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Objectives The purposes of this study were to measure a safe zone and a path for ultra–minimally invasive sonographically guided carpal tunnel release with a 1‐mm incision in healthy volunteers and then test the procedure in cadavers. Methods First, a previously reported sonographic zone was defined as the space between the median nerve and the closest ulnar vascular structure. Axially, the safest theoretical cutting point for carpal tunnel release was set by bisecting this zone. Magnetic resonance imaging was used for axially determining the limits of the sectors (origin at the cutting point) that did not enclose structures at risk (arteries and nerves) and coronally for determining whether our release path could require directions that could potentially compromise safety (origin at the pisiform's proximal pole). Second, in cadavers, we performed ultra–minimally invasive sonographically guided carpal tunnel release from an intracarpal position through a 1‐mm antebrachial approach. Efficacy (deepest fibrous layer release rate), safety (absence of neurovascular or tendon injury), and damage to any anatomy superficial to transverse carpal ligament were assessed by dissection. Results All 11 of our volunteers (22 wrists) had safe axial sectors located volar and radially of at least 80.4º (considered safe). Release path directions were theoretically safe (almost parallel to the longitudinal axis of the forearm). In 10 cadaver wrists, ultra–minimally invasive sonographically guided carpal tunnel release was effective (100% release rate) and safe without signs of intrusion into the superficial anatomy. Conclusions Ultra–minimally invasive sonographically guided carpal tunnel release in a safe sonographic zone may be feasible The technique preserves the superficial anatomy and diminishes the damage of a surgical approach.

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Cerebrospinal fluid (CSF) and serum levels of 22 amino acids were studied in 13 patients with dementia of the Alzheimer type (DAT), 13 patients with vascular dementia (VD) and 15 age-matched controls. We found significantly reduced levels of glutamate in CSF samples from DAT patients compared to VD and control subjects, but CSF levels of aspartate were found to be significantly elevated in the two groups of dementia studied. Moreover, CSF concentrations of tyrosine, leucine and phenylalanine were significantly increased in VD patients in comparison with those in DAT patients and control subjects. Our results showed a wide increase in CSF/serum amino acid ratios in DAT and VD groups compared to controls. However, no differences were found in CSF/serum ratios between dementia groups. These changes show evidence for a possible disorder of amino acid metabolism with different patterns in these two dementia types.

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Several substances related to the neurodegenerative diseases of Alzheimer and Parkinson, such as hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42, have been shown to induce apoptosis in tumoral cell lines and rat neurons but not in human neurons. Moreover, the role of mitochondria (membrane potential) during neuronal apoptosis is still a matter of debate. We present here, for the first time, in cultured human cortical neurons that the DNA fragmentation induced by these substances was preceded by a decrease of the mitochondrial membrane potential. We have also examined the antiapoptotic effect of the antioxidants glutathione, N-acetyl-cysteine and ascorbic acid. All these antioxidants inhibited the apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42, since they were able to inhibit completely the mitochondrial membrane potential depolarization and the DNA fragmentation.