RESUMEN
INTRODUCTION: Muscle weakness determines functional impairment in spastic cerebral palsy (SCP). Measurement of specific force (SF) allows for strength comparison with unimpaired populations (controls) accounting for neural (activation and coactivation), architectural (fascicle length and pennation angle), and structural differences (moment arm length). METHODS: Medial gastrocnemius (MG) SF (and its determinants) was assessed in both paretic and non-paretic legs of 11 men with SCP and 11 age-matched controls during plantarflexion maximal voluntary isometric contraction (MVIC). RESULTS: SCP fascicles were 28% longer than control fascicles (P < 0.05). Pennation angle of SCP patients was 41% smaller than in controls. The physiological cross-sectional area of SCP MG patients was 47% smaller than in controls (P < 0.05). There was no difference in SF between controls and SCP patients. CONCLUSIONS: Weakness in SCP is primarily attributable to deficits in agonist activation and muscle size; consequently, SF measured in the MG is similar between SCP and controls. Muscle Nerve 56: 298-306, 2017.
Asunto(s)
Parálisis Cerebral/complicaciones , Debilidad Muscular/etiología , Debilidad Muscular/patología , Músculo Esquelético/fisiopatología , Tendón Calcáneo/inervación , Tendón Calcáneo/fisiopatología , Adolescente , Adulto , Articulación del Tobillo , Estudios de Casos y Controles , Parálisis Cerebral/patología , Estimulación Eléctrica , Electromiografía , Humanos , Contracción Isométrica/fisiología , Masculino , Movimiento/fisiología , Rango del Movimiento Articular , Estadísticas no Paramétricas , Torque , Adulto JovenRESUMEN
INTRODUCTION: Muscle weakness is present in the paretic limbs of individuals with cerebral palsy (CP). We aimed to determine what neuromuscular factors contribute to weakness in adults with CP during isometric maximal voluntary contractions (iMVCs). METHODS: Gastrocnemius anatomical cross-sectional area (ACSA) and agonist and antagonist activation were measured in 11 CP and 11 control adult men during plantarflexion iMVC. RESULTS: Plantarflexion iMVC torque of the paretic leg was 42% and 52% less than in the non-paretic and control limbs, respectively. The paretic gastrocnemius ACSA was smaller than in the control group only. Paretic agonist activation was less than the non-paretic and control groups, whereas antagonist coactivation was higher. Multiple regression analysis revealed muscle activation accounted for 57% of variation in paretic plantarflexion iMVC torque. CONCLUSIONS: In individuals with CP, muscle weakness in the paretic limb is attributed primarily to impaired neural activation and, to a lesser degree, ACSA.