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SECTION III
Central & Peripheral Neurophysiology
two components of pain pathways. From VPL nuclei in the
thalamus, fibers project to SI and SII. This is the pathway
responsible for the
discriminative
aspect of pain, and is also
called the
neospinothalamic tract.
In contrast, the pathway
that includes synapses in the brain stem reticular formation and
centrolateral thalamic nucleus projects to the frontal lobe, lim-
bic system, and insula. This pathway mediates the
motiva-
tional-affect
component of pain and is called the
paleospinothalamic tract.
In the central nervous system (CNS), visceral sensation
travels along the same pathways as somatic sensation in the
spinothalamic tracts and thalamic radiations, and the cortical
receiving areas for visceral sensation are intermixed with the
somatic receiving areas.
CORTICAL PLASTICITY
It is now clear that the extensive neuronal connections de-
scribed above are not innate and immutable but can be
changed relatively rapidly by experience to reflect the use of
the represented area. Clinical Box 11–1 describes remarkable
changes in cortical and thalamic organization that occur in re-
sponse to limb amputation to lead to the phenomenon of
phantom limb pain.
Numerous animal studies point to dramatic reorganization
of cortical structures. If a digit is amputated in a monkey, the
cortical representation of the neighboring digits spreads into
the cortical area that was formerly occupied by the represen-
tation of the amputated digit. Conversely, if the cortical area
representing a digit is removed, the somatosensory map of the
digit moves to the surrounding cortex. Extensive, long-term
deafferentation of limbs leads to even more dramatic shifts in
somatosensory representation in the cortex, with, for exam-
ple, the limb cortical area responding to touching the face.
The explanation of these shifts appears to be that cortical con-
nections of sensory units to the cortex have extensive conver-
gence and divergence, with connections that can become
weak with disuse and strong with use.
Plasticity of this type occurs not only with input from cuta-
neous receptors but also with input in other sensory systems.
For example, in cats with small lesions of the retina, the corti-
cal area for the blinded spot begins to respond to light striking
other areas of the retina. Development of the adult pattern of
retinal projections to the visual cortex is another example of
this plasticity. At a more extreme level, experimentally routing
visual input to the auditory cortex during development cre-
ates visual receptive fields in the auditory system.
PET scanning in humans also documents plastic changes,
sometimes from one sensory modality to another. Thus, for
example, tactile and auditory stimuli increase metabolic activ-
ity in the visual cortex in blind individuals. Conversely, deaf
individuals respond faster and more accurately than normal
individuals to moving stimuli in the visual periphery. Plastic-
ity also occurs in the motor cortex. These findings illustrate
the malleability of the brain and its ability to adapt.
EFFECTS OF CNS LESIONS
Ablation of SI in animals causes deficits in position sense and in
the ability to discriminate size and shape. Ablation of SII causes
deficits in learning based on tactile discrimination. Ablation of
SI causes deficits in sensory processing in SII, whereas ablation
of SII has no gross effect on processing in SI. Thus, it seems clear
that SI and SII process sensory information in series rather than
in parallel and that SII is concerned with further elaboration of
sensory data. SI also projects to the posterior parietal cortex
(Figure 11–3), and lesions of this association area produce com-
plex abnormalities of spatial orientation on the contralateral
side of the body.
In experimental animals and humans, cortical lesions do
not abolish somatic sensation. Proprioception and fine touch
are most affected by cortical lesions. Temperature sensibility
is less affected, and pain sensibility is only slightly altered.
Only very extensive lesions completely interrupt touch sensa-
tion. When the dorsal columns are destroyed, vibratory sensationCLINICAL BOX 11–1
Phantom Limb Pain
In 1551, a military surgeon, Ambroise Pare, wrote, ”... the
patients, long after the amputation is made,
say they still
feel pain in the amputated part. Of this they
complain
strongly, a thing worthy of wonder and almost incredible
to
people who have not experienced this.” This is perhaps the
earliest description of
phantom limb pain.
Between 50%
and 80% of amputees experience phantom sensations, usu-
ally pain, in the region of their amputated limb. Phantom
sensations may also occur after the removal of body parts
other than the limbs, for example, after amputation of the
breast, extraction of a tooth
(phantom tooth pain),
or re-
moval of an eye
(phantom eye syndrome).
Numerous the-
ories have been evoked to explain this phenomenon. The
current theory is based on evidence that the brain can reor-
ganize if sensory input is cut off. The
ventral posterior tha-
lamic nucleus
is one example where this change can occur.
In patients who have had their leg amputated, single neu-
ron recordings show that the thalamic region that once re-
ceived input from the leg and foot now respond to stimula-
tion of the stump (thigh). Others have demonstrated
remapping of the somatosensory cortex. For example, in
some individuals who have had an arm amputated, stroking
different parts of the face can lead to the feeling of being
touched in the area of the missing limb. Spinal cord stimula-
tion has been shown to be an effective therapy for phantom
pain. Electric current is passed through an electrode that is
placed next to the spinal cord to stimulate spinal pathways.
This interferes with the impulses ascending to the brain and
lessens the pain felt in the phantom limb. Instead, amputees
feel a tingling sensation in the phantom limb.