0% found this document useful (0 votes)
71 views2 pages

Etiology: Molecular Mimicry - Myelin-Reactive

Multiple sclerosis is an autoimmune disease characterized by inflammation, demyelination, and gliosis in the central nervous system. It commonly presents with sensory disturbances, pain, visual issues, motor impairment, coordination and balance problems, speech and swallowing difficulties, and bladder and bowel dysfunction. Diagnosis involves evidence of lesions disseminated in space and time via MRI or other tests. While treatments can help control symptoms and reduce relapse rates, MS has no cure.

Uploaded by

Julia Salvio
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
71 views2 pages

Etiology: Molecular Mimicry - Myelin-Reactive

Multiple sclerosis is an autoimmune disease characterized by inflammation, demyelination, and gliosis in the central nervous system. It commonly presents with sensory disturbances, pain, visual issues, motor impairment, coordination and balance problems, speech and swallowing difficulties, and bladder and bowel dysfunction. Diagnosis involves evidence of lesions disseminated in space and time via MRI or other tests. While treatments can help control symptoms and reduce relapse rates, MS has no cure.

Uploaded by

Julia Salvio
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 2

Malignant (Marburg) – rapid onset, almost continual 

MULTIPLE SCLEROSIS progression


Trigeminal neuralgia (tic douloureux) –
demyelination of sensory division of trigeminal
 Autoimmune disease characterized by nerve
inflammation, selective demyelination, and  Hyperpathia – hypersensitivity to minor sensory
gliosis. stimuli
 First defined by Dr. Jean Charcot in 1868 Four major disease courses:  Headache
o Paralysis  Relapsing-remitting (RRMS) – m/c, ~85% of pts  Neuropathic pain – demyelinating lesions in
o Charcot’s Triad: o Relapses followed by remissions, lack of spinothalamic tracts/sensory roots
 Scanned speech – brainstem progression between  (+) Lhermitte’s sign – post column damage in
 Intention tremor – motor  Secondary-progressing (SPMS) – some RRMS the SC; electric shock-like pain down the spine
pathways/cerebellum may progress to SPMS upon neck flexion
 Nystagmus – nerves of the eyes o Begins with relapsing-remitting course Visual – 80% of pts
 Onset usually 20-40 y/o followed by progression to steady and  Improves c/in 4-12 wks
 W>M, 2-3:1 irreversible decline  Optic neuritis – inflammation of the optic nerve;
Etiology o Progressive axonal loss rather than new icepick-like pain behind the eye c
 3% in a sibling lesions blurring/graying of vision/blindness in one eye,
 5% in a fraternal twin  Primary-progressive (PPMS) – 10% of cases, scotoma may appear
later onset (40 y/o)  Marcus Gunn pupil – paradoxical dilation of both
 25% in an identical twin
o Nearly continuous worsening of the pupils when light is shone in affected eye
 Molecular mimicry – myelin-reactive
disease from onset  Nystagmus – cerebellum/central vestibular
lymphocytes activated by the immune system
during exposure to virus  Progressive-relapsing (PRMS) – 5% of pts pathway; involuntary cyclical movements of the
o Progressive from onset and steady eyeball
 Implicated virus
o Measles deterioration, with occasional acute  Internuclear ophthalmoplegia (INO) –
attacks demyelination of pontine medial longitudinal
o Epstein-Barr virus
Exacerbating Factors – new and recurrent MS fasciculus; lateral gaze palsy on affected side,
o Chlamydia pneumoniae
symptoms lasting > 24 hrs nystagmus of opposite abducting eye
o Canine distemper
 Overall health  Diplopia – double vision
o Human herpesvirus-6
 Viral/bacterial infections (cold, flu, UTI, sinus Motor – UMN signs (paresis, spasticity, brisk tendon
 Risk of MS may be ↑ in vit. D deficiency and
infection) reflexes, involuntary flexor and extensor spasms,
smoking
 Disease of major organ systems (hepatitis, clonus, Babinski’s sign, exaggerated cutaneous
Pathophysiology
pancreatitis, asthma attacks) reflexes, loss of precise autonomic control)
Immune Autoantige  Stress  Weakness – loss of orderly recruitment and ↓
response ns  Pseudoexacerbation – temporary worsening of firing rate modulation
MS symptoms, usually c/in 24 hrs o Asthenia and ataxia in pts c cerebellar
Gliosis Demyelinati
o Uthoff’s symptoms – adverse reaction to lesions
on
heat  Spasticity – 75% of cases
Symptoms o Certain antidepressants (SSRIs) can
Lesion Type I
Sensory exacerbate spasticity
Type II  Hypesthesia, numbness  Fatigue – 75-95% of pts; subjective lack of
 Paresthesia physical/mental energy perceived to interfere c
Type Pain – 80% of pts, 55% clinically significant usual and desired activities
III  Paroxysmal limb pain – dysesthesia common in o Results of central activation failure
Disease Course
Benign – pt remains fully functional 15 yrs p onset the LE, m/c type of pain Coordination and Balance
o Fewer than 20% of cases  Ataxia – dysmetria (undershoot/overshoot),
dyssynergia (loss of synergy),
dysdiadochokinesia (rapid alternating  Constipation – m/c GI complaint; lesions  Antidepressants
movements) affecting control of gastrocolic reflex PT Examination
 Postural tremor during sitting/standing o Spasticity of pelvic floor muscles,  Complete musculoskeletal and neurologic
 Intention tremor – involuntary, rhythmic, inactivity assessment
shaking movements when purposeful o Bowel impaction – serious complication Exercise Training
movements are attempted Sexual – 91% of men, 72% of women  Emphasis on maintenance of general
Gait and Mobility Diagnosis conditioning
 ~50% of pts c RRMS require some form of  Dissemination of lesions in space and time  Best exercise for task is the task itself.
assistance during walking 15 yrs p diagnosis  Lab tests: MRI, EP, LP c CSF analysis Important Prognostic Signs
 Ataxic gait – staggering, uneven steps, poor o MRI is highly sensitive, 95%  Male
foot placement, uncoordinated limb o Bright spots in new lesions (preceding 6  Initial presentation over 35 y/o
movements, frequent loss of balance wks)  Motor/cerebellar dysfunction
 Scissoring gait – spasticity of the adductor o Black holes in more long-term disease  Rapid disease progression
muscles activity (gadolinium-enhanced)  Polysymptomatic onset
Speech and Swallowing  VEP is most sensitive indicator of optic nerve
 Dysarthria dysfunction Expanded Disability Status Scale for Patients with MS
 Dysphonia  Elevated immunoglobulin (IgG) in CSF
 Aspiration pneumonia – wet voice quality c Medical Management
gurgling, sounds of congestion, fever Acute Relapses
Cognitive - ~50% of pts  Corticosteroids (methylprednisolone) shorten
 Short-term memory, attention and duration of exacerbations
concentration, information processing, Spasticity
executive functions, visuospatial functions,  Oral baclofen (Lioresal)
verbal fluency  Tizanidine
 Dantrolene sodium
Depression - ~50% of pts  Diazepam
Emotional
 Carbamazepine – paroxysmal spasms
 Pseudobulbar Affect
 Botulinum toxin
 Euphoria Pain
Bladder - ~80% of lesions  Neuropathic pain – tricyclic antidepressants
 Spastic/small
 Paroxysmal pain – carbamazepine,
 Flaccid/big amitriptyline, phenytoin, diazepam, gabapentin
 Dyssynergic/conflicting – problem c  Dysesthesia – amitriptyline, imipramine,
coordination between bladder and sphincter desipramine
contraction  Trigeminal neuralgia – antiepileptic drugs
 Types of incontinence (carbamazepine)
o Urge – overactive bladder  Mild painkillers (acetaminophen, ibuprofen)
o Stress – poor bladder closure Fatigue
o Overflow – poor contraction/urethral  Amantadine, Modafinil
blockage Tremor
o Functional – medications/health  Hydroxizine, propranolol, buspirone,
problems making it hard to reach the ondansetron, primidone
bathroom  Anti-nausea drugs for dizziness and vertigo
Bowel Cognitive and Emotional Impairments

You might also like

pFad - Phonifier reborn

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.

Note: This service is not intended for secure transactions such as banking, social media, email, or purchasing. Use at your own risk. We assume no liability whatsoever for broken pages.


Alternative Proxies:

Alternative Proxy

pFad Proxy

pFad v3 Proxy

pFad v4 Proxy