Venous leg ulcers (VLU) generally have slow healing rates (HR) and frequent recurrence rates (RR). The underlying etiology is venous hypertension. The present observational cohort study was to determine healing and RR in VLU treated with ultrasound-guided foam sclerotherapy (UGFS). One hundred and eighty VLU were treated with polidocanol microfoam monthly under ultrasound control. Median follow-up was 30 months (range: 17-40). One hundred seventy-two (95.6%) ulcers healed during the study. The overall twenty-four week HR was 79.4% and was significantly higher (95.1%) in patients with isolated great saphenous vein incompetence than in those with great saphenous vein plus perforator (91.7%) or exclusive perforator incompetence (78.9%) (p¿<¿0.01). Patients without deep vein incompetence had a significantly higher 6-month HR (89.8%) than those with (67.4%) (p¿<¿0.01). Multivariate analysis identified the following independent risk factors: chronicity¿>¿12 months (OR 7.69), area¿>¿6¿cm(2) (OR 4.24), lipodermatoesclerosis (OR 12.22), history of¿>¿3 previous ulcers (OR 5.57) and history of deep vein thrombosis (OR 6.18). One, two and three year ulcer RR were 8.1%, 14.9%, and 20.8%, respectively. Isolated perforator incompetence and previous history of venous surgery were significantly (p¿=¿0.03) associated with a higher RR. VLU treated with microfoam sclerotherapy are associated with high HR and low mid-term RR.

The tegmental pedunculopontine nucleus (PPN) is a basal ganglia-related structure that has recently gained renewed interest as a potential surgical target for the treatment of several aspects of Parkinson's disease. However, the underlying anatomical substrates sustaining the choice of the PPN nucleus as a surgical candidate remain poorly understood. Here, we characterized the chemical phenotypes of different subtypes of PPN efferent neurons innervating the rat parafascicular (PF) nucleus. Emphasis was placed on elucidating the impact of unilateral nigrostriatal denervation on the expression patterns of the mRNA coding the vesicular glutamate transporter type 2 (vGlut2 mRNA). We found a bilateral projection from the PPN nucleus to the PF nucleus arising from cholinergic and glutamatergic efferent neurons, with a small fraction of projection neurons co-expressing both cholinergic and glutamatergic markers. Furthermore, the unilateral nigrostriatal depletion induced a bilateral twofold increase in the expression levels of vGlut2 mRNA within the PPN nucleus. Our results support the view that heterogeneous chemical profiles account for PPN efferent neurons innervating thalamic targets. Moreover, a bilateral enhancement of glutamatergic transmission arising from the PPN nucleus occurs following unilateral dopaminergic denervation, therefore sustaining the well-known hyperactivity of the PF nucleus in parkinsonian-like conditions. In conclusion, our data suggest that the ascending projections from the PPN that reach basal ganglia-related targets could play an important role in the pathophysiology of Parkinson's disease.

GABAergic neurons within the internal division of the globus pallidus (GPi) are the main source of basal ganglia output reaching the thalamic ventral nuclei in monkeys. Following dopaminergic denervation, pallidothalamic-projecting neurons are known to be hyperactive, whereas a reduction in GPi activity is typically observed in lesioned animals showing levodopa-induced dyskinesia. Besides the mRNAs coding for GABAergic markers (GAD65 and GAD67), we show that all GPi neurons innervating thalamic targets also express transcripts for the isoforms 1 and 2 of the vesicular glutamate transporter (vGlut1 and vGlut2 mRNA). Indeed, dual immunofluorescent detection of GAD67 and vGlut1/2 confirmed the data gathered from in situ hybridization experiments, therefore demonstrating that the detected mRNAs are translated into the related proteins. Furthermore, the dopaminergic lesion resulted in an up-regulation of expression levels for both GAD65 and GAD67 mRNA within identified pallidothalamic-projecting neurons. This was coupled with a down-regulation of GAD65/67 mRNA expression levels in GPi neurons innervating thalamic targets in monkeys showing levodopa-induced dyskinesia. By contrast, the patterns of gene expression for both vGlut1 and vGlut2 mRNAs remained unchanged across GPi projection neurons in control, MPTP-treated and dyskinetic monkeys. In summary, both GABAergic and glutamatergic markers were co-expressed by GPi efferent neurons in primates. Although the status of the dopaminergic system directly modulates the expression levels of GAD65/67 mRNA, the observed expression of vGlut1/2 mRNA is not regulated by either dopaminergic removal or by continuous stimulation with dopaminergic agonists.