Novel anatomical findings with implications on the etiology of the piriformis syndrome.

PURPOSE: The cause of the piriformis-related pelvic and extra-pelvic pain syndromes is still not well understood. Usually, the piriformis syndrome is seen as extra-pelvic sciatica caused by the entrapment of the sciatic nerve by the piriformis in its crossing through the greater sciatic foramen. However, the piriformis muscle may compress additional nerve structures in other regions and cause idiotypic pelvic pain, pelvic visceral pain, pudendal neuralgia, and pelvic organ dysfunction. There is still a lack of detailed description of the muscle origin, topography, and its possible relationships with the anterior branches of the sacral spinal nerves and with the sacral plexus. In this research, we aimed to characterize the topographic relationship of the piriformis with its surrounding anatomical structures, especially the anterior branches of the sacral spinal nerves and the sacral plexus in the pelvic cavity, as well as to estimate the possible role of anatomical piriformis variants in pelvic pain and extra-pelvic sciatica. METHODS: Human cadaveric material was used accordingly to the Swiss Academy of Medical Science Guidelines adapted in 2021 and the Federal Act on Research involving Human Beings (Human Research ACT, HRA, status as 26, May 2021). All body donors gave written consent for using their bodies for teaching and research. 14 males and 26 females were included in this study. The age range varied from 64 to 97 years (mean 84 ± 10.7 years, median 88). RESULTS: three variants of the sacral origin of the piriformis were found when referring to the relationship between the muscle and the anterior sacral foramen. Firstly, the medial muscle origin pattern and its complete covering of the anterior sacral foramen by the piriformis muscle is the most frequent anatomical variation (43% in males, 70% in females), probably with the most relevant clinical impact. This pattern may result in the compression of the anterior branches of the sacral spinal nerves when crossing the muscle. CONCLUSIONS: These new anatomical findings may provide a better understanding of the complex piriformis and pelvic pain syndromes due to compression of the sacral spinal nerves with their somatic or autonomous (parasympathetic) qualities when crossing the piriformis.

Innervation of the clavicular part of the deltoid muscle by the lateral pectoral nerve.

INTRODUCTION: The innervation pattern of the clavicular head of the deltoid muscle and its corresponding topography was investigated via cadaveric dissection in the present study, focusing on the lateral pectoral nerve. MATERIALS AND METHODS: Fifty-eight upper extremities were dissected and the nerve supplies to the deltoid muscle and the variability of the lateral pectoral and axillary nerves, including their topographical patterns, were noted. RESULTS: The clavicular portion of the deltoid muscle received a deltoid branch from the lateral pectoral nerve in 86.2% of cases. Two topographical patterns of the lateral pectoral nerve were observed, depending on the branching level from the brachial plexus: a proximal variant, where the nerve entered the pectoral region under the clavicle, and a distal variant, where the nerve entered the pectoral region from the axillary fossa around the caudal border of the pectoralis minor. These dissection findings were supported by histological confirmation of peripheral nerve tissue entering the clavicular part of the deltoid muscle. CONCLUSIONS: The topographical variations of the lateral pectoral nerve are relevant for orthopedic and trauma surgeons and neurologists. These new data could revise the interpretation of deltoid muscle atrophy and of thoracic outlet and pectoralis minor compression syndromes. They could also explain the residual anteversion function of the arm after axillary nerve injury and deficiency, which is often thought to be related to biceps brachii muscle function.

HDAC1/2-Dependent P0 Expression Maintains Paranodal and Nodal Integrity Independently of Myelin Stability through Interactions with Neurofascins.

The pathogenesis of peripheral neuropathies in adults is linked to maintenance mechanisms that are not well understood. Here, we elucidate a novel critical maintenance mechanism for Schwann cell (SC)-axon interaction. Using mouse genetics, ablation of the transcriptional regulators histone deacetylases 1 and 2 (HDAC1/2) in adult SCs severely affected paranodal and nodal integrity and led to demyelination/remyelination. Expression levels of the HDAC1/2 target gene myelin protein zero (P0) were reduced by half, accompanied by altered localization and stability of neurofascin (NFasc)155, NFasc186, and loss of Caspr and septate-like junctions. We identify P0 as a novel binding partner of NFasc155 and NFasc186, both in vivo and by in vitro adhesion assay. Furthermore, we demonstrate that HDAC1/2-dependent P0 expression is crucial for the maintenance of paranodal/nodal integrity and axonal function through interaction of P0 with neurofascins. In addition, we show that the latter mechanism is impaired by some P0 mutations that lead to late onset Charcot-Marie-Tooth disease.

Microglia at center stage: a comprehensive review about the versatile and unique residential macrophages of the central nervous system.

Microglia cells are the unique residential macrophages of the central nervous system (CNS). They have a special origin, as they derive from the embryonic yolk sac and enter the developing CNS at a very early stage. They play an important role during CNS development and adult homeostasis. They have a major contribution to adult neurogenesis and neuroinflammation. Thus, they participate in the pathogenesis of neurodegenerative diseases and contribute to aging. They play an important role in sustaining and breaking the blood-brain barrier. As innate immune cells, they contribute substantially to the immune response against infectious agents affecting the CNS. They play also a major role in the growth of tumours of the CNS. Microglia are consequently the key cell population linking the nervous and the immune system. This review covers all different aspects of microglia biology and pathology in a comprehensive way.

Parvalbumin-like immunostaining in the cat inferior colliculus. Light and electron microscopic investigation.

The presence of the calcium-binding protein parvalbumin (PV) was studied in neuronal elements of the cat's inferior colliculus (IC) by means of light and electron microscopic immunocytochemistry. Immunostaining of PV was detected in all three main parts of the IC. Several subtypes of large neurons that differed in size and shape were immunostained, comprising approx. 15% of the total number of PV-containing neurons. Approx. half of the labeled neurons were medium sized. Two types of small neurons were found to be PV synthesizing, and comprised approx. 35% of the total PV-containing population. Ultrastructurally, many dendrites were heavily immunolabeled, and the reaction product was present in dendritic spines as well. Several types of synaptic boutons contained reaction product, and terminated on both labeled and unlabeled postsynaptic targets forming asymmetric and symmetric synapses. Approx. 70% of all PV-immunolabeled terminals contained round synaptic vesicles and formed asymmetric synapses. The majority of these boutons were of the "large round" type and corresponded to the terminals of cochlear nuclei. A lower number were of the "small round" type, and were probably corticotectal terminals. The remaining 30% of PV-containing terminals contained pleomorphic or elongated vesicles and formed symmetric synapses. These terminals corresponded with "P" and "F1" bouton types. Part of these boutons appeared to arise from nuclei of the lateral lemniscus and the superior olive, and a certain percentage likely represented endings of inhibitory interneurons.