Expert-driven Chêneau applications: Description and in-brace corrections

In-brace correction and compliance are the main predictors of a successful outcome of brace treatment in the management of patients with idiopathic scoliosis. The latest CAD/CAM- or module-based bracing concepts related to a proper classification have led to better in-brace corrections and have made the braces easier to wear for the patient. However, even the latest developments on the market do not ensure successful treatment in every case. Thoracic curves with Cobb angles less than 50° may be treated with the best likelihood of success utilizing the latest Chêneau derivates, enabling a real 3D correction that includes sagittal correction of the spine, when patient compliance can be achieved. The successful application of the braces demands a proper classification of curve patterns. The percentage of in-brace correction of the Cobb angle correlates with the end result and consequently is a good indicator for brace quality. However, other factors, such as 3D correction or the absolute reduction of the Cobb angle (i.e., in rigid curves over 50°), might also be important indicators.     

Repetitive TMS over the human oculomotor cortex: comparison of 1-Hz and theta burst stimulation

The aim of the study was to compare the effect duration of two different protocols of repetitive transcranial magnetic stimulation (rTMS) on saccade triggering. In four experiments, two regions (right frontal eye field (FEF) and vertex) were stimulated using a 1-Hz and a theta burst protocol (three 30Hz pulses repeated at intervals of 100ms). The same number of TMS pulses (600 pulses) was applied with stimulation strength of 80% of the resting motor threshold for hand muscles. Following stimulation the subjects repeatedly performed an oculomotor task using a modified overlap paradigm, and saccade latencies were measured over a period of 60min. The results show that both 1-Hz and theta burst stimulation had inhibitory effects on saccade triggering when applied over the FEF, but not over the vertex. One-hertz rTMS significantly increased saccade latencies over a period of about 8min. After theta burst rTMS, this effect lasted up to 30min. Furthermore, the decay of rTMS effects was protocol-specific: After 1-Hz stimulation, saccade latencies returned to a baseline level much faster than after theta burst stimulation. We speculate that these time course differences represent distinct physiological mechanisms of how TMS interacts with brain function.     

The selective nicotinic acetylcholine receptor alpha7 agonist JN403 is active in animal models of cognition, sensory gating, epilepsy and pain

Several lines of evidence suggest that the nicotinic acetylcholine receptor α7 (nAChR α7) is involved in central nervous system disorders like schizophrenia and Alzheimer's disease as well as in inflammatory disorders like sepsis and pancreatitis. The present article describes the in vivo effects of JN403, a compound recently characterized to be a potent and selective partial nAChR α7 agonist. JN403 rapidly penetrates into the brain after i.v. and after p.o. administration in mice and rats. In the social recognition test in mice JN403 facilitates learning/memory performance over a broad dose range. JN403 shows anxiolytic-like properties in the social exploration model in rats and the effects are retained after a 6 h pre-treatment period and after subchronic administration. The effect on sensory inhibition was investigated in DBA/2 mice, a strain with reduced sensory inhibition under standard experimental conditions. Systemic administration of JN403 restores sensory gating in DBA/2 mice, both in anaesthetized and awake animals. Furthermore, JN403 shows anticonvulsant potential in the audiogenic seizure paradigm in DBA/2 mice. In the two models of permanent pain tested, JN403 produces a significant reversal of mechanical hyperalgesia. The onset was fast and the duration lasted for about 6 h. Altogether, the present set of data suggests that nAChR α7 agonists, like JN403 may be beneficial for improving learning/memory performance, restoring sensory gating deficits, and alleviating pain, epileptic seizures and conditions of anxiety.     

Clinical diagnosis compared to classification criteria in in a cohort of 54 patients with systemic sclerosis and associated disorders

OBJECTIVE: To compare clinical diagnosis with two validated classification criteria for systemic sclerosis (SSc) in a cohort of Swiss patients with SSc and associated disorders. METHODS: Charts of 54 patients with SSc and associated disorders were reviewed and compared with data obtained at a thorough clinical examination using a standardised protocol (Raynaud's phenomen [RP], skin involvement, nailfold capillary microscopy and determination of autoantibody pattern). RESULTS: According to patient records 6 patients had diffuse cutaneous SSc (dcSSc), 23 limited cutaneous SSc (lcSSc) and 20 were not classified. Two patients had mixed connective tissue disease (MCTD) and 3 overlap syndromes. At the time of clinical examination, 7 patients showed dcSSc (6 plus 1 patient originally classified as lcSSc), 26 lcSSc (20 plus 6 originally not classified) and 16 patients had severe RP which was arbitrarily classified as Raynaud's syndrome (RS). 15 of the latter 16 were antinuclear antibody positive and 7 exhibited pathological nailfold capillaries. On the basis of LeRoy and Medsger's criteria, 6 of these patients could be further classified as limited SSc (lSSc). Of 49 sera tested, 14 contained centromere antibodies at clinical examination, 16 Scl-70, 5 RNA-pol, 1 Ku, 12 antibodies with unknown specificity, and one serum was autoantibody negative. CONCLUSIONS: A substantial number of patients with minor cutaneous manifestations do not fulfil ACR classification criteria, though they have typical clinical signs of SSc. Characteristic features in these patients are presence of Raynaud's phenomenon, antinuclear antibodies and pathological changes in nailfold capillary microscopy. Application of the diagnostic criteria recently proposed by LeRoy and Medsger makes it possible to name many of these patients. The use of these criteria is recommended for clinical management.     

JNK is activated but does not mediate hippocampal neuronal apoptosis in experimental neonatal pneumococcal meningitis

Pneumococcal meningitis is associated with caspase 3-dependent apoptosis of recently post-mitotic immature neurons in the dentate gyrus of the hippocampus. The death of these cells is implicated in the learning and memory deficits in patients surviving the disease. The stress-activated protein kinase c-Jun N-terminal kinase (JNK) has been shown to be an important mediator of caspase 3-dependent neuronal apoptosis. However, whether JNK is involved in hippocampal apoptosis caused by pneumococcal meningitis has so far not been investigated. Here we show in a neonatal rat model of pneumococcal meningitis that JNK3 but not JNK1 or JNK2 is activated in the hippocampus during the acute phase of infection. At the cellular level, JNK3 activation was accompanied in the dentate gyrus by markedly increased phosphorylation of its major downstream target c-Jun in early immature (Hu-positive) neurons, but not in migrating (doublecortin-positive) neurons, the cells that do undergo apoptosis. These findings suggested that JNK may not be involved in pneumococcal meningitis-induced hippocampal apoptosis. Indeed, although intracerebroventricular administration of D-JNKI-1 or AS601245 (two highly specific JNK inhibitors) inhibited c-Jun phosphorylation and protein expression in the hippocampus, hippocampal apoptosis was unaffected. Collectively, these results demonstrate that JNK does not mediate hippocampal apoptosis in pneumococcal meningitis, and that JNK may be involved in processes unrelated to apoptosis in this disease.