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Article: Rolf Jorde, Knut Waterloo, Hilde Storhaug, Audhild Nyrnes, Johan Sundsfjord, and Trond Geir Jenssen Neuropsychological function and symptoms in subjects with subclinical hypothyroidism and the effect of thyroxine treatment J Clin Endocrinol Metab 2005; 0: jc.2005-1775v1 [Abstract]

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Neuropsychological function in subjects with subclinical hypothyroidism

Rolf Jorde, Knut Waterloo, Hilde Storhaug, Audhild Nyrnes, Johan Sundsfjord, and Trond G. Jenssen   (3 January 2006)

Neuropsychological Function in Subjects with Subclinical Hypothyroidism

James V Hennessey, Jennifer Duncan Davis and Geoffrey Tremont   (19 December 2005)

Neuropsychological function in subjects with subclinical hypothyroidism 3 January 2006
Rolf Jorde, Professor Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway, Knut Waterloo, Hilde Storhaug, Audhild Nyrnes, Johan Sundsfjord, and Trond G. Jenssen Send letter to journal: Re: Neuropsychological function in subjects with subclinical hypothyroidism rolf.jorde{at}unn.no Rolf Jorde, et al.	Dr. Hennessey's points are well taken. The groups he suggests should also be thoroughly studied. In general, it is important for clinical studies to describe meticulously the subjects included, and in this respect, we believe his comment shows that we have been successful.
Neuropsychological Function in Subjects with Subclinical Hypothyroidism 19 December 2005
James V Hennessey, Endocrinologist Brown Medical School/Rhode Island Hospital, Jennifer Duncan Davis and Geoffrey Tremont Send letter to journal: Re: Neuropsychological Function in Subjects with Subclinical Hypothyroidism jhennessey{at}lifespan.org James V Hennessey, et al.	In the study of Jorde et al., there was no difference in neuropsychological functioning or hypothyroid symptoms in individuals with subclinical hypothyroidism with a TSH 3.5–10.0 mIU/L compared to healthy controls. Not surprisingly, thyroxine substitution had no effect. Although the authors conclude that thyroxine treatment should not be initiated for a mildly elevated serum TSH level, we believe that, the study did not conclusively address the impact of mild hypothyroidism on neuropsychological functioning. First, subjects with TSH values in the goal range, but “without obvious clinical symptoms of hypothyroidism” were excluded. The individuals excluded are the group of greatest interest to study in terms of neuropsychological functioning and thyroxine treatment response. Second, the mean TSH in this sample was 5.6 mIU/L, indicating that participants with TSH values in the 3.5-5.0 mIU/L range were overrepresented. Therefore, the sample appears to have been biased toward a group with milder thyroid hormone deficiency who may have been less likely to have neuropsychological symptoms. Third, the authors excluded patients on thyroid medication with undertreated hypothyroidism and individuals over age 80 years, both of which might have been informative. All of these factors may have biased the results toward not finding a relationship between subclinical hypothyroidism and neuropsychological symptoms. We think that the most appropriate conclusions from this study are that there are no cognitive or emotional changes or responses to thyroxine in individuals who are asymptomatic with TSH levels ranging from 3.5-10 mIU/L. Future studies should address neuropsychological functioning in symptomatic individuals with TSH ranging from 3.5-10 mIU/L, the group most likely to be treated based on current practice. Furthermore, studies should examine differences across age cohorts to determine if the potential for cognitive sequelae is greater in affected older adults.