The brachial plexus - explaining its morphology and variability by a generic developmental model.

In classic anatomy teaching, the brachial plexus generally features as an enigmatic rote-learned structure, leaving the student with a feeling of complexity. The notion of complexity may increase in dissections, where plexuses significantly differing from the standard plexus model are readily found. This raises questions: what determines the existence and prevalence of variants and to what degree should they be considered anomalous? A model linking brachial plexus morphology and its variability to causative morphological parameters which would also standardize plexus description and teaching would be beneficial. The present study aims to provide such a model by analyzing the context of plexus development and applying this model in the analysis of plexus variability in anatomical specimens. Based on a thorough literature review, a generic developmental model was formulated and different factors of variability defined. In 56 plexuses, the proposed generic principles of plexus variability were found consistent with the variations encountered. Summarized, the modeled generic principles are as follows. Brachial plexus axon bundles grow out into an environment of chemical tracer paths in which constraints and obstacles are present: the geometry of the arm bud, cartilaginous bone precursors and vessels. The overall constancy of these factors generates a gross plexus outline, while the variability in these factors gives rise to typical plexus variations. The usefulness of the model derives from the fact that the variability of the main morphologically determining factors is not random but is the expression of the possibilities of the embryological substrate. Within the model, the major plexus morphological determinant is the segmental position of the subclavian artery, which is determined by the segment level of the intersegmental artery from which it develops. Normally, the subclavian artery develops from intersegmental artery i7. However, the subclavian artery can develop from inferior or superior segmental levels, from intersegmental artery i8 or i6, and possibly also from i9 or i5. Each of these arterial variants creates a typical, morphologically distinct, predictable plexus configuration. Superimposed on these basic plexus configurations, the underlying embryological substrate may develop further variability by integrating remnants of other intersegmental arteries into the arterial network. The resulting plexus configurations are further modified by local factors, e.g. the splitting of outgrowing axon bundles around vessels. A large split in the lateral cord around a large vein or veins crossing from lateral to medial, tangentially cranially over the subclavian artery was found in 54% of the 56 investigated BP and therefore might be added to plexus teaching. The distinct plexus morphologies associated with the subclavian artery segmental levels were further found associated with, among others, typical variations in the pectoral nerves and their ansas; these associations were also modeled. The presented models could allow brachial plexus rote learning to be replaced by a more insightful narrative of formative principles suitable for teaching. Clinically, improved understanding of the relationship between plexus variability and the local anatomical environment should be relevant to brachial plexus surgery and reconstruction.

Etiological musculo-skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist.

A case study is presented in which a focal hand dystonia seems to have developed in the right hand of a classical guitarist as a result of a neuromuscular peripheral defect caused by trauma. The trauma was a near total perforation of the first web space by a splinter. Healing was uneventful without apparent functional complications. Two years later the patient noticed difficulties in extending the index in playing, for which he received various unsuccessful treatments during seven years. However, we found more severe dystonic symptoms (cocontractions) in the thumb than in the index during playing, which correlated with an undiagnosed insufficiency in the flexor pollicis brevis (FPB). This defect allowed proposing a biomechanical analysis of compensations for diminished thumb control in playing, which would explain the dysfunction in the index in playing as overcompensation for the thumb problem. If this analysis is correct, the etiology of the case can be traced back to underlying multiarticular control problems in the thumb caused by an insufficient FPB. This defect was considered irrepairable. It was concluded that even with knowledge of the underlying cause, a potentially successful treatment of the dystonia might not exist in this case. The case would demonstrate that task-specific hand dystonias can arise as overcompensations for (peripheral) neuro-musculoskeletal defects. The case is illustrated by videos of playing and functional thumb tests.