# Clinical and structural disconnectome evaluation in a case of optic aphasia

## TL;DR

This paper presents a case study of a patient with optic aphasia, linking her visual naming difficulties to brain damage and disconnection between brain hemispheres.

## Contribution

The study provides a detailed clinical and structural disconnectome analysis of optic aphasia through a single case with left occipital and splenial damage.

## Key findings

- The patient's behavioral data suggest semantic access from visual input is preserved.
- Structural disconnectome analysis revealed involvement of the splenium in the patient's condition.
- Findings support a visuo-verbal callosal disconnection model for optic aphasia.

## Abstract

Optic Aphasia (OA) and Associative Visual Agnosia (AVA) are neuropsychological disorders characterized by impaired naming on visual presentation. From a cognitive point of view, while stimulus identification is largely unimpaired in OA (where access to semantic knowledge is still possible), in AVA it is not. OA has been linked with right hemianopia and disconnection of the occipital right-hemisphere (RH) visual processing from the left hemisphere (LH) language areas.

In this paper, we describe the case of AA, an 81-year-old housewife suffering from a deficit in naming visually presented stimuli after left occipital lesion and damage to the interhemispheric splenial pathway. AA has been tested through a set of tasks assessing different levels of visual object processing. We discuss behavioral performance as well as the pattern of lesion and disconnection in relation to a neurocognitive model adapted from Luzzatti and colleagues (1998). Despite the complexity of the neuropsychological picture, behavioral data suggest that semantic access from visual input is possible, while a lesion-based structural disconnectome investigation demonstrated the splenial involvement.

Altogether, neuropsychological and neuroanatomical findings support the assumption of visuo-verbal callosal disconnection compatible with a diagnosis of OA.

The online version contains supplementary material available at 10.1007/s00429-024-02818-z.