Impairments in gait kinematics and postural control may not correlate with dopamine transporter depletion in individuals with mild to moderate Parkinson's disease

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by the loss of dopamine, an important neurotransmitter involved in regulating movement. Nuclear medicine imaging methods such as single‐photon emission computed tomography (SPECT) combined with radiotracers can obtain the density of this neurotransmitter. This reduced density leads to classic PD symptoms, such as bradykinesia, tremor and stiffness, consequently affecting walking and postural control. The aim of this study was to verify the correlation between disorders of gait kinematics and postural instability with dopamine depletion in individuals with mild to moderate PD. This is a descriptive, observational cross‐sectional study. Subjects were assessed for spatiotemporal gait parameters by a three‐dimensional motion capture system, for postural control by stabilometry on a force plate. Dopamine depletion was verified through 99mTc‐TRODAT‐1 (SPECT‐CT) examination. The subjects were in the off‐stage of levodopa in all analysis. We evaluated 71 individuals, 32 with mild to moderate PD (HY 2 and 2.5) and 39 healthy individuals matched for gender, age, and height. There was a significant difference between the groups regarding the spatiotemporal variables of gait, as well as in the stabilometric variables. However, there was no correlation between these disturbances and the uptake values of 99mTc‐TRODAT‐1. The results indicate that there is no correlation between gait impairments and postural instability of individuals with mild to moderate PD and the dopaminergic depletion measured through the 99mTc‐TRODAT‐1 (SPECT‐CT).

The relationship between cognitive decline and motor dysfunction in Parkinson’s disease: A focused mini‐review on cognitive‐locomotor dual‐task interference

“…Unlike bradykinesia and rigidity, truncal dysfunction has been shown not to correlate with dopaminergic loss. 52 reported that the PPN oscillation was altered by a postural/locomotor situation during "ON" state. However, these dynamic state-dependent neural oscillatory changes were diminished during "OFF" state.…”

“…Unlike bradykinesia and rigidity, truncal dysfunction has been shown not to correlate with dopaminergic loss 52 . These findings suggest that lesions of non‐dopaminergic neurons, such as cholinergic neurons in the pedunculopontine nucleus (PPN), 53 may also play an important role in gait and postural impairment in PD.…”

“…Unlike bradykinesia and rigidity, truncal dysfunction has been shown not to correlate with dopaminergic loss. 52 These findings suggest that lesions of non-dopaminergic neurons, such as cholinergic neurons in the pedunculopontine nucleus (PPN), 53 may also play an important role in gait and postural impairment in PD. Aside from the basal ganglia networks, it has been suggested that impaired functional and anatomical connections between the PPN and the cerebral cortex are associated with motor-cognitive interaction.…”

Dual-task walking reduces lower limb range of motion in individuals with Parkinson’s disease and freezing of gait: But does it happen during what events through the gait cycle?

“…Reductions in step length could be accompanied by a decrease in lower limb range of motion (RoM) [14,15]. A previous study evaluated lower limb RoM (sagittal plane) in people with PD without FOG and control individuals during a single gait [16]. Individuals with PD showed a reduced RoM of hips, knees, and ankles when compared to healthy controls [16].…”

“…A previous study evaluated lower limb RoM (sagittal plane) in people with PD without FOG and control individuals during a single gait [16]. Individuals with PD showed a reduced RoM of hips, knees, and ankles when compared to healthy controls [16]. However, the correlation between spatiotemporal parameters and lower limb RoM and the effects of dual-task gait on lower limb RoM in people with FOG were not investigated yet.…”