In their overview of the diagnosis of multiple sclerosis (MS), Charles Poser and Vasna Brinar (Nov 24, p 1746)1 highlight the difficulties that MRI has created for neurologists, but some key issues are not discussed.
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.2 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.3 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. I have seen a patient 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,4 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.5
Poser and Brinar, 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.
Philip B James
Ninewells Hospital and Medical School, Dundee DDI 9SY, UK
1 Poser CM, Brinar VV. Problems with diagnostic criteria for multiple sclerosis. Lancet 2001; 358: 1746-47. [Text]
2 Levy DE. Transient CNS deficits: a common benign syndrome in young adults. Neurology 1988; 38: 831-36. [PubMed]
3 Wang WZ, Olsson T, Kostulas V, Hojeberg B, Ekkre HP, Link H. Myelin antigen reactive T cells in cerebrovascular disease. Clin Exp Immunol 1992; 88: 157-62. [PubMed]
4 Kermode AG, Thompson AJ, Tofts P, et al. Breakdown of the blood-brain barrier precedes symptoms and other MRI signs of new lesions in multiple sclerosis. Brain 1990; 113: 1477-89. [PubMed]
5 Fischer BH, Marks M, Reich T. Hyperbaric-oxygen treatment of multiple sclerosis: a randomised, placebo controlled, double-blind study. N Engl J Med 1983; 308: 181-86. [PubMed]