Psychological Medicine



Original Article

Structural brain correlates of IQ changes in bipolar disorder


S. D. BRUNO a1, K. PAPADOPOULOU a1, M. CERCIGNANI a1, L. CIPOLOTTI a1 and M. A. RON a1c1
a1 Institute of Neurology, University College London, UK

Article author query
bruno sd   [PubMed][Google Scholar] 
papadopoulou k   [PubMed][Google Scholar] 
cercignani m   [PubMed][Google Scholar] 
cipolotti l   [PubMed][Google Scholar] 
ron ma   [PubMed][Google Scholar] 

Abstract

Background. There is increasing evidence that cognitive deficits are present in bipolar disorder (BP), but their neural correlates have not been fully explored. The aim of this study is to correlate structural brain abnormalities with cognitive performance in BP and to explore differences between clinical subtypes.

Method. Thirty-six BP patients (13 men, 23 women) with a mean age of 39 years (range 21–63 years) underwent neuropsychological testing and imaging. Twenty-five patients had bipolar disorder I (BP I) and 11 had bipolar disorder II (BP II). Patients with co-morbid psychiatric diagnosis, drug and alcohol abuse or systemic illness were excluded. Correlations between cognitive performance and structural brain changes were explored using high-resolution anatomical imaging and magnetization transfer imaging (MTI).

Results. In the whole BP group the difference between estimated pre-morbid IQ and current IQ was significantly correlated with left-sided reduction of the magnetization transfer ratio (MTR) in the superior temporal gyrus, uncus and para-hippocampal gyrus. In BP II patients the areas where these correlations were significant extended to the right superior and middle temporal gyri, cingulate gyrus, pre-cuneus and adjacent frontal and parietal white matter. The volume of superior temporal white matter was also correlated with IQ difference in this subgroup.

Conclusions. The study highlights the association between fronto-temporal abnormalities and decline in IQ in BP. The more extensive abnormalities present in BP II patients suggest that persistent depression, rather than mania, may be a key pathophysiological factor or that BP II represents a clinical phenotype with a higher risk of developing cognitive abnormalities.

(Published Online February 10 2006)


Correspondence:
c1 Box 15, Institute of Neurology, Queen Square, London WC1N 3BG, UK. (Email: [email protected])


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