Objective. Intracortical microelectrode arrays (MEA) can be used as part of a brain-machine interface system to provide sensory feedback control of an artificial limb to assist persons with tetraplegia. Variability in functionality of electrodes has been reported but few studies in humans have examined the impact of chronic brain tissue responses revealed postmortem on electrode performance in vivo. Approach. In a tetraplegic man, recording MEAs were implanted into the anterior intraparietal area and Brodmann's area 5 (BA5) of the posterior parietal cortex and a recording and stimulation array was implanted in BA1 of the primary somatosensory cortex (S1). The participant expired from unrelated causes seven months after MEA implantation. The underlying tissue of two of the three devices was processed for histology and electrophysiological recordings were assessed. Main results. Recordings of neuronal activity were obtained from all three MEAs despite meningeal encapsulation. However, the S1 array had a greater encapsulation, yielded lower signal quality than the other arrays and failed to elicit somatosensory percepts with electrical stimulation. Histological examination of tissues underlying S1 and BA5 implant sites revealed localized leptomeningeal proliferation and fibrosis, lymphocytic infiltrates, astrogliosis, and foreign body reaction around the electrodes. The BA5 recording site showed focal cerebral microhemorrhages and leptomeningeal vascular ectasia. The S1 site showed focal tissue damage including vascular recanalization, neuronal loss, and extensive subcortical white matter necrosis. The tissue response at the S1 site included hemorrhagic-induced injury suggesting a likely mechanism for reduced function of the S1 implant. Significance. Our findings are similar to those from animal studies with chronic intracortical implants and suggest that vascular disruption and microhemorrhage during device implantation are important contributors to overall array and individual electrode performance and should be a topic for future device development to mitigate tissue responses. Neurosurgical considerations are also discussed.

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Pathological diagnosis of solitary fibrous tumor (SFT) in the pediatric population is challenging, as it occurs uncommonly in this age-group and resembles other spindle cell neoplasms. SFT contains a NAB2-STAT6 fusion gene, which can be reliably detected using STAT6 immunohistochemistry. Positive staining is highly sensitive and specific. We sought to investigate the utility of STAT6 immunohistochemistry, to show how commonly SFT was historically recognized at 3 academic pediatric institutions, to reclassify them when appropriate, and to demonstrate features of major mimics of SFT. Our series included cases with a previous diagnosis of SFT or for which SFT was among key considerations, from 3 major academic pediatric hospitals seen over the past 30 years. Of 18 tumors identified, only 3 tumors from 2 patients demonstrated positive STAT6 staining as well as the typical histology and immunophenotype seen in SFT. The remaining 15 tumors were reclassified based on morphology, additional immunohistochemistry and fluorescence in situ hybridization as desmoid-type fibromatosis (3 tumors), nerve sheath/neural tumors (3 tumors), low-grade fibromyxoid sarcoma, medallion-like dermal fibroma, poorly differentiated Sertoli cell tumor, nodular/proliferative fasciitis, calcifying fibrous tumor, aneurysmal bone cyst of soft tissue, STAT6-negative SFT with adipocytic differentiation, undifferentiated small round blue cell tumor, and scar (1 tumor each). Our study confirms that SFT is rare in the pediatric population and that it is potentially overdiagnosed. STAT6 immunohistochemistry is recommended to confirm the diagnosis of SFT in the pediatric population.

Congenital hemangiomas (CH) are rare vascular tumors of the neonate, with an estimated incidence of less than 0.5%. 1 CH are present at birth and may involute to varying degrees over the first 2-12 months of age. 2 Based on the course and degree of involution, CH are subdivided into rapidly, partially, and non-involuting subtypes. [3][4][5] Complications of CH are rare and primarily related to high-flow vasculature that may initially be present before the involution phase begins. The most common sequela of this includes ulceration and bleeding, particularly in the peripartum period. 6,7 High-output congestive heart failure can rarely result from intralesional shunting in larger CH, particularly those within visceral organs. Increased blood flow can also lead to a mild coagulopathy, evidenced by hypofibrinogenemia and thrombocytopenia. 2,[8][9][10][11] These findings are usually transient and less severe than Kasabach-Merritt phenomenon (KMP), which occurs most commonly in patients with kaposiform hemangioendotheliomas (KHE) and less so with tufted angiomas (TA). 12 Typically, CH can be managed supportively and expectantly.However, in cases requiring intervention, a lack of evidence in favor of medical therapies was found. 2 Corticosteroids, propranolol, and vincristine have been used with minimal success, and only embolization and surgical resection have been shown to be definitive. 9,13,14 We present a rare, and sadly lethal, case of a neonate with a large CH and severe, overwhelming coagulopathy and multiorgan failure.Treatment options, which were carefully weighed for our patient, are