Questions and Answers
Question # 32
Why is auditory perception "spared," and tactile and visual perception
impaired, in the NLD syndrome?
Background. The "white matter" model (Rourke, 1982, 1987,
1989, 1995; Rourke, van der Vlugt & Rourke, 2002) was proposed
and developed as a theoretical explanation of the content and
neurodevelopmental dynamics of the NLD syndrome (see NLD Content
and Dynamics). White matter (or myelin) serves as "coverings" for
the active parts of neurons. These coverings are known to be
quite crucial for the normal development and functioning of neurons
(e.g., they can affect how well and how fast different signals can
travel, and how well neurons can communicate with each other).
Damage to them, especially during the early phases of neuronal
development, is thought to have significant negative implications
for normal neuronal and cognitive development and functioning (see
NLD and Neurological Disease). With this as background, the
following answers to this question are offered.
Answers. If there is a general or fairly widespread
deterioration/damage of white matter in the brain, it would
be expected that the tactile (touch) and visual modalities
would be affected more adversely than would the auditory
modality. This is expected in the case for the tactile system
because the somatosensory tracts stretch from the cerebral
mantle down into the brainstem, thus traversing the entire vertical axis of the brain, and then some (Casey & Rourke,
2002). Analogous to this situation is the fact that the
visual tracts stretch from the most anterior to the most
posterior regions of the brain, thus traversing a good portion
of the horizontal axis of the brain. It should be clear that
adverse events causing general or fairly widespread deterioration
of white matter would be expected to damage these somatosensory
and visual tracts at one or more points. Such damage would be
expected to cripple the entire tactile and visual systems to a
greater or lesser extent (Casey & Rourke, 2002).
The auditory system, on the other hand, is
"blessed" with some rather short connections on the ipsilateral
sides of the brain. For example, there are some connections to
the primary auditory projection area in the left and right
temporal lobes that project in a fairly direct route from the
left ear and right ear, respectively; these are relatively
short distances in comparison to those traversed by the tactile
and visual projections. More generally, the entire auditory
system is much more “compact” than are either the somatosensory
or the visual systems. Also, there is evidence to suggest that
the auditory pathways are myelinated much earlier than are the
visual pathways. Finally, the auditory system, post-natally,
becomes fully myelinated and fully functioning earlier than does
the visual system. This may confer some advantage to the auditory
system in that perturbations that affect the development of
myelination and that occur after the rather full myelination of
the auditory system would have no effect on it. However, this
state of affairs might still affect the development of myelination
in the not yet fully mature (myelinated) visual system. In a
sense, this is analogous to a kind of "first in, last out" scenario.
These anatomical differences would suggest,
a priori, that the tactile and visual systems are, in a very real
sense, more in harm’s way than are the auditory systems, at least
with respect to the failure to develop, destruction, and/or
dysfunction of white matter. That said, this does not preclude significant perturbations of myelin in auditory systems; it just
renders them less likely vis-a-vis those expected, under such
conditions, in the tactile and visual systems. Indeed, early
general and severe perturbations of white matter would be expected
to have very deleterious affects upon the auditory systems and,
by extension, linguistic development. All of this was envisioned
in the earliest formulation of the white matter model (Rourke,
1982), and has been elaborated upon in subsequent versions of it (Rourke, 1987, 1988, 1989, 1995; Rourke et al., 2002).
Casey, J. E., & Rourke, B. P., (2002).
Somatosensory perception in children. In S. J. Segalowitz & I.
Rapin(Eds.), Handbook of neuropsychology, Vol. 8: Child
neuropsychology (2nd ed., pp. 385-403). Amsterdam: Elsevier.
Rourke, B. P. (1982). Central processing
deficiencies in children: Toward a developmental neuropsychological
model. Journal of Clinical Neuropsychology, 4, 1-18.
Rourke, B. P. (1987). Syndrome of nonverbal
learning disabilities: The final common pathway of white-matter
disease/dysfunction? The Clinical Neuropsychologist, 1,
Rourke, B. P. (1988). The syndrome of nonverbal
learning disabilities: Developmental manifestations in neurological
disease, disorder, and dysfunction. The Clinical Neuropsychologist,
Rourke, B. P. (1989). Nonverbal learning disabilities:
The syndrome and the model. New York: Guilford Press.
Rourke, B. P. (1995). Introduction and overview:
The NLD/white matter model. In B. P. Rourke (Ed.), Syndrome of nonverbal
learning disabilities: Neurodevelopmental manifestations (pp. 1-26).
New York: Guilford Press.
Rourke, B. P., van der Vlugt, H., & Rourke, S. B.
(2002). Practice of child-clinical neuropsychology: An introduction.
Lisse, The Netherlands: Swets & Zeitlinger.