Botulinum Toxin A has been the main treatment for spasticity since the beginning of the 1990s. Surprisingly, there is still no consensus regarding injection parameters or, importantly, how to determine which muscles to target to improve specific functions. The aim of this study was to develop a systematic approach to determine this, using the example of the arm flexion pattern. We first determined anatomical landmarks for selective motor block of the brachialis nerve, using 20 forearms from 10 fresh cadavers in Ecole Europ eenne de Chirurgie and a university-based dissection centre, Paris, France. We then carried out selective blocks of the motor nerves to the brachialis, brachioradialis and biceps brachii in patients with stroke with an arm flexion pattern, in a University Rehabilitation Hospital, Garches, France. We measured: the resting angle of the elbow angle in standing (manual goniometer), active and passive range of extension, and spasticity using the Held and Tardieu and the Modified Ashworth scales. Range of passive elbow extension was also measured with the shoulder in 90°of flexion. The resting angle of the elbow in standing decreased by 35.0°(from 87.6 AE 23.7 to 52.6 AE 24.2°) with inhibition of brachialis, by a further 3.9°(from 52.6 AE 24.2 to 48.7 AE 23.7°) with inhibition of brachioradialis and a further 14.5°(from 48.7 AE 23.7to 34.2 AE 20.7°) with inhibition of biceps brachii. These results were consistent with the clinical evaluation of passive elbow range of motion with the shoulder at 90°. Sequential blocking of the nerves to the three main elbow flexors revealed that the muscle that limited elbow extension the most, was brachialis. This muscle should be the main target to improve the arm flexion pattern. These results show that it is important not simply to inject the most superficial or powerful muscles to treat a spastic deformity. A comprehensive assessment is required. The strategy proposed in this paper should increase the effectiveness of botulinum toxin injections by ensuring that the relevant muscles are targeted.

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The retrotrapezoid nucleus (RTN) is a hub for respiratory chemoregulation in the mammal brainstem that integrates chemosensory information from peripheral sites and central relays. Chemosensitive neurons of the RTN express specific genetic and molecular determinants, which have been used to identify RTN precise location within the brainstem of rodents and nonhuman primates. Based on a comparative approach, we hypothesized that among mammals, neurons exhibiting the same specific molecular and genetic signature would have the same function. The co‐expression of preprogalanin (PPGAL) and SLC17A6 (VGluT2) mRNAs with duplex in situ hybridization has been studied in formalin fixed paraffin‐embedded postmortem human brainstems. Two specimens were processed and analyzed in line with RTN descriptions in adult rats and macaques. Double‐labeled PPGAL+/SLC17A6+ neurons were only identified in the parafacial region of the brainstem. These neurons were found surrounding the nucleus of the facial nerve, located ventrally to the nucleus VII on caudal sections, and slightly more dorsally on rostral sections. The expression of neuromedin B (NMB) mRNA as a single marker of chemosensitive RTN neurons has not been confirmed in humans. The location of the RTN in human adults is provided. This should help to develop investigation tools combining anatomic high‐resolution imaging and respiratory functional investigations to explore the pathogenic role of the RTN in congenital or acquired neurodegenerative diseases.

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