Imaging gait disorders in parkinsonism: a review

Abstract

Gait difficultiesdincluding freezing of gaitdare frequent and disabling symptoms of advanced Parkinson's disease and other parkinsonian syndromes. They respond poorly to current medical and surgical treatments, making patient management very difficult. The underlying pathophysiology remains largely unknown. The late onset of levodopa resistance of Parkinson's disease gait abnormalities has been suggested to result from the progressive extension of the degenerative process to non-dopaminergic structures involved in locomotion, such as cortico-frontal and brainstem networks. Deficiencies in other neurotransmission systems, involving acetylcholine, serotonin or norepinephrine, have also been evoked. Neuroimaging tools appear well suited to decipher the cerebral substrates of parkinsonian gait disorders and their modulation by dopaminergic medication or deep brain stimulation. Here the main functional and metabolic neuroimaging studies aimed at identifying these cerebral networks are reviewed, in both healthy subjects and parkinsonian patients. After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. The most promising methods to examine gait difficulties and their response to currently available treatments are then discussed.

The role of prefrontal cortex during postural control in Parkinsonian syndromes a functional near-infrared spectroscopy study

“…Interestingly, in PD, decreased cholinergic innervations in the pedunculopontine nucleus and in the thalamus, but not in the cortical regions, affect postural control (Muller et al, 2013). The close connection between the pedunculopontine nucleus and the thalamus with the prefrontal cortex (Maillet et al, 2012) could contribute to the explanation of the increased oxygenation of the prefrontal cortex to maintain postural control in patients with PS. Neuropathological studies have reported that older adults with parkinsonian signs not due to PD have specific neuronal loss in the substantia nigra (Ross et al, 2004; Buchman et al, 2012), that projects via the striatum and the thalamus to the prefrontal cortex (Obeso et al, 2008; Krack et al, 2010).…”

Using Motor Imagery to Study the Neural Substrates of Dynamic Balance

“…Three different imagery perspectives are considered, including kinaesthetic imagery, our perspective of interest. In this imagery perspective, subjects are instructed to imagine themselves performing a given action from ‘within’, that is, trying to mentally perceive the associated sensations and muscle contractions [27]. This perspective recruits the neural networks involved in programming the actual actions.…”

Deep Brain Stimulation and L-DOPA Therapy: Concepts of Action and Clinical Applications in Parkinson's Disease

“…Irrespective of task (motor imagery of gait or stance), during the STN-DBS stimulation OFF condition the activity in sensorimotor cortex, SMA and cerebellum is increased, while during the stimulation ON condition, bilateral STN, precuneus, inferior parietal cortex and cerebellum are activated (92). During both STN-DBS conditions, imagery of gait increased the neural activity in SMA and superior parietal lobule (93). The improvement of imagined gait during the STN-DBS ON condition was linked to the increase in rCBF in the pedunculopontine nucleus/mesencephalic locomotor region without significant modulation of cortical and cerebellar locomotor areas (92).…”