Diagnosis and treatment of multiple sclerosis
BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7540.525 (Published 02 March 2006) Cite this as: BMJ 2006;332:525Data supplement
Diagnostic Criteria for Multiple Sclerosis (McDonald Criteria)
The National MS Society of America convened an international panel chaired by Professor W. Ian McDonald to update the Poser Criteria for the diagnosis of MS and in April 2001 recommended the following criteria which makes use of MRI imaging in making diagnostic conclusions:
Clinical Presentation
Additional Data Needed
- 2 or more attacks (relapses)
- 2 or more objective clinical lesions
None; clinical evidence will suffice
(additional evidence desirable but must be consistent with MS)- 2 or more attacks
- 1 objective clinical lesion
Dissemination in space, demonstrated by:
- or a positive CSF and 2 or more MRI lesions consistent with MS
- or further clinical attack involving different site
- 1 attack
- 2 or more objective clinical lesions
Dissemination in time, demonstrated by:
- MRI
- or second clinical attack
- 1 attack
- 1 objective clinical lesion
(monosymptomatic presentation)
Dissemination in space by demonstrated by:
- MRI
- or positive CSF and 2 or more MRI lesions consistent with MS
and
Dissemination in time demonstrated by:
- MRI
- or second clinical attack
Insidious neurological progression
suggestive of MS
(primary progressive MS)Positive CSF
and
Dissemination in space demonstrated by:
- MRI evidence of 9 or more T2 brain lesions
- or 2 or more spinal cord lesions
- or 4-8 brain and 1 spinal cord lesion
- or positive VEP with 4-8 MRI lesions
- or positive VEP with <4 brain lesions plus 1 spinal cord lesion
and
Dissemination in time demonstrated by:
- MRI
- or continued progression for 1 year
What Is An Attack?
- Neurological disturbance of kind seen in MS
- Subjective report or objective observation
- 24 hours duration, minimum
- Excludes pseudoattacks, single paroxysmal episodes
Determining Time Between Attacks
- 30 days between onset of event 1 and onset of event 2
How Is "Abnormality" In Paraclinical Tests Determined?
- Magnetic resonance imaging (MRI) Three out of four:
- 1 Gd-enhancing or 9 T2 hyperintense lesions if no Gd-enhancing lesion
- 1 or more infratentorial lesions
- 1 or more juxtacortical lesions
- 3 or more periventricular lesions
- Cerebrospinal fluid (CSF)
- Oligoclonal IgG bands in CSF (and not serum)
- or elevated IgG index
- Evoked potentials (EP)
- Delayed but well-preserved wave form
- A Gd-enhancing lesion demonstrated in a scan done at least 3 months following onset of clinical attack at a site different
from attack,
or - In absence of Gd-enhancing lesions at 3 month scan, follow-up scan after an additional 3 months showing Gd-lesion or new T2 lesion.
(1 spinal cord lesion = 1 brain lesion)
- Cerebrospinal fluid (CSF)
- Oligoclonal IgG bands in CSF (and not serum)
- or elevated IgG index
- Evoked potentials (EP)
- Delayed but well-preserved wave form
- A Gd-enhancing lesion demonstrated in a scan done at least 3 months following onset of clinical attack at a site different
from attack,
or - In absence of Gd-enhancing lesions at 3 month scan, follow-up scan after an additional 3 months showing Gd-lesion or new T2 lesion.
- Evoked potentials (EP)
- Delayed but well-preserved wave form
- A Gd-enhancing lesion demonstrated in a scan done at least 3 months following onset of clinical attack at a site different
from attack,
or - In absence of Gd-enhancing lesions at 3 month scan, follow-up scan after an additional 3 months showing Gd-lesion or new T2 lesion.
What Provides MRI Evidence Of Dissemination In Time?
- A Gd-enhancing lesion demonstrated in a scan done at least 3 months following onset of clinical attack at a site different
from attack,
or - In absence of Gd-enhancing lesions at 3 month scan, follow-up scan after an additional 3 months showing Gd-lesion or new T2 lesion.
Ongoing research
Research now looks at neuroprotection, repair and recovery mechanisms in the brain as well as the process of CNS damage. The new treatments have shown promise in the short term but the important questions are all long term, so long term outcomes are essential in evaluating the cost effectiveness of current and future therapies. The genetic predisposition, geographical distribution and potential trigger mechanism for the disease are all areas of current research.
Related articles
- Letter Published: 16 March 2006; BMJ 332 doi:10.1136/bmj.332.7542.668-b
- Letter Published: 16 March 2006; BMJ 332 doi:10.1136/bmj.332.7542.668-a
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