ABNORMAL ACCESS OF AXIAL VIBROTACTILE INPUT TO DEAFFERENTED SOMATOSENSORY
CORTEX IN HUMAN UPPER LIMB AMPUTEES.
John JM Kew; Peter W Halligan; John C Marshall; Richard E Passingham; John C
Rothwell; Michael C Ridding; C David Marsden and David J Brooks.
MRC Cyclotron Unit, Hammersmith Hospital, London, UK, MRC Human Movement
and Balance Unit, Institute of Neurology, London, UK Neuropsychology Unit,
Radcliffe Infirmary, and Rivermead Rehabilitation, Centre, Oxford, UK,
Department of Experimental Psychology, University of Oxford, Oxford, UK.
APStracts 4:0043N, 1997.
ABSTRACT
1. Two human subjects with total deafferentation of one upper limb secondary
to traumatic multiple cervical root avulsions were studied. Both subjects
developed a supernumerary phantom limb in the early post-injury period, and
both subsequently underwent elective, above elbow amputation of the flail,
anaesthetic limb. 2. In each subject psychophysical study revealed an area of
skin in the anterior pectoral region ipsilateral to the amputation, vibratory
or tactile stimulation of which elicited referred sensations (RS) in the
phantom limb. This ectopic representation of the phantom limb was similarly
responsive to vibrotactile stimulation (VS) and pressure stimulation (PS). 3.
The cortical correlates of these referred phantom sensations were explored
using positron emission tomographic (PET) measurements of regional cerebral
blood flow (rCBF) during VS of the ectopic phantom representation ipsilateral
to the amputation. For comparison, rCBF measurements were also made during VS
of an homologous part of the pectoral region ipsilateral to the intact arm,
stimulation of which was not associated with referred phantom sensations. A
voxel-based correlation analysis was subsequently used to study the functional
connectivity of activated cortical regions. 4. VS of both pectoral regions was
consistently associated with significant activation of the contralateral
second somatic sensory (SII) cortex. Additional ipsilateral SII activation was
present during VS of both pectoral regions in one of the subjects, and during
VS of the pectoral region adjacent to the amputation in the other. In the
former subject contralateral thalamic activation was present during VS of both
pectoral regions. 5. VS of the pectoral region adjacent to the intact arm was
associated with significant activation of the dorsal part of the contralateral
primary somatosensory (S1) cortex in a position consistent with the S1 trunk
area. In contrast, VS of the ectopic phantom representation in the pectoral
region ipsilateral to the amputation was associated with activation of the
contralateral S1 cortex which extended from the level of the trunk
representation ventrally over distances of 20 mm and 12 mm in the two subjects
respectively. 6. The area of S1 cortex significantly activated during VS of
the digits in a normal control subject was coextensive with the ventral S1
region abnormally activated during VS of the ectopic phantom representation in
the two amputees. This finding suggests that in the amputees the deafferented
digit or hand/arm area can be activated by sensory input from the pectoral
region. 7. Correlation analysis showed an abnormal pattern of intrinsic
connectivity within the deafferented S1 hand/arm area of both amputees. In one
subject the deafferented S1 was functionally connected with three times as
many S1 voxels as the normally afferented S1. This abnormal functional
connectivity extended in both the rostro-caudal and ventro-dorsal dimensions.
8. The results demonstrate that sensory input delivered to the axial body
surface may gain access to the S1 hand/arm area in some humans who have
suffered extensive deafferentation of this area. They also provide evidence
that somatotopic reorganization of S1 may, in part, be related to changes in
intracortical connectivity. The findings are consistent with the hypothesis
that deafferentation of an area of S1 cortex may result in susceptibility of
this area to previously dormant inputs from body surfaces represented in
immediate adjacent parts of S1. Alterations in functional connectivity between
these adjacent areas of cortex, mediated via deafferentation-induced changes
in intracortical GABAergic inhibition, provide a plausible explanation for
such plasticity.
Received 6 March 1996; accepted in final form 9 January 1997.
APS Manuscript Number J181-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 5 February 1997