Median nerve injuries in adults, repaired with nerve suture, lead to incomplete functional
recovery despite improved surgical technique. This results in a reduction in quality of life,
poorer working ability and a considerable expense for society. Misrouting of axons at the
suture site connects regenerating axons to the wrong distal end organs. When distorted
signals are conveyed to the dorsal root ganglia, spinal cord, thalamus and the somatosensory
cortex, somatotopic maps at all levels become reorganised in a disorderly fashion. Children
often regain full sensory function after median nerve injury and repair despite impaired
conduction across the injured segment. There is growing evidence that cortical plasticity is
the main mechanism behind the superior recovery seen in young patients, but the exact
pattern of reorganisation and its impact on functional recovery are not fully understood.
The general aim of this thesis was to investigate various aspects of cortical plasticity, in
particular the response to median nerve injury. To this end we used two non-invasive brain
imaging techniques, functional magnetic resonance imaging (fMRI) and
magnetoencephalography (MEG). In Paper I we investigated the concept of audio-tactile
interaction in a healthy population. We found an increased overlap between cortical
activation areas (fMRI) in patients trained with coupled tactile and auditory stimuli indicating
modulation of cortical plasticity induced by cross-modal training. In Paper II we studied ageand time-dependent effects on cortical activity patterns in patients with median nerve injury
by correlating age at the time of injury and time passed since injury to sensory function, and
cortical activation. We found a time-dependent decline in the size of the cortical activation
area during stimulation of both the median and the ulnar nerve (fMRI). Furthermore, there
was greater ipsilateral activation in the patient group than in a control group from a previous
study. However, the results were not conclusive on this point because the stimulation
paradigms differed between the two studies (event-related in the present and block paradigm
in the previous study). Paper III was performed using MEG in order to further study cortical
plasticity in patients with median nerve injury. We found decreased N1 and P1 amplitudes
during stimulation of the injured median nerve, and an increase in these amplitudes during
ulnar nerve stimulation. Paper IV was designed to reveal any possible differences in
lateralisation of cortical activation after median nerve injury and to see if this was influenced
by the stimulus paradigm used. By means of a laterality index (LI) the extent of contra- and
ipsilateral activation was calculated. LI is decreased (more ipsilateral activation) in patients
with a median nerve injury compared to controls. This means that median nerve injury causes
a shift of activity from the contralateral to the ipsilateral SI. The type of stimulus paradigm
(event-related or block) did not affect LI. Our findings add to the evolving knowledge of the
cortical plasticity following median nerve injury
