This document discusses myelin, its composition and function. It describes how myelin forms a sheath around neurons, insulating them and allowing rapid nerve impulse propagation. Cholesterol and proteins like myelin basic protein are important myelin components. Myelination begins in fetal development and continues through life. Diseases like multiple sclerosis involve demyelination through autoimmune or other processes. The document examines MS in terms of epidemiology, pathogenesis, clinical presentation and investigations like CSF analysis and MRI that are used in diagnosis.
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.
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...
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.
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...
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.
FA is a very rare, genetic, recessive disease, affecting 1/50,000 people.
Originates from mutations in the “coding” of the mitochondria.
Discovered by Nicholaus Friedreich in the early 1860’s.
Both parents must have the dominant trait for a 25% chance of an offspring possessing the disease.
Not necessarily a disease that kills you, but eventually a wheelchair and regular assistance will be required.
Onset before age 20-25 year.
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.
FA is a very rare, genetic, recessive disease, affecting 1/50,000 people.
Originates from mutations in the “coding” of the mitochondria.
Discovered by Nicholaus Friedreich in the early 1860’s.
Both parents must have the dominant trait for a 25% chance of an offspring possessing the disease.
Not necessarily a disease that kills you, but eventually a wheelchair and regular assistance will be required.
Onset before age 20-25 year.
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
A wonderful and interesting presentation on Multiple Sclerosis! It includes videos, pictures and great insight into the possible cure for MS. I truly hope whoever downloads it enjoys it as much as I do. Blessings!
Scott Johnson - Myelin Repair Foundation, Speaker at the marcus evans Discovery Summit Fall 2011 in Las Vegas, delivers his presentation on Carving a New Niche for Non-Profits: Filling the Translational Gap for Novel Treatments for Diseases with Unmet Needs
Multiple sclerosis (MS) or disseminated sclerosis is an auto immune disease characterized by chronic inflammation, demyelination, and scaring of the myelin sheath of the brain and spinal cord
Early Symptoms of MS
• Blurred or double vision
• Thinking problems
• Clumsiness or a lack of coordination
• Loss of balance
• Numbness
• Tingling
• Weakness in an arm or leg
No two people have exactly the same symptoms of MS.
You may have a single symptom, and then go months or years without any others. A problem can also happen just one time, go away, and never return. For some people, the symptoms become worse within weeks or months.
Common Symptoms of MS
These are the most common changes to the mind and body in someone with MS:
Unusual sensations: People with MS often say they feel a "pins and needles" sensation. They may also have numbness, itching, burning, stabbing, or tearing pains. About half of people with MS have these uncomfortable symptoms. Fortunately, they can be managed or treated.
Bladder problems: About 8 in 10 people have bladder problems, which can be treated. You may need to pee often, urgently, need to go at night, or have trouble emptying your bladder fully. Bowel problems, especially constipation, are also common.
Trouble walking: MS can cause muscle weakness or spasms, which make it harder to walk. Balance problems, numb feet, and fatigue can also make walking hard.
Dizziness: It's common to feel dizzy or lightheaded. You usually won't have vertigo, or the feeling that the room is spinning.
Fatigue: About 8 in 10 people feel very tired. It often comes on in the afternoon and causes weak muscles, slowed thinking, or sleepiness. It's usually not related to the amount of work you do. Some people with MS say they can feel tired even after a good night's sleep.
Muscle spasms: They usually affect the leg muscles. For about 40% of people they are an early symptom of MS. In progressive MS, muscle spasms affect about 6 in 10 people. You might feel mild stiffness or strong, painful muscle spasms.
Sexual trouble: These include vaginal dryness in women and erection problems in men. Both men and women may be less responsive to touch, have a lower sex drive, or have trouble reaching orgasm.
Speech problems: Sometimes MS can cause people to pause a long time in between words and have slurred or nasal speech. Some people also develop swallowing problems in more advanced stages of MS.
Treatments for attacks
Corticosteroids, such as oral prednisone and intravenous methylprednisolone,plasma exchange (plasmapheresis) are prescribed to reduce nerve inflammation.
Treatments are avaliable to slow the progression of the disease, interferons,immuno suppressants immno modulators . Anyway treatment for MS is highly coastly
Dealing with angry patients and family memberspadma puppala
Angry patients can evoke fight or flight responses in medical professionals. Inability to diffuse situation in a professional manner can lead to disastrous consequences. Here are few tips to effectively diffuse the situation
This presentation mainly explains about the type of patients that are encountered in day to day practice as well as how each of them should be handled to improve the communication between a doctor and the patient.
A brief description about Demyelination topics by Dr Sabu Augustine for MBBS Students in Medical school.
References from textbooks and other presentations.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
1.multiple sclerosis
1. Dr. Anzil Mani Singh Maharjan
Resident Phase- B
Department of Neurology
BSMMU
2. Myelin
Myelin forms a
layer, the myelin
sheath around
the axon of
a neuron
It is an outgrowth
of a type of glia
cell
3. Myelin composition
Cholesterol is an essential constituent of myelin
Myelinated axons appear white, hence the the
term "white matter" of the brain
Some of the proteins are myelin basic
protein, myelin oligodendrocyte glycoprotein,
and proteolipid protein
The intertwining hydrocarbon chains
of sphingomyelin serve to strengthen the myelin
sheath
4. Myelination
The production of the myelin sheath is called
myelination
In humans, myelination begins in the 14th week of
fetal development
During infancy, myelination occurs quickly and
continues through the adolescent stages of life
Schwann cells supply the myelin for peripheral
neurons
Oligodendrocytes myelinate the axons of the CNS
neurons
5. Myelin Function
• Provides insulation
Propagate nerve
impulses rapidly in a
saltatory fashion
Voltage-gated Na+
channels found at the
nodes of Ranvier
Na+ influx
Current cannot flow
outward in myelinated
internodal segments
6. Myelin Diseases
Demyelination is the
process of damage to the
myelin or oligodendroglial
cell
◦ Autoimmune- MS
◦ Infectious- PML
◦ Toxic and metabolic
◦ Vascular processes –
Binswanger
Dysmyelination - a primary
biochemical abnormality of
myelin formation exists
◦ Hereditary disorders-
Leukodystrophies
7. Classification of the Inflammatory
Demyelinative Diseases
I. Multiple sclerosis
Chronic relapsing encephalomyelopathic form
Acute multiple sclerosis (Marburg disease)
Primary and secondary progressive types
Diffuse cerebral sclerosis (Schilder disease
and concentric sclerosis of Balo
8. Classification of the Inflammatory
Demyelinative Diseases
II.Acute disseminated encephalomyelitis
A.Postinfectious: Following measles, chickenpox, smallpox,
mumps, rubella, influenza,Mycoplasma
B.Postvaccinal : Following rabies or smallpox
III. Neuromyelitis optica (Devic disease)
IV. Acute and subacute necrotizing
hemorrhagic encephalitis
A. Acute encephalopathic form
B. Subacute encephalitis
9.
10. Introduction
British as “disseminated sclerosis”
French as “sclérose en plaques”
MS is a chronic condition characterized clinically
by episodes of focal disorders of the:
◦ Optic nerves
◦ Spinal cord
◦ Brain
remit to a varying extent and recur over a period of
many years
12. Pathology
Hallmark of MS is the cerebral or spinal
plaque, which consists of a discrete region
of demyelination
Relative preservation of axons
Atrophy and ventricular dilatation
Disruption of BBB but vessel wall is
preserved
13. Pathology (Gross)
Active plaques appear whitish
yellow or pink with somewhat indistinct borders
Older plaques appear translucent with a blue-gray
discoloration and sharply demarcated margins
Plaques are small (1-2 cm) but may become confluent,
generating large plaques
Develop in a perivenular distribution
Most frequently in the periventricular white matter,
brainstem, and spinal cord
15. Histopathology
Active plaques reveals
perivascular infiltration of
lymphocytes
(predominantly T cells)
and macrophages, with
occasional plasma cells
In the plaque, myelin is
disrupted, resulting in
myelin debris found in
clumps or within lipid-laden
macrophages
Reactive astrocytes are
prominent in plaques
Demyelination
area
Venule
17. Epidemiology
Age of Onset
◦ Mean and median age of
onset in relapsing forms of
MS is age 29 to 32
◦ Primary progressive MS
(PPMS) has a mean age
of onset of 35 to 39
◦ Can occur as late as the
seventh decade
◦ 5% of cases of MS have
their onset before age 18
Sex Distribution
◦ F>M
◦ 2 : 1
18. Epidemiology
Geographical Distribution
MS is a location-related
illness with a latitude
gradient
High-frequency areas with
prevalence of 60 -100 per
100,000 or more, include
◦ All of Europe (including
Russia)
◦ Southern Canada
◦ Northern United States
◦ New Zealand
◦ SE portion of Australia
The highest reported rate of
300 per 100,000 occurring
in the Orkney Islands
19. Epidemiology
Race
Determinant of MS risk
White extraction, especially from Northern Europe are
the most susceptible
People of Asian, African, or Amerindian origin have the
lowest risk
Other groups are variably intermediate
Migration after puberty no increased risk
Migration before childhood increased risk
21. Pathogenesis
The cause of MS remains undetermined
Possible Etiologies include
◦ Infection
◦ Enviromental factors
◦ Autoimmunity
◦ Genetic Susceptibility
22. Pathogenesis
Infection
Little direct evidence supports the concept of a
role for viral infection
Human T-cell lymphotropic virus type 1 [HTLV1]
Human herpesvirus 6 (HHV6)
Epstein-Barr virus (EBV)
Chlamydia pneumoniae
Environmental Factors
Sunlight exposure during growth
Vitamin D
Epidemiological data supportive
23. Pathogenesis
Autoimmunity
Break down of tolerance (unresponsiveness of the
immune system)
By means of molecular mimicry between self-antigens
and foreign antigens
Myelin basic protein (MBP), the target for
autoimmune attack
T cells that respond to MBP are found in the
peripheral blood possibly at higher levels in MS
patients with active disease
24. Pathogenesis
Genetic susceptibility
The risk of familial recurrence in MS is 15%
Highest risk in first-degree relatives (age-adjusted risk):
4–5% for siblings and
2–3% for parents or offspring
Monozygotic twins have a concordance rate of 30%
The genes that predispose to MS are incompletely defined
Inheritance appears to be polygenic, with influences from
◦ Genes for human leucocyte antigen (HLA) typing
◦ Interleukin receptors
◦ CLEC16A (C-type lectin domain family 16 member A)
◦ CD226 genes
26. Clinical Manifestations
Multiple sclerosis is classically described as a relapsing
remitting disorder
MS may display marked clinical heterogeneity. This
variability includes
◦ age of onset
◦ mode of initial manifestation
◦ frequency
◦ severity
◦ sequelae of relapses
◦ extent of progression
◦ Cumulative deficit over time
High degree of variability and the difficulty in predicting
the course and severity make MS one of the most
puzzling CNS disease
28. Clinical Manifestations
Early Symptoms
Onset over hours or days
Motor or sensory system involvement in 50 % of
patients
Symptoms of tingling of the extremities and tight band-like
sensations around the trunk
Dragging or poor control of one or both legs to a spastic
or ataxic paraparesis
Early Signs
The tendon reflexes are retained and later become
hyperactive
Extensor plantar reflexes
Disappearance of the abdominal reflexes
Varying degrees of deep and superficial sensory loss
may be associated
29. Clinical Manifestations
The patient will complain of weakness,
incoordination, or numbness and tingling in one
lower limb
But the examination will reveal
◦ Bilateral Babinski signs
◦ Bilateral corticospinal tract signs
◦ Posterior column disease
30. Clinical Manifestations
Several syndromes typical of MS and may
be the initial manifestation :
(1) Optic neuritis
(2) Transverse myelitis
(3) Cerebellar ataxia - nystagmus and ataxia
(4) Various brainstem syndromes (vertigo, facial
pain or numbness, dysarthria, diplopia)
◦ These syndromes may pose a diagnostic
dilemma as these do occur in other diseases
too
31. Clinical Manifestations
Paresthesia or numbness of an entire arm or leg
Facial pain often simulating tic douloureux
Disorders of micturition
Cervical myelopathy- slowly progressive with
weakness and ataxia
32. Clinical Manifestations
Diplopia
◦ Medial longitudinal fasciculi
◦ Internuclear ophthalmoplegia
◦ Paresis of the medial rectus on attempted lateral
gaze, with a coarse nystagmus in the abducting
eye
◦ Usually bilateral
The presence of bilateral internuclear
ophthalmoplegia in a young adult is
virtually diagnostic of MS
33. Clinical Manifestations
Myokymia or paralysis of facial muscles
Deafness, tinnitus, unformed auditory hallucinations
(because of involvement of cochlear connections)
Vomiting (vestibular connections), and, rarely, stupor
and coma
Vertigo of central type
Dull, aching low back pain
Sharp, burning, poorly localized, or lancinating radicular
pain, localized to a limb or discrete part of the trunk
34. Clinical Manifestations
Lhermitte sign
Flexion of the neck may
induce a tingling, electric
shock like feeling down
the shoulders and back
Frequent occurrence of
this phenomenon in MS
Due to an increased
sensitivity of
demyelinated axons to
the stretch or pressure
on the spinal cord
induced by neck flexion
35. Clinical Manifestations
Uhthoff phenomenon
Transient worsening of function with
increased body temperature
Due to a drop below the safety threshold for
conduction because of physiological
changes involving the partially
demyelinated axon
36. Clinical Manifestations
Established Stage of the Disease
50 % will manifest a clinical picture of mixed or
generalized type with signs pointing to involvement of
the optic nerves, brainstem, cerebellum, and spinal cord
30 to 40 % will exhibit only varying degrees of spastic
ataxia and deep sensory changes in the extremities,
i.e., essentially a spinal form of the disease
5 % have a predominantly cerebellar or brainstem–
cerebellar form occurs
37. Clinical Manifestations
Cognitive impairment
Progressive decline, is present in perhaps one-half
of patients with long-standing MS
Reduced attention
Diminished processing speed and executive
skills
Memory decline
Language skills and other intellectual functions
are preserved
38. Clinical Manifestations
The most characteristic clinical course of MS
is the occurrence of relapses
Relapses can be defined as
◦ acute or subacute onset of clinical dysfunction
◦ that usually reaches its peak from days to
several weeks,
◦ followed by a remission during which the
symptoms and signs usually resolve partially or
completely
The minimum duration for a relapse has been
arbitrarily established at 24 hours
39. Clinical Manifestations (Course)
1. Relapsing-remitting (RRMS):
Clearly defined relapses with full recovery or with sequelae and
residual deficit on recovery
The periods between disease relapses are characterized by a
lack of disease progression
2. Secondary progressive (SPMS):
Initial relapsing remitting disease course followed by progression
with or without occasional relapses, minor remissions, and plateaus
3. Primary progressive (PPMS):
Disease progression from onset, with occasional plateaus and
temporary minor improvements allowed
4. Progressive relapsing (PRMS):
Progressive disease from onset, with clear acute relapses with or
without full recovery
The periods between relapses are characterized by continuing
progression
43. CSF ANALYSIS
Cytology
In 1/3 of with an acute onset or
an exacerbation, there may be a
slight to moderate mononuclear
pleocytosis (6 to 20 or less than
50 cells/mm3)
In rapidly severe demyelinating
disease of the brainstem, the
total cell count may reach or
exceed 100, and rarely 1,000,
cells/mm3
In the hyperacute cases, the
greater proportion of these may
be polymorphonuclear
leukocytes
44. CSF ANALYSIS
Protein
40 % of patients, the total protein content of the
CSF is increased slightly
Not more than 100 mg/dL
In two-thirds of patients, the proportion of gamma
globulin (mainly IgG) is increased (greater than
12 percent of the total protein)
IgG index obtained by measuring albumin and
gamma globulin in both the serum and CSF
45. CSF ANALYSIS
Oligoclonal bands
Gamma globulin proteins in the CSF of
patients with MS are synthesized in the
CNS
They migrate in agarose electrophoresis
as abnormal discrete populations, so-called
oligoclonal bands
The most widely used CSF test for the
confirmation of the diagnosis
Show several bands in the CSF in more
than 90 percent of cases of MS
But they are not always found with the
first attack or even in the later stages of
the disease
46. Magnetic Resonance Imaging
MRI is the most helpful ancillary examination
in the diagnosis of MS
Reveal asymptomatic plaques in the
cerebrum, brainstem, optic nerves, and spinal
cord
T2-weighted images show :
◦ Hyperintense well-demarcated lesions
◦ Multiple and asymmetrical
◦ Periventricular surface in location
48. Magnetic Resonance Imaging
The presence
lesions in the
corpus callosum is
diagnostically
useful
This structure is
spared in many
other disorders
Midsagittal FLAIR image
49. Magnetic Resonance Imaging
In sagittal images
extension of the lesion
outward from the
corpus callosum in a
fimbriated pattern and
have been termed
“Dawson fingers”
These areas may
extend into the
centrum semiovale
and may reach the
convolutional white
matter
Sagittal FLAIR image
51. Newer Imaging Tecniques
MAGNETIC RESONANCE SPECTROSCOPY
◦ a tool that derives MRI signal from
multiple metabolites
◦ A high choline (Cho) peak is indicative of
an increase in membrane turnover, as can
be seen in demyelination and
remyelination
DIFFUSION TENSOR IMAGING
HIGH-FIELD-STRENGTH MRI
52. Evoked Potentials
EPs are CNS electrical events
generated by peripheral stimulation of a
sensory organ
Are useful
◦ To determine abnormal function that may
be clinically unapparent
◦ When the clinical data point to only one
lesion in the CNS mainly in the early
stages of the disease or in the spinal form
Commonly used EPs are
1. Visual Evoked response (VEPs)
2. Somatosensory evoked potentials (SSEPs)
3. Brainstem auditory-evoked responses (BAER)
53. Comparison of Sensitivity of
Laboratory Testing
Investigations Sensitivity
VER 80%-85%
BAER 50%-65%
SSEP 65%-80%
OCB 85%-95%
MRI 90%-97%
56. Differential diagnosis
The differential diagnosis of MS in the setting
of a young adult with two or more clinically
distinct episodes of CNS dysfunction with at
least partial resolution is limited
Problems arise with
◦ Atypical presentations
◦ Monophasic episodes
◦ Progressive illness
◦ The unusual nature of some sensory symptoms
may result in a misdiagnosis of conversion
disorder
59. Treatment
Treatment of the MS patient should be directed toward these
basic goals:
Relief or modification of symptoms
Shortening the duration or limiting the residual effects of an
acute relapse
Reducing the frequency of relapses
Preventing disability progression or slowing its pace
Supporting family and patient, alleviating social and economic
effects, and advocating for the disabled or handicapped
60. Symptomatic Treatment
Spasticity
Baclofen a GABA agonist Daily divided doses of 20 to 120 mg and
occasionally .Intrathecal baclofen via an implanted pump
Tizanidine a centrally active α2-noradrenergic agonist, gradually
increased starting with 2 mg at bedtime
Benzodiazepines
Dantrolene sodium rarely
4-Aminopyridine and 3,4-diaminopyridine (3,4-DAP) block
potassium channels in the axolemma
Botulinum toxin type A (Botox) injections into spastic or
contracted muscles may also be effective in selective cases
61. Symptomatic Treatment
Tremor
Weighted wrist bracelets and specially adapted utensils are
nonpharmaceutical options
Most attempts at pharmacological amelioration of tremor fail
Isoniazid
Primidone
Carbamazepine
Gabapentin
Topiramate
Clonazepam
Propranolol
Ondansetron
62. Symptomatic Treatment
Fatigue
Amantadine 100 mg twice a day
Modafinil - a wakefulness promoting agent
Methylphenidate 10 to 60 mg/day in 2 to 3 divided dose
SSRIs
Fluoxetine 10 to 20 mg once twice daily
Bupropion
63. Symptomatic Treatment
Bladder Dysfunction
Initial steps in managing bladder dysfunction include
◦ fluid management,
◦ timed voiding
◦ use of a bedside commode
Hyperreflexic bladder without outlet obstruction
◦ Oxybutynin,Tolterodine,Trospium,Darifenacin,solifenacin,
Desmopressin
Imipramine for enuresis
Detrusor hyperreflexia with outlet obstruction may respond
Credé maneuvers terazosin hydrochloride
Intermittent catheterization
Chronic indwelling catheterization may be required
Surgical correction-augmentation of bladder capacity with an
exteriorized loop of bowel
64. Symptomatic Treatment
Depression
SSRIs are the medications of choice
Fluoxetine
Amitriptyline, 25 to 100 mg daily
Sexual Dysfunction
Sildenafil 25 to 100 mg 1 hour before sexual
intercourse for erectile dysfunction
65. Symptomatic Treatment
Cognitive Impairment
Interferon beta-1a SC
L-amphetamine
Modafinil
Donepezil
Cognitive-behavioral therapy
Family and individual counseling
Strategies to improve day-to-day function
Job modifications and accommodations
66. Treatment of Acute Attacks
Acute attacks are typically treated with corticosteroids
Indications for treatment of a relapse include
functionally disabling symptoms with objective evidence
of neurological impairment
Short courses of IV methylprednisolone – 500 to 1000
mg daily for 3 to 5 days
◦ With or without a short prednisone
S/Es include psychiatric changes, predilection for
infections,GI disturbances,anaphylactoid reactions,
Increased incidence of fracture
68. Disease-Modifying Treatments
Emerging Therapies
Laquinimod
Orally active synthetic immunoregulator
Oral fumarate/BG-12
Induces apotosis of activated T cells
Teriflunomide
Is a metabolite of leflunomide
Alemtuzumab
Humanized monoclonal anti-body against CD52 antigen expressed in all
lymphocytes
Rituximab
A chimeri murine-human monoclonal antibody directed against CD30
antigen on B lymphocytes
69. Treatment-Rehabilitation
Referral to
physical,occupational and
speech therapists
1.Physical therapy
Evaluate and train the patient
in appropriate exercise
programs to :
◦ decrease spasticity
◦ maintain range of motion
◦ strengthen muscles
◦ improve coordination
Mechanical aids, such as
ankle-foot orthoses, also can
be useful in spasticity
management.
70. Treatment-Rehabilitation
2. Speech therapy
3.Occupational therapy
• Assessment of the patient's
functional abilities in completing
activities of daily living
•Evaluate for adaptive equipment
and assistive technology needs
72. Prognosis
Prognostic indicators:
MS appears to follow a more benign course in women than in men
Onset at an early age is a favorable factor, whereas onset at a later
age carries a less favorable prognosis
RRMS is more common in younger patients, and PPMS and SPMS
are more common in the older age group
Relapsing form of the disease is associated with a better prognosis
than progressive disease
Among initial symptoms, impairment of sensory pathways or ON has
a favorable prognostic feature
Pyramidal and particularly brainstem and cerebellar symptoms carry
a poor prognosis
Devic disease, Baló concentric sclerosis, and particularly Marburg
disease are more fulminant variants of MS, with early disability and
even death