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30 Cards in this Set

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MS: general definition?
Chronic and progressive inflammatory CNS disorder in which focal lymphocytic infiltration leads to the destruction of oligodendrocytes and the demyelination of axons
MS: general progression?
Initially, the inflammation is transient and some remyelination occurs, but over time microglial and astrocytic activation is thought to result in a chronic inflammatory response which results in widespread pathology.
MS: general cause?
Autoimmuneish - The activated T cell mediated response is believed to be triggered by a variety of agents. Autoreactive lymphocytes cross the BBB and attack myeline basic or other proteins expressed by oligodendrocytes and possibly neurons.
Plaques of MS: location?
Any CNS tissue can be affected (therefore any pathways can be affected)
Proclivity for the deep white matter of the hemispheres surrounding the lateral ventricles
General MS presentation/timeline
Alternating periods of exacerbations (characterized by active plaques where there is microglial and astrocytic activation and inflammation) and remissions (when inflammation decreases)
What is responsible for any remyelination occurring in MS? Describe the process.
OPCs in the surrounding areas that differentiate into mature myelin-producing oligodendrocytes. Remyelination is sparse and myelin sheaths are thin. Believed to contribute to periods of remission early in the course of the disorder.
How do plaques change over time and what does this result in?
Active plaques evolve into 'old' plaques where astrocytes lay down scars. Appears to be deleterious to the recruitment of OPCs from surrounding tissue, so no remyelination occurs.
Common signs/symptoms of MS
Paresthesias
Ocular symptoms: blurry vision, eye pain, blind spots
Motor (weakness) and cerebellar (ataxia) signs/symptoms
Lhermitte's sign
What is the most common cause of ocular symptoms in MS?
Optic neuritis (inflammation associated with demyelination of the optic nerve)
What is Lhermitte's sign in MS?
If the dorsal columns of the spinal cord are involved, flexion of the neck (which cases stretching of the dorsal columns) can elicit a painful, electric-like sensation down the spine.
How is a clinical diagnosis of MS made?
If the individual has attacks at two or more different times and shows evidence of at least 2 separate lesions in the CNS (separated in time sand space)
Lab testing in MS
Oligoclonal bands (bands of IgG on electrophoresis of CSF indicating production of autoantibodies within the CNS)
Plaque imaging
MRI
MRI with gadolinium will show focal enhancement of active plaques
Four courses of MS
Benign
Relapsing remitting
Secondary progressive
Primary progressive
Describe benign MS.
Mild infrequent exacerbations with full recovery
Describe relapsing remitting MS.
Episodes of exacerbations and remissions during which not all symptoms resolve completely. Relapses are often more severe than in the benign group, and can become more severe with time.
Describe secondary progressive MS.
Relapsing/remitting disease begins to gradually worsen over time with resulting accumulation of neurological signs and symptoms. Relapses become more severe while remissions are less complete, shorter in duration, and eventually non-existent.
Describe primary progressive MS.
No periods of remission. Disease begins with a slow progression of neurological deficits; problems gradually worsen over time.
List general therapy of MS
Immunomodulatory agents
Avoidance of possible triggers (heat, infections, etc.)
Treatment of spasticity/rigidity
Treatment of depression (tricyclics, SSRIs)
Treat for fatigue
Treatment for chronic neuropathic pain state
What is the purpose of immunomodulatory agents with MS?
Don't affect the ultimate progression of the disease, but decrease the number of flare-ups.
What is Uhthoff's sign?
Worsening of symptoms in MS patients which occurs after taking a hot bath or participating in vigorous exercise.
What are potential causes for the chronic neuropathic pain state in MS?
Chronic inflammation of axons or destruction of neurons of the pain pathway
GB: cells affected? general progression?
Schwann cells in the PNS (axons are spared)
Rapid in onset, remyelination occurs over time
GB: cause?
Immune-related demyelination following viral illness, enteritis, or other infections
GB: most common symptoms?
Paresthesias and weakness
Areflexia
Respiratory failure and autonomic dysfunction
Contrast the weakness in MS and GB.
Weakness in GB is an ascending weakness and may be bilateral
What causes respiratory failure in GB?
Demyelination of the phrenic and intercostal nerves
What causes autonomic dysfunction in GB? What does this result in?
Demyelination of the sympathetic and vagus nerves

Can lead to cardiac arrhythmias, tachycardia, postural hypotension, and HTN
CSF of GB
Elevated protein
Normal or only slightly elevated number of cells
Treatment of GB
Hospitalization until weakness subsides
Monitor respiratory function, intubation may be necessary