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Colin Russell asks "If Mono Sclerosis was diagnosed as a pre-curser to Multiple Sclerosis, would you prefer to be told as soon as Mono Sclerotic damage was identified together with your clinical symptoms or would you prefer to wait until the Multiple lesions had formed for the diagnosis to be conclusive?"
Anyone opting for the Mono Sclerosis diagnosis has a far better chance of managing their symptoms and progression of the illness by looking at the alternative therapy options available.
Include the disease modifying drugs available and we may see MS being stopped in its tracks at the Mono stage, therefore maintaining a quality of life for all concerned.
Here's the tricky bit
Disease modifying drugs cost money. Delaying diagnosis of MS untill multiple scarring has occured buys time. Neurologists have decided between themselves that anyone diagnosed with MS must then wait untill they have two significant relapses within a twelve month period to meet the criteria for their perscription.
Define "significant"
I don't know which group of geniuses came up with that criteria or how and when they arrived at it or how often it is reviewed but, needless to say, this criteria only helps to keep down the cost of drug therapy for people with MS.
Most MS people spoken to are not aware of this and they need to know the importance of keeping the Neurocare team informed of their condition every time they have a relapse, however "significant", get it noted and recorded by the medical team.
The inclusion of controls in MRI studies has shown that apparently symptomless single and multiple lesions are common, as are transient neurological disturbances in young people.
The natural history of the underlying disease is for most patients to recover. Patients with clinical signs represent the tip of the iceberg and disability relates to the site of lesions and axonal loss, rather than the volume of tissue involved.
MRI has also shown that in most patients presenting with a monosclerotic event, such as optic neuritis, multiple sites are active. This suggests that the blood-brain barrier is damaged at multiple sites at the same time, qualifying for the pathological description of a subacute disseminated vasculopathy.
However, because of the non-sense of an arbitrary requirement for dissemination in time, with a minimum interval of a month, these patients cannot be labelled as having MS, despite having multiple lesions. It is suggested that immunological markers provide confirmation, but they are all found, and at the same levels, in stroke patients after a single event. Since the tendency is for stroke patients to improve, the autoimmune features might represent a reparative not a pathological process.
The terms multiple and sclerosis refer to areas of glial scarring and the consequences for treatment of adopting an end-stage pathological description as a diagnosis are obvious. There can be no certainty that the disability from one attack will resolve.A patient can be permanently blind after bilateral optic neuritis and another with permanent paraplegia after clinically isolated acute transverse myelitis. The window of opportunity for effective treatment can be measured in hours.
Opening of the blood-brain barrier precedes the onset of symptoms, and MR spectroscopy has shown lactate and, therefore, hypoxia in acute lesions. Increasing the plasma oxygen tension may relieve the hypoxia and by inducing vasoconstriction assist in the restoration of endothelial function. Oxygen delivered under hyperbaric conditions is the only agent to improve symptoms in patients with chronic long-term disease.
Neurologists, in objecting to what has been termed a mechano-diagnosis based on MRI, state that waiting for a second episode might be a better course of action. It may be for the neurologist, but it is not for the patient!
The aim of this web site is for Mono Sclerosis to be recognised as the first stage of Multiple Sclerosis and to be treated as soon as Mono Sclerotic symptoms present themselves.
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