Demyelination

- Acute bilateral painful decrease of vision (optic neuritis)
- Spinal injury symptoms (myelitis)
- Females > males
- Monophasic or recurrent

Antibodies against astrocyte’s aquaporin-4 protein may be present (NMO-immunoglobulin G [IgG] test)

Neurologic sequelae tend to be more severe and permanent than multiple sclerosis

Similar to acute multiple sclerosis:
1. IV steroids
2. Plasmapheresis

- Headache
- Impaired cognition
- Seizures

MRI:T2 sequence presents concentric layers of demyelination

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Treatment: similar to acute multiple sclerosis
Prognosis: generally fatal

- Presents 2 wk after infection or vaccination (usually against rabies)
- Monophasic deterioration with variable symptoms (among which are fever, seizures, confusion)
- Usually children

1. MRI: lesions all over brain including basal ganglia and thalami
2. CSF: increased protein and lymphocytes

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1. High-dose steroids
2. Plasmapheresis
3. IV IgG
Prognosis: mortality of 20%

- Optic neuritis/sensory motor symptoms/internuclear ophthalmoplegia
-Two attacksin different places and different times
- Females > males
- Three clinical types:
– Relapsing remitting
– Primary progressive
– Secondary progressive (initially relapsing remitting)
-Clinical signs
– Uhthoff’s sign (symptoms worsen when temperature is higher)
– Lhermitte’s sign (sense of current along the spine when bending the neck)

1. MRI: white matter lesions:
- Acute lesion is enhancing
- Chronic lesion is a black hole in T2
- Spares basal ganglia and thalamus
2. CSF: increased protein + oligoclonal bands

Prevalence increases with distance from equator

Acute phase:
1. Steroids
2. Plasmapheresis (if no response to steroids)
3. IV immunoglobulins (if contraindication to steroids or plasmapheresis)
Preventative:
1. Interferon beta (may produce flulike symptoms and liver dysfunction)
2. Daclizumab/ocrelizumab (for relapsing–remitting and primary progressive type)
3. Mitoxantrone (for secondary progressive type)