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Multiple sclerosis is a demyelination illness of the CNS and Spinal cord. The immune system targets the myelin sheath that protects the fibre nerves. When the myelin sheath is the subject of attack, a communication error between the nerves and brain occur. The level of damage depends on the extent of injury to the nerves and the types of targeted nerves. One of the most severe repercussions of MS is losing the ability to walk; otherwise, other people with the condition; would have developed symptoms much later and first entered a state of remission. Common signs of multiple sclerosis include numbness, a tingling sensation in the limbs and an electric shock in the neck.




Clinically isolated syndrome (CIS) is the initial sign of neurological dysfunction such as fever or infection for the first 24 hours. An MRI scan indicates numerous areas of lesions to the spinal cord and brain, a tell-tale sign of multiple sclerosis.

Relapses of multiple sclerosis attacks characterise Relapsing-remitting MS (RRMS). People usually experience these types of MS attacks in their 20s or 30s. In between these episodes or flare-ups, there is a state of remission the body goes into. In about 10-20 years, the disease advances to a secondary progressive form. Returning multiple sclerosis causes eye pain, incontinence, fatigue, lack of sexual desire, stiff muscles and depression.

Primary progressive MS (PPMS) is a stage of advanced neurological deterioration. There are different phases of PPMS, the first being active along with the disease’s progression and then non-active with evidence of progression.

Secondary progressive MS (SPMS) presents the after-effects of relapse when multiple sclerosis reaches a severe stage of deterioration. There is no form of relapse after SPMS, which means the disease will decline even further.

There is no specific remedy for multiple sclerosis. Treatment focuses on the recovery of a person after multiple attacks and significantly slows down the disease's progression. 



“Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin.”

By this definition, TIA, which lasts < 24 hours, and patients with stroke symptoms caused by subdural haemorrhage, tumours, poisoning, or trauma are excluded.


  • Thrombosis is an In situ obstruction of an artery.

  • Embolism result from particles of debris originating elsewhere that blocks arterial access to a particular brain region.

  • Systemic hypoperfusion is a more general circulatory problem, manifesting itself in the brain and perhaps other organs.

  • Haemorrhagic stroke due to intracerebral haemorrhage or subarachnoid haemorrhage.

Data compiled by AHA show that strokes due to ischemia, intracerebral haemorrhage and subarachnoid haemorrhage are 87%, 10%, and 3 %, respectively.


The brain contains little or no energy stores and relies on blood for its delivery. During a stroke, reduction of blood flow to the brain results in a deprivation of glucose and oxygen.

The region that directly surrounds the vessel is most affected.

Central core irreversibly damaged and necrosis if ischemia is long enough. (Infarct), brain blood flow is reduced.

Cells which receive oxygen and glucose by diffusion from collaterals are viable. (Penumbra), 20 -30 ml/100gr/min

Experimental studies report that the infarct is formed 3-12 h after initiation of ischemia and continues to develop even after 24h, although at a much slower rate.

By definition, neuroprotection is an effect that may result in salvage, recovery or regeneration of the nervous system, its cells, structure and function.

Neuroprotection is specifically defined as the "protection of neurons" and is a strategy used to potentially protect the brain in several different cerebral conditions, including Parkinson’s disease, traumatic brain injury and ischemic stroke.

Neuroprotection is perhaps best exemplified by strategies designed to prevent cells from undergoing apoptosis.

There are currently no approved treatments for the myriad of damaging pathological processes that persist in the brain long after the acute stage, which are:

  • Inflammation

  • Excitotoxicity

  • Oxidative stress

  • Apoptosis

  • Oedema that results from disruption of the blood-brain barrier.

A common feature evident in most neuroprotection studies is that beneficial outcomes are far greater when the therapy is commenced earlier in the disease process.

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