Posterior interosseous neuropathy: the diagnostic benefits of a multimodal approach to investigation.
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ABSTRACT:
SUBMITTER: Lawley AR
PROVIDER: S-EPMC4831403 | biostudies-other | 2016 Apr
REPOSITORIES: biostudies-other
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Project description:Although rare, posterior interosseous nerve (PIN) palsy can occur in patients with a closed proximal forearm fracture and may present in a delayed fashion after initial trauma. In this case series, three cases of posterior interosseous nerve (PIN) injury following proximal forearm fractures are presented and discussed. Our literature search yielded six studies concerning PIN injury in radial head/neck fractures and proximal forearm fractures. Out of a total of 8 patients, 7 patients were treated non-operatively and in one patient a PIN release was performed. One patient was lost to follow-up, all other 7 patients showed successful recovery. A treatment algorithm for PIN palsy after proximal forearm fractures is provided. Based on our experience and what we found in literature, it seems safe to treat PIN palsies conservatively.
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Project description:UnlabelledComplex hand trauma presents multifaceted problems for the surgeon. Soft tissue defects of the upper extremity must be carefully assessed to determine the most appropriate method of coverage of hand. In this article, the reversed posterior interosseous flap was used for coverage of the hand. The injured areas include: dorsum of the hand (10 cases), the wrist (3 cases) and the dorsal thumb (2 cases). All flaps survived completely and none exhibited venous compromise. All donor sites were skin grafted. The reversed posterior interosseous flap is a versatile option for coverage of moderate sized defects of the hand and is specifically indicated for coverage of injuries of the wrist, dorsal hand and dorsal thumb.Electronic supplementary materialThe online version of this article (doi:10.1007/s12593-011-0042-y) contains supplementary material, which is available to authorized users.
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Project description:The radial nerve and posterior interosseous nerve (PIN) are prone to injury at multiple sites. Electrodiagnostic (EDx) studies may only identify the most proximal lesion. Nerve ultrasound could augment EDx by visualizing additional pathology.This investigation was a retrospective examination of ultrasound and EDx from 26 patients evaluated for posterior cord/radial/PIN lesions.Eighteen of 26 patients had abnormalities on EDx (15 radial, 2 PIN, 1 posterior cord). Ultrasound identified 15 of 18 (83%) of the EDx abnormalities and provided additional diagnostic information. In 6 of 15 (40%) patients with EDx evidence of radial neuropathy, ultrasound identified both radial nerve enlargement and additional, unsuspected PIN enlargement (53% to 339% enlarged vs. unaffected side). Ultrasound also identified: nerve (dis)continuity at the trauma site (n = 8); and nerve tumor (n = 2; 1 with normal EDx).In radial neuropathy, ultrasound often augments EDx studies and identifies a second lesion in the PIN. Further studies are required to determine the etiology and significance of this additional distal pathology.
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Project description:Introduction: Taxanes are a class of chemotherapeutics commonly used to treat various solid tumors, including breast and ovarian cancers. Taxane-induced peripheral neuropathy (TIPN) occurs in up to 70% of patients, impacting quality of life both during and after treatment. TIPN typically manifests as tingling and numbness in the hands and feet and can cause irreversible loss of function of peripheral nerves. TIPN can be dose-limiting, potentially impacting clinical outcomes. The mechanisms underlying TIPN are poorly understood. As such, there are limited treatment options and no tools to provide early detection of those who will develop TIPN. Although some patients may have a genetic predisposition, genetic biomarkers have been inconsistent in predicting chemotherapy-induced peripheral neuropathy (CIPN). Moreover, other molecular markers (eg, metabolites, mRNA, miRNA, proteins) may be informative for predicting CIPN, but remain largely unexplored. We anticipate that combinations of multiple biomarkers will be required to consistently predict those who will develop TIPN. Methods: To address this clinical gap of identifying patients at risk of TIPN, we initiated the Genetics and Inflammatory Markers for CIPN (GENIE) study. This longitudinal multicenter observational study uses a novel, multimodal approach to evaluate genomic variation, metabolites, DNA methylation, gene expression, and circulating cytokines/chemokines prior to, during, and after taxane treatment in 400 patients with breast cancer. Molecular and patient reported data will be collected prior to, during, and after taxane therapy. Multi-modal data will be used to develop a set of comprehensive predictive biomarker signatures of TIPN. Conclusion: The goal of this study is to enable early detection of patients at risk of developing TIPN, provide a tool to modify taxane treatment to minimize morbidity from TIPN, and improved patient quality of life. Here we provide a brief review of the current state of research into CIPN and TIPN and introduce the GENIE study design.
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Project description:We are reporting our 10-year experience with 68 patients. Sixty-six flaps were of fasciocutaneous type and two were of osteofasciocutaneous type. These flaps were used for volar and dorsal traumatic hand defects, first web space reconstruction, thumb reconstruction, and repair of congenital anomalies. Sixty flaps (88.24%) had complete uneventful take-up. Four flaps developed partial necrosis, whereas four flaps suffered complete necrosis. The single most important factor for flap survival in our experience has been inclusion of at least two perforators to supply the skin pedal. The proximal flap dissection has a learning curve and all of our poor results were in the early part of our experience. We believe that posterior interosseous fasciocutaneous flap (PIF) is a versatile and reliable option for the challenging problems of hand soft-tissue coverage.
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Project description:Young adult APOE-?4 carriers show increased activity in posterior regions of the default mode network (pDMN), but how this is related to structural connectivity is unknown. Thirty young adults (one half of whom were APOE-?4 carriers; mean age 20 years) were scanned using both diffusion and functional magnetic resonance imaging. The parahippocampal cingulum bundle (PHCB)-which links the pDMN and the medial temporal lobe-was manually delineated in individual participants using deterministic tractography. Measures of tract microstructure (mean diffusivity and fractional anisotropy) were then extracted from these tract delineations. APOE-?4 carriers had lower mean diffusivity and higher fractional anisotropy relative to noncarriers in PHCB, but not in a control tract (the inferior longitudinal fasciculus). Furthermore, PHCB microstructure was selectively associated with pDMN (and medial temporal lobe) activity during a scene discrimination task known to be sensitive to Alzheimer's disease. These findings are consistent with a lifespan view of Alzheimer's disease risk, where early-life, connectivity-related changes in specific, vulnerable "hubs" (e.g., pDMN) lead to increased neural activity. Critically, such changes may reflect reduced network efficiency/flexibility in APOE-?4 carriers, which in itself may portend a faster decline in connectivity over the lifespan and ultimately trigger early amyloid-? deposition in later life.
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Project description:ObjectivesTo develop a reliable, reproducible rat model of posterior ischemic optic neuropathy (PION) and study the cellular responses in the optic nerve and retina.MethodsPosterior ischemic optic neuropathy was induced in adult rats by photochemically induced ischemia. Retinal and optic nerve vasculature was examined by fluorescein isothiocyanate–dextran extravasation. Tissue sectioning and immunohistochemistry were used to investigate the pathologic changes. Retinal ganglion cell survival at different times after PION induction, with or without neurotrophic application, was quantified by fluorogold retrograde labeling.ResultsOptic nerve injury was confirmed after PION induction, including local vascular leakage, optic nerve edema, and cavernous degeneration. Immunostaining data revealed microglial activation and focal loss of astrocytes, with adjacent astrocytic hypertrophy. Up to 23%, 50%, and 70% retinal ganglion cell loss was observed at 1 week, 2 weeks, and 3 weeks, respectively, after injury compared with a sham control group. Experimental treatment by brain-derived neurotrophic factor and ciliary neurotrophic factor remarkably prevented retinal ganglion cell loss in PION rats. At 3 weeks after injury, more than 40% of retinal ganglion cells were saved by the application of neurotrophic factors.ConclusionsRat PION created by photochemically induced ischemia is a reproducible and reliable animal model for mimicking the key features of human PION.Clinical relevanceThe correspondence between the features of this rat PION model to those of human PION makes it an ideal model to study the pathophysiologic course of the disease, most of which remains to be elucidated. Furthermore, it provides an optimal model for testing therapeutic approaches for optic neuropathies.
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