Objective: Our study aims to examine the state of praxis within the structure of motor impairments in patients with Parkinson’s disease (PD).

Background: PD is a multisystem progressive disorder characterized by alpha-synuclein accumulation and neurotransmitter imbalance, leading to motor and non-motor syndromes. Classical movement disorders (bradykinesia, rigidity, tremor) are caused by subcortical dysfunction; however, higher mental functions, including praxis, may also be affected in PD. According to studies (Leiguarda et al., 1997), apraxia in PD is not a direct consequence of motor disorders.

Method: The study included 37 patients diagnosed with PD according to the clinical criteria. Patients underwent a comprehensive neurological examination, including assessment using the UPDRS and MoCA scales. Assessment of apraxia included tests for kinesthetic, kinetic, spatial and regulatory apraxia.

Results: The mean age was 64.5±10.4 years. There were 9 men (24.3%) and 28 women (75.7%). The mean Hoehn and Yahr stage of PD was 3.25. The mean MoCA score was 22.6; UPDRS –

35,18; Pearson correlation coefficient: r = -0.455. Although none of the correlations achieved statistical significance, the Spearman rank correlation coefficient was higher for UPDRS –

apraxia (ρ = 0.261) than for MoCA – apraxia (ρ = -0.123). The  apraxia were recorded in the 37 patients with PD (a single patient could exhibit several types simultaneously in 29,73% of cases).Statistical analysis confirmed that the distribution of apraxia types significantly differs from a uniform distribution (p = 0.000224). Kinetic apraxia occurred significantly more often (37,84%). Motor impairments were predominantly right-sided, while apraxia was more often bilateral (p =0.000216).

Conclusion: Our study supports the view that the mechanisms underlying the development of apraxia differ from those underlying the development of motor symptoms of parkinsonism. The absence of the correlation between apraxia and the severity of rigidity, tremor, and bradykinesia, as well as its bilateral nature, confirm that apraxia is not a direct consequence of elementary motor disorders. These findings support the hypothesis of distinct pathogenetic mechanisms for motor deficits, cognitive decline and praxis impairments in PD.

References: 1. Leiguarda RC, Pramstaller PP, Merello M, Starkstein S, Lees AJ, Marsden CD. Apraxia in Parkinson’s disease, progressive supranuclear palsy, multiple system atrophy and neuroleptic-induced parkinsonism. Brain. 1997 Jan;120 (Pt 1):75-90. doi: 10.1093/brain/120.1.75. PMID: 9055799

2. Antonen EG, Kruchek MM, Bagdasaryan RT. Apraxia in Parkinson’s disease. Neurological bulletin. 2020; 52(5):12. doi: 10.26295/OS.2020.67.72.002

3. Vanbellingen T, Kersten B, Van Hemelrijk B, Van de Winckel A, Bertschi M, Müri R, De Weerdt W, Bohlhalter S. Comprehensive assessment of gesture production: a new test of upper limb apraxia (TULIA). Eur J Neurol. 2010 Jan;17(1):59-66. doi:10.1111/j.1468-1331.2009.02741.x. Epub 2009 Jul 9. PMID: 19614961

4. Stamenova V, Roy EA, Black SE. Limb apraxia in corticobasal syndrome. Cortex. 2011 Apr;47(4):460-72. doi: 10.1016/j.cortex.2010.04.010. Epub 2010 May 8. PMID: 20580354. PMCID: PMC4134687

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MDS Abstracts - https://www.mdsabstracts.org/abstract/the-spectrum-of-praxis-impairments-in-patients-with-parkinsons-disease/