# Gerstmann’s Syndrome and Limb Apraxia: A Single Case Study

## TL;DR

This case study explores Gerstmann’s syndrome and limb apraxia in a patient with a left hemisphere brain lesion, revealing consistent symptoms and specific brain regions involved.

## Contribution

The study provides new insights into the neural correlates of Gerstmann’s syndrome and limb apraxia through detailed clinical and neuroanatomical analysis.

## Key findings

- The patient consistently displayed the four core symptoms of Gerstmann’s syndrome over time.
- Limb apraxia persisted alongside Gerstmann’s syndrome symptoms.
- Neuroanatomical analysis identified damage in the left parietal cortex and disconnections in fronto-parietal networks.

## Abstract

Gerstmann’s syndrome (GS) represents a still debated clinical condition, in terms of both symptoms’ evolution and neural correlates. In depth, repeated neuropsychological assessments along with advanced methods of lesion analysis can contribute to a better understanding of the syndrome and clinical diagnosis.

The study reports a patient suffering from GS and limb apraxia following a left hemisphere lesion. Two in-depth assessments, at two and four months from the lesion onset, in addition to video material, document the symptoms over time. An in-depth analysis of the grey and white matter lesions was carried out with 3D reconstruction and a disconnection map.

The patient shows the characteristic tetrad of GS symptoms in both subacute and chronic phases, in the absence of other clinically relevant sensorimotor or cognitive deficits. Limb apraxia persists over time as well. The neuroanatomical investigation shows the involvement of cortical damage in the inferior parietal cortex that extends to the superior parietal cortex, anteriorly to the peri-rolandic area and medially to the precuneus. Furthermore, disconnections in the fronto-parietal networks and the corpus callosum were identified.

This single case study supports previous neuropsychological evidence and neuroanatomical findings on healthy participants, suggesting a core neural network underlying the four GS symptoms, which involves the left superior parietal lobe, the intraparietal cortices and the white matter parietal and fronto-parietal tracts. Furthermore, the involvement of the three branches of the superior longitudinal fasciculus explains the co-occurrence of limb apraxia.