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J Neurol Neurosurg Psychiatry 1998;65:748-754 doi:10.1136/jnnp.65.5.748
  • Paper

The human motor cortex after incomplete spinal cord injury: an investigation using proton magnetic resonance spectroscopy

  1. B K Puria,
  2. H C Smithb,
  3. I J Coxa,
  4. J Sargentonia,
  5. G Savicc,
  6. D W Maskillb,
  7. H L Frankelc,
  8. P H Ellawayb,
  9. N J Daveyb
  1. aRobert Steiner MRI Unit, Imperial College School of Medicine, Hammersmith Hospital, London, UK, bDivision of Neuroscience and Psychological Medicine, Imperial College School of Medicine, Charing Cross Hospital, London, UK, cNational Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Buckinghamshire, UK
  1. Dr NJ Davey, Department of Sensorimotor Systems, Division of Neuroscience and Psychological Medicine, Imperial College School of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF. Telephone 0044 181 846 7284; fax 0044 181 846 7338; email n.davey{at}ic.ac.uk
  • Received 16 October 1997
  • Revised 10 February 1998
  • Accepted 20 April 1998

Abstract

OBJECTIVES (1) A biochemical investigation of the motor cortex in patients with incomplete spinal cord injury and normal control subjects using proton magnetic resonance spectroscopy (MRS). (2) To relate any altered biochemistry with the physiological changes in corticospinal function seen after spinal cord injury.

METHODS a group of six patients with incomplete spinal cord injury who showed good recovery of motor function were selected. The patients were compared with five healthy control subjects. Electromyographic (EMG) responses of thenar muscles to transcranial magnetic stimulation (TMS) of the motor cortex showed that inhibition of cortical output was weaker in the patients than the controls. Proton MRS data were collected from a plane at the level of the centrum semiovale. Two 4.5 cm3 voxels in the motor cortex and a third voxel in the ipsilateral occipital cortex were examined in the patients and control subjects.

RESULTS The mean level ofN-acetylaspartate (NAA), expressed relative to the creatine (Cr) peak (NAA/Cr), was significantly increased in the motor cortex of the patients compared with their ipsilateral occipital cortex or either cortical area in the controls. No differences between patients and controls were seen for any of the other metabolite peaks (choline (Cho), glutamate/glutamine (Glx) or the aspartate component of NAA (AspNAA)) relative to Cr. Choline relative to Cr (Cho/Cr) was higher in the motor cortex of the control subjects than in their ipsilateral occipital cortex. This difference was not present in the patients.

CONCLUSIONS Raised NAA/Cr in the motor cortex of the patients probably results from increased NAA rather than a decrease in the more stable Cr. The possible relevance of a raised NAA/Cr ratio is discussed, particularly with regard to the changed corticospinal physiology and the functional recovery seen in the patients.

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