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Numb rats walk – a behavioural and fMRI comparison of mild and moderate spinal cord injury

Authors

  • Christoph P. Hofstetter,

    1. Department of Neuroscience Karolinska Institutet, Retziusv. 8, B2:4, 17172 Solna, Stockholm, Sweden
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    • *

      C.P.H. and P.S. contributed equally to this work.

  • Petra Schweinhardt,

    1. Department of Neuroscience Karolinska Institutet, Retziusv. 8, B2:4, 17172 Solna, Stockholm, Sweden
    2. Department of Human Anatomy and Genetics, Oxford University, UK
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    • *

      C.P.H. and P.S. contributed equally to this work.

  • Tomas Klason,

    1. Department of Neuroscience Karolinska Institutet, Retziusv. 8, B2:4, 17172 Solna, Stockholm, Sweden
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  • Lars Olson,

    1. Department of Neuroscience Karolinska Institutet, Retziusv. 8, B2:4, 17172 Solna, Stockholm, Sweden
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  • Christian Spenger

    1. Department of Neuroscience Karolinska Institutet, Retziusv. 8, B2:4, 17172 Solna, Stockholm, Sweden
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: Dr Christoph Hofstetter, as above.
E-mail: Christoph.Hofstetter@neuro.ki.se

Abstract

Assessment of sensory function serves as a sensitive measure for predicting the functional outcome following spinal cord injury in patients. However, little is known about loss and recovery of sensory function in rodent spinal cord injury models as most tests of sensory functions rely on behaviour and thus motor function. We used functional magnetic resonance imaging (fMRI) to investigate cortical and thalamic BOLD-signal changes in response to limb stimulation following mild or moderate thoracic spinal cord weight drop injury in Sprague–Dawley rats. While there was recovery of close to normal hindlimb motor function as determined by open field locomotor testing following both degrees of injury, recovery of hindlimb sensory function as determined by fMRI and hotplate testing was only seen following mild injury and not following moderate injury. Thus, moderate injury can lead to near normal hindlimb motor function in animals with major sensory deficits. Recovered fMRI signals following mild injury had a partly altered cortical distribution engaging also ipsilateral somatosensory cortex and the cingulate gyrus. Importantly, thoracic spinal cord injury also affected sensory representation of the upper nonaffected limbs. Thus, cortical and thalamic activation in response to forelimb stimulation was significantly increased 16 weeks after spinal cord injury compared to control animals. We conclude that both forelimb and hindlimb cortical sensory representation is altered following thoracic spinal cord injury. Furthermore tests of sensory function that are independent of motor behaviour are needed in rodent spinal cord injury research.

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