Secondary Progressive MS Trial of Lamotrigine Tested For Neuroprotection Benefits

A recently completed study at University College London Hospital suggests that administration of certain drugs can block the entry of sodium ions in nerve cells that in turn can prevent aggressive nerve cell damage. The research team proposed that delaying nerve cell destruction can limit the rate of disability in secondary progressive MS patients. The supporting study, which was completed after two years of testing, was aimed at employing nerve cell blockers like lamotrigine to monitor the rate of worsening disability in secondary progressive MS patients.

The Primary Outcome of this double-blind interventional study was to monitor changes in the volume of the whole brain with the help of the Loseff method using MRI technology (to monitor cerebral atrophy due to loss of axons). Secondary Outcomes for the study included monitoring the changes in the volume of whole brain with the help of Brain Boundary Shift Integral; the rate of atrophic changes in the spinal cord; appearance of new high intensity lesions on an MRI scan; ratio calculation of new T1 and T2 lesions; and the overall rate of changes in the MS Functional Composite and Impact Scale.

The cerebral and spinal volumes and cross-sectional area of the cervical spinal cord were tested at baseline, at 12 months into the study, and towards the end of the study period (24^th month). Brain volume was measured more periodically at the 6^th and 18 month marks, as well as at the 12 and 24 month marks. The clinical visits were planned for every 3 months.

Details of the Study:

The research team enrolled 120 patients with a positive history of MS and a progressive course of illness as seen in secondary progressive MS patients (patients with frequent episodes of clinical relapses resulting in disability were excluded). The study sample was divided into a test group and control groups, and the patients were randomly selected to receive either placebo or lamotrigine.

The research team explained that degenerative spinal or cerebral diseases can respond fairly well to neuroprotective treatments. The cause of disease progression in multiple sclerosis is degeneration of nerve axons. Previous research projects conducted by investigators at the University College London Hospitals have concluded that inflammatory mediators like nitric oxide can contribute to axonal degeneration. Various in-vitro studies confirm that blocking the activity of sodium channels can reduce the degeneration of axonal processes. Several pharmacological agents are currently available that are used to block sodium channels in the brain tissue (like phenytoin and flecainide in addition to lamotrigine).

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