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agate
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 Posted: Mon Oct 02, 2006 6:56 pm Post subject: (Abstract)Lamotrigine in SPMS |
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From the 22nd Congress of ECTRIMS (European Committee for Treatment and Research in Multiple Sclerosis), Madrid, 9/29/06:
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Neuroprotection
Friday, September 29, 2006, 15:30 - 17:00
A randomised controlled trial of neuroprotection with lamotrigine in secondary progressive multiple sclerosis
J. Furby, T. Hayton, K.J. Smith, D.R. Altmann, R. Brenner, J. Chataway, N.C. Fox, R.A.C. Hughes, D.H. Miller, R. Kapoor (London, UK)
Background: There is good evidence that the primary cause of disability is neuro-axonal degeneration within the CNS. Experimental work by members of our group has established that axons may degenerate upon exposure to the inflammatory mediator nitric oxide. The mechanism of the damage implies that protection might be afforded by the novel approach of partially blocking sodium channels.
Our group and others have demonstrated that drugs including flecainide, phenytoin and lamotrigine can reduce axonal degeneration when optic nerves or spinal roots are exposed to nitric oxide, and in experimental autoimmune encephalomyelitis.
Consequently, we have initiated a clinical trial to assess whether the sodium channel blocker lamotrigine has a neuroprotective, disease- modifying effect on a) the rate of axonal degeneration and b) the accumulation of disability in patients with secondary progressive multiple sclerosis (SPMS).
Methodology: We are recruiting 120 people with SPMS, in whom progression rather than relapse is the major cause of increasing disability, into a double-blind, parallel group, controlled trial lasting two years. Random allocation will be made to receive treatment with either extended release lamotrigine (GlaxoSmithKline) or placebo.
The primary endpoint will be an effect of treatment on cerebral atrophy, which correlates with other MR markers of axonal loss, and which can be measured reliably and sensitively using recently developed MR techniques.
The trial is powered to detect a 60% beneficial effect on the rate of development of cerebral atrophy.
Secondary endpoints include effects of treatment on spinal cord atrophy and on clinical measurements of impairment/disability. MR measures of brain volume and scores of clinical impairment/disability will be determined at entry, and after 6, 12, 18 and 24 months. Cervical spinal cord cross-sectional area will be measured at entry, and after 12 and 24 months.
Utilization of results: A phase II trial of sodium channel blockade in SPMS is timely, given recent advances arising from experimental and imaging work. Our results are likely to help with the design of future trials of neuroprotection in MS, and a successful outcome would demonstrate a novel, safe neuroprotective strategy to reduce long-term disability.
Supported by the MS Society of GB&NI |
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