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Question #30


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Questions and Answers

 

Question # 30

Why do persons who exhibit symptoms of significant traumatic brain injury (TBI) often present with a pattern of neuropsychological assets and deficits that is suggestive of right cerebral hemisphere dysfunction?

Does this have any implications with respect to the presence or absence of NLD in such persons?


As regards the first question, there are several reasons for this finding, not all of which are mutually exclusive. Some of these are as follows:

(1) There is a greater proportion of white/grey matter in the right than in the left cerebral hemisphere (Goldberg & Costa, 1981). Hence, an event, such as significant TBI, that can cause extensive neuronal stretching and shearing (and, in consequence, some degree of damage and/or dysfunction of myelin), is likely to cause much more disruption of systems within the right than of those within the left cerebral hemisphere.

(2) Systems within the right hemisphere are inferred to be principally responsible for intermodal integration and dealing with novel information within a developmental context (Goldberg & Costa, 1981; Rourke, 1982, 1987, 1988, 1989, 1995; Rourke, van der Vlugt, & Rourke, 2002). Most psychological tests that are thought to be "sensitive" to right hemisphere functioning (or deficit) are more novel in nature (e.g., Wechsler Block Design) than are those thought typically to reflect left hemisphere functioning (e.g., Wechsler Vocabulary). The latter (verbal) types of tests tend to be those that tap into overlearned, rote, verbal information that is "crystallized" to the point that it becomes somewhat impervious to perturbations of general white matter dysfunction. The systems within the right hemisphere are not thought to be specialized for, or capable of, this sort of intramodal functioning. Thus, if there are general white matter perturbations as a result of TBI, it is very likely that skills and abilities thought to be mediated primarily by systems within the right hemisphere will appear to be more impaired than are those thought to be mediated primarily by systems within the left hemisphere. This is, in one very important sense, the truth. However, this "truth" is not a reflection of more damage within the right hemisphere, but rather of more functional deficit of the skills and abilities subserved primarily by systems within the right hemisphere. In this sense, the basis for the exhibited "lateralized" deficits is functional/physiological in nature and does not necessarily imply more structural damage within the right cerebral hemisphere.

(3) Obviously, significant TBI may be confined to the right cerebral hemisphere. In such cases, one often sees the principal deficits as very similar, or even identical, to deficits that are among those considered to be primary in the NLD syndrome (see NLD Content and Dynamics): outstanding visual-spatial-organizational deficits; and, a predominance of somatosensory and psychomotor deficits on the left side of the body.

(4) As outlined in Question #29, children who exhibit the NLD syndrome (and, hence, may be suffering from significant impairment of right hemisphere systems) are very likely to "rush in where angels fear to tread," including out from between parked cars and into roadways filled with speeding vehicles. Similarly, they are more prone to fall from swings, slides, bicycles, and so on than are children who are developing their psychomotor, somatosensory, and visual-spatial-organizational skills at a normal rate. Thus, it may be the case that some children who appear to be suffering from greater impairment in skills and abilities thought to be mediated primarily by systems within the right cerebral hemisphere as a result of significant TBI were, in fact, deficient in these skills and abilities prior to the TBI they sustained.

In answer to the second question, all of the points (1) through (4) above, are relevant. More specifically, a decision regarding the framing of an inference with respect to the presence or absence of NLD prior to TBI involves a considered judgment regarding pre-TBI neuropsychological and psychosocial dimensions. One feature of particular interest regarding the framing of such an inference of pre-TBI NLD is the very wide diversity of psychosocial outcomes that are evident following TBI in both children (Butler, Rourke, Fuerst, & Fisk, 1997; Hayman-Abello, Rourke, & Fuerst, 2003) and adults (Warriner, Rourke, Velikonja, & Metham, 2003). One of these psychosocial outcomes (internalized psychopathology) is seen most frequently in persons with NLD (Casey, Rourke, & Picard, 1991; Pelletier, Ahmad, & Rourke, 2001; Rourke, 2000; Tsatsanis, Fuerst, & Rourke, 1997). But many post-TBI psychosocial outcomes are completely normal and most abnormal outcomes are seen only rarely in persons with NLD. These considerations have a number of clinical ramifications, some of which are as follows.

Clinical Implications. For adolescents and young adults who are thought to exhibit symptoms consistent with significant TBI plus a pattern of neuropsychological assets and deficits that would be consistent with NLD prior to their TBI, the bases for a reasonable inference of pre-TBI NLD are at least three-fold. Such persons usually present with the following: (1) a pattern of post-TBI neuropsychological assets and deficits that is concordant with NLD (with added features commonly seen in TBI); (2) levels and patterns of academic performance (e.g., superior single-word reading and spelling within a context of outstandingly impaired mechanical arithmetic performance) very often seen in persons with NLD; and, (3) a pre-TBI pattern of psychosocial functioning (internalized psychopathology) that is typical of persons at this age who have exhibited NLD for a very long period of time. If such conditions obtain, it is reasonable to infer the presence of a clinical comorbidity that a colleague of mine is wont to characterize as "measles (i.e., NLD) and a broken leg (i.e., TBI)." That said, it must be acknowledged that determinations of this particular type of comorbidity are fraught with difficulty, even for very experienced clinical neuropsychologists.



References

Butler, K., Rourke, B. P., Fuerst, D. R., & Fisk, J. L. (1997). A typology of psychosocial functioning in pediatric closed-head injury. Child Neuropsychology, 3, 98-133.

Casey, J. E., Rourke, B. P., & Picard, E. M. (1991). Syndrome of nonverbal learning disabilities: Age differences in neuropsychological, academic, and socioemotional functioning. Development and Psychopathology , 3, 331-347.

Goldberg, E., & Costa, L. D. (1981). Hemispheric differences in the acquisition and use of descriptive systems. Brain and Language, 14, 144-173.

Hayman-Abello, S. E., Rourke, B. P., & Fuerst, D. R. (2003). Psychosocial status after pediatric traumatic brain injury: A subtype analysis using the Child Behavior Checklist. Journal of the International Neuropsychological Society, 9, 887-898.

Pelletier, P. M., Ahmad, S. A., & Rourke, B. P. (2001). Classification rules for Basic Phonological Processing Disabilities and Nonverbal Learning Disabilities: Formulation and external validity. Child Neuropsychology , 7, 84-98.

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. (2000). Neuropsychological and psychosocial subtyping: A review of investigations within the University of Windsor laboratory. Canadian Psychology, 41, 34-50.

Rourke, B. P., van der Vlugt, H., & Rourke, S. B. (2002). Practice of child-clinical neuropsychology: An introduction. Lisse, The Netherlands: Swets & Zeitlinger.

Tsatsanis, K. D., Fuerst, D. R., & Rourke, B. P. (1997). Psychosocial dimensions of learning disabilities: External validation and relationship with age and academic functioning. Journal of Learning Disabilities, 30, 490-502.

Warriner, E. M., Rourke, B. P., Velikonja, D., & Metham, L. (2003). Subtypes of emotional and psychosocial sequelae in patients with traumatic brain injury. Journal of Clinical and Experimental Neuropsychology, 25, 904-917.


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