A brief description about Demyelination topics by Dr Sabu Augustine for MBBS Students in Medical school.
References from textbooks and other presentations.
neurological disorders of demyelination, for generalized idea as a seminar work for university, department of pathophysiolog.
for more information feel free to contact me
neurological disorders of demyelination, for generalized idea as a seminar work for university, department of pathophysiolog.
for more information feel free to contact me
This presentation is a comprehensive & updated presentation that delves deeply into Multiple Sclerosis. It is intended for healthcare professionals and features the Anatomy and Physiology, Common Etiology, a focused review of the disease Pathophysiology, Prevalence & Morbidity, Clinical Manifestations, Diagnostics, Classification & Prognosis, Treatment (Both current and experimental), Nutrition, and Psychosocial issues and resources available to patients. It is very rich in details, diagrams (on every slide), and interactive content when in slide presentation mode. The presentation has also hyperlinks to videos (3 D Patho) and controversial treatments. Finally, it concludes with a Case Study to highlight the clinical application.
Please note that you're welcome to use any slides as long as you reference my post when you do so to maintain the integrity of authorship
If interested in detailed answers, please email: aamirdash@yahoo.com
Thanks, Ahmad
This presentation is a comprehensive & updated presentation that delves deeply into Multiple Sclerosis. It is intended for healthcare professionals and features the Anatomy and Physiology, Common Etiology, a focused review of the disease Pathophysiology, Prevalence & Morbidity, Clinical Manifestations, Diagnostics, Classification & Prognosis, Treatment (Both current and experimental), Nutrition, and Psychosocial issues and resources available to patients. It is very rich in details, diagrams (on every slide), and interactive content when in slide presentation mode. The presentation has also hyperlinks to videos (3 D Patho) and controversial treatments. Finally, it concludes with a Case Study to highlight the clinical application.
Please note that you're welcome to use any slides as long as you reference my post when you do so to maintain the integrity of authorship
If interested in detailed answers, please email: aamirdash@yahoo.com
Thanks, Ahmad
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.
references:
Phases and Phenotypes of Multiple Sclerosis By Orhun H. Kantarci, MD.
Diagnosis of Multiple Sclerosis By Jiwon Oh, MD, PhD, FRCPC
Nature Reviews | Disease Primers
Multiple sclerosis Massimo Filippi1,2*, Amit Bar- Or3, Fredrik Piehl4,5,6, Paolo Preziosa1,2, Alessandra Solari7, Sandra Vukusic8 and Maria A. Rocca1,2
Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system). In MS , the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body.
Imaging of spinal cord acute myelopathiesNavni Garg
This presentation provides a comprehensive review of imaging of causes of acute myelopathies and a systemic approach for narrowing down the differentials
Here is very good and amazing presentation on Multiple sclerosis ..its about brain
read this carefully and work on this because the work on brain is very good for future research...
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
1. BY
DR SABU AUGUSTINE
ASSOCIATE PROFESSOR
DEPT. OF GENERAL MEDICINE
DEMYELINATION
Dr Sabu Augustine
Associate Professor
Dept Of General Medicine
Dr S.M C.S.I Medical College, Karakonam, Trivandrum
3. INTRODUCTION
• Demyelinating diseases comprise of diseases of central
and peripheral nervous system in which disruption of
myelin is a dominant feature.
• whether a primary biochemical abnormality of myelin
exists (dysmyelinating) or
• whether some other process damages the myelin or
oligodendroglial cells (demyelinating).
• Demyelinating diseases include autoimmune, infectious,
toxic, metabolic, and vascular processes; dysmyelinating
diseases in which a primary abnormality of the formation
of myelin exists include several hereditary disorders.
4.
5. PARTS OF A NEURON
• Cell Body
– Contains the nucleus
• Dendrites
– Receptive regions; transmit
impulse to cell body
– Short, often highly branched
– May be modified to form receptors
• Axons
– Transmit impulses away from cell body
– Axon hillock; trigger zone
• Where action potentials first develop
– Presynaptic terminals (terminal boutons)
• Contain neurotransmitter substance (NT)
• Release of NT stimulates impulse in
next neuron
– Bundles of axons form nerves
6. MYELIN AND WHITE MATTER
• The gray matter primarily contains neurons and their
processes, the white matter is composed predominantly of
myelinated bundles of axons
• The oligodendroglial cell membrane is the source of the
myelin sheath, which is a tightly wrapped, multilayered
membrane composed of a repeating structure characterized
by lipid- cytoplasm-lipid-water and which ensheathes
axons.
• Any process, including metabolic injury or ischemia, that changes
the chemical composition of myelin will result in a less stable
structure that is more susceptible to injury .
7. MYELIN AND WHITE MATTER
• Neuroglial cells, namely oligodendrocytes,
astrocytes, and microglia, are primarily
responsible for the maintenance or “well- being”
of the white matter- by providing structural and
nutritional support of neurons, regulating the
extracellular environment, and acting as
scavenger cells.
• As white matter becomes myelinated, it appears
hyperintense on T1-weighted and hypointense on
T2-weighted images relative to gray matter
9. Normal myelinated
axon
nodes of Ranvier
• Lipid-rich myelin sheath
produced by oligodendrocytes
• Axon insulation
• Sodium channels clustered at
• Increased conduction speed and
metabolic efficiency
Demyelination
or block
cytoskeleton
• Decreased conduction velocity
• Destablization of axonal
• Remodelling of internodal
membrane
• Progressive axonal loss
11. DEFINITION
• Multiple sclerosis is a chronic progressive,
degenerative disorder of the CNS
characterized by disseminated demyelination
of the nerve fibres of the brain and spinal
cord.
• Multiple sclerosis (MS) is characterized by a
triad of inflammation, demyelination, and
gliosis (scarring); the course can be relapsing-
remitting or progressive.
12. EPIDEMIOLOGY
• MS is 2-3 times more common in women
than men.
• MS is predominantly a disease of young adults
with a mean age of onset around 30 years old.
13. AETIOLOGY & RISK FACTORS
• The aetiology of MS remains poorly
understood.
• Like most inflammatory conditions of
unknown aetiology, the cause is thought to be
due to an abnormal immune reaction to an
unknown environmental trigger in a
genetically predisposed individual.
14. RISK FACTORS
Risk factors that may be associated with triggering an
autoimmune response that subsequently leads to the
disease.
• Viral infections: several viruses linked with MS.
Increased risk of MS following Epstein-Barr virus (EBV)
infection (i.e. glandular fever)
• Geographic latitude: prevalence of MS increases the
greater the distance north or south from the equator.
Migration after puberty carries risk from former
geographic location.
• Sunlight exposure: inverse relationship between MS,
sunlight exposure and vitamin D levels.
• Other: obesity during adolescence, smoking, gender
(females at increased risk).
15. PATHOPHYSIOLOGY
• MS is an inflammatory, demyelinating disease
of the CNS, which is characterised by the
presence of plaques.
• In MS, oligodendrocytes are destroyed, which
leads to demyelination and can cause axonal
loss.
16. Classical plaque sites
• Optic nerves: affects 40% during course of disease.
Presenting demyelinating event in 20%.
• Spinal cord: affects 50-75% during course of disease.
Majority associated with concomitant brain lesions.
Predilection for cervical spine.
• Brainstem: may present with ophthalmoplegia (e.g.
intranuclear ophthalmoplegia - discussed below).
• Cerebellum: characteristically causes ataxia and gait
disturbance.
• Juxtacortical white matter (near the cerebral cortex).
• Periventricular white matter (near the ventricular
system).
17. • The BBB prevent entrance of T cells into the nervous
system.
The blood–brain barrier is normally not permeable to
these types of cells, unless triggered by infection or a
virus, which decreases the integrity of the tight junctions.
When the blood–brain barrier regains its integrity, usually
after infection or virus has cleared, the T cells are trapped
inside the brain.
Blood-brain
barrier
breakdown
• The immune system attacks the nervous system, forming
plaques or lesions.
Commonly involves white matter.
Destroys oligodendrocytes- causing demyelination
Remyelination occurs in early phase but not completely.
Repeated attacks lead to fewer remyelination.
Autoimmunology
• T-cells attacks on myelin triggers inflammatory processes,
stimulating other immune cells and soluble factors like
cytokines and antibodies.
Leaks form in the BBB cause swelling, activation of
macrophages, and more activation of cytokines and other
destructive protein
Inflammation
18. CLASSIFICATION
• There are eight types of multiple sclerosis. They
are:
• Progressive Relapsing (PRMS)
• Secondary Progressive (SPMS)
• Primary Progressive (PPMS)
• Relapsing / Remitting (RRMS)
• Benign
• Spinal form
• Neuromyelitis optica
• Marburg variant
19.
20. 13-03-2016 DEMYELINATING DIS
•changes in sensation (33%)
•Optic neuritis (20%)
•Weakness(exercise induced) (13%)
•double vision- internuclear opthalmoplegia (7%)
•unsteadiness while walking (5%)
•and balance problems (3%)
Lhermitte's sign (25-40%) is an electrical
sensation that runs down the back and into the
limbs and is produced by bending the neck
forwards. The sign suggests a lesion of the dorsal
columns of the cervical cord or of the caudal
medulla.
Uhthoff's phenomenon is the worsening of
neurologic symptoms in multiple sclerosis when
the body gets overheated from hot weather,
exercise, fever,
The most common initial symptoms
CLINICAL FEATURES
21. CLINICAL FEATURES
• Clinical features associated with MS are
determined by plaque locations within the
CNS.
Visual- Optic neuritis and Eye movement
abnormalities.
• Optic neuritis characteristically presents with
partial or total unilateral visual loss that
develops over days.
22. • Eye movement disorders may be due to
brainstem lesions that affect cranial nerves or
the pathways that connect visual tracts
together.
• Two commonly seen are INO and Abducens
palsy.
23. INO: disorder of conjugate lateral gaze due to demyelination of the
medial longitudinal fasciculus (MLF). MLF is heavily myelinated.
Connects the abducens nucleus complex with the contralateral
oculomotor nucleus. If affected, when looking to the right, the
right eye will abduct but the left will remain central (failure in
adduction).
24. Motor & coordination
• The prominent motor feature in MS is progressive
paraparesis and evidence of upper motor neuron signs
(Spasticity, reduced power, hyper-reflexia).
• Motor and coordination abnormalities may present as
a typical clinical syndrome such as
transverse myelitis
or
cerebellar syndrome (ataxia, slurred speech, intension
tremor, nystagmus, vertigo and clumsiness).
25. Sensory & autonomic
• Sensory symptoms are common in MS and seen
in almost all patients during the course of the
disease.
• Paraesthesia
• Pain
• Heat sensitivity (Uhthoff phenomenon)
• Sexual dysfunction
• Bladder & bowel dysfunction
26. Cognitive & psychological
• Cognitive impairment,
depression and fatigue
are all extremely
common.
• depression can have a
negative impact on
memory, attention, and
concentration.
27. DIAGNOSIS
• MS is primarily a clinical diagnosis, which is
supported by the use of MRI.
• There is no pathognomonic test for MS. All labs
are nonspecific and are to be interpreted within
the clinical picture.
• Lesions scattered in time and space”; a lesion
must occur in different locations in the CNS at
different points of time.
• The diagnosis of MS is based on the clinical
presentation (called an ‘attack’ or ‘relapse’),
which is then confirmed by objective clinical
evidence.
28. DIAGNOSIS
• MS attack: defined simply as an episode of
neurological symptoms that relate to an
inflammatory demyelinating lesion. Lasts > 24
hours with or without recovery. Typically sensory
disturbances, motor weakness, or visual
complaints. There must be more than 30 days
between attacks to count as a separate episode.
• Objective clinical evidence: identification of an
abnormality (usually on clinical examination or
MRI), which corresponds to the anatomical
location suggested by the current, or past,
symptoms of a MS attack.
29. Revised McDonald criteria
• The McDonald criteria was revised in 2017
and it is based on the principle that
demyelinating lesions (in brain +/- spinal cord)
are disseminated in time and space.
• In other words, two independent clinical
attacks would be evidence of dissemination in
time and two separate lesions on MRI would
be evidence of dissemination in space.
30. INVESTIGATIONS
• Additional investigations can be used to help
support the diagnosis and exclude an alternative
pathology.
Cerebral Spinal Fluid (CSF) Examination
• Increased in Protein (myelin basic, 25%),
Oligoclonal IgG bands (greatest sensitivity), IgG
and WBCs.
• The test is considered positive if oligoclonal
bands identified in the CSF are not present in the
serum. Therefore, a paired serum sample should
be taken at the time of the lumbar puncture.
31. VEP (Visual Evoked Potentials) (high sensitivity
along with MRI)
• VER involves measuring electrical activity via a
transducer over the occipital cortex in response
to a light stimulus.
• not useful during acute episodes.
BAER (Brainstem Auditory Evoked Response)
• Investigates the pontine area displaying an
absence or delay of wave formation secondary
to the demyelinating process
SEP (Sensory Evoked Potentials)
•Prolongation of absolute peak or interpeak
latency
Evoked potentials
32. MANAGEMENT
• MS management is broadly divided into
general care, managing acute relapses and
disease modifying therapies.
• The principle management of an acute relapse
or ‘attack’ in RRMS is the use of
corticosteroids.
• Before treating a relapse, it is essential to rule
out infection, which can lead to a
deterioration in symptoms.
33. Medications
• Immunomodulator agents- Disease modifying.
• Corticosteroids (Methylprednisolone).
• Agents to Alter the Course of theDisease.
Interferon-A
Interferon-B
Glatiramer acetate
• Immunosuppression agents are reserved for
patients with unresponsive disabling MS.
34. Mental function (Hmf): Mild cognitive changes, apathy,
inattention, depression, euphoria
Upper motor neuron weakness
Uthoff's phenomenon
Language: Dysarthria
Tingling numbness
Trigeminal neuralgia
Intention tremors
Internuclear ophthalmoplegia
Posterior column features
Pulfrich phenomenon (sense of disorientation in moving traffic)
Lesions disseminated in time and space
Exercise worsens symptom
Mnemonic to remember
35. • Sensory: Posterior column involvement
Cerebellar signs
Lhermitte sign
Exercise worsens symptoms
Remitting features
Optic neuritis
Oligoclonal bands in CSF electrophoresis
Spasticity
Internuclear ophthalmoplegia
Immunotherapy (Disease modifying drugs): ABC –
Interferon Beta-1A, Interferon Beta-1B, Copaxone
(Glatiramer)
Incontinence (bowel and bladder involvement)
Steroids for acute exacerbation
Mnemonic to remember