Background: Brain plasticity occurs as a result of sensory and motor adaptation to increased
or altered use and leads to reorganization of the respective representations [1].
Plasticity of the adult human brain following deafferentation has only been assessed
functionally, revealing functional reorganization of somatosensory and motor cortices
[2, 3]. Only a few reports exist reporting plasticity of groß brain structure [4].
In this study we explored whether structural brain plasticity occurs after amputation
of the upper limb. Methods: We investigated a 33-year-old, right-handed male patient with an amputation of the
right forearm following severe trauma. Fifteen weeks after amputation he received
a myoelectric prosthesis which was regularly used. After removing signal uniformities,
all scans were registered to the first scan using rigid-body transformation. Remaining
local differences were then minimized by applying high-resolution deformations [5]
and the local volume changes were calculated using the Jacobian determinant [6]. Results: Significant volume loss was detected in the primary motor cortex (M1), primary somatosensory
cortex (S1), and in the superior parietal cortex contralateral to the amputated limb.
Further volume loss was seen in the supplementary motor area (SMA), and the ipsilateral
primary motor cortex and bilaterally in the cerebellum and the brain stem. Discussion: This case report is the first indication of structural brain plasticity in the adult
human brain following limb deafferentation. The data suggest that loss of sensory
input and lack of motor output leads not only to a functional reorganization, but
may also cause a change of groß brain structure. The regions with volume loss cover
most parts of the motor system such as M1, S1, SMA, superior parietal cortex, cerebellum,
and brain stem. Thus, short-term changes occur not only in the functional but also
in the structural organization of the motor and sensorimotor system. This is in line
with current observations of short-term structural changes as a consequence of intensive
training [7]. References: [1] Black JE et al. PNAS 1990; 87: 5568–5572. [2] Elbert T, Heim S. Nature 2001;
411:139. [3] Weiss T et al. Neuroreport 1998; 9: 213–216. [4] Hamzei F et al. Neuroreport
2001; 12: 957–962. [5] Gaser C et al. Neuroimage 1999; 10: 107–113. [6] Ashburner
J et al. Hum Brain Map 2000; 9: 212–225. [7] Draganski B et al. Nature 2004; 427:
311–312.
