Noninvasive Neuromodulation in Poststroke Gait Disorders

Abstract

Walking rehabilitation is one of the primary goals in stroke survivors because of its great potential for recovery and its functional relevance in daily living activities. Although 70% to 80% of people in the chronic poststroke phases are able to walk, impairment of gait often persists, involving speed, endurance, and stability. Walking involves several brain regions, such as the sensorimotor cortex, supplementary motor area, cerebellum, and brainstem, which are approachable by the application of noninvasive brain stimulation (NIBS). NIBS techniques, such as repetitive transcranial magnetic stimulation and transcranial direct current stimulation, have been reported to modulate neural activity beyond the period of stimulation, facilitating neuroplasticity. NIBS methods have been largely applied for improving paretic hand motor function and strokeassociated cognitive deficits. Recent studies suggest a possible effectiveness of these techniques also in the recovery of poststroke gait disturbance. This article is a selective review about functional investigations addressing the mechanisms of lower-limb motor system reorganization after stroke and the application of NIBS for neurorehabilitation.

The Promising Role of Neuromodulation in Improving Ischemic Stroke Recovery

“…Due to the many aspects of neuromodulation, different protocols have been created to either facilitate or inhibit neuronal activity. This can modify expression of neuronal proteins, such as neurotransmitters and neurotrophins, which then activate the long-term potentiation pathway [15]. Furthermore, cortical stimulation can influence contralateral and downstream pathways rather than being confined to monosynaptic connections, so high-frequency stimulation in the motor cortex can lead to decreased stretch reflexes in the leg of patients with multiple sclerosis, thereby decreasing spasticity [16].…”

“…This process uses different configured coilsto create an extracranial magnetic field that is powerful enough to influence neuronal activity in a pulse-like manner. The effect that these coils will have directly relates to the frequency of impulses, types of coils, their geometric orientation in relation to the brain, and the distance between the coils themselves and the brain [15]. One method that has been well documented is the use of low-frequency pulses, defined as less than one hertz, to reduce the excitability of neurons and higher frequencies, defined as more than 5 hertz, to increase excitability of neurons [15].…”

“…The effect that these coils will have directly relates to the frequency of impulses, types of coils, their geometric orientation in relation to the brain, and the distance between the coils themselves and the brain [15]. One method that has been well documented is the use of low-frequency pulses, defined as less than one hertz, to reduce the excitability of neurons and higher frequencies, defined as more than 5 hertz, to increase excitability of neurons [15]. Another common protocol uses brief bursts of low-intensity theta frequency stimuli in a continuous patter to decrease motor cortex excitability and high-frequencies to increase it [15].…”

“…One method that has been well documented is the use of low-frequency pulses, defined as less than one hertz, to reduce the excitability of neurons and higher frequencies, defined as more than 5 hertz, to increase excitability of neurons [15]. Another common protocol uses brief bursts of low-intensity theta frequency stimuli in a continuous patter to decrease motor cortex excitability and high-frequencies to increase it [15].…”

“…This physical current is presumed to cause neuronal membrane depolarization or hyperpolarization, depending on the orientation of the electrodes. tDCS has been shown to improve motor function in stroke patients, when coupled with motor training, due to cortical reorganization [4] via ipsilateral and peri-lesional cortex stimulation and modulation of interhemispheric inhibition [15]. It is thought that cathodal stimulation of the unaffected hemisphere will cause a suppression of activity locally, allowing for the transcallosal disinhibition of the affected hemisphere, thereby increasing neuroplastic response to repair itself [17].…”