# Differences in gait apraxia due to reduced regional cerebral blood flow in the supplementary motor area in corticobasal syndrome: a report of two cases

## TL;DR

Two cases of gait apraxia in corticobasal syndrome are linked to reduced blood flow in the supplementary motor area, suggesting this symptom can indicate early-stage disease.

## Contribution

Demonstrates SMA dysfunction via SPECT imaging as a cause of gait apraxia in CBS, offering insights into its pathogenesis.

## Key findings

- Gait apraxia in CBS is associated with SMA hypoperfusion detected via SPECT imaging.
- Distinct SMA regions correlate with specific gait patterns, such as freezing or exaggerated movements.
- Gait apraxia may precede limb apraxia and serve as an early CBS indicator.

## Abstract

Gait apraxia, characterized by difficulties initiating and coordinating walking despite preserved conceptual movement abilities, is a distinct entity from lower limb apraxia. Although gait apraxia has been associated with dysfunction of the frontal lobe, particularly the supplementary motor area (SMA), the specific associated somatotopic organization phenotype remains poorly understood. Corticobasal syndrome (CBS), a clinical phenotype of corticobasal degeneration, commonly presents with upper limb apraxia, while lower limb or gait apraxia has rarely been reported. Herein, we describe two rare cases of CBS presenting with gait apraxia shown to be caused by SMA dysfunction, based on regional cerebral blood flow (rCBF) reduction on single-photon emission computed tomography (SPECT).

Case 1 was of an 82-year-old man who exhibited right-sided apraxic gait with freezing and shuffling patterns, along with SMA hypoperfusion in both the dorsal and pre-SMA regions. Neurological examination revealed mild rigidity, right-sided Babinski sign, and clumsiness in mimicking leg movements. Gait patterns were inconsistent and unresponsive to levodopa treatment or sensory cues. Case 2 was of an 80-year-old man who demonstrated a peculiar gait characterized by exaggerated right leg movements and everted ankle positioning. Hypoperfusion was localized to the left dorsal SMA. Examination findings included rigidity and impaired hand weight perception. Sensory tricks and levodopa provided no benefit.

These cases highlight the role of SMA dysfunction in the pathogenesis of gait apraxia. Variations in rCBF reduction correlated with distinct gait patterns. For example, the freezing gait shown in Case 1 likely resulted from pre-SMA impairment, which is critical for movement initiation, while the exaggerated leg movements in Case 2 reflected dorsal SMA dysfunction, involved in motor execution. These results indicate that gait apraxia, which is often underdiagnosed, should be recognized as a potential early indicator of CBS. Further, these cases suggest that SMA dysfunction, identified through SPECT imaging, underlies the distinct gait patterns seen in CBS patients with apraxic gait. Recognizing these symptoms, even in the absence of weakness or limb apraxia, may aid in early CBS diagnosis and improve clinical management.

The online version contains supplementary material available at 10.1186/s12883-025-04332-z.