Multiple Sclerosis Flashcards
Clinical course in MS
Different clinical patterns, but generally episodic; remitting, relapsing
Symptoms
Visual Muscle weakness Sensory Cerebellar abnormalities Sphincter Mental changes
Aetiology and Pathogenesis
Aetiology: Unknown
Pathogenesis:
Microscopic pathology- active (acute) lesions:
Perivascular cuffing. Infiltration of WBC’s, activation of microglial cells, loss of myelin.
Lymphocytes around venule- inflammatory/ immune response: t lymphocytes and macrophages in the CNS, blood-borne macrophages and activated microglial cells, some B-lymphocytes, plasma cells.
As lesions advance, see macrophages with remnants of myelin in their cytoplasm. Astrocytes become active, proliferate, scarring.
Olgiodendrocytes are responsible for laying myelin on CNS neurons- but cannot do so in MS.
Inactive (chronic) lesions:
Demyelinated neurons, fewer Oligodendrocytes, Axonal degeneration, goiosis/ astrocytosis
Why do signs and symptoms remit/relapse?
- Temporary relapse (weeks/ months) New inflammation new loss of myelin Oedema - remission Inflammation resolved Oedema resolves New sodium channels form Remyelination of axons - short term effects An increase in tempt by 0.5 degrees can cause an increase in spasticity, reduce temperature or drinking a glass of water can cause improvement. Stress Trauma Infections
Why permanent loss of function
Scarring, and degeneration of axons.
Demyelination predisposes axon to injury by inflammatory chemicals?
Aetiology and epidemiology
Related to genetics and environment.
Generally in late 20s, most common in areas populated by Northern Europeans
Theory: MS is a consequence of a common infection. Viral infection followed by molecular mimicry may cause MS. Host immune response against viral Ag, immune cells recognise and attack (self) myelin protein as well (cross reaction, molecular mimicry)
MS trait- more susceptible to develop a cross reaction. Perhaps BBB easily damaged? Strong inflam response in CNS. Reduced
Oligodendrocyte activity.
MS
Progressive disease of the CNS leading to demyelination of axons, and thus leads to loss of impulse. Progressive over space and time. Scattered foci of demyelination and scarring.
