Locomotor deficits and adaptive mechanisms after thoracic spinal cord contusion in the adult rat.
The rat is widely used for modeling human spinal cord injury (SCI) and paraplegia. However, quadruped animals adapt trunk, forelimb and hindlimb movements to compensate for deficits, improving their behavioral scores and complicating the interpretation of spontaneous and treatment-induced function recovery. The kinematics of locomotion was studied in rats, both normal and after SCI (T9 contusion), and variables indicative of hindlimb function were related to brain-spinal cord connections (BSCC) spared during lesioning. Normal animals showed forward velocities characteristic of fast walking. The hind paw was placed approximately three centimeters in front of the hip at the initial contact. Hip height decreased during the first third of hindlimb stance and increased later. Mild and moderate spinal cord contusions destroyed the gray matter and adjacent axons but spared the ventrolateral tracts to various degrees. Injured animals placed the hindpaw in a more caudal position than normal and showed reduced forward velocity and hip height. Knee extension was also impaired, and both hindlimb and forelimb steps were adapted to compensate for the deficits. BSCC was estimated by averaging the transverse area of white matter at the lesion epicenter and the percentage of brain neurons labeled after peroxidase injection into L2 and L3. Recovery of hindlimb motor function was proportional to the amount of BSCC. On average, injured animals retained 18% of BSSC and recovered 23% of hindlimb function. These findings show that kinematic analysis is a reliable tool for assessing locomotor deficits and compensations and suggest limited spontaneous motor plasticity after SCI.
Collazos-Castro
Jorge E
JE
Laboratorio de Reparación Neural, Hospital Nacional de Parapléjicos, SESCAM, Toledo, Spain. jcollazos@sescam.org
López-Dolado
Elisa
E
Nieto-Sampedro
Manuel
M
D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D001370:Axonal Transport; D001696:Biomechanical Phenomena; D003714:Denervation; D004185:Disability Evaluation; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D005552:Forelimb / Q000294:innervation / Q000503:physiopathology; D020233:Gait Disorders, Neurologic / Q000175:diagnosis / Q000503:physiopathology*; D006614:Hindlimb / Q000294:innervation / Q000503:physiopathology; D006735:Horseradish Peroxidase; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology*; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000175:diagnosis / Q000503:physiopathology*; D013904:Thoracic Vertebrae
D006735:Horseradish Peroxidase