Symptoms
These tend to occur in attacks usually lasting several weeks and at least in the first few attacks, remissions that may be total or partial. Symptoms that are more short-lived lasting minutes are only very rarely due to MS. Loss of vision in one eye (optic neuritis), loss of sensation in arms or legs or loss of strength (myelitis) may occur. Double vision, unsteadiness (brainstem lesion) are fairly typical sort of attacks. In some patients but by no means all, a progressive element sets in. In these cases, function of the legs with weakness and unsteadiness (ataxia) and bladder problems sometimes leading to being wheelchair bound, can occur. The range is extreme and simple classifications of MS largely for clinical trial uses has over simplified the situation that does not account for patients who have a single attack in their lifetime to the very rare patients who become disabled very quickly or can even die.

Diagnosis
It remains important to have clinical symptoms that conform to inflammation of the central nervous system such as a myelitis or optic neuritis. Back up support for the diagnosis and simultaneously exclusion of other possibilities would normally be achieved from doing an MRI scan of the head, spine or both and when changes are not characteristic, some Neurologists will also advise a lumbar puncture to look specifically for changes in the immuno-globulin fraction known as oligoclonal bands. In patients with MS, it is possible for either the MRI scan or the lumbar puncture to not show a positive result but almost impossible for both to be negative. The investigations do not give any indication as to prognosis.

Characteristically the MRI scan will show “white dots” within the white matter and if the spinal scan shows anything which it often does not, it will again show “white blobs” characteristic of inflammation. Other tests of an electrical sort known as visual evoked and auditory evoked potentials occasionally get done but have really been superseded by MRI and oligoclonal banding.

Cause
The cause is unknown but the effect is to strip the sheath off the central nervous system neurones that makes them function poorly and slowly. There is also inflammation. In some cases the nerve cells will eventually die. In patients who improve, remyelination must occur but it is always imperfect but fortunately can be enough to allow the symptoms to remit. Like many complex conditions, MS does not run in families in the strict sense of the term though there is a slight increased incidence suggesting that there are pre-disposing genetic factors. However, it seems unlikely that genetics factors on their own can cause the condition and the presumption has always been that there is interaction with a virus through an immunological achilles heel that gives rise to persistent inflammation. Perhaps the immune system in trying to continually rid the body of the virus also attacks the myelinia hypothesis known as molecular mimicry. MS is much less common in countries close to the equator and this is explained on environmental, not genetic grounds as if individuals migrate before late teenage years to the Northern hemispheres, they acquire the increased chances of getting MS.

Treatment
Not all patients require treatment as they may improve under their own steam.

In severe or persistent attacks, a short course of steroids are normally advised. These do not always work and when they do, promptly speed up recovery rather than cause a recovery in patients who would not otherwise have improved in time.

New drugs are becoming available. Beta Interferon is on the market though not always available given its expense. It is normally advised in patients who are having frequent attacks at around 2 a year, particularly if they are quite severe and particularly if complete recovery is not always taking place. It is less clear whether or not it effects increasing disability in the situation of progressive MS no longer having discrete attacks.

In the small percentage of patients who develop severe disability, rehabilitation becomes important. The spinal cord is most at risk and patients should be managed in the same sort of way as if they had had a spinal injury. Attention to bladder function and the best way of managing that is important and dealing with impotence where present can now be addressed. Spasticity can be a considerable problem. Anti spasticity agents need to be treated with objectivity as although they often reduce the spasticity, this does not always improve function as a degree of weakness may result. Baclofen, Dantrolene and Tizanidine can all be employed but the role of the physiotherapist is paramount.

In all patients but perhaps particularly in milder cases after their first attack and just when they have been told the diagnosis, education and support is of importance. This is particularly so as the common view of the disease is that it is always severe and progressive. With the advent particularly of MRI scanning, it is quite clear that benign disease is much commoner than previously thought but this message is yet to get across to the general population or some physicians.

In the majority of patients it is possible to carry on with a normal life including children and careers.

MS Society

MS National Centre
372 Edgware Road
Staples Corner
London NW2 6ND
Tel: 020 8438 0700

MS Helpline: 0808 800 8000

Website: http://www.mssociety.org.uk/