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.
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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.
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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