Dizziness and vertigo are common symptoms in patients visiting neurology clinics and emergency departments, with its incidence increasing with age. Stroke is the most common cause of central dizziness/vertigo, accounting for 3%-5% of acute dizziness/vertigo cases[12]. Unlike peripheral dizziness/vertigo, central dizziness/vertigo is prone to misdiagnosis and carries a higher risk of mortality and poorer prognosis. Damage to central vestibular (such as the vestibular nuclei, cerebellar flocculus, cerebellar nodulus, vestibular thalamus, and insula) or vestibular-related pathways (vestibulo-cortical, vestibulo-spinal, and vestibulo-cerebellar pathways) can lead to vestibular-related symptoms such as dizziness/vertigo, diplopia, oscillopsia, and balance and gait abnormalities, accounting for approximately 30%-60% of posterior circulation strokes[12–13]. Clinically, these patients may not exhibit obvious limb paralysis, but even after dizziness/vertigo symptoms improve, they may still be unable to stand and walk normally, displaying head and eye posture deviations, unstable gait, spatial orientation disorders, and a high risk of falls[4]. This study aims to explore the differences in spatiotemporal gait parameters in stroke patients with vestibular symptoms under different walking speeds, to identify their movement patterns and provide more precise rehabilitation strategies.
The vestibular system perceives body position and external stimuli through peripheral receptors, transmitting vestibular signals to the vestibular centers, and adjusting head and eye movements and body posture to achieve clear and stable vision, postural stability, and accurate spatial orientation[14]. The damaged central vestibular structures in the brainstem, including the dorsal medulla, pontine tegmentum, and midbrain tectum, lead to abnormal utilization and integration of vestibular information in the central nervous system, resulting in dizziness/vertigo, blurred vision, postural instability, and gait abnormalities[12–13]. Walking is a primary form of movement in daily life, and gait is a behavioral characteristic of human walking, serving as an important indicator of motor recovery in stroke patients. Gait analysis objectively describes walking patterns using gait analysis equipment to analyze biomechanical and kinematic features by capturing precise walking characteristics, facilitating more accurate assessments and personalized rehabilitation. Hemiplegic patients typically exhibit gait characteristics such as reduced walking speed, shortened stride length and frequency, increased step width, and altered stance and swing phases. To maintain postural stability, hemiplegic patients often reduce the time spent on the affected limb during the stance phase and prolong the swing phase[15–16]. Studies have shown that bilateral vestibular patients display increased gait variability, shortened stride length and width, prolonged double support phase during walking, and increased trunk sway angle[17]. Our previous study indicated that stroke patients with vestibular symptoms in the posterior circulation exhibit reduced walking speed, shortened stride length and frequency, prolonged double support phase, and increased trunk sway angles in the sagittal and coronal planes compared to normal controls [4]. Thus, stroke patients with vestibular symptoms exhibit a different gait pattern from typical hemiplegic patients.
Vestibular control of balance during walking shows stage-dependent regulation, depending on when the lower limbs contact the ground and the role of muscles in balance control. Specifically, the response of lower limb muscles to vestibular stimulation primarily occurs during the stance phase of the same limb[18–20]. Study confirmed that the medial gastrocnemius muscle, as the primary power source for the foot during normal walking, is sensitive to vestibular input in the late stance phase. The gluteus medius muscle contributes to foot placement strategies, with its activity related to the foot placement of next step and being sensitive to vestibular errors before heel strike[21]. Coherence studies between electromyography (EMG) signals and vestibular electrical stimulation also found that the peak coherence between vestibular electrical stimulation and EMG appears during the double support phase of the gait cycle[21–22]. Therefore, all muscles involved in balance control during movement are coupled with vestibular stimulation at specific periods of the gait cycle, but the maximum net response to vestibular stimulation occurs during the stance phase. Piccolo et al. found that active stepping and accurate foot placement during the terminal double support phase of the gait cycle requires the vestibular system. The brain needs to integrate, and process received vestibular information during the terminal double support phase to determine whether the body has undergone the correct displacement, ensuring a stable walking posture[23]. Therefore, the vestibular system plays a crucial role during the stance phase of the gait cycle. The patient's double support phase increases when vestibular information is impaired.
This study found that, compared to the control, stroke patients with vestibular symptoms had an extended proportion of double support phase under fast walking conditions, while other gait parameters:walking speed, stride length, terminal double support phase, and stride time showed no significant differences. Under slow and normal walking conditions, stroke patients with vestibular symptoms exhibited slower self-selected walking speeds, shorter stride lengths, and longer double support phases, consistent with our previous findings. These results suggest that stroke patients with vestibular symptoms achieve a gait pattern similar to the control group under fast walking conditions by extending the double support phase. However, under normal and slow walking conditions, they enhance walking stability by extending the double support phase, reducing walking speed, and shortening stride length.
Vestibular control of balance during movement decreases with increasing movement speed (from posture to walking to running). The central nervous system inhibits vestibular signals in a speed-dependent manner, supporting spinal mechanisms expressed through muscle synergy to control movement behavior[19, 22]. Research confirms that fast movement behavior is a highly automated process based on spinal locomotor generators, controlled by supraspinal structures that inhibit unstable vestibular inputs. This vestibular inhibition prevents irregular head movements from interfering with the activities of spinal and supraspinal networks controlling fast movement behavior. Compared to fast movement behavior, posture and slow walking rely more on vestibular inputs[24]. Brandt et al. found that patients with unilateral vestibular neuritis tend to deviate to the affected side when walking with their eyes closed, but do not deviate when running[7, 25]. Jahn et al. found that vestibular-evoked compensatory whole-body sway responses during running were reduced compared to walking[26]. Dakin et al. showed that vestibular-muscle coupling reduces with increased walking speed especially during the stance phase of the gait cycle, but appears unaffected during the swing phase[19]. Therefore, vestibular input is differentially regulated based on the walking speed and pattern used. For hemiplegic stroke patients, a common strategy to avoid imbalance and falls is to reduce speed to enhance postural stability. However, studies on the gait of sensory-impaired patients found that these patients (with visual, proprioceptive, and vestibular impairments) typically show greater spatiotemporal gait variability under slow walking conditions and relatively less variability under fast walking conditions. This is because balance and postural regulation during fast walking depend less on sensory system feedback control[27–29]. Thus, postural control of gait during slow walking primarily relies on sensory system feedback. The above studies explain why stroke patients with vestibular symptoms achieve a gait pattern similar to the control group under fast walking conditions, as vestibular input is suppressed, therefore masking the impairment of vestibular information. However, under slow and normal walking conditions, more vestibular feedback is required, and the impaired vestibular information in patients cannot meet walking demands. Consequently, patients extend the support phase time and slow down to increase stability and prevent falls.
Study limitations
This study has several limitations: (1) The sample size is small and not continuously enrolled, possibly introducing selection bias; (2) This study only analyzed temporal and spatial parameters, while kinematic parameters (joint angles, pelvic movement), kinetic parameters (ground reaction forces, moments), and EMG parameters could also provide further information to help analyze patients' gait characteristics; (3) The severity of vestibular function impairment in patients was not graded in detail. Future studies will expand the sample size, include multicenter studies, analyze more comprehensive gait parameters, objectively evaluate vestibular function impairment severity, and explore the correlation between vestibular function and gait parameters to provide objective theoretical support for precise rehabilitation treatment.