Cirrhosis Associated Intracranial Shunting Lesions

Document Type

Conference Proceeding

Publication Date

5-9-2025

Abstract

There is mounting clinical and biochemical evidence that suggests intracranial vascular shunting lesions can develop de novo, via a different pathophysiologic mechanism than conventional arteriovenous malformations (AVMs). A conventional AVM is a nodular collection of arteries with direct fistular connections to venous drainage, creating a nidus of hyperdynamic vascular circulation that is prone to rupture. Conventional AVMs are widely accepted to be congenital lesions that develop secondary to embryologic genetic mutations, though our experience suggests that the pathogenesis of these lesions extends beyond in utero development.

Literature review of SCOPUS and PubMed databases were performed independently (JH, MM). Search modifiers included: hepatic, failure, cirrhosis, arteriovenous, malformation, angiography, shunt, brain, and intracerebral. Articles were included for literature review on the basis of strength of evidence, language, format, and neuroimaging techniques. Consensus on inclusion and exclusion criteria was achieved by the authors. Systematic review was unsuitable for data collection due to lack of quantitative data. Case details were taken retrospectively from a secure electronic medical record.

We propose the classification of a disease entity belonging to the category of intracranial shunting lesions, known as CAISLs (Cirrhosis Associated Intracranial Shunting Lesions). There is strong empirical evidence to suggest CAISLs differ in pathogenesis than conventional arteriovenous malformations. CAISLs likely develop secondary to cirrhosis mediated angiogenic cascades, and have been demonstrated to resolve when the angiogenic signal is terminated by liver transplantation. We propose speculative pathogenetic mechanisms for their development, and potential avenues.

Comments

2025 Research Day Corewell Health West, Grand Rapids, MI, May 9, 2025. Abstract 1653

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