document summarizes neurological manifestations of human immunodeficiency virus (HIV). It discusses how HIV can affect both the central nervous system and peripheral nervous system. Some key points:
- Up to 50% of HIV patients experience clinically apparent neurological disease. Common manifestations involve the brain, meninges, spinal cord, peripheral nerves, and muscles.
- Direct effects of HIV include infection of cells like macrophages, monocytes, microglia, and possibly astrocytes. Indirect effects include opportunistic infections and neoplasms.
- Common CNS manifestations include HIV encephalopathy/dementia, space-occupying lesions, encephalitis, and stroke-like syndromes. Common peripheral
1) Normal pressure hydrocephalus (NPH) is characterized by abnormal gait, urinary incontinence, and dementia. It is most common in the elderly and can be caused by conditions like subarachnoid hemorrhage.
2) Diagnosis involves evaluating symptoms, imaging tests showing disproportionate ventricle enlargement, and tests like lumbar puncture to check CSF pressure and flow.
3) Treatment usually involves surgically placing a CSF shunt if symptoms improve with temporary drainage, with benefits seen in 50-61% of cases but also a high risk of complications.
This document provides an overview of leukodystrophies and discusses their clinical presentation and neuroimaging features. It begins with definitions of leukodystrophies and outlines their age of onset. Common clinical features are then described, including neurological, non-neurological, ophthalmological, and radiological findings. A stepwise approach to the neuroimaging of leukodystrophies is presented, focusing on patterns of white matter involvement that can help differentiate genetic from acquired causes.
This document provides information about acute disseminated encephalomyelitis (ADEM). It defines ADEM as a demyelinating disease of the central nervous system that typically presents as a monophasic disorder with encephalopathy and multifocal neurological symptoms. The document discusses the pathogenesis, clinical features, diagnosis, differential diagnosis and treatment of ADEM. It states that ADEM is usually treated initially with high-dose intravenous corticosteroids over 3-5 days.
This document provides an overview of approaches to diagnosing leukodystrophies. It begins by defining leukodystrophies and differentiating them from other white matter disorders. Clinical features that suggest a leukodystrophy are described. A 3-step MRI approach is outlined involving identifying symmetric white matter involvement, patterns of involvement, and distinctive features. Common leukodystrophies in adults are discussed in detail including clinical presentation, genetics, imaging findings, and diagnostic testing. The document emphasizes a systematic approach to diagnosis utilizing clinical features, imaging, and ancillary tests.
Demyelinating and inflammatory diseasesShivam Batra
Demyelinating diseases involve disruption of myelin in the central and peripheral nervous systems. Multiple sclerosis (MS) is an autoimmune demyelinating disease characterized by inflammatory demyelinating lesions throughout the white matter. MRI is useful for diagnosing MS by demonstrating dissemination of lesions in space and time. Typical MS lesions on MRI appear as oval or linear hyperintensities on T2/FLAIR images surrounding medullary veins and involving the periventricular white matter, corpus callosum, brainstem, and cortical gray matter.
1) Neurological signs that indicate dysfunction in a different area of the brain than would be expected given the location of pathology are known as false localizing signs.
2) False localizing signs can occur due to compression of brain structures distant from the site of a lesion, such as cranial nerve palsies resulting from compression against the skull base.
3) Dysfunction of motor or sensory pathways can also produce false localizing signs, like contralateral hemiparesis from transtentorial herniation compressing the cerebral peduncle.
The document discusses the importance of carefully considering alternative diagnoses to multiple sclerosis (MS) when evaluating patients. Common causes of MS misdiagnosis include nonspecific white matter abnormalities on brain MRI and vague neurological symptoms. Other disorders like neuromyelitis optica spectrum disorders, acute disseminated encephalomyelitis, and inherited disorders can mimic MS clinically and radiologically. A thorough evaluation of demographic, clinical, laboratory, and imaging factors is necessary to avoid misdiagnosis, as an MS diagnosis has significant implications for treatment.
Vitamin B12 deficiency is a common cause of nutritional myelopathy. It presents as slowly progressive myelopathy involving the posterior and lateral spinal cord. Peripheral neuropathy and neuropsychiatric manifestations may also occur. Diagnosis is based on low vitamin B12 levels and elevated methylmalonic acid and homocysteine levels. Treatment involves lifelong parenteral vitamin B12 replacement therapy. Neurological symptoms may improve over months following treatment. Nitrous oxide exposure can also cause vitamin B12 deficient myelopathy, especially in individuals with underlying B12 deficiency.
This document discusses the anatomy, landmarks, measurements, common anomalies, syndromes, and injuries of the craniovertebral junction. It begins with a brief description of the craniovertebral junction's development and components. It then outlines several key anatomical landmarks and measurements used to evaluate the region on imaging. The remainder of the document details various congenital anomalies, developmental abnormalities, syndromes, and acquired conditions that can affect the craniovertebral junction.
Parkinson plus syndrome refers to atypical Parkinsonism syndromes that are more challenging to diagnose than Parkinson's disease due to overlapping symptoms. The document discusses several Parkinson plus syndromes including progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB). It provides details on the epidemiology, clinical features, investigations, treatments, and prognosis of each condition. PSP is characterized by early falls and vertical gaze palsy. CBD presents with asymmetric rigidity and dystonia. MSA involves parkinsonism, cerebellar ataxia, and autonomic dysfunction. DLB involves early
Multiple sclerosis is a chronic disease characterized by inflammation, demyelination, and gliosis in the central nervous system. It affects around 5 million people worldwide. The cause is unknown but involves genetic and environmental factors. Symptoms vary widely and can include sensory disturbances, motor symptoms, visual problems, ataxia, and cognitive impairment. Diagnosis involves demonstrating dissemination of lesions in the CNS over time via MRI imaging or evoked potentials testing, and sometimes analysis of cerebrospinal fluid. There are several disease courses including relapsing-remitting MS, primary progressive MS, and secondary progressive MS. Management aims to reduce inflammation and disability progression.
The document discusses acute disseminated encephalomyelitis (ADEM), a rare inflammatory disease of the central nervous system. ADEM is typically triggered by an environmental stimulus in genetically susceptible individuals. It most commonly affects children between 5-8 years old, with symptoms developing within 2 weeks of a viral or bacterial infection in approximately 50-75% of cases. Diagnosis is based on clinical presentation and MRI findings showing multifocal brain inflammation. Treatment involves high-dose corticosteroids, with plasma exchange or IVIG recommended for non-responders. Most children recover fully, but some have residual symptoms like headaches or behavioral issues.
1. The document discusses various causes of myelopathy including infectious, autoimmune, demyelinating, paraneoplastic, metabolic, toxic, and vascular etiologies.
2. Clinical features, imaging, cerebrospinal fluid analysis and differential diagnosis for different types of myelopathies are provided with key distinguishing factors between compressive vs non-compressive, inflammatory vs non-inflammatory myelopathies.
3. Specific conditions like acute transverse myelitis, neuromyelitis optica, HIV myelopathy, syphilitic myelopathy, and acute disseminated encephalomyelitis are summarized in detail.
Multiple system atrophy is a rare, fatal neurodegenerative disease characterized by parkinsonian or cerebellar features and autonomic dysfunction. It is caused by the accumulation of alpha-synuclein protein in oligodendrocytes throughout the brain and spinal cord. There are no disease-modifying treatments available, so management focuses on alleviating motor symptoms and addressing problems related to autonomic failure and other non-motor issues.
1) Cerebral venous thrombosis (CVT) is an uncommon form of stroke caused by thrombosis of cerebral veins and dural sinuses. It presents with highly variable clinical features including headache, seizures, focal neurological deficits, and altered mental status.
2) Risk factors for CVT include inherited and acquired thrombophilias, pregnancy, oral contraceptive use, and various systemic diseases. Diagnosis is made using neuroimaging techniques like MRI, MRV, and CT venography.
3) Treatment involves anticoagulation with heparin or warfarin for 3-12 months depending on risk factors. Outcomes are generally good with around 80% of patients making a complete or near-complete recovery, but mortality
The craniovertebral junction (CVJ) refers to the occiput, atlas, axis, and supporting ligaments. It is a transition zone between the mobile cranium and spinal column. The CVJ encloses important neural and vascular structures.
Anatomically, the CVJ includes bony structures like the occiput, atlas, and axis along with their articulations and connecting ligaments. It also has muscles, neural elements like the medulla and lower cranial nerves, lymphatics, arteries and veins. Congenital anomalies of the CVJ can occur due to malformations during embryological development.
Radiological evaluation of the CVJ involves measurements and angles on X
Metachromatic leukodystrophy is a rare lysosomal storage disorder caused by a deficiency of the enzyme arylsulfatase A. This leads to a buildup of sulfatide in the body's cells. It is inherited in an autosomal recessive pattern and causes demyelination in the nervous system. Clinical presentations vary by age of onset, but common symptoms include cognitive and behavioral issues. Hematopoietic stem cell transplantation is the primary treatment option.
Motor neuron disease - Etiology, Pathogenesis, Clinical Features, Classificat...Chetan Ganteppanavar
This document discusses motor neuron diseases, including amyotrophic lateral sclerosis (ALS). It provides details on the classification, symptoms, signs, diagnosis, prognosis, and management of ALS and related conditions. Key points include that ALS is characterized by the degeneration of both upper and lower motor neurons, leading to muscle weakness, atrophy, and fasciculations. Diagnosis involves finding signs of both upper and lower motor neuron involvement. Prognosis is typically worse if onset is bulbar or simultaneous in multiple limbs. Treatment focuses on managing symptoms while no treatments have been proven to slow disease progression.
The document discusses the history and key developments in understanding multiple sclerosis from its initial description in 1868 to recent advances in 2001. It covers landmark events such as the discovery of myelin in 1878 and oligoclonal bands in spinal fluid in 1948. The epidemiology, immunopathogenesis, clinical course, diagnosis, and management of multiple sclerosis are also summarized.
Multiple sclerosis (MS) is a demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged.This damage disrupts the ability of parts of the nervous system to communicate, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems
MRI is the gold standard for diagnosing multiple sclerosis (MS). It can detect focal demyelinating lesions appearing as hyperintense areas on T2-weighted MRI. Different MRI sequences like T1, T2, FLAIR, and gadolinium contrast help identify lesions at various stages. MS lesions typically occur in periventricular white matter, corpus callosum, brainstem, and spinal cord. Advanced MRI techniques like MTR, DTI, and MRS provide additional insights into MS pathology by detecting subtle tissue damage. MRI plays a key role in the diagnostic criteria for MS by demonstrating dissemination of lesions in space and time. It is also used as an outcome measure in clinical trials to monitor
The document summarizes proposed updates to MRI criteria for diagnosing multiple sclerosis (MS) by the MAGNIMS group in 2016. The updates aim to 1) expand the definition of dissemination in space to include more lesion locations, 2) revise lesion count requirements, and 3) remove the distinction between symptomatic and asymptomatic lesions. The changes also broaden the criteria's applicability to more age groups and ethnicities. Key revisions include requiring 3+ periventricular lesions instead of 1, considering lesions in the optic nerves, and applying the same dissemination standards to both relapsing-remitting and primary progressive MS. The updates are meant to improve sensitivity while maintaining specificity in MS diagnosis.
The document provides guidance on performing a neurological examination. It emphasizes that obtaining a thorough clinical history is key to making an accurate diagnosis, as it is sometimes the only way to diagnose certain neurological disorders. A neurological examination requires skill and experience to evaluate things like motor function, sensation, cranial nerves, coordination, and the presence of abnormal movements or seizures. The examiner should make the patient comfortable and modify their approach based on the patient's characteristics.
This document summarizes diagnostic criteria for multiple sclerosis (MS) over time. It discusses early criteria by Charcot in 1868, then Schumacher criteria in 1965 which required dissemination in time and space. Poser criteria in 1983 expanded criteria to include supportive laboratory data. McDonald criteria in 2001 and revisions integrated MRI findings and clarified definitions to make diagnosis more accurate and enable earlier diagnosis. Key diagnostic aspects include clinical attacks, dissemination in space and time demonstrated by lesions on MRI or other tests.
Cerebral small vessel disease (CSVD) is a term used to encompass a syndrome of clinical and radiological findings that are thought to result from pathologies in perforating cerebral arterioles, capillaries and venules.
Associated Clinical syndromes like Vascular Dementia or Parkinsonism are treated in isolation, rather than thinking holistically as Cerebral small vessel disease.
Diagnosis till date is largely based on Radiological markers.
Chronic myelogenous leukemia (CML) is a myeloproliferative disorder characterized by increased proliferation of granulocytic cells. The initiating factor of CML is an acquired genetic translocation that fuses the BCR gene on chromosome 22 and the ABL gene on chromosome 9, producing the Philadelphia chromosome and the BCR-ABL fusion gene. This gene encodes for an unregulated tyrosine kinase that drives uncontrolled proliferation of myeloid cells. CML progresses through chronic, accelerated, and blast phases as the disease advances and more immature cells appear in the blood and bone marrow over time. Diagnosis is confirmed by detecting the Philadelphia chromosome or BCR-ABL fusion using techniques like fluorescence in situ hybrid
This document provides an overview of systemic vasculitis for medical residents. It defines vasculitis as inflammation of blood vessels and explains how different types of vasculitis can affect different vessel sizes and organ systems. The document outlines the clinical approach to diagnosing vasculitis through history, physical exam, lab tests, imaging studies and tissue biopsies. It then discusses several specific types of vasculitis in more detail, including giant cell arteritis, granulomatous polyangiitis (Wegener's), and microscopic polyangiitis. The presentation provides information on clinical manifestations, diagnostic criteria, pathology findings, and treatments for these forms of vasculitis.
Chronic myelogenous leukemia (CML) is a type of leukemia characterized by the Philadelphia chromosome, which fuses the BCR and ABL genes. This results in uncontrolled proliferation of granulocytes. CML typically progresses through chronic, accelerated, and blast crisis phases. The chronic phase is often asymptomatic but may include fatigue and splenomegaly. Treatment with tyrosine kinase inhibitors like imatinib has greatly improved prognosis, achieving molecular remission in some cases. Without treatment, survival is 3-5 years in chronic phase and 3-6 months in blast crisis.
AML is characterized by accumulation of abnormal blast cells in the bone marrow and impaired production of normal blood cells. It results from clonal expansion of myeloid precursor cells with reduced ability to differentiate. Treatment involves induction chemotherapy with anthracyclines and cytarabine to achieve complete remission, defined as less than 5% blasts in the bone marrow. Risk is then assessed based on genetics to determine if additional chemotherapy or stem cell transplant is needed.
This document discusses systemic lupus erythematosus (SLE), including its pathophysiology, clinical manifestations, diagnostic criteria, and management. It outlines the 2019 EULAR classification criteria for SLE which uses 7 clinical and 3 immunological criteria weighted from 2 to 10, with a score of 10 or more required for classification. Treatment involves glucocorticoids, antimalarials like hydroxychloroquine, and immunosuppressives depending on disease severity.
1. Systemic sclerosis is a disease characterized by abnormalities of blood vessels, fibrosis of skin and internal organs, and activation of the immune system.
2. It is classified as limited or diffuse cutaneous systemic sclerosis based on the extent of skin involvement and rate of progression.
3. Clinical features include Raynaud's phenomenon, skin thickening, joint and muscle involvement, as well as pulmonary, cardiac, gastrointestinal, and renal complications.
Clinically isolated syndromes (CIS) refer to the first clinical episodes of neurological symptoms suggestive of multiple sclerosis. The document discusses CIS in three parts: definition and clinical features of CIS, risk factors for conversion from CIS to multiple sclerosis, and management of CIS. Regarding clinical features, optic neuritis, transverse myelitis, and brainstem syndromes are highlighted as common presentations of CIS. MRI abnormalities, younger age of onset, smoking, and vitamin D deficiency are identified as risk factors for progression to multiple sclerosis. The management section outlines acute treatment with corticosteroids, use of disease-modifying therapies based on MRI findings, and consideration of vitamin D supplementation.
Neurological manisfestation of pri vasculitis syndromeNeurologyKota
This document discusses several primary vasculitis syndromes that can affect the neurology. It begins by defining vasculitis as inflammation and necrosis of blood vessels. It then discusses several specific types of vasculitis:
- Giant cell arteritis is a cranial vasculitis most common in those over age 50 that can cause headaches, vision issues, and rarely stroke. High dose steroids are the main treatment.
- Polyarteritis nodosa is a systemic necrotizing vasculitis associated with hepatitis infection that commonly causes peripheral neuropathy. Treatment involves steroids and antivirals.
- Wegener's granulomatosis is a necrotizing vasculitis of small vessels associated with cAN
This document provides an overview of primary central nervous system vasculitis (PACNS), including:
1. PACNS is a rare inflammatory disease of blood vessels in the brain that causes varied neurological symptoms. The cause is unknown.
2. Diagnosis is challenging due to non-specific symptoms but may involve MRI, lumbar puncture, angiography, and brain biopsy. Brain biopsy provides the most definitive diagnosis but is not always possible.
3. Treatment typically involves high-dose corticosteroids combined with immunosuppressants like cyclophosphamide to induce remission, followed by corticosteroid-sparing drugs to maintain remission. Prognosis is generally good if patients respond to initial treatment
This document provides information on systemic lupus erythematosus (SLE) for physicians. It discusses the disease characteristics, diagnostic criteria, common signs and symptoms, and treatment approach. Key points include: SLE is an autoimmune disease that can affect multiple organs; it predominantly affects women of childbearing age; the ACR diagnostic criteria require 4 of 11 criteria to be met, including malar rash, arthritis, serositis, kidney disorder, blood abnormalities and positive ANA; common signs include painful or swollen joints, rashes, fever and fatigue; diagnosis involves screening tests like CBC, urinalysis and ANA, along with specialty tests depending on symptoms.
This document discusses chronic myeloid leukemia (CML). It defines CML as a stem cell disease characterized by excessive blood granulocytes and the Philadelphia chromosome - a translocation between chromosomes 9 and 22. CML progresses through chronic, accelerated and blast crisis phases. Symptoms include fatigue and splenomegaly. Diagnosis involves blood tests, bone marrow biopsy and detecting the Philadelphia chromosome. Treatment includes tyrosine kinase inhibitors, interferon and chemotherapy.
Primary central nervous system vasculitis (PACNS) is a rare disorder characterized by inflammation of blood vessels in the brain and spinal cord. It presents with non-specific symptoms like headache, cognitive impairment, and focal neurological deficits. Diagnosis involves neuroimaging showing multifocal lesions, angiography revealing vessel narrowing and dilation, and brain biopsy detecting immune cell infiltration of vessel walls. While the cause is unknown, infectious agents may trigger PACNS. Treatment involves immunosuppression but prognosis depends on disease severity and response to treatment.
This document discusses multiple sclerosis (MS), including:
1) Epidemiology shows it is most common in young white women at northern latitudes and those with Scandinavian ancestry or vitamin D deficiency.
2) Diagnosis relies on clinical patterns and exclusion of other causes, supported by MRI, CSF, and evoked potential studies showing lesions in white matter tracts.
3) The 2010 McDonald criteria provide guidelines for diagnosing MS based on demonstrations of dissemination of lesions in space and time through clinical attacks and imaging/laboratory results.
Neuro ophthalomology of Multiple sclerosisAmr Hassan
This document discusses the neuro-ophthalmological presentations of multiple sclerosis (MS), including optic neuritis as a common symptom. It begins with an overview of MS, covering etiology, pathogenesis, diagnosis, clinical course, and treatment options. It then focuses on ophthalmological manifestations of MS, emphasizing optic neuritis as the most frequent presentation. Specific symptoms, signs, differential diagnoses, and evaluation of optic neuritis are reviewed in detail. The role of the ophthalmologist in early detection and diagnosis of MS is highlighted.
Vasculitis refers to a group of diseases characterized by inflammation of blood vessels. The document defines and classifies different types of vasculitis based on vessel size. It discusses the pathophysiology, clinical features, investigations and management of vasculitis. Giant cell arteritis is provided as an example of large vessel vasculitis that predominantly affects branches of the temporal and ophthalmic arteries in older individuals, with headaches, jaw pain and risk of vision loss as key clinical features.
This document provides a review of neurosarcoidosis. It begins with defining sarcoidosis and neurosarcoidosis as involving non-caseating granulomas in the nervous system. It then discusses the epidemiology, clinical manifestations such as cranial neuropathies and meningitis, diagnostic criteria including biopsy evidence, and treatment primarily with corticosteroids. The review concludes with highlighting the challenges of diagnosing and managing neurosarcoidosis given the lack of randomized controlled trials and importance of raising awareness of this condition.
This document provides an outline for a course on childhood acute lymphoblastic leukemia (ALL). It covers the definition and epidemiology of ALL, risk factors, clinical presentation, diagnosis, management including treatment phases, complications, prognosis, and prevention. ALL is the most common childhood cancer characterized by excessive lymphoblasts. It peaks between ages 2-3 and has a survival rate over 85% with current treatments over 2-3 years consisting of induction, intensification, and maintenance chemotherapy, along with intrathecal therapy targeting the central nervous system. Complications can include tumor lysis syndrome, infections, and secondary cancers. Prognosis depends on risk factors like age and white blood cell count. Prevention focuses on limiting environmental exposures like benz
Similar to Diagnosis and red flags in Multiple sclerosis (20)
Parkinsonism is a clinical syndrome and, typically, when the condition
appears to be idiopathic and responsive to levodopa therapy, is referred
to as Parkinson’s disease1
• The four cardinal features of the parkinsonian syndrome are:2
– Bradykinesia
– Muscular rigidity
– Resting tremor
– Postural instability (and gait impairment)
• These features are not always observed in every patient, at any given
time
To make a diagnosis of PD, the physician must distinguish between
different forms of parkinsonism:1
– Parkinson’s disease
– Secondary parkinsonism
– Parkinsonism as part of another neurodegenerative disorder (e.g., multiple
system atrophy, progressive supranuclear palsy, corticobasal degeneration, or
Lewy body dementia)
SCALES COMMONLY USED IN
PARKINSON’S DISEASE
RESEARCH
SCALES COMMONLY USED IN
PARKINSON’S DISEASE
RESEARCH
Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkin’s disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection / acquired immune deficiency syndrome (AIDS). Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication.
In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities.
Sequencing in management of Multiple sclerosisAmr Hassan
Sequencing of DMTs for individual multiple sclerosis patients should be designed in such a way to maximize disease control and minimize risk based on the mechanism of action, pharmacokinetic and pharmacodynamic properties of each therapy. This includes the DMT patients are being switched from to those they are being switched to. The reversibility of immune system effects should be a key consideration for DMT sequence selection. This feature varies across DMTs and should factor more prominently in decision making as newer treatments become available for the prevention of disability accumulation in patients with progressive MS. In this short review, we discuss the landscape of existing therapies with an eye to the future when planning for optimal DMT sequencing. While no cure exists for MS, efforts are being directed toward research in neuroregeneration with the hope for positive outcomes.
A neuromuscular disorder that leads to weakness of skeletal muscles.
Symptoms
Causes
Prevention
Complications
Common tests & procedures
Neurological examination:
Repetitive nerve stimulation test:
Antibody test:
Pulmonary function tests (PFTs): To check any breathing difficulty.
CT scan: To rule out a presence of tumor in thymus.
Magnetic resonance imaging (MRI): MRI of the chest is performed to rule out a presence of tumor in thymus.
Edrophonium (Tensilon) test:
Medication
Procedures
Nutrition
Prediction of outcome of Multiple sclerosisAmr Hassan
Prediction of outcome of Multiple sclerosis
An understanding of the natural history of multiple sclerosis(MS) in a patient is important to begin proper treatment at the correct time, especially when there is a high risk for poor prognosis. Factors that predict unfavorable prognosis are a primary or secondary progressive course, older age at disease onset, short interval between first and second attacks, initial cerebellar or pyramidal symptoms, a large number of functional systems involved at onset, moderate to severe disability within the first 2 years, and the presence of typical plaques or greater lesion volume shown by magnetic resonance imaging results during the first 5 years. However, there are no established laboratory tests able to predict long-term prognosis.
Lifestyle modification in epilepsy
Lifestyle Modifications
Lifestyle modifications can include:
Adequate sleep: Fatigue is one of the most common seizure triggers, and disrupted sleep can make the brain more vulnerable to misfiring.
Avoiding drugs and alcohol: These can be triggers for seizures in patients with epilepsy. Even one or two drinks can provoke seizures.
Minimizing emotional stress: Although there is not definitive proof that stress causes seizures, those who maintain healthy stress levels have reported that they believe it reduces their risk.
Frequency of exercise: In addition to a range of health benefits, regular exercise can help reduce risk of seizure. However, you should consult your physician before starting a new exercise routine, as some exercise can, rarely, cause seizures.
Childhood demyelinating syndromes
In the past decade, the number of studies related to demyelinating diseases in children has exponentially increased. Demyelinating disease in children may be monophasic or chronic. Typical monophasic disorders in children are acute disseminated encephalomyelitis and clinically isolated syndromes, including optic neuritis and transverse myelitis. However, some cases of acute disseminated encephalomyelitis or clinically isolated syndrome progress to become chronic disorders, including multiple sclerosis and neuromyelitis optica. This review summarizes the current knowledge on monophasic and chronic demyelinating disorders in children, focusing on an approach to diagnosis and management.
This document discusses diabetic polyneuropathy. It begins with an agenda outlining the topics to be covered: epidemiology, clinical presentation, pathogenic mechanisms, diagnosis, and treatment. Some key points include:
- Up to 50% of diabetics may develop symptomatic neuropathy 20 years after diagnosis. The risk increases the longer a person has diabetes.
- Neuropathic pain symptoms can include burning, tingling sensations, allodynia, and hyperalgesia. The pain is usually chronic.
- Pathogenic mechanisms include metabolic and vascular factors that damage nerve fibers over time, such as hyperglycemia, oxidative stress, impaired blood flow. This can lead to endoneurial hypoxia, ATP depletion and nerve damage.
Excessive daytime sleepiness
The most common causes of excessive daytime sleepiness are sleep deprivation, obstructive sleep apnea, and sedating medications. Other potential causes of excessive daytime sleepiness include certain medical and psychiatric conditions and sleep disorders, such as narcolepsy.
Vagal Nerve stimulation
Vagus nerve stimulation (VNS) is a medical treatment that involves delivering electrical impulses to the vagus nerve. It is used as an add-on treatment for certain types of intractable epilepsy and treatment-resistant depression. Frequent side effects include coughing and shortness of breath. Serious side effects may include trouble talking and cardiac arrest.
Dystonia
Dystonia is a movement disorder in which your muscles contract involuntarily, causing repetitive or twisting movements.
The condition can affect one part of your body (focal dystonia), two or more adjacent parts (segmental dystonia) or all parts of your body (general dystonia). The muscle spasms can range from mild to severe. They may be painful, and they can interfere with your performance of day-to-day tasks.
Dystonia: Causes, Types, Symptoms, and Treatments
Trigeminal neuralgia is sudden, severe facial pain. It's often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums.
Trigeminal neuralgia
Contents
Overview
Symptoms
Causes
Diagnosis
Treatment
Nootropics and smart drugs are natural or synthetic substances that can be taken to improve mental performance in healthy people.
They have gained popularity in today’s highly competitive society and are most often used to boost memory, focus, creativity, intelligence and motivation.
Here’s a look at the ]best nootropics and how they enhance performance.
This document provides an overview of eye movements and disorders of eye movements. It begins with an agenda that covers topics like cranial nerves controlling eye movements, extraocular muscles, examining ocular motility, ophthalmoplegia, diplopia, gaze pathways, and types of nystagmus and non-nystagmus eye oscillations. It then defines different types of eye movements including fast and slow movements. The document discusses various physiological and pathological causes of nystagmus and other eye oscillations. It provides details on infantile, acquired, vestibular, downbeat, upbeat and other types of nystagmus. The document concludes with examining techniques for gaze, saccades, pursuit, convergence and other
Basics of Neuroradiology
Neuroradiology is an essential tool in management of patients with neurological and neurosurgical disorders. The aim of this presentation will be to acquaint the reader to understand how images are formed on a computed tomography (CT) and magnetic resonance imaging (MRI) along with a review of the relevant neuroanatomy. This understanding will be helpful to the reader in interpretation of images and diagnosis of various neurological disorders.
This document discusses the development of new antiepileptic drugs and therapies. It begins by showing the increasing number of licensed antiepileptic drugs over time since 1840. It then discusses the need for new drugs that improve seizure control, safety, and compliance while reducing side effects. New drugs discussed include Brivaracetam, eslicarbazepine acetate, perampanel, and cannabidiol. New delivery methods explored are intranasal, inhaled, and transdermal formulations. Non-drug therapies discussed include responsive neurostimulation, seizure detection devices, and trigeminal nerve stimulation. The document emphasizes that continued progress requires both evolutionary drugs that improve existing treatments as well as revolutionary drugs with novel mechanisms of
Zonisamide is an antiseizure drug that was launched in Japan in 1989 and the United States in 2000. It is chemically classified as a sulfonamide. Zonisamide blocks voltage-sensitive sodium channels and T-type calcium channels, increasing GABA inhibition of seizures. Clinical studies showed zonisamide resulted in seizure freedom rates of 79.4% at 26 weeks and 67.7% at 52 weeks. Common adverse effects include ataxia, dizziness, and weight loss. Zonisamide is particularly useful for seizures like Lennox-Gastaut syndrome and infantile spasms.
stem cell transplantation in pediatric neurology Amr Hassan
This document discusses stem cell therapy for pediatric neurological disorders. It defines stem cells as undifferentiated cells that can self-renew or commit to differentiation. Sources of stem cells include embryos, umbilical cord, and adults. Embryonic stem cells are derived from the blastocyst inner cell mass, while umbilical cord stem cells include mesenchymal and hematopoietic stem cells and were first successfully transplanted in 1989. Adult stem cells reside in tissue niches and include hematopoietic, neural, endothelial and other types. Stem cell therapy aims to generate new tissue through regeneration and repair. Limitations include variability in isolation, integration and functional outcomes. Various cell types have been used in cerebral
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
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.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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
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- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
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
4. Multiple Sclerosis Diagnosis
4
• Diagnosis relies on clinical judgment.
• MS is extremely variable.
• There is no specific test.
• The diagnosis has dramatic implications.
6. How to diagnose MS?
6
Clinical:
• History and examination.
• Evidence of CNS
involvement.
• Dissemination in space
and time.
Paraclinical:
• Neuroimaging.
• Evoked potentials.
• CSF analysis.
8. Diagnostic Criteria
• Dawson criteria: 1916
• Schumacher criteria: 1965
• Poser criteria: 1983
• McDonald criteria: 2001
• McDonald criteria: 2005
• McDonald criteria: 2010
All criteria require dissemination in time and space
9. Summarized Diagnostic Criteria
1. Dissemination in space: Objective evidence
of neurological deficits localized to two
separate parts of the CNS
2. Dissemination in Time:
Onset of neurological deficits separated by
at least one month
3. Rule out other explanations!
2010
2014
10. Diagnostic Criteria 2005
• Incorporate use of MRI
• Clinically Isolated Syndrom + MRI
Dissemination in space + MRI
Dissemination on time =
Earlier MS Diagnosis
August
DIS
DIT
November
11. New Diagnostic Criteria 2010
• Incorporate use of MRI
• Clinically Isolated Syndrom + MRI
Dissemination in space + MRI
Dissemination on time =
Earlier MS Diagnosis
August
DIS
DIT
August
21. Diagnostic tools
21
CSF examination:
• Abnormal in 85% to 90% of patients with MS.
• Elevated total IgG, an elevated IgG ratio, an increased IgG synthesis
rate,
• Presence of two or more oligoclonal bands in the CSF that are not
present in a simultaneously drawn serum sample
22. CSF examination
22
IgG index:
• [IgGCSF/albuminCSF]/[IgGserum/albuminserum]
MS patients elevated IgG index (>1.7). (normal is <0.77)
25. Mental map for diagnosis of MS
25
Clinical/Paraclinical/Imaging
Typical for MS
Fulfills Criteria
Atypical for MS
Red Flags Present
Work Up for Alternative
Diagnoses
Clinical/Imaging Follow
Up
Alternative Diagnosis
Established
Further clinical/imaging
typical for MS
MS Diagnosis
Typical for MS
not Fulfilling Criteria
Clinical/Imaging Follow
Up
27. Red flags
27
• Major red flags point fairly definitively to a non-MS diagnosis
• Intermediate red flags point to poor agreement and uncertainty
among raters about the weighting of the flag for differential
diagnosis in MS
• Minor red flags suggest that a disease other than MS should be
considered and fully explored, but an MS diagnosis is not excluded.
41. Clinical Red Flags
41
• Fever at the onset.
• Dermatologic involvement , other than psoriasis.
• Endocrinologic disease other than autoimmune
thyroid disease.
47. Labs UPON red flags
47
CNS Inflammatory/Autoimmune Disease:
• ANA,CRP, Anti DS DNA,C3,C4, ANCA panel, Chest CT, eye exam,
conjunctival biopsy, Pathergy skin test (Behcet's), Skin biopsy
if suspicious rash present, CTA, angiogram .
CNS Infection:
• Brucella antibodies, HIV test, HTLV1, and CSF antibodies (if isolated
myelopathy with a lesion on spinal MRI), ESR, small bowel biopsy
for whipple .
48. Labs UPON red flags
48
CNS Neoplasm/ Infiltrative Disorder:
• CSF cytology and flow cytometry, CXR, CT Chest AbdomenPelvis,
Pelvic ultrasound, Mammogram, LDH, skeletal series, bone scan,
Brain biopsy.
CNS vasculopathy/Ischemic Disease:
• Notch3 mutations in CADASIL , MRA, CTA, standard angiogram,
thrombophilia panel, Lupus anticoagulant .
49. Labs UPON red flags
49
Dysmyelinating/ Metabolic Disorders:
• Lumbar puncture
• EMG/NCVs
• biochemical studies
• buccal or rectal mucosa biopsy for electron microscopy if neuronal
ceroid lipofuscinosis (NCL) suspected
• Brain biopsy (rarely needed): fingerprint profiles, curvilinear and
rectilinear bodies by E.M. in NCL oligodendrocytes; diffuse white
matter gliosis by light microscopy in NCL.
50. Labs UPON red flags
50
Urine/blood for biochemical studies, including levels of:
• WBC arylsulfatase A, Very long chain fatty, Fasting arterial lactate,
Quantitative plasma amino acid and Urine organic acid analyses.
Nutritional deficiency/Toxicity:
• Vitamin B12, Copper and Zinc Levels, Ceruloplasmin, Folate, Heavy
metal screen.
52. 52
“The most common reason for falsely
attributing a patient’s symptoms to
multiple sclerosis is faulty
interpretation of the magnetic
resonance imaging.”
Famous Dictum
Loren A. Rolak
2007
55. MRI Red Flags (Major)
55
Calcifications on CT
scans
28 Cysticercosis; toxoplasmosis, mitochondrial disorders
Selective involvement of
the anterior temporal and
inferior frontal lobe
27 CADASIL
Lacunar infarcts 27
Hypertensive ischemic disease; CADASIL; Susac
syndrome
Persistent Gd-
enhancement and
continued enlargement of
lesions
27 Lymphoma; glioma; vasculitis; sarcoidosis
56. MRI Red Flags (Major)
56
Simultaneous
enhancement of all lesions
26 Vasculitis; lymphoma; sarcoidosis
T2-hyperintensity in the
dentate nuclei
26 Cerebrotendinous xanthomatosis
T1-hyperintensity of the
pulvinar
25 Fabry disease; hepatic encephalopathy; manganese toxicity
Large and infiltrating
brainstem lesions
24 Behçet's disease; pontine glioma
Predominance of lesions
at the cortical/subcortical
junction
23
Embolic infarction; vasculitis; progressive multifocal
leukoencephalopathy
57. MRI Red Flags (Intermediate)
57
Hydrocephalus 23
Sarcoidosis or other chronic meningitis;
lymphoma or other CNS neoplasm
Punctiform parenchymal enhancement 23 Sarcoidosis; vasculitis
T2-hyperintensities of U-fibers at the vertex,
external capsule and insular regions
22 CADASIL
Regional atrophy of the brainstem 21
Behçet's disease; adult onset Alexander's
disease
Diffuse lactate increase on brain MRS 21 Mitochondrial disease
Marked hippocampal and amygdala atrophy 21 Hyperhomocystinemia
Symmetrically distributed lesions 20 Leukodystrophy
T2-hyperintensities of the basal ganglia,
thalamus and hypothalamus
20
Behçet's disease; mitochondrial
encephalomyopathies; Susac's
syndrome; acute disseminated
encephalomyelitis
58. MRI Red Flags (Intermediate)
58
Diffuse abnormalities in the
posterior columns of the cord
20
B12 deficiency; copper deficiency;
paraneoplastic disorder
Lesions across GM/WM
boundaries
19
Hypoxic-ischemic conditions;
vasculitis; systemic lupus erythematosus
T2-hyperintensities of the
temporal pole
19 CADASIL
Complete ring enhancement 18 Brain abscess; glioblastoma; metastatic cancer
Central brainstem lesions 17
Central pontine myelinolysis; hypoxicischemic
conditions; infarct
59. MRI Red Flags (Intermediate)
59
Predominant brainstem and
cerebellar lesions
1 7 Behçet's disease; pontine glioma
Lesions in the center of CC,
sparing the periphery
1 7 Susac's syndrome
Dilation of the Virchow-Robin
spaces
15
Hyperhomocystinemia;
primary CNS angiitis
Cortical/subcortical lesions
crossing vascular territories
14
Ischemic leukoencephalopathy; CADASIL;
vasculitis
60. MRI Red Flags (Intermediate)
60
Large lesions with absent or rare
mass effect and enhancement
1 3 Progressive multifocal leukoencephalopathy
No “occult” changes in the NAWM 1 3 Lyme disease, isolated myelitis, CADASIL
No enhancement 8
Progressive multifocal leukoencephalopathy; ischemic
lesions; metachromatic leukodystrophy
No optic nerve lesions 9
Metastatic carcinoma; gliomatosis cerebri;
toxoplasmosis
No spinal cord lesions 10
Multiple infarcts; vasculitis; progressive multifocal
leukoencephalopathy
Large lesions 11
Glioblastoma; lymphoma; progressive multifocal
leukoencephalopathy
No T1 hypointense lesions (black
holes)
11
Ischemic degenerative leukoencephalopathy;
progressive multifocal leukoencephalopathy
Marked asymmetry of WM lesions 12 Glioblastoma; lymphoma; cerebral infarction
64. 64
Normal Aging
• Periventricular caps
and bands
• Mild atrophy with
widening of sulci and
ventricles
• Punctate and
sometimes even
confluent lesions in the
deep white matter
(Fazekas I and II).
66. These white matter changes are classified
according to Fazekas:
66
• Mild - punctate WMLs: Fazekas I)
• Moderate - confluent WMLs: Fazekas II - in the deep white
matter can be considered normal in aging.
• Severe - extensive confluent WMLs: Fazekas III - always
abnormal.
83. 83
MRI Red Flags
Poorly defined lesion border/ U fiber involvement
Progressive Multifocal Leukoencephalopathy
84. 84
Tumefactive MS
• Post-gadolinium, there may
be some peripheral
enhancement, often with an
incomplete ring.
• These lesions can be
distinguished from gliomas or
intraparenchymal abscesses,
which typically have a
closed-ring enhancement.
96. D.D. OF M.S. IN MRI
96
1. Age-related changes
2. Acute disseminated encephalomyelitis
3. CNS vasculitis
4. Behçet disease
5. Sjögren syndrome
6. Sarcoidosis
7. Metastatic neoplasm
8. CADASIL (cerebral autosomal dominant arteriopathy with
subcortical infarcts and leukoencephalopathy)
9. Binswanger disease
10. Migrainous ischemia
97. D.D. OF M.S. IN MRI
97
11. Cerebrovascular disease
12. Progressive multifocal leukoencephalopathy
13. Inherited white matter diseases
14. Effects of radiation therapy or drugs
15. CNS lymphoma
16. Lyme disease
17. HTLV-1 infection
18. CNS lupus
19. Mitochondrial encephalopathies
20. Antiphospholipid antibody syndrome
98. Mental map for diagnosis of MS
98
Clinical/Paraclinical/Imaging
Typical for MS
Fulfills Criteria
Atypical for MS
Red Flags Present
Work Up for Alternative
Diagnoses
Clinical/Imaging Follow
Up
Alternative Diagnosis
Established
Further clinical/imaging
typical for MS
MS Diagnosis
Typical for MS
not Fulfilling Criteria
Clinical/Imaging Follow
Up