MS can't explain any lower motor or peripheral nerve signs such as Hypotonia or HYPOREFLEXIA

DEMYELINATION;
CNS ( Brain & Spinal cord) myelin sheath is made up of Oligodendrocytes, whereas the myelin sheath of nerves ( peripheral a& cranial ) is made up of Schwann cells, so CNS demyelination such as MS doesn’t affect peripheral nervous system. Hence MS can’t explain any lower motor or peripheral nerve signs such as Hypotonia or HYPOREFLEXIA etc.

Demyelination is due to antibody mediated attack ( type II immune response ) , so CSF mainly has globulins and very few lymphocytes if any. Protein / Cell dissociation. Infections has more cells and type of cells depends on type of infection.

Being an immune disease, it’s more prevalent in females of reproductive age & may have relapsing / remitting pattern. However some time disease never goes in remission and keeps progressing. Immunosuppression is needed to control the disease, steroids such as short term ُAcute measure and other Immunosuppression on long term.

Demyelination is loss of volume rather than oedema etc, hence it does NOT explain raised ICP or mass effect or headache.
Demyelination is white matter problem hence doesn’t explain Grey matter irritation and can’t explain seizures.
Demyelination can be ُAcute ( confused with stroke), subacute ( confused with infection or tumours ) or chronic to confuse with degenerative disease.

Demyelination plaques can be asymptomatic and silent , hence we need MRI to detect all the plaques, symptomatic or asymptomatic to demonstrate disseminated in place and may be necessary to help think of demyelination presenting with one or two symptomatic lesions which can be confused with stroke or tumour. Demonstration of multiple plaques favours demyelination. Commonly involved areas are cerebellum, Peri ventricular & peri Callosal etc. Evoked potentials also help to detect subclinical lesions by shoring slow conduction velocity in visual or other sensory pathways within CNS.

Demyelination can also be disseminated in time. So the first episode especially if not involving mutinous ares, needs high suspicion about MS whereas subsequent lesions make it easier to think of MS.

Brainstem and Cerebellar involvement usually indicates poor prognosis whereas sparing of these areas has good prognosis. Relapsing remitting pattern has good prognosis. Less number of plaques also means good prognosis.