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Neurological and Psychiatric disorders Mindmap am Demyelinating disorders, erstellt von Cher Bachar am 24/05/2013.
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neurological and psychiatric disorders
neurological and psychiatric disorders
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Cher Bachar
vor mehr als 11 Jahre
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106783
mind_map
2016-03-02T00:30:59Z
Demyelinating disorders
Classification
Multiple sclerosis
(MS)
post infecious
encephalomyelitis
progressive multifocal
leucoencephalophy
toxic and nutritional
disorders
leucodystrophies
Disorders affecting solely or
predominately the peripheral nervous
system
Multiple sclerosis (MS)
Etiology and
incidence
onset- 20-45yr
women are more affected
cause?
immunological abnormalities
genetic suseptibility
low sun levels- more risk
autoimmune attack
T-cells
Macrophages
secret inflammatory
cytokines and chemikines
results in demyelination and
impairement in signal coduction
strip myelin
Stage 1- inflammatory phase
Stage 2- degenerative phase
T cells, macrophages-
cytokines, chemokines
T-cells- excess
glutamate release
remyelination failure- recovery
requires a sequence of
steps- cell interaction
Clinical features
Mechanisms
Diagnosis
MRI imaging
oligoclonal presence in
CSF and serum
Oligoclonal band test
CNS lesions- disseminated
in more than one area
Management
muscle training
plagues or islands of demyelination
primarily in white matter
periventricular regions
optic nerves
spinal cord
subcortical white matter
cerebral cortex (most
cases)
brainstem
cerebellum
Types
95% have IgG in the CSF
isoelectric focusing using agarose gels
S-ve, C-ve= normal
S-ve, C+ve= MS
S+ve, C+ve= Guillain-Barre syndrome
S+ve, C+ve= viral encephalitis
symptoms
remitting relapsing
secondary progressive
Primary progressive (<15%)
Progressive relapsing (<5%)
complete
partial
relapses
no relapses
Acute- supression of inflammation
minimizing handicap
Reduce relapse + suppress ongoing disease activity
Control muscle tone
drugs
corticosteriods
interferon-B, glatiramer acetate, natalizumab
history of relapses
and remissions
Blood tests
Periventricular leukomalacia (PVL)
loss of myelinating oligodendrocytes
(OLs) and OL progenitor cells (OPCs)
Oxidative damage
Excitotoxicity
Pro-inflammatory cytokines
Genetic alterations
OPC
express NG2 and PDGFαR
myelin production-
energy-ATP-dependent
byproduct- hydrogen peroxide
cause DNA degradation and OL apoptosis
peroxisomes- present in OL
byproduct- hydrogen peroxide
Cellular metabolism
myelin synthetic
enzymes require iron
free radical formation
Sphingolipids - apoptosis
contain Death
receptors (DRs)
apoptotic cascades
ceramide - second messenger
activates DRs- OL apoptosis
amyloid-β peptide
elevated gluatamte
OLs / immature OLs
CNS pathalogy
macrophages and microglia
>> prolonged activation of receptors
high Ca levels
activating enzymes
that degrade
cytoskeletal proteins
causing mitochondrial disruption leading
to reactive oxygen species production
studies- OLs and myelin are
vulnerable to Glu excitotoxicity
AMPAR/ NMDAR present in OLs
evidence
AMPAR vs NMDAR
cytokines IL-1β, IL-2,
interferon γ (IFNγ), and TNFα
direct and/or indirect
TNFα - p55 TNF receptor
TNFα - microglial and
macrophage activation
activate SMase-
leading to ceramide
up-regulate the transcription factor p53
cell death receptors
irradiation-induced OL death
Alexander’s disease
mutations in the astrocyte glial fibrillary
acidic protein (GFAP) gene
Adrenoleukodystrophy
defect in the ABCD1 gene
Neurodegeneration
transition into the progressive
disease phase - critical loss of
axon density
MRI, MRS, pathological studies
Hypothesis
inflammation-related mechanisms might
over time initiate an autonomous
neurodegenerative process
that (adaptive or innate) immune
mechanisms in the nonlesional white
matter might substantially contribute to
the extent of neuroaxonal damage
that Wallerian and retrograde degeneration initiated
by axonal transections in focally demyelinated
lesions may explain the wealth of neuroaxonal loss
observed
alternative hypothesis considers MS as a primary
degenerative disease in individuals in whom certain
features of their immune system favor a very strong,
albeit secondary, immune response
early stages
pathological substrate(s) of the
progressive disease phase
Neuroaxonal dysfunction or demise
meningeal inflammation
correlated with neuronal/ axonal loss
ongoing adaptive immune cell
infiltration correlated with APP
T-cells- induce
neuronal damage
enhanced microglia activation
inflammatory response in nonlesioned tissues,
and upregulated inflammatory pathways
neuroaxonal cytoskeleton
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106783
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2016-03-02T00:30:59Z
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