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The post-operative realm for hepatic transplant patients presents many challenges, but of them all, we take a deeper dive into an increased risk of associated cerebrovascular events. Cerebrovascular diseases, such as cerebral arteriovenous malformation (AVM), are a leading cause of death following a liver transplant. We present a unique case of a liver transplant patient who presented with no brainstem reflexes three months into the post-transplant period. Imaging studies revealed a ruptured AVM within the foramen magnum and cervicomedullary junction, as well as substantial cerebral hemorrhage. While establishing the exact cause of the AVM is not as trivial as it may appear, side effects associated with post-transplantation management regimens and possible congenital factors do shed some light on notable considerations. Given the potential damage associated with ruptured AVMs, poor patient outcomes are unfortunately not as rare as one would hope. This case highlights a rare but highly possible occurrence for cerebrovascular complications, specifically AVM rupture linked to liver transplantation and the systemic changes associated with a procedure as invasive as liver transplantation.

Spinal cord injury (SCI), particularly of the traumatic variety, is a relatively common condition that disproportionately affects the elderly. Cases of SCI with nontraumatic etiologies in the geriatric population have increased over the last 20 years, however. Pannus formation, resulting from chronic inflammation of the spine, is one such etiology that may progress to SCI and potentially result in rapid neurological degeneration. Here we describe a case of an elderly woman who presented with a sudden onset of quadriplegia without a history of trauma. Radiography revealed upper cervical instability and fracture due to the presence of a large erosive pannus formation. Unfortunately, in the context of severe SCI, the reversibility of neurological decline is not always guaranteed. Additionally, surgical intervention is not always appropriate, especially among the elderly population, where medical management and end-of-life care are more often delivered.

The entorhinal cortex and hippocampus are interconnected brain regions required for episodic learning and memory. For this functional encoding, correct assembly of specific synaptic connections across this circuit is a critical component during development. To guide the connection specificity that exists between neurons requires a multitude of circuit building molecular components, including the latrophilin family of synaptic cell adhesion molecules (Lphn1-3; gene symbols ADGRL1-3). Of this genetic family, Lphn2 (ADGRL2) exhibits a unique topographical and cell-type specific expression patterning in the entorhinal cortex and hippocampus that mirrors connectivity. To investigate the role of Lphn2 in a specific cell-type in this circuit, we here created a transgenic mouse (Lphn2fl/fl;pOXR1-Cre) with targeted Lphn2 deletion in medial entorhinal cortex layer III neurons (MECIII). Using these mice, we find two major input/output circuitry pathways to be topographically shifted with Lphn2 deletion in MECIII neurons that include MECIII axon projections to contralateral MEC layer I, and presubiculum axons to ipsilateral MEC layer III. To test the behavioral consequences of these circuitry alterations, we investigated varying entorhinal cortex dependent behaviors, revealing selective deficits in spatial-temporal sequence recognition. Taken together, this study demonstrates that Lphn2 expression in MECIII neurons is necessary for the accurate assembly of MEC topographical circuits that support episodic learning.

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