This document discusses cerebrovascular disease and stroke. It defines stroke and transient ischemic attack, and describes the main types of stroke as ischemic or hemorrhagic. Risk factors for ischemic stroke are discussed, including modifiable factors like hypertension and non-modifiable factors like age. The anatomy of brain blood vessels and circulation is outlined. Clinical presentations of strokes in different vascular territories are summarized, such as left middle cerebral artery infarction causing right-sided hemiparesis and sensory loss.
This document summarizes the examination of the sensory system and neurogenic bladder. It describes evaluating superficial, deep, and cortical sensations. It also discusses speech disorders like dysarthria and different types. Language examination and aphasia are mentioned. Neurogenic bladder is examined, including lesions affecting the reflex arc at different levels causing atonic, motor atonic, or autonomic bladders. Lesions above the reflex arc can cause retention, incontinence, or automatic bladder function.
Motor neuron diseases (MNDs) are a group of progressive neurological disorders that predominantly or exclusively affect upper motor neurons, lower motor neurons, or both. There are several classifications of MND including sporadic or inherited forms, and those involving combined upper and lower motor neuron involvement (such as amyotrophic lateral sclerosis), pure lower motor neuron involvement (such as spinal muscular atrophy), or pure upper motor neuron involvement (such as primary lateral sclerosis). Common clinical features include muscle weakness, wasting, and fasciculations depending on the type and location of motor neuron involvement. Investigations help differentiate MNDs from other conditions and there is currently no cure, though some treatments can help manage symptoms.
1. The document discusses the approach to evaluating and managing a comatose patient. It defines consciousness and the components of arousal and content of consciousness.
2. Evaluation of a comatose patient involves obtaining a detailed history, performing a physical exam including neurological assessment of pupil size and reactivity, eye and motor movements, and determining the level of coma.
3. Management begins with addressing airway, breathing, and circulation (ABCs), treating potentially life-threatening metabolic disorders, evaluating for increased intracranial pressure, and providing supportive care measures.
This document discusses cerebrovascular disease and stroke. It defines stroke and transient ischemic attack, and describes the main types of stroke as ischemic or hemorrhagic. Risk factors for ischemic stroke are discussed, including modifiable factors like hypertension and non-modifiable factors like age. The anatomy of brain blood vessels and circulation is outlined. Clinical presentations of strokes in different vascular territories are summarized, such as left middle cerebral artery infarction causing right-sided hemiparesis and sensory loss.
This document summarizes the examination of the sensory system and neurogenic bladder. It describes evaluating superficial, deep, and cortical sensations. It also discusses speech disorders like dysarthria and different types. Language examination and aphasia are mentioned. Neurogenic bladder is examined, including lesions affecting the reflex arc at different levels causing atonic, motor atonic, or autonomic bladders. Lesions above the reflex arc can cause retention, incontinence, or automatic bladder function.
Motor neuron diseases (MNDs) are a group of progressive neurological disorders that predominantly or exclusively affect upper motor neurons, lower motor neurons, or both. There are several classifications of MND including sporadic or inherited forms, and those involving combined upper and lower motor neuron involvement (such as amyotrophic lateral sclerosis), pure lower motor neuron involvement (such as spinal muscular atrophy), or pure upper motor neuron involvement (such as primary lateral sclerosis). Common clinical features include muscle weakness, wasting, and fasciculations depending on the type and location of motor neuron involvement. Investigations help differentiate MNDs from other conditions and there is currently no cure, though some treatments can help manage symptoms.
1. The document discusses the approach to evaluating and managing a comatose patient. It defines consciousness and the components of arousal and content of consciousness.
2. Evaluation of a comatose patient involves obtaining a detailed history, performing a physical exam including neurological assessment of pupil size and reactivity, eye and motor movements, and determining the level of coma.
3. Management begins with addressing airway, breathing, and circulation (ABCs), treating potentially life-threatening metabolic disorders, evaluating for increased intracranial pressure, and providing supportive care measures.
Epilepsy is a brain disorder characterized by recurrent seizures. It is defined as having two or more unprovoked seizures or one seizure with a high risk of recurrence. Seizures occur due to abnormal excessive neuronal activity in the brain. Epilepsy can be caused by genetic factors, structural abnormalities, infections, tumors or other injuries to the brain. It is classified based on seizure type, location in the brain, underlying cause, and associated medical syndromes. Diagnosis involves taking a detailed history, EEG, brain imaging and sometimes neurological testing to identify the type and cause of seizures. Conditions with similar presentations need to be considered in the differential diagnosis.
This document provides information on examining the 12 cranial nerves. It describes the pathway of smell for the olfactory nerve and how to test for smell. It discusses examining the optic nerve by testing visual acuity, color vision, visual fields, and the fundus. The document outlines how to test the oculomotor, trochlear, and abducent nerves by examining eye movements. It also describes examining the trigeminal, facial, vestibulocochlear, glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves by testing motor function, reflexes, and sensory abilities.
This document discusses the cranial nerves, beginning with an overview of their anatomy and numbering. It then provides mnemonics to remember the names and functions of the cranial nerves. The majority of the document discusses the anatomy and examination of specific cranial nerves, including the olfactory, optic, oculomotor, trochlear, abducent, and trigeminal nerves. It describes their pathways, functions, lesions, and how to examine things like visual acuity, visual fields, eye movements, and sensation.
This document provides guidance on performing a neurological history and examination. It begins with an introduction on the importance of the history and building rapport with the patient. The document then outlines the key components of a neurological history, including personal history, chief complaint, history of present illness, past medical history, and family history. It provides examples of questions to ask within each component. For the physical examination, it describes how to analyze symptoms related to motor function, sensation, coordination, and other neurological domains. It also reviews models for localizing neurological lesions based on their cause, location in the central or peripheral nervous system, and other characteristics. The overall document serves as a reference for neurology trainees on obtaining a thorough neurological history and focused physical examination
This document discusses various reflexes examined in neurology. It describes deep reflexes of the upper and lower limbs, as well as superficial reflexes like plantar reflexes. A scale is provided to rate reflexes. Pathological reflexes are also outlined, such as Hoffman's sign and frontal release signs seen with diffuse frontal lobe lesions. Lower limb pathologic reflexes like plantar grasp are explained. Typical reflex patterns seen with upper motor neuron lesions are summarized. The document concludes by thanking the reader and providing contact information for the neurology lecturer who authored the document.
1. The cerebellum is located in the posterior cranial fossa and consists of three lobes and three functional subdivisions that control different movements.
2. Ataxia is incoordination of voluntary motor activity without weakness that can be cerebellar, sensory, or vestibular in nature and can result from various hereditary, toxic, vascular, inflammatory, or degenerative causes.
3. Examination of patients with ataxia involves tests of coordination, balance, speech, and eye movements to localize the source and assess severity.
This document discusses the classification and characteristics of various movement disorders. It begins by classifying movement disorders as either hyperkinetic (increased movement) or hypokinetic (decreased movement). It then provides details on specific disorders such as Parkinson's disease, chorea, athetosis, tremor, tics, and others. For Parkinson's disease, it discusses epidemiology, pathophysiology, cardinal manifestations including tremor, bradykinesia, rigidity and postural instability, non-motor symptoms, investigation, and treatment options including pharmacologic, non-pharmacologic and surgical therapies. It also provides information on the causes, characteristics and classification of chorea, athetosis, tremor, and t
The sensory system examination is divided into evaluating superficial sensation, deep sensation, and cortical sensations. Superficial sensation tests pain, touch, and temperature using pin pricks, cotton, and hot/cold test tubes to detect hemihypothesia, level of lesion, stocking glove patterns, and radicular loss. Deep sensation evaluates joint position, vibration, and muscle strength. Cortical sensations include tactile localization, two-point discrimination, graphosthesia, stereognosis, and sensory attention.
This document summarizes the components of a motor system examination, including muscle state, tone, power, and coordination. It describes how to evaluate each component, such as inspecting for muscle wasting or fasciculations, testing tone using maneuvers like Gower's sign, grading strength using the MRC scale, and assessing coordination through finger-nose and heel-knee tests. It also differentiates between types of abnormal tone like spasticity and rigidity. The overall motor exam is divided into inspection of muscle and skeletal features, assessment of tone, strength, and coordination through specific physical exam techniques.
This document summarizes the cranial nerves IX through XII that innervate the head and neck region. It describes the motor, sensory and autonomic functions of the glossopharyngeal (CN IX), vagus (CN X), accessory (CN XI) and hypoglossal (CN XII) nerves. It also discusses lesions of these nerves and their resulting clinical presentations. Pseudobulbar and true bulbar palsy are defined based on whether the lesion is upstream or within the motor nuclei of these cranial nerves. Common causes of each condition are provided.
This document summarizes the steps for performing a thorough motor system examination. It outlines how to inspect muscles for wasting, deformities, involuntary movements, and trophic changes. It describes how to assess muscle tone, power, coordination, reflexes, and gait. Abnormal findings are defined, including pathological reflexes like Babinski's sign. The exam involves a full evaluation of muscle and nerve function in the upper and lower limbs as well as the trunk.
This document discusses various types of myopathies, including muscular dystrophies, inflammatory myopathies, and channelopathies. It provides details on inherited conditions like Duchenne muscular dystrophy, myotonic dystrophy, and limb girdle muscular dystrophy. It also covers acquired myopathies such as those caused by drugs, endocrine disorders, inflammation, and malignancy. Clinical features, investigations, and management are outlined for different myopathies.
This document discusses neuromuscular junction disorders, focusing on Myasthenia Gravis. Myasthenia Gravis is an autoimmune disorder causing muscle weakness and fatigue. It results from antibodies destroying acetylcholine receptors at the neuromuscular junction, reducing signal transmission. Symptoms include drooping eyelids, facial weakness, difficulty swallowing and limb weakness. Diagnosis involves tests like repetitive nerve stimulation and response to medication like pyridostigmine. Treatment includes pyridostigmine, steroids, immunosuppressants and sometimes plasma exchange or IV immunoglobulin for severe cases. Thymectomy may also help by removing the source of antibody production in the thymus.
The document discusses various syndromes associated with lesions in different areas of the brainstem. It describes syndromes related to lesions of the posterior cerebral artery including Dejerine-Roussy syndrome and Claude's syndrome. It also summarizes syndromes caused by lesions in specific areas of the pons including the basis pontis, ventral pons, dorsal pons, and ventral medial pons. Syndromes involving the medulla are also outlined such as Wallenberg's lateral medullary syndrome and medial medullary syndrome. Finally, it provides an overview of the anatomy and blood supply of the midbrain and medulla.
The thalamus is the largest part of the diencephalon and acts as a relay station for sensory and motor signals sent to and from the cerebral cortex. It contains several nuclei that process different sensory modalities like somatosensory, visual, and auditory input. The thalamus also influences voluntary movements, mood, memory, and arousal. Damage to the thalamus can result in sensory and motor deficits like thalamic pain syndromes as well as language and emotional issues.
This document discusses hemifacial spasm, a condition where there are intermittent, involuntary contractions of muscles on one side of the face innervated by the facial nerve. It is usually caused by vascular compression of the facial nerve root. The document covers the epidemiology, clinical features, diagnostic workup, differential diagnosis, medical and surgical management options like microvascular decompression surgery, and outcomes of treating hemifacial spasm.
Peripheral neuropathy can be caused by damage to peripheral nerves outside of the brain and spinal cord. Symptoms may include numbness, tingling, pain or weakness in the hands, feet, arms and legs. Peripheral neuropathy has many potential causes including diabetes, nutritional deficiencies, toxins, infections and autoimmune disorders. Evaluation may involve neurological exams, nerve conduction studies and biopsies. Treatment depends on the underlying cause but aims to relieve symptoms and prevent further nerve damage when possible.
This document provides information to help localize neurological deficits based on symptoms and signs. It discusses localization in the upper motor neuron system including the cortex, corona radiata, internal capsule, brainstem, and spinal cord. It also discusses localization in the lower motor neuron system including the anterior horn, root/plexus, and nerves. Localization is guided by features like patterns of weakness, sensory loss, reflex changes, and specific cranial nerve involvement.
The document provides an overview of approaches to diagnosing and classifying ataxia. It begins by defining ataxia and discussing tests to differentiate various causes, including cerebellar ataxia, sensory ataxia, cortical ataxia, labyrinthine ataxia, and others. It then discusses the approach to cerebellar ataxia in adults, including considering mode of onset, progression, focal/symmetric involvement, and localizing the lesion. Acquired causes like infection, autoimmune, nutritional deficiencies and more are discussed. Inherited ataxias like autosomal dominant SCA types 1-3 and others are also summarized.
This document discusses demyelinating diseases, specifically multiple sclerosis. It describes the key features of MS, including that it is a chronic disease characterized by episodes of focal neurological disorders that remit and recur over many years. The diagnosis can be uncertain early on but becomes more accurate as lesions disseminate throughout the central nervous system. The document outlines the pathogenesis of MS, which involves an autoimmune reaction triggered by viral infection that results in destruction of the myelin sheath. Diagnostics include examination of cerebrospinal fluid and MRI of the brain and spine to detect lesions. Variants such as acute disseminated encephalomyelitis are also mentioned.
Epilepsy is a brain disorder characterized by recurrent seizures. It is defined as having two or more unprovoked seizures or one seizure with a high risk of recurrence. Seizures occur due to abnormal excessive neuronal activity in the brain. Epilepsy can be caused by genetic factors, structural abnormalities, infections, tumors or other injuries to the brain. It is classified based on seizure type, location in the brain, underlying cause, and associated medical syndromes. Diagnosis involves taking a detailed history, EEG, brain imaging and sometimes neurological testing to identify the type and cause of seizures. Conditions with similar presentations need to be considered in the differential diagnosis.
This document provides information on examining the 12 cranial nerves. It describes the pathway of smell for the olfactory nerve and how to test for smell. It discusses examining the optic nerve by testing visual acuity, color vision, visual fields, and the fundus. The document outlines how to test the oculomotor, trochlear, and abducent nerves by examining eye movements. It also describes examining the trigeminal, facial, vestibulocochlear, glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves by testing motor function, reflexes, and sensory abilities.
This document discusses the cranial nerves, beginning with an overview of their anatomy and numbering. It then provides mnemonics to remember the names and functions of the cranial nerves. The majority of the document discusses the anatomy and examination of specific cranial nerves, including the olfactory, optic, oculomotor, trochlear, abducent, and trigeminal nerves. It describes their pathways, functions, lesions, and how to examine things like visual acuity, visual fields, eye movements, and sensation.
This document provides guidance on performing a neurological history and examination. It begins with an introduction on the importance of the history and building rapport with the patient. The document then outlines the key components of a neurological history, including personal history, chief complaint, history of present illness, past medical history, and family history. It provides examples of questions to ask within each component. For the physical examination, it describes how to analyze symptoms related to motor function, sensation, coordination, and other neurological domains. It also reviews models for localizing neurological lesions based on their cause, location in the central or peripheral nervous system, and other characteristics. The overall document serves as a reference for neurology trainees on obtaining a thorough neurological history and focused physical examination
This document discusses various reflexes examined in neurology. It describes deep reflexes of the upper and lower limbs, as well as superficial reflexes like plantar reflexes. A scale is provided to rate reflexes. Pathological reflexes are also outlined, such as Hoffman's sign and frontal release signs seen with diffuse frontal lobe lesions. Lower limb pathologic reflexes like plantar grasp are explained. Typical reflex patterns seen with upper motor neuron lesions are summarized. The document concludes by thanking the reader and providing contact information for the neurology lecturer who authored the document.
1. The cerebellum is located in the posterior cranial fossa and consists of three lobes and three functional subdivisions that control different movements.
2. Ataxia is incoordination of voluntary motor activity without weakness that can be cerebellar, sensory, or vestibular in nature and can result from various hereditary, toxic, vascular, inflammatory, or degenerative causes.
3. Examination of patients with ataxia involves tests of coordination, balance, speech, and eye movements to localize the source and assess severity.
This document discusses the classification and characteristics of various movement disorders. It begins by classifying movement disorders as either hyperkinetic (increased movement) or hypokinetic (decreased movement). It then provides details on specific disorders such as Parkinson's disease, chorea, athetosis, tremor, tics, and others. For Parkinson's disease, it discusses epidemiology, pathophysiology, cardinal manifestations including tremor, bradykinesia, rigidity and postural instability, non-motor symptoms, investigation, and treatment options including pharmacologic, non-pharmacologic and surgical therapies. It also provides information on the causes, characteristics and classification of chorea, athetosis, tremor, and t
The sensory system examination is divided into evaluating superficial sensation, deep sensation, and cortical sensations. Superficial sensation tests pain, touch, and temperature using pin pricks, cotton, and hot/cold test tubes to detect hemihypothesia, level of lesion, stocking glove patterns, and radicular loss. Deep sensation evaluates joint position, vibration, and muscle strength. Cortical sensations include tactile localization, two-point discrimination, graphosthesia, stereognosis, and sensory attention.
This document summarizes the components of a motor system examination, including muscle state, tone, power, and coordination. It describes how to evaluate each component, such as inspecting for muscle wasting or fasciculations, testing tone using maneuvers like Gower's sign, grading strength using the MRC scale, and assessing coordination through finger-nose and heel-knee tests. It also differentiates between types of abnormal tone like spasticity and rigidity. The overall motor exam is divided into inspection of muscle and skeletal features, assessment of tone, strength, and coordination through specific physical exam techniques.
This document summarizes the cranial nerves IX through XII that innervate the head and neck region. It describes the motor, sensory and autonomic functions of the glossopharyngeal (CN IX), vagus (CN X), accessory (CN XI) and hypoglossal (CN XII) nerves. It also discusses lesions of these nerves and their resulting clinical presentations. Pseudobulbar and true bulbar palsy are defined based on whether the lesion is upstream or within the motor nuclei of these cranial nerves. Common causes of each condition are provided.
This document summarizes the steps for performing a thorough motor system examination. It outlines how to inspect muscles for wasting, deformities, involuntary movements, and trophic changes. It describes how to assess muscle tone, power, coordination, reflexes, and gait. Abnormal findings are defined, including pathological reflexes like Babinski's sign. The exam involves a full evaluation of muscle and nerve function in the upper and lower limbs as well as the trunk.
This document discusses various types of myopathies, including muscular dystrophies, inflammatory myopathies, and channelopathies. It provides details on inherited conditions like Duchenne muscular dystrophy, myotonic dystrophy, and limb girdle muscular dystrophy. It also covers acquired myopathies such as those caused by drugs, endocrine disorders, inflammation, and malignancy. Clinical features, investigations, and management are outlined for different myopathies.
This document discusses neuromuscular junction disorders, focusing on Myasthenia Gravis. Myasthenia Gravis is an autoimmune disorder causing muscle weakness and fatigue. It results from antibodies destroying acetylcholine receptors at the neuromuscular junction, reducing signal transmission. Symptoms include drooping eyelids, facial weakness, difficulty swallowing and limb weakness. Diagnosis involves tests like repetitive nerve stimulation and response to medication like pyridostigmine. Treatment includes pyridostigmine, steroids, immunosuppressants and sometimes plasma exchange or IV immunoglobulin for severe cases. Thymectomy may also help by removing the source of antibody production in the thymus.
The document discusses various syndromes associated with lesions in different areas of the brainstem. It describes syndromes related to lesions of the posterior cerebral artery including Dejerine-Roussy syndrome and Claude's syndrome. It also summarizes syndromes caused by lesions in specific areas of the pons including the basis pontis, ventral pons, dorsal pons, and ventral medial pons. Syndromes involving the medulla are also outlined such as Wallenberg's lateral medullary syndrome and medial medullary syndrome. Finally, it provides an overview of the anatomy and blood supply of the midbrain and medulla.
The thalamus is the largest part of the diencephalon and acts as a relay station for sensory and motor signals sent to and from the cerebral cortex. It contains several nuclei that process different sensory modalities like somatosensory, visual, and auditory input. The thalamus also influences voluntary movements, mood, memory, and arousal. Damage to the thalamus can result in sensory and motor deficits like thalamic pain syndromes as well as language and emotional issues.
This document discusses hemifacial spasm, a condition where there are intermittent, involuntary contractions of muscles on one side of the face innervated by the facial nerve. It is usually caused by vascular compression of the facial nerve root. The document covers the epidemiology, clinical features, diagnostic workup, differential diagnosis, medical and surgical management options like microvascular decompression surgery, and outcomes of treating hemifacial spasm.
Peripheral neuropathy can be caused by damage to peripheral nerves outside of the brain and spinal cord. Symptoms may include numbness, tingling, pain or weakness in the hands, feet, arms and legs. Peripheral neuropathy has many potential causes including diabetes, nutritional deficiencies, toxins, infections and autoimmune disorders. Evaluation may involve neurological exams, nerve conduction studies and biopsies. Treatment depends on the underlying cause but aims to relieve symptoms and prevent further nerve damage when possible.
This document provides information to help localize neurological deficits based on symptoms and signs. It discusses localization in the upper motor neuron system including the cortex, corona radiata, internal capsule, brainstem, and spinal cord. It also discusses localization in the lower motor neuron system including the anterior horn, root/plexus, and nerves. Localization is guided by features like patterns of weakness, sensory loss, reflex changes, and specific cranial nerve involvement.
The document provides an overview of approaches to diagnosing and classifying ataxia. It begins by defining ataxia and discussing tests to differentiate various causes, including cerebellar ataxia, sensory ataxia, cortical ataxia, labyrinthine ataxia, and others. It then discusses the approach to cerebellar ataxia in adults, including considering mode of onset, progression, focal/symmetric involvement, and localizing the lesion. Acquired causes like infection, autoimmune, nutritional deficiencies and more are discussed. Inherited ataxias like autosomal dominant SCA types 1-3 and others are also summarized.
This document discusses demyelinating diseases, specifically multiple sclerosis. It describes the key features of MS, including that it is a chronic disease characterized by episodes of focal neurological disorders that remit and recur over many years. The diagnosis can be uncertain early on but becomes more accurate as lesions disseminate throughout the central nervous system. The document outlines the pathogenesis of MS, which involves an autoimmune reaction triggered by viral infection that results in destruction of the myelin sheath. Diagnostics include examination of cerebrospinal fluid and MRI of the brain and spine to detect lesions. Variants such as acute disseminated encephalomyelitis are also mentioned.
epidemiology and pathophysiology of multiple sclerosis Balqees Majali
Multiple sclerosis (MS) is a chronic inflammatory disease that affects the central nervous system. It has four clinical forms and is more common in females than males. The exact cause is unknown but is believed to involve both genetic and environmental factors. Pathologically, MS is characterized by lesions throughout the white matter of the brain and spinal cord caused by inflammation and the loss of myelin. These lesions can be either actively demyelinating or chronically demyelinated. While the disease course and prognosis can vary between individuals, it generally involves periods of relapse followed by remission or a progressive decline over time.
MRI in evaluation of white matter diseases like multiple sclerosis, leukodystrophies, demyelination, dysmyelination, ADEM, leukoencephalopathies, van der knaap disease, ALD, MLD, Krabbes disease, Leighs disease, Vanishing white matter disease, Canavan disease, Alexander disease
This document provides an overview of demyelinating diseases of the central nervous system, with a focus on multiple sclerosis. It discusses the etiology, pathogenesis, clinical features, diagnosis, treatment and management of multiple sclerosis. Key points include: MS results from an autoimmune attack on the myelin sheath surrounding nerves in the brain and spinal cord; diagnosis involves evidence of lesions disseminated in space and time via MRI or other tests; and treatments include steroids for acute attacks and disease-modifying drugs such as interferons to reduce relapse rates long-term.
This document provides an overview of various demyelinating diseases of the central nervous system. It begins by defining demyelinating diseases as those involving disruption of myelin, which forms an insulating sheath around axons. It then classifies and describes several specific diseases, including acute disseminated encephalomyelitis (ADEM), inflammatory demyelinating pseudotumor, multiple sclerosis (MS), neuromyelitis optica, central pontine myelinolysis, HIV encephalopathy, progressive multifocal leukoencephalopathy (PML), and others. For each disease, it discusses clinical features, magnetic resonance imaging (MRI) findings, differential diagnoses, and pathology where relevant.
Multiple sclerosis (MS) is a chronic disease that damages the protective sheath surrounding nerve fibers in the brain and spinal cord. The immune system mistakenly attacks this sheath. Symptoms vary but can include vision problems, muscle weakness, and impaired coordination. The cause is unknown but likely involves genetic and environmental factors. Diagnosis involves ruling out other conditions and looking for lesions in the brain and spinal cord by MRI or lumbar puncture. There is no cure for MS but treatments can help manage symptoms and reduce relapses. Lifestyle changes and medications aim to reduce inflammation and manage symptoms like pain, fatigue, and bladder problems. Prognosis depends on the type and severity of early symptoms.
Multiple sclerosis is a chronic disease that damages the protective sheath surrounding nerve fibers in the brain and spinal cord. The immune system attacks this sheath, called myelin, which causes communication problems between the brain and body. The cause is unknown but likely involves genetic and environmental factors. Symptoms vary depending on the location of damage but can include numbness, vision problems, weakness, and impaired coordination. Diagnosis involves neurological exams, MRI images showing lesions in the brain and spine, and analysis of cerebrospinal fluid. While there is no cure, treatments aim to reduce frequency and severity of attacks and manage symptoms. Prognosis depends on the specific symptoms and disease progression in early years.
Multiple sclerosis: Introduction, Risk Factors, Diagnosis and TreatmentEnriqueAlvarez93
Introduction about Multiple Sclerosis.
Risk factors affect to Multiple Sclerosis.
When to Suspect Multiple Sclerosis.
Evaluation and Diagnosis of Multiple Sclerosis.
How to treatment of Multiple Sclerosis.
Treatment of Multiple Sclerosis with Monoclonal Antibody.
This document discusses demyelinating diseases of the nervous system, specifically focusing on multiple sclerosis (MS). It provides details on the structure and function of myelin sheaths, describes different types of demyelinating diseases including genetic myelinopathies and autoimmune myelinoclasthies like MS. It discusses the epidemiology, pathogenesis, clinical forms and manifestations of MS, including characteristic signs like retrobulbar neuritis, internuclear ophthalmoplegia, and Lhermitte's sign. MRI images of MS lesions in the brain and spinal cord are also included.
The document describes a case of a 14-year old boy who developed abnormal movements and weakness following treatment for snake bite with anti-venom serum (ASV). MRI later revealed lesions in the basal ganglia. He was diagnosed with acute disseminated encephalomyelitis (ADEM) caused by an immune response to the anti-venom. Steroid treatment improved his symptoms and he recovered fully after 3 months. ADEM is an inflammatory demyelinating condition that can be triggered by infections or vaccines and presents with polyneurological symptoms.
Multiple sclerosis (neurology) dr sikander aliMuhammad Ali
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system characterized by inflammation and nerve damage. It commonly affects women under 30 years old in temperate climates. Symptoms include visual problems, numbness, weakness, and impaired coordination. While relapses may be followed by remission, over time disability accumulates without treatment. The cause is unknown but involves immune-mediated damage to myelin. Diagnosis is clinical based on dissemination of lesions in time and space. MRI is used to identify lesions. Treatment focuses on reducing relapse rate and progression with steroids, interferons, glatiramer acetate or monoclonal antibodies.
Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy that causes weakness and diminished reflexes as the immune system attacks the nerves. It is usually preceded by a viral or bacterial infection. There are different subtypes depending on whether the myelin sheath or axons are affected. Diagnosis involves physical exam, lumbar puncture showing elevated proteins, and electrodiagnostic studies. Treatment involves plasma exchange or IV immunoglobulin to modulate the immune system. Most patients require hospitalization but most make a full recovery, though some experience long-term weakness or paralysis.
This document provides information about multiple sclerosis (MS), including:
- MS is an immune-mediated disease that attacks the myelin sheath surrounding nerves in the central nervous system.
- Symptoms vary between individuals but can include fatigue, mobility issues, sensory changes, and cognitive difficulties. Diagnosis involves ruling out other conditions and detecting lesions in the brain and spinal cord.
- Treatment involves managing relapses, symptoms, and slowing disease progression using disease-modifying therapies like interferons that aim to reduce inflammation. Prognosis depends on individual characteristics but the disease course is generally unpredictable.
Myasthenia gravis for students part onePratap Tiwari
This document discusses myasthenia gravis (MG), an autoimmune disorder characterized by weakness and fatigability of skeletal muscles due to dysfunction of the neuromuscular junction (NMJ). It is divided into two parts. Part one covers the epidemiology, clinical features, and types of MG. It describes how MG results from autoantibodies that reduce acetylcholine receptors at the NMJ, causing weakness that typically fluctuates throughout the day. Part two will cover the diagnostic approach and management of MG.
Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system characterized by inflammation, demyelination, axonal loss and gliosis. It is considered an autoimmune disease where the body's immune system attacks the protective myelin sheath surrounding the nerves. There are several types including relapsing-remitting MS where patients experience clearly defined attacks followed by periods of remission, primary progressive MS where symptoms worsen from the onset without remission, and secondary progressive MS where an initial relapsing-remitting course transitions to progressive worsening over time. Symptoms vary between patients and over time but can include sensory impairment, visual impairment, motor impairment, cognitive issues, and bladder/bowel
This document provides an overview of the management of multiple sclerosis (MS). It describes MS as a chronic inflammatory demyelinating disease of the central nervous system that predominantly affects women aged 20-40. The main phenotypes discussed are relapsing-remitting MS, clinically isolated syndrome, secondary progressive MS, and primary progressive MS. Diagnosis involves dissemination of lesions in time and space based on clinical symptoms and MRI findings. Treatment aims to reduce relapse rates and disability progression through disease-modifying therapies like interferons, glatiramer acetate, fingolimod, natalizumab, and dimethyl fumarate. Symptomatic treatments are also discussed.
Multiple sclerosis and newer concept in management till 2014 maydrnikhilver
This document provides information about Multiple Sclerosis (MS), including what it is, possible causes, types, diagnosis, treatment and newer concepts in management. It defines MS as a chronic neurological disorder affecting the central nervous system, where myelin is destroyed in the brain and spinal cord. The exact cause is unknown but is believed to involve immunological, viral, environmental and genetic factors. Diagnosis involves clinical symptoms and tests like MRI, CSF examination and evoked potentials. Treatment includes managing acute attacks, reducing disease activity through medications, and symptom management. Newer oral medications and concepts in disease-modifying therapies are discussed.
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
The chapter Lifelines of National Economy in Class 10 Geography focuses on the various modes of transportation and communication that play a vital role in the economic development of a country. These lifelines are crucial for the movement of goods, services, and people, thereby connecting different regions and promoting economic activities.
Temple of Asclepius in Thrace. Excavation resultsKrassimira Luka
The temple and the sanctuary around were dedicated to Asklepios Zmidrenus. This name has been known since 1875 when an inscription dedicated to him was discovered in Rome. The inscription is dated in 227 AD and was left by soldiers originating from the city of Philippopolis (modern Plovdiv).
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
Philippine Edukasyong Pantahanan at Pangkabuhayan (EPP) CurriculumMJDuyan
(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 𝟏)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐄𝐏𝐏 𝐂𝐮𝐫𝐫𝐢𝐜𝐮𝐥𝐮𝐦 𝐢𝐧 𝐭𝐡𝐞 𝐏𝐡𝐢𝐥𝐢𝐩𝐩𝐢𝐧𝐞𝐬:
- Understand the goals and objectives of the Edukasyong Pantahanan at Pangkabuhayan (EPP) curriculum, recognizing its importance in fostering practical life skills and values among students. Students will also be able to identify the key components and subjects covered, such as agriculture, home economics, industrial arts, and information and communication technology.
𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐍𝐚𝐭𝐮𝐫𝐞 𝐚𝐧𝐝 𝐒𝐜𝐨𝐩𝐞 𝐨𝐟 𝐚𝐧 𝐄𝐧𝐭𝐫𝐞𝐩𝐫𝐞𝐧𝐞𝐮𝐫:
-Define entrepreneurship, distinguishing it from general business activities by emphasizing its focus on innovation, risk-taking, and value creation. Students will describe the characteristics and traits of successful entrepreneurs, including their roles and responsibilities, and discuss the broader economic and social impacts of entrepreneurial activities on both local and global scales.
3. Multiple sclerosis
"It is an immune-mediated inflammatory
demyelinating disease of the central nervous
system characterized by remissions and relapses
and causing chronic disability."
• Disseminated in time and place, The
hallmark of MS is symptomatic episodes
that occur months or years apart and
affect different anatomic locations. See
the image below.
• Characterized by relapses and remissions or
a progressive course.
4. MRI of the head of a 35-year-old
man with relapsing-remitting
multiple sclerosis. MRI reveals
multiple lesions with high T2
signal intensity and one large
white matter lesion. These
demyelinating lesions may
sometimes mimic brain tumors
because of the associated edema
and inflammation.
5. Common sites of demyelination:
• Optic nerve
• Around lateral ventricles,
• Corpus callosum,
• Cortical-subcortical junction,
• Brainstem,
• Cerebellum
• Cervical cord.
6. Etiology and risk factors:
1-genetic factors:
A. Sex: Women are more likely to have MS than men by a 2:1 ratio.
B. Racial Group: Whites are more than twice as likely as other races to develop MS
C. Family History: First-degree relatives are generally greater risk of developing MS than the general
population.
D. Genetic factors : Association with certain HLA types e.g. HLA-DR2
2- environmental factors:
• Latitude: above and below 40° latitude, MS is more common.
• Socioeconomic : It is least common in the lower class and in rural residence.
• Infection: Viral infections may include shingles, chicken pox, measles, or certain herpes
• Factors with the strongest evidence for involvement in MS are Epstein-Barr virus (EBV}, infectious
mononucleosis, smoking, and latitude/vitamin D.
7. Pathogenesis
• Macrophages engulf unknown antigen --
> represent it surface of macrophages on
HLA Dr2 and become APC
• APC is adhesion with T lymphocytes.
(CD4 cells) by T cell receptors and HLA
dr2
Signal 1 stimulation
• APC release B7 protein and CD4 release
CD28
Signal 2 stimulation
8. APCs engulf the
unknown antigen
It expresses a piece of that antigen on its
membrane surface on MHC 2 complex.
Another name for MHC 2 complex is HLA DR2
(S
igna l 1 s
timula tion)
Antigen
MHC 2 complex
APCs presents
the antigen to a
T- helper cell
T- helper cell has a receptor
that can recognize that antigen
anywhere else in the body.
CD4+ molecules connect the
APCs to T- helper cells
CD4+
When this
connection
occurs
T- helper cells release
cytokines and start
proliferating.
(S
igna l 2 s
timula tion)
The T- helper cells have a very particular
TCR that recognizes that specific antigen
Strangely this antigen may resemble
or have a very similar configuration to
a protein that is present within Myelin
Myelin Basic Protein
Antigen ͌
So, T cell Receptors are now
recognizing that antigen and
also other proteins within our
bodies that maybe mimic that
antigen. It is called Molecular
Mimicry.
IL-2
IL-12
IL-27
IFN-ϒ
9. APC
APC (HLA DR2 ) release cytokines
IL 12 & gamma interferon T
helper 1 (cell mediated) release
gamma interferon, TNF B stimulate
macrophage to release TNF alpha
APC ( HLA DR2 ) release
cytokines IL4, IL10 T
helper 2 (cell humoral)
stimulation B cells. release
autoantibodies
T cells (CD4 cells)
T cells release IL2
autoactivation of CD25
more activation
T cells S1P1 receptor & alpha 4
integrin lymph node S1P1
receptor enter T cells inside lymph
node internalization for more
proliferation exist from LN
10.
11. CNS is a Target
• To enter BBB alpha 4 integrin adhesion
with VCAM 1 upregulation of MMP
open BBB T cells enters CNS
• T cells adhesion with microglia
• Signal 1 and 2. repeated inside CNS
• TNF alpha
• Auto antibodies complement fixation
destructed myelin , oligodendrocytes and
open BBB again
12. clinical pattern of MS:
1. Relapsing- remitting MS (RRMS, 85%):
• Attacks with complete/ incomplete recovery.
• Stable course (no progression) between attacks.
2. Secondary progressive MS (SPMS):
• Initially relapsing-remitting, then progression± attacks
3. Primary progressive MS (PPMS):
• Gradual decline • No attacks.
4. Progressive relapsing MS (PRMS):
• Initial gradual deterioration.
• Subsequent episodes.
Relapses are defined as new or worsening neurologic
symptoms that occur in the absence of fever or
infection, last over 24 hours, and are preceded by 30
days of relative neurologic stability.
13. Recent MS phenotypes
1) RRMS: active or not active
2) Progressive disease (PPMS or SPMS):
a) Active and with progression.
b} Active and without progression.
c) Not active and with progression.
d) Not active and without progression (stable
disease}.
14. Clinical Manifestations of MS
Attacks lasting> 24 hours, spaced at least 1 month apart
1} Cognitive and Affective Symptom:
• Abnormalities of working memory, attention, speed of information processing, and executive function.
• Affective disorders: Depression ,Hypomania or mania.
2} Cranial Nerve Manifestations: (brain stem affection)
Visual Manifestations: very common, usually unilateral, or bilateral.
A) optic or retro bulbar neuritis :
• unilateral or bilateral.
• Acute to subacute loss of visual acuity.
• Pain in or behind the eye, increase with eye movement.
• Tender eyeball on pressure.
• Color vision deficits & field defect due to lesion in optic nerve, chiasma, or tract.
15. B)Ocular Nerves:
• 6th nerve palsy, 3rd or isolated 4th palsies
(infrequent}.
• Internuclear ophthalmoplegia
(pathognomonic) ( lag of adducting eye,
& nystagmus of abducting eye during
horizontal ocular movements} due to
medial longitudinal bundle (MLB} lesion
diplopia without squint.
• Horizontal and vertical gaze palsies
16. • One and half syndrome (horizontal gaze
palsy to one side + impaired adduction to
other}.
• Nystagmus
17. C)Trigeminal neuralgia: Unilateral or bilateral.
• Plaque in pons affecting; nuclei or nerve.
• Brisk jaw is common.
D) Auditory and vestibular manifestations; vertigo .
E) Dysphagia and dysarthria: due to pseudo bulbar palsy.
F) VII nerve palsy : hemifacial spasm
18. 3) Motor Manifestations:
1. Fatigability .
2. UMNL:
• Weakness, commonest paraparesis "may be monoparesis, hemiparesis, quadriparesis."
• Marked spasticity most disabling ~ painful spasms ..
• Deep reflexes are markedly increased with clonus.
• lost abdominal reflexes as early sign.
• Extensor planter response.
3. Incoordination: cerebellar affection~ Ataxia (common); manifestations as intention tremors, ataxia
gait, titubation; truncal ataxia, dysarthria, nystagmus.
19. 4) Sensory Manifestations:
a) Deep sensation due to posterior column affection especially cervical segment.
1. Paresthesia, tingling and numbness.
2. Sense of swelling or tight bandage in the limb and trunk. ·'
3. Impaired vibration deep sensation sense of position.
4. lhermitte's symptom and sign; electric like pain in the back and shoulder on bending the neck.
b) Superficial sensation: paresthesia and numbness; level "ascending," Brown
Squared syndrome.
c) Cortical sensations: impaired.
20. 5) Autonomic Involvement:
A) bladder: due to UMNL: urgency, hesitancy, precipitancy, increase residual volume, nocturia, and
recurrent urinary tract infection.
B) Sexual dysfunction: impotence, fatigue, loss of libido, or may be psychogenic.
C) Constipation or fecal incontinence.
6) Myelopathy :
A) Acute transverse myelitis : paraparesis , sensory level , autonomic manifestation
B) Chronic progressive myelitis in progressive pattern
21. Uhthoff's phenomenon
Uhthoff's phenomenon (also known as Uhthoff sign or Uhthoff syndrome) is described as temporary,
short-lived (less than 24 hours), and stereotyped worsening of neurological function among multiple
sclerosis patients in response to increases in core body temperature.
It causes a decrease in the speed of action potentials in the central nervous
system (CNS). Heat may increase the time when voltage-gated sodium channels
are inactivated, which delays further action potentials. This is worsened by the
demyelination caused by MS.
22. Diagnosis of multiple sclerosis in adults :
1-MRI: has improved the diagnostic accuracy of multiple sclerosis
A. Acute lesion : observed as Gadolinium enhancement, appears as a very early sign of the formation of a new lesion
and is perhaps a marker of inflammation.
Site of patches :
Periventricular white matter,
• deep white matter
• centrum semiovale
• corpus callosum (Dawson fingers).
• posterior optic radiation.
• juxtacortical .
• Brain stem , cerebellar & midbrain .
• Cervical spinal segment.
B. Chronic lesions : hyperintensity also without Gadolinium enhancement
C. MS Plaque as a hyperintense area in T2 weighted images. The relationship between the number of T2-weighted
lesions and the degree of clinical disability is poor.
25. 2-Evoked potentials:
Detect whether there is any problem of slowing or
blockade of conduction in the auditory, visual, or
somatosensory, motor pathways.
Visual Evoked potentials :Delays in latencies indicate
demyelination in the anterior visual pathways.
• They are abnormal in 80- 90% with definite MS.
• They Can reveal clinically silent MS lesions in the visual
pathway.
27. Three Categories of Treatment
Treatment of Exacerbations
Disease modifying drugs
Specific MS symptom treatment
28. Treatment of relapse: ( during attack )
Treatment of exacerbations must be done with glucocorticoids to Reduce swelling and inflammation
in the plaques of demyelination, accelerate recovery.
- Intravenous methylprednisolone (pulse therapy) 0.5-1gm/day for five days, followed by a short
course of oral prednisone.
Complications of corticosteroid :
a) Fluid retention and hypokalemia.
b) Gastric ulcer and hemorrhage.
c) Psychosis, anxiety and insomnia.
d) Infections.
e) Osteoporosis and avascular necrosis of the head of femur.