Impulse control behavior in GBA-mutated parkinsonian patients

J Neurol Sci. 2021 Feb 15:421:117291. doi: 10.1016/j.jns.2020.117291. Epub 2020 Dec 21.

Abstract

Objective: To assess the prevalence and phenomenology of Impulse control behavior (ICB) in Parkinson's disease (PD) patients carrying mutations in the β-glucocerebrosidase (GBA) gene.

Background: GBA mutations are a common genetic factor predisposing to PD. ICB is among the most disabling non-motor complications of PD. The occurrence of ICB in PD patients carrying GBA gene mutations (GBA-PD) has not been yet established.

Methods: Forty-six patients with clinically definite PD (23 GBA-PD and 23 non-mutated patients, NM-PD) were screened for ICB. Diagnosis was clinically and rating based on a specific questionnaire (QUIP-RS). Other demographic and clinical variables did not differ between groups.

Results: ICB occurred more frequently in GBA-PD patients (52.2%) compared to NM-PD (13%) and the total QUIP-RS score was higher in the GBA-PD group. Hypersexuality and compulsive shopping were the most prevalent ICB types occurring in GBA patients. ICB occurred only in one GBA-PD patient on levodopa monotherapy and in 11 patients taking dopamine agonists, either monotherapy or combined with levodopa (the corresponding figures in NM-PD patients were 0 and 3). Most GBA-PD patients were heterozygous for two common genetic variants, without appreciable difference in their ICB profile.

Conclusion: ICB is more common in GBA-PD patients compared to NM-PD. Dopamine agonist therapy may be synergic to GBA carrier status for ICB occurrence.

Keywords: Dopamine agonists; Genotype-phenotype correlation; Glucocerebrosidase; Impulse control disorders; Parkinson's disease.

MeSH terms

  • Dopamine Agonists / therapeutic use
  • Glucosylceramidase* / genetics
  • Heterozygote
  • Humans
  • Levodopa
  • Mutation / genetics
  • Parkinson Disease* / drug therapy
  • Parkinson Disease* / epidemiology
  • Parkinson Disease* / genetics

Substances

  • Dopamine Agonists
  • Levodopa
  • Glucosylceramidase