Myelin is a lipid-rich insulating sheath produced by oligodendrocytes (CNS) and Schwann cells (PNS) that enables rapid saltatory conduction of action potentials along myelinated axons. Demyelination disrupts this conduction, causing neurological deficits whose pattern depends on the location and distribution of myelin loss. In multiple sclerosis (MS), autoreactive T-cells and B-cells cross the BBB and attack CNS myelin, forming perivenular inflammatory plaques predominantly in periventricular white matter, optic nerves, corpus callosum, brainstem, and spinal cord. The disease follows different patterns: relapsing-remitting (85% at onset; distinct attacks with recovery), secondary progressive (gradual disability accumulation after RRMS phase), and primary progressive (steady decline from onset without relapses). Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy of the PNS, typically post-infectious (Campylobacter jejuni most common trigger). Molecular mimicry between pathogen epitopes and ganglioside components of peripheral nerve myelin (GM1, GD1a, GQ1b) triggers antibody-mediated complement activation and macrophage-mediated myelin stripping. GBS presents as ascending symmetric weakness, areflexia, and potential respiratory failure over days to weeks. Distinguishing CNS from PNS demyelination is critical: MS has upper motor neuron signs (hyperreflexia, Babinski, spasticity) while GBS...