MS

let's talk about multiple sclerosis. it is a chronic inflammatory disorder of the CNS. There are multiple plaques of demyelination within the brain and spinal cord where the plaques a disseminated both in time and place.

Prevalence
it's prevalence varies being directly proprortional to distance of residence from equator. MS is a rarity at the equator but a common neurological disease of young adults at north america and europe.

Aetiology and Pathogenesis
Although the mechanism is unknown, there is an inflammatory process in white matter of the brain and cord mediated by CD4 T cells.in active lesions there is an increase in inflammatory cells, active myelin degeneration and and phagocytosis. An initial inflammatory demyelinating event may prime autoreactive cellular and humoral immune responses against myelin. antibody-mediated demyelination probably develops early in MS. First degree realtives of a [atirnt have an increased chance of developing MS, without a clear-cut  pattern of inheritance. No known links between MS and infection exists but abnormal immune response in many MS patents produces increased titres of serum and CSF antibodies to many common viruses particularly measles.

Pathology
Plaques of demyelination, initially 2-10 mm in size, are the important features. Plaques are perivenular often occurs at distinct CNS sites: optic nerves, periventricular region, the brainstem and its cerebellar connections and the cervical cords. Acute relapses are caused by focal inflammatory  demyelination, which causes conduction block and it is relieved when inflammation stops and remyelination occurs. nevertheless, if the damage is severe, secondary axonal destruction will occur. In the cord, destruction of the anterior horn cells by the plaques is rare. So, focal muscle wasting like small hand muscles is uncommon. plaques are not seen in myelin sheath of peripheral nerves.

Clinical features
age of onset commonly is between 20-45 years and more common in women. 3 characteristic common presentaitons of relapsing and remitting MS are:

- optic neuropathy - blurring of vision in one eye develops over hours to days and mild ocular pain usually occur. The optic disc appearance depends on the site of plaques within optic nerve (optic neuritis/retrobulbar neuritis) Worsening of vision of optic neuritis during fever, hot weather, or after exercise occur as central conduction is slowed when body temperature increased(Uthoff's phenomenon).

- brainstem demyelination - Acute MS in brainstem causes combinations of diplopia, vertigo, facial numbness, dysarthria, or dysphagia. Pyramidal signs in the limbs occur  when the corticospinal tracts are involved.

- spinal cord lesion - spastic paraparesis developing over days or weeks is a common features of plaque in cervical or thoracic cord. this causes difficulty in walking and lower limb numbness. Lhermitte's sign may present and urinary symptoms are common

Unusual presentations for MS include epilepsy, trigeminal neuralgia, tonic spasms, and organic psychosis.

Investigations
-MRI of brain and cord shows multiple plaques in periventricular region, corpus callosum, brainstem, and cervical cord. Head MRI also shows lesion while plaques are rarely seen with CT
-CSF examination shows oligoclonal IgG bands in 80% patients with MS. CSF cell count might be raised (5-60 mononuclear cells/mm^3)
-Evoked responses delay in visual evoked response is seen in optic neuropathy.

MS therapies
include
- Steroids (short course) for remission of acute relapse
- beta interferon (INF-beta1b and 1a) for preventing relapse and disability
- Immunosuppressants and antineoplastic drugs (azathioprine, cyclophosphamide)
- Immunomodulator (Glatiramer acetate) to reduce relapse frequency
- Natalizumab, monoclonal antibody that inhibits migration of leukocytes into CNS


all are taken from Kumar and Clark
you can see im getting lazy to type as the post goes but it is easier to read with bullet points and less writing.