Abnormal cutaneous flexor reflex activity during controlled isometric plantarflexion in human spinal cord injury spasticity syndrome

• Published in: Spinal cord 2016-09, Vol.54 (9), p.687-694
• Main Authors: Gómez-Soriano, J, Bravo-Esteban, E, Pérez-Rizo, E, Ávila-Martín, G, Galán-Arriero, I, Simón-Martinez, C, Taylor, J
• Format: Article
• Language: English
• Subjects: 692/1807; 692/617; Adult; Anatomy; Biomedical and Life Sciences; Biomedicine; Electromyography; Female; Human Physiology; Humans; Male; Middle Aged; Muscle Contraction - physiology; Muscle Spasticity - etiology; Muscle, Skeletal - physiopathology; Neurochemistry; Neuropsychology; Neurosciences; original-article; Reaction Time - physiology; Reflex, Abnormal - physiology; Skin - physiopathology; Spinal Cord Injuries - complications; Statistics, Nonparametric; Torque; Young Adult
• ISSN: 1362-4393; 1476-5624
• DOI: 10.1038/sc.2016.9

Study design: Although abnormal cutaneous reflex (CR) activity has been identified during gait after incomplete spinal cord injury (SCI), this activity has not been directly compared in subjects with and without the spasticity syndrome. Objectives: Characterisation of CR activity during controlled rest and ‘ramp and hold’ phases of controlled plantarflexion in subjects with and without the SCI spasticity syndrome. Design: Transverse descriptive study with non-parametric group analysis. Setting: SCI rehabilitation hospital. Methods: Tibialis Anterior (TA) reflexes were evoked by innocuous cutaneous plantar sole stimulation during rest and ramp and hold phases of plantarflexion torque in non-injured subjects ( n =10) and after SCI with ( n =9) and without ( n =10) hypertonia and/or involuntary spasm activity. Integrated TA reflex responses were analysed as total (50–300 ms) or short (50–200 ms) and long-latency (200–300 ms) activity. Results: Total and long-latency TA activity was inhibited in non-injured subjects and the SCI group without the spasticity syndrome during plantarflexion torque but not in the SCI spasticity group. Furthermore, loss of TA reflex inhibition during plantarflexion correlated with time after SCI (ρ=0.79, P =0.009). Moreover, TA reflex activity inversely correlated with maximum plantarflexion torque in the spasticity group (ρ=−0.75, P =0.02), despite similar non-reflex TA electromyographic activity during plantarflexion after SCI in subjects with (0.11, 0.08–0.13 mV) or without the spasticity syndrome (0.09, 0.07–0.12 mV). Conclusions: This reflex testing procedure supports previously published evidence for abnormal CR activity after SCI and may characterise the progressive disinhibition of TA reflex activity during controlled plantarflexion in subjects diagnosed with the spasticity syndrome.