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29 Cards in this Set

  • Front
  • Back

What characterizes MS

Progressive demyelination or sclerosis of the white matter in the brain, spinal cord, and/or optic nerve


Plaques seen throughout CNS

MS symptoms pattern

Often follow an exacerbation and remission

MS risk factors

Women


Colder northern climates


European descent


Age 20-40


Affected first-degree relative

Cause of MS

Unknown


Genetic risk in individuals with certain MHC polymorphisms


Supports autoimmune etiology, but an immune attack on virally infected oligodendrocytes is also suspected

What happens as MS exacerbations occur?

Neural fxn is lost permanently

MS pathophysiology

Demyelination = slowed or blocked conduction


Early lesions occur as small areas of inflammation, but progresses to become firm demyelinated plaques, absent of oligodendrocytes



Why does MS get remission periods

If initial inflammation subsides, neural function may return


Lasts months to years with incomplete recovery from relapses (rarely steady progression from onset)



MS manifestations

Initially see: weakness, numbness, burning, tingling, unsteady limb


May disappear after a few days to weeks (but examination shows residual defects)Vary considerably between individuals


MRI shows presence of multiple lesions in brain or spinal cord


CSF has lymphocytosis and elevated Ab's

MS treatment

Remission or partial remission can be induced with glucocorticoids, immunosuppression, or interferon

MS drug therapy

Corticosteroids


Immunosuppressive therapy


Immunomodulators


Muscle relaxants


CNS stimulants


Acetylcholinesterase inhibitors


Tricyclic antidepressants


Anti-seizure drugs

Immunomodulators

Do we have to know???

Parkinsonism

Clinical syndrome characterized by tremor, rigidity, bradykinesia, and postural inability


Sometimes, mild intellectual deterioration



Causes of Parkinsonism

Most common is Parkinson's Disease (idiopathic)


Others: encephalitis, severe CO poisoning, MPTP, and neuroleptic drug toxicity

Extrapyramidal effect

Can do voluntary movements, but see defects in lower brain actions (arm swings, tremors)


Excessive ACh stimulated inhibition of motor cortex

Connection between dopamine and voluntary movements

Reduced dopamine = more inhibition on voluntary movements


Therefore, we needs neurons to either make more dopamine or block ACh

Why do Parkinson's symptoms occur

Imbalance between the amount of ACh and dopamine secreted in the basal nuclei (need balance between activation and inhibition)


Destruction of dopaminergic neurons in substantia nigra


Results in excessive ACh stimulated inhibition of motor cortex



What usually controls movement

Movement "programs" from the motor cortex are normally inhibited by GABA secreted from the basal nuclei onto the thalamus



What controls the amount of GABA produced

Increased by ACh


Decreased by dopamine

Manifestations of Parkinson's

Tremor


Rigidity and bradykinesia


Postural instability

Parkinson's tremors

More pronounced at rest


Enhanced by stress or anxiety


Usually begins in 1 limb (hands) but can be present in all limbs



Parkinson's - rigidity and bradykinesia

Increased resistance to passive movement


Slow voluntary movements


Reduction in automatic extrapyramidal movements (not swinging arms)


Effective movement can sometimes be regained in an emergency

Parkinson's - postural instability

Person tends to lean forward


Shuffles


Complicated by slow voluntary movements

Parkinson's treatment

No cure


Restore balance bw ACh and dopamine

Parkinson's complications

Increase as disease progresses


Motor symptoms


Weakness


Akinesia


Neuro problems


Depression, anxiety


Dementia

Surgical care of Parkinson's

Deep brain stimulation

Myasthenia graves patho

Autoimmune


Make Ab that bind to, block, and destroy ACh receptors at the postsynaptic neuromuscular junction



Myasthenia graves symptoms

Only affects skeletal muscles


Don't have sensory nerve attack

Guillon barre

Affects peripheral motor nerves


See both muscle and sensory problems

Amyotrophic lateral sclerosis

Scarring in laterocorticospinal tract of spinal cord


Without muscle growth (profound muscle atrophy) throughout body