Development of a Neurosurgical Cadaver Laboratory despite Limited Resources.

OBJECTIVE: Our neurosurgical program did not have a cadaver laboratory. The need to create one arose following a decrease in elective cranial cases at our institution after Hurricane Maria. Many neurosurgical programs are in countries where financial support for projects such as developing a cadaver research laboratory cannot be expected from their parent institutions. This article describes how, despite limited resources, a neurosurgical cadaver dissection laboratory can be created and maintained to promote resident education and stimulate future research. MATERIALS AND METHODS: The University of Puerto Rico Institutional Review Board evaluated and approved the proposal for creating a neurosurgical cadaver laboratory. The process to establish the laboratory was broken into steps. After obtaining the basic materials, the laboratory was created. RESULTS: The creation of our neurosurgical cadaver laboratory was divided into discrete steps that can be undertaken by any institution with a similar goal. First, a suitable workspace was identified. Second, the surgical instruments and equipment required to perform dissections were obtained. Third, cadaveric specimens for dissection and for practicing surgical approaches were acquired. Last, documentation regarding the laboratory's development was maintained, and an expansion plan was created. We created a dissection laboratory by gathering decommissioned or donated operating room equipment, seeking out contributions from other institutions, and, sometimes, by monetary contribution from the faculty or residents. CONCLUSION: Clear goals, interdepartmental collaboration, and a high degree of motivation were essential in creating, despite limited resources, a working neurosurgical cadaver laboratory to improve resident education.

Radiologic Features with Pathologic Correlation of an Unusual Large Intraosseous Skull Cavernous Hemangioma.

BACKGROUND Intraosseous cavernous skull hemangiomas are rare benign vascular tumors that are usually found incidentally on imaging, with an asymptomatic and slow-growing course. We present a case in which the patient had a mass on her forehead for many years, which began to grow rapidly after head trauma. Imaging characteristics play a crucial role in the diagnosis and description of this disease, and in differentiating it from other more common calvarial lesions that may present with a similar clinical picture. Here, we report an unusual presentation of a large skull hemangioma and discuss the different radiologic imaging findings and pathologic correlations. CASE REPORT A 58-year-old female with history of a lump on her forehead since childhood, which began to grow rapidly after experiencing a closed-head injury. Due to its large size, she went on to seek further management. Radiologic images revealed a frontal skull lesion suggestive of an intraosseous hemangioma. She underwent embolization of the tumor, and 2 days later underwent bilateral frontal craniectomy and cranioplasty. Histopathologic findings confirmed this diagnosis. CONCLUSIONS Intraosseous skull hemangioma may be confidently diagnosed and differentiated from other skull lesions by its imaging characteristics. An accurate diagnosis is essential to selecting correct management and avoiding complications.

aPKC-Mediated Persistent Increase in AMPA/NMDA Ratio in the VTA Participates in the Neuroadaptive Signal Necessary to Induce NAc Synaptic Plasticity After Cocaine Administration.

Chronic cocaine exposure produces enduring neuroadaptations in the brain's reward system. Persistence of early cocaine-evoked neuroadaptations in the ventral tegmental area (VTA) is necessary for later synaptic alterations in the nucleus accumbens (NAc), suggesting a temporal sequence of neuroplastic changes between these two areas. However, the molecular nature of the signal that mediates this sequential event is unknown. Here we used the behavioral sensitization model and the aPKC inhibitor of late-phase LTP maintenance, ZIP, to investigate if a persistent increase in AMPA/NMDA ratio plays a role in the molecular mechanism that allows VTA neuroadaptations to induce changes in the NAc. Results showed that intra-VTA ZIP microinfusion successfully blocked cocaine-evoked synaptic enhancement in the VTA and the expected AMPA/NMDA ratio decrease in the NAc following cocaine sensitization. ZIP microinfusions also blocked the expected AMPA/NMDA ratio increase in the NAc following cocaine withdrawal. These results suggest that a persistent increase in AMPA/NMDA ratio, mediated by aPKCs, could be the molecular signal that enables the VTA to elicit synaptic alterations in the NAc following cocaine administration.