Questions and Answers
Question #32


Questions and Answers

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, 209-234.

Rourke, B. P. (1988). The syndrome of nonverbal learning disabilities: Developmental manifestations in neurological disease, disorder, and dysfunction. The Clinical Neuropsychologist, 2, 293-330.

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.

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