Questions and Answers
Question #41


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Questions and Answers

 

Question # 41

What are the relationships among NLD, Asperger's Syndrome (AS), and High Functioning Autism (HFA)?


(1) Virtually all persons with AS exhibit Definite or Probable NLD (See Question #10 for characterizations of Definite and Probable NLD).

(2) No persons with HFA exhibit Definite or Probable NLD.

These conclusions are based upon extensive research on this topic (See the AS section of NLD and Neurological Disease for these references.)

Below are data that can be used to constitute a (hopefully) straightforward demonstration of conclusions (1) and (2). (See NLD Content & Dynamics for NLD Assets and Deficits.)

SOME PRINCIPAL NLD ASSETS & DEFICITS (14-YEAR-OLD; yes=Deficit no=No Deficit)


Neuropsychological & Neurolinguistic Assets

AS
HFA

auditory perception
no
no

auditory attention
no
???
auditory memory
no
???

language output
no
yes
language assoc.
no
yes
language form
no
yes




Neuropsychological & Neurolinguistic Deficits

somatosensory
???
???
psychomotor
yes
no
visual-spatial
yes
no
deal with novelty
yes
yes

tactile attention
yes
???
visual attention
yes
no

exploration
yes
no

tactile memory
yes
???
visual memory
yes
???

concept-formation
yes
no
problem-solving
yes
no

language content
yes
???
language function
yes
???

............................................................................



Neuropsychological & Neurolinguistic
Assets and Deficits: 2 Summaries

1. ASSETS & DEFICITS

(yes= exhibited; no= not exhibited)

ASSETS


YES
NO
???

AS
6
0
0

HFA
1
3
2

DEFICITS


YES
NO
???

AS
12
0
1

HFA
1
6
6



2. POSITIVE (+) AND NEGATIVE (-) NLD INDICATORS



+
-
???

AS
18
0
1

HFA
2
8
9




Observations.

(1) These data and summaries would certainly be consistent with the Conclusions enunciated above. This may be especially apparent in (2) above that summarizes the positive and negative characteristics of NLD in AS and HFA.

(2) These Conclusions would support the notion that AS and HFA do no not lie on some sort of "spectrum." Indeed, the so-called "Autistic Spectrum" may not include AS.

(3) One important limitation of this (informal) study is that there are too many ???, especially for HFA. Additional research should rectify this situation.

(4) The Academic and Psychosocial Assets of AS and HFA are characterized in terms of their similarity to NLD (yes= deficit; no= no deficit):

AS
HFA

Academic Assets

read single words
no
yes

spell words
no
yes

Academic Deficits

reading comp.
yes
???
arithmetic
yes
yes
............................................................................
Psychosocial Asset

social intent
no
yes

Psychosocial Deficits

social perception
yes
yes

social competence
yes
yes

intnlzd. psypathol.
yes
???

............................................................................




These data are too incomplete to allow for confident generalizations and conclusions.

However, it is notable that the psychosocial deficits of AS and HFA are quite similar. That said, it would seem highly probable that the sources of these deficits are quite distinct, and have much to do with the fairly long time that persons with AS (and NLD) attempt to establish social contacts, as opposed to the reluctance of persons with HFA ever to try. Thus, the psychosocial deficits of persons with AS (and NLD) may very well be the direct result of their continuing, but failing, attempts at socializing. Whereas, the deficits of those with HFA are the direct result of not trying to perform in these areas. A similar difference in the etiology of social perception deficits would also seem very likely.

Bottom Line. NLD would appear to constitute a "final common pathway" for AS, as it does for many types of neurological disease, disorder, and dysfunction (see NLD and Neurological Disease); it is clear that HFA does not. That is, the behavioural phenotype of AS is very similar to that evident in disorders such as Williams syndrome, early shunted hydrocephalus, Triple X syndrome, Sotos syndrome, and significant damage/lesions confined to the right cerebral hemisphere; the behavioural phenotype of HFA has very little in common with these and all other neurological diseases and disorders in which NLD is clearly evident in their behavioural phenotypes. It would be of interest to carry out analyses similar to those contained herein to determine the extent to which the NLD syndrome is evident in their phenotypes. Among other things, such analyses would allow for a "ranking" of these diseases that may reveal interesting "clusters," such as those of various genetic etiologies.

............................................................................

What are some of the important therapeutic implications of the differences between HFA and those neurological disorders such as AS whose behavioural phenotypes include NLD?

It is clear that behavioural techniques involving the systematic application of rewards and consequences have achieved quite positive results for many, if not the majority of, youngsters with autism.

Such regimens are clearly inappropriate for children who exhibit NLD (see Question #21), including those diagnosed with AS. Insight-oriented dynamic psychotherapy is also counterproductive (Question #23). Virtually all therapeutic approaches to NLD that have been shown to have some success involve intensive concentration on skill learning and anxiety reduction, which are intimately related (see Question #16).

It is clear that treatment plans for persons who exhibit NLD need to be highly individualized (Question #31), and that any system that ignores this (e.g., one that relies on rewards and consequences) would be expected to be, at best, a failure and, at worst, counterproductive. Dynamic psychotherapy for youngsters with NLD and their families can, and often does, lead to very negative consequences (e.g., Question #20). The individualization of treatment plans for adults must also take into consideration their particular needs (Question #40).

The neurodevelopmental unfolding of NLD is quite predictable, especially with respect to psychosocial dynamics (Question #18), transient psychosocial “comorbidities” (Question # 7), and those of a more entrenched and serious nature (Question #33, #38).

Bottom line. This very brief overview of the therapeutic needs of persons with HFA versus those who exhibit NLD (e.g., those with AS) would suggest strongly that making the distinctions suggested above between and among these disorders is very helpful, indeed necessary, if therapeutic gains are to be made. As was stated above with respect to the enormous differences extant between persons with HFA and those with AS, it is clear that they do not belong on any sort of therapeutic continuum or spectrum. Their intervention needs appear as orthogonal to one another as are their patterns of neuropsychological assets and deficits. Maintaining otherwise will simply turn out to be counterproductive for achieving any significant degree of adaptive development for these persons.

Final Note. Many students of AS and NLD seem to think that they are one and the same. Of course, they are not. Reflections on the relevant sections above and the NLD and Neurological Disease section will show this assertion of identity to be absurd.

Perhaps a little example from Aristotle’s Logic will be of assistance within this context. Consider the following non-sequitur:

All apples are fruit.
Therefore, all fruit are apples.

Applied to the current considerations:

All persons with AS exhibit NLD.
Therefore, all persons with NLD have AS.

I rest my case.

References

Ellis, H. D. (1994). A preliminary study of right-hemisphere cognitive deficits and impaired social judgment among young people with Asperger syndrome. European Journal of Child and Adolescent Psychiatry, 3, 255-266.

Ellis, H. D., & Gunter, H. L. (1999). Asperger syndrome: A simple matter of white matter? Trends in Cognitive Sciences, 3, 192-200.

Gunter, H. L., Ghaziuddin, M., & Ellis, H. D. (2002). Asperger syndrome: Tests of right hemisphere functioning and interhemispheric communication. Journal of Autism and Developmental Disorders, 32, 263-281.

Klin, A., Sparrow, S. S., Volkmar, F., Cicchetti, D. V., & Rourke, B. P. (1995). Asperger syndrome. In B. P. Rourke (Ed.), Syndrome of nonverbal learning disabilities: Neurodevelopmental manifestations (pp. 93-118). New York: Guilford Press.

Klin, A., Volkmar, F. R., Sparrow, S. S., Cicchetti, D. V., & Rourke, B. P. (1995). Validity and neuropsychological characterization of Asperger syndrome: Convergence with Nonverbal Learning Disabilities syndrome. Journal of Child Psychology and Psychiatry, 36, 1127-1140.

Lincoln, A. et al. (1998). Neurobiology of Asperger syndrome: Seven case studies and quantitative magnetic responance imaging findings. In E. Schopler, G. B. Mesibov, & L. J. Kunce (Eds.), Asperger syndrome or high functioning autism? (pp.145-160). New York, Plenum.

McKelvey, J. R., Lambert, R., Mottron, L., & Shevell, M.I. (1995). Right-hemisphere dysfunction in Asperger’s syndrome. Journal of Child Neurology, 10, 310-314.

Molina, J. L., Ruata, J. M., & Soler, E. P. (1986). Is there a right-hemisphere dysfunction in Asperger’s syndrome? British Journal of Psychiatry, 148, 745-746.

Nass, R., & Gutman, R. (1997). Boys with Asperger’s disorder, exceptional verbal intelligence, tics, and clumsiness. Developmental Medicine and Child Neurology, 39, 691-695.

Rourke, B. P., & Tsatsanis, K. D. (2000). Syndrome of Nonverbal Learning Disabilities and Asperger syndrome. In A. Klin, F. Volkmar, & S. S. Sparrow (Eds.), Asperger syndrome (pp. 231-253). New York: Guilford Press.

Stevens, D. E., & Moffitt, T. E. (1988). Neuropsychological profile of an Asperger's syndrome case with exceptional calculating ability. The Clinical Neuropsychologist, 2, 228-238.

Tsatsanis, K.D. (2003). Outcome research in Asperger syndrome and autism. Child & Adolescent Psychiatric Clinics of North America, 12(1), 47-63.

Tsatsanis, K.D. (2004). Heterogeneity in learning style in Asperger syndrome and high-functioning autism. Topics in Language Disorders, 24(4), 260-270.

Tsatsanis, K.D., Foley, C., & Donehower, C. (2004). Contemporary outcome research and programming guidelines for Asperger syndrome and high-functioning autism. Topics in Language Disorders, 24(4), 249-259.

Volkmar, F. R., & Cohen, D. J. (1991). Nonautistic pervasive developmental disorders. Psychiatry, 2, 1-12.

Witt, J. N. (1996). Diagnostic issues in the neuropsychological and neurobehavioral assessment of a 12-year-old boy seen following epilepsy surgery. Archives of Clinical Neuropsychology, 11, 465-466.



NOTE:

THE INTERESTED READER MAY ALSO WISH TO CONSULT THE FOLLOWING FOR CASE STRUDIES THAT ILLUSTRATE TYPICAL FINDINGS IN YOUNGSTERS WITH MANY TYPES OF NEUROLOGICAL DISEASE DISORDER, AND DYSFUNCTION, INCLUDING AS, WHEREIN THE SYNDROME OF NLD FORMS A SIGNIFICANT PART OF THEIR BEHAVIOURAL PHENOTYPE:

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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