Questions and Answers
Question #43


Questions and Answers

Questions and Answers


Question # 43

You assign Traumatic Brain Injury (TBI) to Level 3 in the NLD and Neurological Disease section. Does this hold any implications for the psychosocial disturbances that may follow TBI?

We have conducted several studies of adults and children with TBI. Some of the results of these investigations can be construed as having implications that bear upon this general issue. [Before reviewing these, it would be well for the reader to examine the material contained in Question #30.]

One of these studies dealt with a 40-year follow-up of soldiers who had suffered penetrating missile wounds to the brain and had, subsequently, developed a seizure disorder resulting from these (Tellier, Adams, Walker, & Rourke, 1990). It was found that the vast majority of these soldiers were living what appeared to be very adaptive life-styles. Indeed, all but a few were quite satisfied with their lives, and did not appear to have suffered any long-term negative psychosocial sequelae of their injuries and/or accompanying seizure disorders. Of interest, those who presented with significant psychopathology were, without exception, soldiers whose lesion was in the right cerebral hemisphere-a result predictable from our early neurodevelopmental model (Rourke (1982) and subsequent extensions of the NLD/White Matter theory (Rourke, 1987, 1988, 1989, 1995a; Rourke, van der Vlugt, & Rourke, 2002).

In another investigation, we examined reliable subtypes of psychosocial functioning in children who had undergone TBI (Butler, Rourke, Fuerst, & Fisk, 1997). In this study, we demonstrated that the psychosocial consequences (subtypes) of this type of brain injury in older children and adolescents were virtually identical to the psychosocial subtypes evident in children with learning disabilities (LD; Rourke & Fuerst, 1991, 1992, 1996) and those with below-average IQ (Ralston, Fuerst, & Rourke, 2003), with one exception: One subtype appeared that we had not observed in children with LD. These results have been replicated using a completely different measure of psychosocial functioning (Hayman-Abello, Rourke, & Fuerst, 2003). Thus, from a psychosocial perspective, there were several quite distinct subtypes clearly evident. These covered the psychosocial spectrum from completely normal, through mild, moderate, and severe forms of psychopathology.

One of the very important conclusions of this investigation: There was no connection between the supposed severity of brain injury and the severity of negative psychosocial outcome. The ordinary hypotheses regarding the positive correlation between the severity of TBI and the severity of psychosocial disturbance following TBI were clearly not supported.

Another study involved a similar analysis of psychosocial subtypes among adults who had suffered TBI (Warriner, Rourke, Velikonja, & Metham, 2003). Analysis of the results of this study indicated very clearly that there were several quite distinct subtypes of psychosocial functioning in evidence, varying from completely normal, through mild, moderate, and severe. Again, it was clear that the psychosocial sequelae of TBI are diverse. There is no single psychosocial “response” to such brain injury.

A Related Note. The results of a recent investigation by Collins, Rourke, Rothermel, and Chugani (under review) provided strong support for the view that children with epilepsy can be meaningfully categorized into six psychosocial subtypes. These ranged from essentially normal to significant psychosocial disturbances characterized by internalizing psychopathology, and, to a lesser extent, externalizing psychopathology. The relationship between subtype assignment and patterns of cerebral glucose metabolism in a subsample of the participants using PET was also examined. Results from the PET study indicated that four of the subtypes were differentiated from controls by decreased glucose metabolism, mainly in right frontal, bilateral cerebellar, and to a lesser extent right temporal regions. Thus, specific subtypes of psychosocial functioning in children with epilepsy seem to be associated with specific patterns of cerebral metabolic dysfunction. It is also of note that the principal differentiations among the psychosocial subtypes involved children whose apparently epileptogenic foci were in the right cerebral hemisphere.


(1) In some instances, it is probable that brain impairment resulting from TBI has an effect upon psychosocial functioning.

(2) SOME persons with severe TBI do not exhibit any evidence of psychosocial disturbance. Thus, brain impairment of a significant degree need not be accompanied by clinically significant psychosocial disturbance. At the same time, some persons with mild TBI do exhibit clinically significant, severe types of psychosocial disturbance.

(3) Evidence of severe or moderate or mild psychosocial disturbance does not map onto (correlate positively with) coincidental degrees of brain impairment, however defined. Psychosocial disturbance of a mild, moderate, or severe degree is not associated with coincidental mild, moderate, or severe TBI.

(4) It is also clear that the relationship between severity of TBI and vocational outcomes in adults is not simple (Paniak, Shore, Rourke, Finlayson, Rourke, & Moustacalis, 1992). And there is quite clear evidence of psychosocial subgroups in adults with TBI who are involved in Workmen’s Compensation (Millikin, Shore, Rourke, Salmon, & Celinski, in press).

(5) There are distinct subtypes of psychosocial functioning in children with epilepsy. Four of these subtypes can be differentiated from controls by decreased glucose metabolism in different brain regions.

(6) Much of the evidence cited herein would suggest that lesions of the right cerebral hemisphere are partcularly salient with respect to the presence of moderate to severe psychosocial disturbance. This conclusion would be entirely consistent with deductions that derive from the NLD/White Matter model (See Rourke et al. [2002] for the most recent formulation of this model).

(7) Although the syndrome of NLD would appear to be quite probable following some types of TBI (e.g., those involving extensive white matter perturbations, especially within the right cerebral hemisphere), it is necessary to determine, through a comprehensive neuropsychological assessment, if such be the case (See Question #37). Even then, it is quite probable that other dimensions of the injuries sustained in TBI (e.g., significant focal disruptions) may eventuate in dimensions of neuropsychological and psychosocial impairment that are quite unrelated to those expected in persons who exhibit NLD. Put simply: It is possible to have “measles” (e.g., significant white matter perturbations that cause NLD) and a “broken leg” (e.g., significant focal lesions such as those that may cause particular forms of aphasia) (See Question #7 and #34 for other examples of the “measles”/“broken leg” metaphor). It seems obvious that it would be most propitious for treatment considerations if both sets of cirumstances and their likely psychosocial implications were known.

For a fuller picture of the context within which our studies of psychosocial functioning and its relationships with brain impairment and NLD, the reader may wish to consult Rourke (2008a, 2008b).

Clinical Implications, General. The overwhelming evidence of marked diversity of psychosocial sequelae following TBI, including completely normal psychosocial functioning in persons classified as having maintained severe TBI, has at least one clinical implication: The assessment of psychosocial functioning following TBI is desirable, and probably necessary. Formulating inferences about--and establishing psychosocial treatment plans for--persons with TBI solely, or even partially, on the basis of their supposed severity of brain impairment cannot be justified from a scientific point of view. Failure to consider this in the practice of neuropsychiatry and other areas of health and psychosocial service provision for persons with TBI is quite likely to be counterproductive.

Clinical Implications

(1) Recommended Forms of Intervention. Consider the case of a person who exhibits the syndrome of NLD (perhaps, as a result of of diffuse white matter perturbations) and a form of treatable linguistic disturbance/aphasia (perhaps, as a result of a focal lesion involving the left fronto-temporal region). This is a not uncommon clinical picture following significant TBI.

I would recommend giving consideration to the following modes of intervention:

For NLD: cognitive-behaviorural interventions aimed at developing nessary and desirable adaptive skills.

For the Linguistic/Aphasic dimensions: Appropirate speech/language therapy.

For any type or degree of psychosocial disturbance: Supportive counselling plus appropairate forms of cognitive-behavioural therapy; these may include therapeutic targets such as anxiety-reduction, desensitization, and a host of other issues.

(2) Forms of intervention not recommended.

I have found that two forms of intervention for persons exhibiting NLD are completely without merit, and often counterproductive:

(a) A “discipline” plan with clear rewards and consequences (See Question #21) and insight-oriented dynamic psychotherapy (See Question #23). That said, it is probable that these therapeutic approaches may be quite beneficial for other dimensions of behavioural and psychosocial disturbances that may follow TBI.

Concluding Note. This discussion has been confined, almost exclusively, to a review of relevant studies that have been carried out in, or in conjunction with, our laboratory. I think it would be interesting to test the hypotheses nascent within this discussion through the use of data generated in other relevant literature. Finally, designing studies that test these hypotheses would probably be fruitful (See Question #42). For examples of this in other areas, see Question #15 and #16.


Collins, D.W., Rourke, B.P., Rothermel, R., & Chugani, H. (under review). Psychosocial subtyping and brain metabolism in children with epilepsy.

Goldberg, E., & Costa, L. D. (1981). Hemisphere 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.

Millikin, C. P., Shore, D., Rourke, B. P.,, Salmon, J. D., & Celinski, M. (in press). Empirically derived MCMI and MCMI-II subgroups in two Workers' Compensation traumatic brain injury samples. Archives of Clinical Neuropsychology,

Paniak, C. E., Shore, D. L., Rourke, B. P., Finlayson, M.A.J., & Moustacalis, E. (1992). Long-term vocational functioning after severe closed-head injury: A controlled study. Archives of Clinical Neuropsychology, 7, 529-540.

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 neurologicaldisease, 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. (1995a). 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. (Ed.). (1995b). Syndrome of nonverbal learning disabilities: Neurodevelopmental manifestations. New York: Guilford Press.

Rourke, B. P. (2008, in press). Is neuropsychology a (psycho)social science? Journal of Clinical and Experimental Neuropsychology,

Rourke, B. P. (2008, in press). Neuropsychology as a (psycho)social science: Implications for research and clinical practice.Canadian Psychology,

Rourke, B.P., & Fuerst, D. R. (1991). Learning disabilities and psychosocial functioning: A neuropsychological perspective. New York: Guilford Press.

Rourke, B. P., & Fuerst, D. R. (1992). Psychosocial dimensions of learning disability subtypes: Neuropsychological studies in the Windsor Laboratory. School Psychology Review, 21, 360-373.

Rourke, B. P., & Fuerst, D. R. (1996). Psychosocial dimensions of learning disability subtypes. Assessment , 3, 277-290.

Rourke, B. P., van der Vlugt, H., & Rourke, S. B. (2002). Practice of child-clinical neuropsychology: An introduction. New York: Taylor & Francis.

Tellier, A., Adams, K. M., Walker, A. E., & Rourke, B. P. (1990). Long-term effects of severe penetrating head injury on psychosocial adjustment level. Journal of Consulting and Clinical Psychology, 58, 531-537.

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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