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a Robert Steiner MRI Unit, Imperial College School of
Medicine, Hammersmith Hospital, London, UK, b Division of Neuroscience and
Psychological Medicine, Imperial College School of Medicine, Charing
Cross Hospital, London, UK, c National Spinal Injuries
Centre, Stoke Mandeville Hospital, Aylesbury, Buckinghamshire, UK
Correspondence to: 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 and in revised form 10 February 1998;
Accepted 20 April 1998
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 of
N-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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