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connections had been established in foetal life, they hardly changed in adult-
hood. The only areas of the adult brain capable of reorganization were those
involved in learning and memory processes.
The picture has changed radically in the past decades; indeed, recent evi-
dence demonstrates that the brain is capable of remarkable and widespread
adaptive changes in response to peripheral injuries ( Davis et al., 2011; Jain,
Florence, & Kaas, 1998; Navarro et al., 2007 ). In fact, an injured nerve stops
to function normally and this occurrence results in the reorganization of the
projections to the CNS. While it is likely that this reorganization following
injury takes place in the cortex, plastic changes may also occur in subcortical
structures such as the thalamus, brainstem relay nuclei, and spinal cord
( Lewin & McMahon, 1993 ). Plasticity of central connections may be pos-
itive, that is, compensate the lack in target reinnervation, but may also result
in maladaptive changes, such as neuropathic pain, hyperreflexia, dystonia,
and phantom limb awareness ( Navarro et al., 2007 ).
The response of the CNS to altered peripheral inputs may take many
forms and include changes in ongoing or stimulus-evoked activity, neuro-
chemical changes, functional alterations of excitatory and inhibitory con-
nections, atrophy and degeneration of normal substrates, sprouting of
new connections, and reorganization of somatosensory and motor maps
( Davis et al., 2011; Navarro et al., 2007 ).
Plasticity of the somatosensory system has been extensively studied, and
it has been shown that dramatic changes in the organization of cortical
topography of the S1 area (primary somatosensory cortex) occur in response
to a peripheral nerve injury ( Donoghue & Sanes, 1987 ). It has been dem-
onstrated that following peripheral nerve lesion in adult monkeys, the area
in the somatosensory cortex corresponding to the deafferented body parts of
the S1 became responsive to inputs from neighboring body parts ( Merzenich
et al., 1983 ). Although this form of cortical plasticity is well documented
across several sensory systems and in several species, such as cats, raccoons,
rodents, and bats, the understanding of the underlying mechanisms remains
an active area of research ( Pelled, Chuang, Dodd, & Koretsky, 2007 ).
In the motor system, changes in cortical representation also occur after
peripheral injury; following amputation or peripheral nerve lesions, the area
from which stimulation evoked movements of the adjacent body parts
enlarged and the threshold for eliciting these movements
is reduced
( Donoghue & Sanes, 1988; Sanes, Suner, & Donoghue, 1990 ).
The hypothesis that also visceral afferents exert a significant influence on
the CNS plasticity has been investigated by many researchers, even if little is
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