Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2019
Excessive short-latency stretch reflexes in the calf muscles do not cause postural instability in patients with hereditary spastic paraplegia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
van Lith B J H, de Niet M, van de Warrenburg B P C, Geurts A C, Weerdesteyn V
Аннотация
OBJECTIVE: To identify the role of hyperexcitable short-latency stretch reflexes (SLRs) on balance control in people with hereditary spastic paraplegia (PwHSP).
METHODS: Sixteen PwHSP with triceps surae spasticity and 9 healthy control subjects were subjected to toes-up support-surface perturbations. EMG data were recorded from gastrocnemius, soleus and tibialis anterior. Furthermore, center-of-mass trajectories were recorded.
RESULTS: PwHSP were less able to withstand the perturbations. Triceps surae SLRs (40-80 ms post perturbation) in PwHSP were increased compared to healthy subjects. Furthermore, a sustained triceps surae EMG activity at 220-320 ms post perturbation was observed in PwHSP, whereas control subjects demonstrated suppression of triceps surae activity. Center of mass trajectories started to diverge between PwHSP and controls only after ∼500 ms, with greater excursions being observed in the PwHSP.
CONCLUSIONS: The present results confirm that balance control is impaired in PwHSP. However, the late instant of center of mass divergence argues against a direct, causative role of hyperexcitable SLRs in the triceps surae.
SIGNIFICANCE: We postulate that enhanced short-latency stretch reflexes of the triceps surae do not underlie poor balance control in PwHSP. Instead, we suggest the lack of suppression of later triceps surae activity to be the main cause.
METHODS: Sixteen PwHSP with triceps surae spasticity and 9 healthy control subjects were subjected to toes-up support-surface perturbations. EMG data were recorded from gastrocnemius, soleus and tibialis anterior. Furthermore, center-of-mass trajectories were recorded.
RESULTS: PwHSP were less able to withstand the perturbations. Triceps surae SLRs (40-80 ms post perturbation) in PwHSP were increased compared to healthy subjects. Furthermore, a sustained triceps surae EMG activity at 220-320 ms post perturbation was observed in PwHSP, whereas control subjects demonstrated suppression of triceps surae activity. Center of mass trajectories started to diverge between PwHSP and controls only after ∼500 ms, with greater excursions being observed in the PwHSP.
CONCLUSIONS: The present results confirm that balance control is impaired in PwHSP. However, the late instant of center of mass divergence argues against a direct, causative role of hyperexcitable SLRs in the triceps surae.
SIGNIFICANCE: We postulate that enhanced short-latency stretch reflexes of the triceps surae do not underlie poor balance control in PwHSP. Instead, we suggest the lack of suppression of later triceps surae activity to be the main cause.