MS Flashcards
What is MS?
chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system mistakenly attacks the protective sheath (myelin) that covers nerve fibers, leading to inflammation and damage. This myelin damage disrupts the normal flow of electrical impulses along the nerves, leading to various neurological symptoms.
RRMS
The most common form, characterized by clear attacks (relapses) of new or worsening symptoms followed by periods of partial or complete recovery (remissions).
* pathophysiology: demyelination, inflammation, axonal injury, astrocyte hyperplasia
PPMS
Characterized by a gradual worsening of symptoms without distinct relapses or remissions.
* clinically rare
* progressive and cumulative steady deterioation
* not interrupted by periods of remissions, continuous deterioration of disability with or without seizures
SPMS
Initially starts as RRMS but transitions to a more steadily progressive form.
* after 10-15 years, approx 50% RRMS progresses to SPMS
* relapsing-remitting course followed by progressive deterioration
Risk factors for MS
- Genetic factors, in particular the distribution of the HLA- DRB1 haplotype, might account in part for the latitudinal gradient, but environmental risk factors that vary with latitude might also be involved.
- Environmental The most well-established risk factors are
- Epstein–Barr virus (EBV) infection in adolescence and early adulthood,
- tobacco exposure through active or passive smoking,
- a lack of sun exposure, low vitamin D levels and
- obesity during adolescence
Pathology of MS
- Demyelinating disease
- auto-immune inflammatory reaction resulting in destruction of myelin and reduction in # of oligodendricites
- Proliferation of astrocytes lay day fibrous scar tissue forming a plaque resulting in no potential for re-myelination
- scars/lesions form in CNS, rarely affects PNS
- lesions commmonly affect white matter in optic nerve, brain stem, basal ganglia, spinal cord
PRMS
- clinically rare
- gradual development and aggravation, occasional recurrence
- continuous progression between two relapses
Pathological hallmark of all MS
- focal plaques (also known as lesions), which are areas of demyelination that are typically located around postcapillary venules and are characterized by breakdown of the blood–brain barrier (BBB).
- The mechanisms of BBB breakdown are incompletely understood but seem to involve direct effects of pro-inflammatory cytokines and chemokines (such as TNF, IL-1β and IL-6) produced by resident cells and endothelial cells, as well as indirect cytokine-dependent and chemokine-dependent leukocyte-mediated injury
- The dysregulation of the BBB increases the trans-endothelial migration of activated leukocytes, including macrophages, T cells and B cells, into the CNS, which leads to further inflammation and demyelination, followed by oligodendrocyte loss, reactive gliosis and neuro-axonal degeneration
Astrocyte hyperplasia
- Previously thought only to react later, at post inflammatory stage to form glial scar
- now considered early players and highly active in early to late lesion pathology
- recuits lymphocytes, contributes to tissue damage, confine inflammation, promote lesion repair
Benign MS (Clinically isolated syndrome)
- to denote those patients whose first clinical presentation has characteristics of inflammatory demyelination that could be MS but who do not fulfil its diagnostic criteria
Charcot’s neurological triad
Well known trio of symptoms with MS are Charcot’s neurological triad = dysarthria, nystagmus, intention tremor
Symptoms of MS
- Charcot’s neurological triad
- nystagmus
- optic nerve plaques (reduced vision in one of both eyes), optic neuritis (blurred vision or dark spots in centre of vision)
- dysarthria (reduced or impaired speech)
- intention tremor (plaques along motor pathways in spinal cord affecting outbound signals of muscle control)
- muscle weakness, spasms, tremor, ataxia, paralysis
- spasticity
- foot drop
- fatigue
- decreased skin sensation
- paraesthesia
- L’Hermitte’s (specific sensory signal with electric shock down the back and radiating to limbs when person flexes neck)
- bladder & bowel, sexual dysfunction
- hyper or hypotonia, clonus
- muscle atrophy
- decreased proprioception
- changes in reflexes
- ataxia
- decrease in balance
- diplopia
- decrease in visual acuity
- dysarthria
- cognitive deficits
- emotional issues
Meds for MS
- Meds more effective to RRMS
- Corticosteroids (supress inflammation)
- copaxone (reduce frequency of relapses)
- interferon (decrease inflammation and prevent nerve damage)
- immunosupresants (used to target inflammation)
- anti-spastic meds (reduce tone, increase ROM, decrease pain as result)
- teriflunomide (dampens immune response)
Physio management
- improve joint ROM & integrity
- increase motor function
- increase muscle strength
- improve postural control and balance
- improve gait
- increased aerobic capacity
- manage fatigue
- reduce pain
- improve sensation
Spasticity in MS
- leads to decreased ROM & flexibility
- occurs in quad, hams, adductors, neck muscles
Treatment - stretch & strength affected muscles
- positioning is important
- education
