Characterization of Major Complications of Bridge Plating of Distal Radius Fractures at a Level I Trauma Center.

BACKGROUND: Comminuted, markedly displaced distal radius fractures can cause instability requiring advanced stabilization with dorsal bridge plating. However, published complication rates of bridge plating widely vary. We hypothesize that complications of bridge plating of distal radius fractures are more prevalent than published rates. METHODS: A retrospective review was performed on all patients at an academic level I trauma center treated with a bridge plate for a distal radius fracture from 2014 to 2022. RESULTS: Sixty-five wrists were included in the final analysis: average age 53 years, male 51%, average plate retention 4 months, and average follow-up 6 months. Carpal tunnel release (CTR) was performed at time of primary procedure in 7 (10%) cases. Radial height, radial inclination, dorsal tilt, and ulnar variance were all significantly improved (P < .001). Grip strength, flexion, extension, and supination were significantly limited (P < .03). Twenty-one patients (32%) developed 35 major complications requiring unplanned reoperation, including mechanical hardware-related complication (15%), deep infection (11%), nonunion/delayed union (9%), adhesions (6%), median neuropathy (6%), symptomatic arthritis (5%), and tendon rupture (2%). Plate breakage occurred in 3 patients (5%) and was always localized over the central drill holes of the bridge plate. CONCLUSIONS: Major complications for bridge plating of distal radius fractures were higher at our institution than previously published. Plate breakage should prompt reconsideration of plate design to avoid drill holes over the wrist joint. Signs and symptoms of carpal tunnel syndrome should be carefully assessed at initial presentation, and consideration for concomitant CTR should be strongly considered.

Case Report of Transgender Patient with Gonadotropic Dysfunction Secondary to Craniopharyngioma: Toward Improving Understanding of Biopsychosocial Dynamics of Gender Identity in Neurosurgical Care.

BACKGROUND: There is a paucity of information in the literature linking possible neuroendocrinologic repercussions of anterior pituitary insufficiency from tumor-associated mass effect with gender identity in transindividuals. The authors present the case of a 26-year-old transgender woman who was found to have a sellar/suprasellar neoplasm after reporting loss of vision in a bitemporal distribution. CASE DESCRIPTION: Magnetic resonance imaging demonstrated a 2.6-cm complex cystic and solid sellar/suprasellar mass, suggestive of craniopharyngioma, intimately associated with the pituitary stalk. Importantly, this radiographic diagnosis was made 2 years following the initiation of gender-affirming hormone therapy (HT). Laboratory testing following radiographic diagnosis demonstrated evidence of diffuse anterior pituitary insufficiency with decreased morning cortisol, free thyroxine, insulin-like growth factor-1, and testosterone. Following optimization with the endocrinology team, the patient was taken to the operating room for expanded endonasal resection of tumor with lumbar drain insertion and nasoseptal flap coverage. Gross total resection was achieved with marked improvement in vision noted following surgery. The patient continued her HT following surgery. CONCLUSIONS: In hindsight, the neuroendocrinologic manifestations of the craniopharyngioma may have influenced distressing pubertal experiences that distanced her from her assigned male sex, as well as the desired effects of feminization HT in this patient, ultimately delaying her presentation to the neurosurgery service and diagnosis of craniopharyngioma. As the first report of the neurosurgical evaluation and treatment of a transgender patient with anterior pituitary insufficiency secondary to craniopharyngioma, this case examines the biopsychosocial interplay between the development of gender identity and the neuroendocrinologic manifestations of craniopharyngioma.

Characterization of a novel rat model of X-linked hydrocephalus by CRISPR-mediated mutation in L1cam.

OBJECTIVE: Emergence of CRISPR/Cas9 genome editing provides a robust method for gene targeting in a variety of cell types, including fertilized rat embryos. The authors used this method to generate a transgenic rat L1cam knockout model of X-linked hydrocephalus (XLH) with human genetic etiology. The object of this study was to use diffusion tensor imaging (DTI) in studying perivascular white matter tract injury in the rat model and to characterize its pathological definition in histology. METHODS: Two guide RNAs designed to disrupt exon 4 of the L1cam gene on the X chromosome were injected into Sprague-Dawley rat embryos. Following embryo transfer into pseudopregnant females, rats were born and their DNA was sequenced for evidence of L1cam mutation. The mutant and control wild-type rats were monitored for growth and hydrocephalus phenotypes. Their macro- and microbrain structures were studied with T2-weighted MRI, DTI, immunohistochemistry, and transmission electron microscopy (TEM). RESULTS: The authors successfully obtained 2 independent L1cam knockout alleles and 1 missense mutant allele. Hemizygous male mutants from all 3 alleles developed hydrocephalus and delayed development. Significant reductions in fractional anisotropy and axial diffusivity were observed in the corpus callosum, external capsule, and internal capsule at 3 months of age. The mutant rats did not show reactive gliosis by then but exhibited hypomyelination and increased extracellular fluid in the corpus callosum. CONCLUSIONS: The CRISPR/Cas9-mediated genome editing system can be harnessed to efficiently disrupt the L1cam gene in rats for creation of a larger XLH animal model than previously available. This study provides evidence that the early pathology of the periventricular white matter tracts in hydrocephalus can be detected in DTI. Furthermore, TEM-based morphometric analysis of the corpus callosum elucidates the underlying cytopathological changes accompanying hydrocephalus-derived variations in DTI. The CRISPR/Cas9 system offers opportunities to explore novel surgical and imaging techniques on larger mammalian models.

Impaired neural differentiation and glymphatic CSF flow in the Ccdc39 rat model of neonatal hydrocephalus: genetic interaction with L1cam.

Neonatal hydrocephalus affects about one child per 1000 births and is a major congenital brain abnormality. We previously discovered a gene mutation within the coiled-coil domain-containing 39 (Ccdc39) gene, which causes the progressive hydrocephalus (prh) phenotype in mice due to lack of ependymal-cilia-mediated cerebrospinal fluid (CSF) flow. In this study, we used CRISPR/Cas9 to introduce the Ccdc39 gene mutation into rats, which are more suitable for imaging and surgical experiments. The Ccdc39prh/prh mutants exhibited mild ventriculomegaly at postnatal day (P)5 that progressed into severe hydrocephalus by P11 (P<0.001). After P11, macrophage and neutrophil invasion along with subarachnoid hemorrhage were observed in mutant brains showing reduced neurofilament density, hypomyelination and increased cell death signals compared with wild-type brains. Significantly more macrophages entered the brain parenchyma at P5 before hemorrhaging was noted and increased expression of a pro-inflammatory factor (monocyte chemoattractant protein-1) was found in the cortical neural and endothelial cells in the mutant brains at P11. Glymphatic-mediated CSF circulation was progressively impaired along the middle cerebral artery from P11 as mutants developed severe hydrocephalus (P<0.001). In addition, Ccdc39prh/prh mutants with L1 cell adhesion molecule (L1cam) gene mutation, which causes X-linked human congenital hydrocephalus, showed an accelerated early hydrocephalus phenotype (P<0.05-0.01). Our findings in Ccdc39prh/prh mutant rats demonstrate a possible causal role of neuroinflammation in neonatal hydrocephalus development, which involves impaired cortical development and glymphatic CSF flow. Improved understanding of inflammatory responses and the glymphatic system in neonatal hydrocephalus could lead to new therapeutic strategies for this condition.This article has an associated First Person interview with the joint first authors of the paper.