A clinico-anatomical dissection of the magnocellular and parvocellular pathways in a patient with the Riddoch syndrome

TL;DR

A patient with Riddoch syndrome shows selective visual deficits and hallucinations due to damage to specific visual pathways, not the primary visual cortex.

Contribution

Demonstrates that Riddoch syndrome can result from damage to optic radiations, not just V1, and highlights differential vulnerability of magnocellular and parvocellular pathways.

Findings

Patient YL showed Riddoch syndrome symptoms despite intact V1, indicating optic radiation damage.

High-resolution fMRI revealed strong magnocellular but weak parvocellular responses in V1.

Patient reported visual hallucinations of moving stimuli, suggesting functional parvocellular pathway disruption.

Abstract

The Riddoch syndrome is thought to be caused by damage to the primary visual cortex (V1), usually following a vascular event. This study shows that damage to the anatomical input to V1, i.e., the optic radiations, can result in selective visual deficits that mimic the Riddoch syndrome. The results also highlight the differential susceptibility of the magnocellular and parvocellular visual systems to injury. Overall, this study offers new insights that will improve our understanding of the impact of brain injury and neurosurgery on the visual pathways.

The Riddoch syndrome, characterised by the ability to perceive, consciously, moving visual stimuli but not static ones, has been associated with lesions of primary visual cortex (V1). We present here the case of patient YL who, after a tumour resection surgery that spared his V1, nevertheless showed symptoms of the Riddoch syndrome. Based on our testing, we postulated that the magnocellular (M) and parvocellular (P) inputs to his V1 may be differentially affected. In a first experiment, YL was presented with static and moving checkerboards in his blind field while undergoing multimodal magnetic resonance imaging (MRI), including structural, functional, and diffusion, acquired at 3 T. In a second experiment, we assessed YL’s neural responses to M and P visual stimuli using psychophysics and high-resolution fMRI acquired at 7 T. YL’s optic radiations were partially damaged but not severed. We found extensive activity in his visual cortex for moving, but not static, visual stimuli, while our psychophysical tests revealed that only low-spatial frequency moving checkerboards were perceived. High-resolution fMRI revealed strong responses in YL's V1 to M stimuli and very weak ones to P stimuli, indicating a functional P lesion affecting V1. In addition, YL frequently reported seeing moving stimuli and discriminating their direction of motion in the absence of visual stimulation, suggesting that he was experiencing visual hallucinations. Overall, this study highlights the possibility of a selective loss of P inputs to V1 resulting in the Riddoch syndrome and in hallucinations of visual motion.

The online version contains supplementary material available at 10.1007/s00429-024-02774-8.

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