N-acetylaspartate normalization in bipolar depression after lamotrigine treatment

Objectives: The aim of the present study was to examine N-acetylaspartate (NAA), a general marker of neuronal viability, and total NAA (tNAA), the combined signal of NAA and N-acetylaspartylglutamate, in bipolar depression before and after lamotrigine treatment. Given that NAA is synthesized through direct acetylation of aspartate by acetyl-coenzyme A-l-aspartate-N-acetyltransferase, we hypothesized that treatment with lamotrigine would be associated with an increase in NAA level. Methods: Patients with bipolar depression underwent two-dimensional proton magnetic resonance spectroscopy of the anterior cingulate at baseline (n = 15) and after 12 weeks of lamotrigine treatment (n = 10). A group of age-matched healthy controls (n = 9) underwent scanning at baseline for comparison. Results: At baseline, patients with bipolar depression had significantly lower NAA [mean standard deviation (SD) = 1.13 (0.21); p = 0.02] than controls [mean (SD) = 1.37 (0.27)]. Significant increases in NAA [mean (SD) = 1.39 (0.21); p = 0.01] and tNAA [mean (SD) = 1.61 (0.25); p = 0.02] levels were found after 12 weeks of lamotrigine treatment. Conclusions: These data suggest an NAA deficit in bipolar depression that is normalized after lamotrigine treatment. Future research is warranted to evaluate whether baseline NAA level is a potential biomarker for identifying lamotrigine response patterns and whether this functional brain change has an associated clinical response

N-acetylaspartate normalization in bipolar depression after lamotrigine treatment

Objectives: The aim of the present study was to examine N-acetylaspartate (NAA), a general marker of neuronal viability, and total NAA (tNAA), the combined signal of NAA and N-acetylaspartylglutamate, in bipolar depression before and after lamotrigine treatment. Given that NAA is synthesized through direct acetylation of aspartate by acetyl-coenzyme A-l-aspartate-N-acetyltransferase, we hypothesized that treatment with lamotrigine would be associated with an increase in NAA level. Methods: Patients with bipolar depression underwent two-dimensional proton magnetic resonance spectroscopy of the anterior cingulate at baseline (n = 15) and after 12 weeks of lamotrigine treatment (n = 10). A group of age-matched healthy controls (n = 9) underwent scanning at baseline for comparison. Results: At baseline, patients with bipolar depression had significantly lower NAA [mean standard deviation (SD) = 1.13 (0.21); p = 0.02] than controls [mean (SD) = 1.37 (0.27)]. Significant increases in NAA [mean (SD) = 1.39 (0.21); p = 0.01] and tNAA [mean (SD) = 1.61 (0.25); p = 0.02] levels were found after 12 weeks of lamotrigine treatment. Conclusions: These data suggest an NAA deficit in bipolar depression that is normalized after lamotrigine treatment. Future research is warranted to evaluate whether baseline NAA level is a potential biomarker for identifying lamotrigine response patterns and whether this functional brain change has an associated clinical response

Development of a compact rectenna for wireless powering of a head-mountable deep brain stimulation device

Design of a rectangular spiral planar inverted-F antenna (PIFA) at 915 MHz for wireless power transmission applications is proposed. The antenna and rectifying circuitry form a rectenna, which can produce dc power from a distant radio frequency energy transmitter. The generated dc power is used to operate a low-power deep brain stimulation pulse generator. The proposed antenna has the dimensions of 10 mm × 12.5 mm × 1.5 mm and resonance frequency of 915 MHz with a measured bandwidth of 15 MHz at return loss of -10 dB. A dielectric substrate of FR-4 of εr = 4.8 and δ = 0.015 with thickness of 1.5 mm is used for both antenna and rectifier circuit simulation and fabrication because of its availability and low cost. An L-section impedance matching circuit is used between the PIFA and voltage doubler rectifier. The impedance matching circuit also works as a low-pass filter for elimination of higher order harmonics. Maximum dc voltage at the rectenna output is 7.5 V in free space and this rectenna can drive a deep brain stimulation pulse generator at a distance of 30 cm from a radio frequency energy transmitter, which transmits power of 26.77 dBm