Background <p>Freezing of gait (FOG) is a symptom that occurs in Parkinson’s disease (PD) and various other gait disorders. Primary progressive freezing of gait (PPFG) disorder is a rare clinical syndrome in which FOG persists for at least three years without any other clinical symptoms. We report a patient with long-lasting isolated FOG accompanied by marked parietal cortical atrophy to explore its potential pathophysiological significance.</p> Case presentation <p>A 55-year-old man presented with a one-year history of FOG and recurrent unprovoked falls. Neurological examinations revealed FOG without signs of parkinsonism. While dopamine transporter (DAT) imaging showed normal uptake, brain magnetic resonance imaging (MRI) demonstrated marked bilateral parietal lobe atrophy without brainstem atrophy. Five years later, FOG persisted with mild parkinsonism, consistent with the diagnosis of PPFG. Follow-up MRI and DAT imaging revealed no interval changes. Single-case voxel-based morphometry demonstrated reduced volume in the right superior parietal lobe and left superior occipital gyrus, and neuropsychological testing indicated preserved cognition across all domains.</p> Conclusion <p>This case illustrates a rare presentation of long-standing isolated FOG associated with localized parietal cortical atrophy. These findings suggest that involvement of the parietal cortex may contribute to the pathophysiology of FOG.</p>

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A notable case of primary progressive freezing of gait associated with parietal cortical atrophy

  • Su Hyeon Ha,
  • Dallah Yoo,
  • Il Ki Hong,
  • Hyug-Gi Kim,
  • Kyung Mi Lee,
  • Tae-Beom Ahn

摘要

Background

Freezing of gait (FOG) is a symptom that occurs in Parkinson’s disease (PD) and various other gait disorders. Primary progressive freezing of gait (PPFG) disorder is a rare clinical syndrome in which FOG persists for at least three years without any other clinical symptoms. We report a patient with long-lasting isolated FOG accompanied by marked parietal cortical atrophy to explore its potential pathophysiological significance.

Case presentation

A 55-year-old man presented with a one-year history of FOG and recurrent unprovoked falls. Neurological examinations revealed FOG without signs of parkinsonism. While dopamine transporter (DAT) imaging showed normal uptake, brain magnetic resonance imaging (MRI) demonstrated marked bilateral parietal lobe atrophy without brainstem atrophy. Five years later, FOG persisted with mild parkinsonism, consistent with the diagnosis of PPFG. Follow-up MRI and DAT imaging revealed no interval changes. Single-case voxel-based morphometry demonstrated reduced volume in the right superior parietal lobe and left superior occipital gyrus, and neuropsychological testing indicated preserved cognition across all domains.

Conclusion

This case illustrates a rare presentation of long-standing isolated FOG associated with localized parietal cortical atrophy. These findings suggest that involvement of the parietal cortex may contribute to the pathophysiology of FOG.