Aims and Scope
Vagus nerve stimulation (VNS) has been used for the treatment of drug-resistant epilepsy, especially in patients who are not candidates for surgical intervention. In fact, it was approved by the US FDA in 1997 as an adjunctive treatment for medically intractable epilepsy.
In this study, we investigated the efficacy of VNS in drug-resistant epilepsy associated with structural brain lesions (SBLs).
We retrospectively analyzed the effect of VNS on 25 patients diagnosed with intractable epilepsy-associated SBL, and compared the results to 19 patients with intractable epilepsy and normal neuroimaging. All patients underwent VNS insertion at the National Neurosciences Institute, King Fahad Medical City (Riyadh, Saudi Arabia) between 2008 and 2018.
The response rate (RR) for patients with drug-resistant epilepsy-associated SBL was 24% after 3 months, 36% after 6 months, and 48% after 1 year, reaching 76% over time. The mean follow-up period was 63.3 months. For non-SBL patients, the RR was 10.5% after 3 months, 36.8% after 6 months, and 47.4% after 1 year, reaching 73.7% over time. The mean follow-up period was 59.2 months. There was no statistically significant difference between the two groups regarding RR, VNS settings, and other parameters, including anti-epileptic drug use and demographics data.
VNS is strongly considered for intractable epilepsy in SBL patients, especially if they are not candidates for surgical intervention. Over time, those patients will receive increased benefits from VNS therapy.
October 28, 2020
- September 22, 2020
- September 08, 2020
- August 20, 2020
- July 27, 2020
- July 27, 2020
- June 16, 2020
Omega-3 Hastens and Omega-6 Delays the Progression of Neuropathology in a Murine Model of Familial ALSEdward F. Boumil, Rishel Brenna Vohnoutka, Yuguan Liu, Sangmook Lee, Thomas B Shea
Amyotrophic lateral sclerosis (ALS) is a progressive disease of motor neurons that has no cure or effective treatment. Any approach that could sustain minor motor function during terminal stages would improve quality of life.
We examined the impact of omega-3 (Ω-3) and Ω-6, on motor neuron function in mice expressing mutant human superoxide dismutase-1 (SOD-1), which dominantly confers familial ALS and induces a similar sequence of motor neuron decline and eventual death when expressed in mice.
Mice received standard diets supplemented with equivalent amounts of Ω-3 and Ω-6 or a 10x increase in Ω-6 with no change in Ω-3 commencing at 4 weeks of age. Motor function and biochemical/histological parameters were assayed by standard methodologies.
Supplementation with equivalent Ω-3 and Ω-6 hastened motor neuron pathology and death, while 10x Ω-6 with no change in Ω-3 significantly delayed motor neuron pathology, including preservation of minor motor neuron function during the terminal stage.
In the absence of a cure or treatment, affected individuals may resort to popular nutritional supplements such as Ω-3 as a form of “self-medication”. However, our findings and those of other laboratories indicate that such an approach could be harmful. Our findings suggest that a critical balance of Ω-6 and Ω-3 may temporarily preserve motor neuron function during the terminal stages of ALS, which could provide a substantial improvement in quality of life for affected individuals and their caregivers.
December 22, 2017
- December 19, 2017
- November 16, 2017
- September 30, 2017
- September 26, 2017
- April 17, 2017
- December 30, 2016