Objective:
To identify networks causally involved in new-onset synesthesia.
Background:
Synesthesia offers a unique perspective on the brain’s integration of sensory input across modalities. Defining the structures involved in synesthesia may also provide insight into conditions such as schizophrenia, autism, and savant syndrome that are also associated with persistent disruptions of perception and sensory experiences.
Design/Methods:
We conducted a literature search to identify studies of new-onset synesthesia following focal brain injury with traceable neuroimaging. We leveraged resting-state fMRI data from 1,000 healthy controls to generate lesion connectivity maps for each lesion. The FSL Permutation Analysis of Linear Models (PALM) tool was used to perform voxelwise one-sample t-tests that assessed the consistency of functional connectivity (FC) to synesthesia-associated lesions (family-wise error p < 0.05). Nodes and networks with significant associations were identified using the Harvard-Oxford structural atlases and Yeo-7 and Buckner-7 functional network parcellations, respectively.
Results:
We identified 27 patients with acquired synesthesia, demonstrating heterogeneous lesion location, however the left amygdala was present in 90% of subjects’ focal injuries. Lesions resulting in synesthesic symptoms displayed positive FC to the amygdala, but also to the hippocampus, putamen, and cerebellar Crus V - which is involved in the somatomotor network - and negative FC to the lateral occipital cortex - a node of the frontoparietal and dorsal attention networks.
Conclusions:
Positive connectivity with associative learning, multimodal integration, and the limbic system suggests that synesthesia may be due to increased cross-talk between sensory and memory systems and over-engagement of circuits that extract meaning from stimuli. In contrast, disruption to attention and control networks may result in decreased inhibitory top-down constraint of sensory interactions. As such, the overarching network identified here is consistent with a framework that synesthesia arises from lesions that both disrupt top-down inhibition and accentuate semantic cross-talk between sensory systems.
Disclaimer: Abstracts were not reviewed by Neurology® and do not reflect the views of Neurology® editors or staff.