Right Frontotemporal Activation by Tonal Memory in Dyslexia, an O 15 PET Study Judith M. Rumsey, Paul Andreason, Alan J. Zametkin, A. Catherine King, Susan D. Hamburger, Tracy Aquino, Ashley P. Hanahan, Anita Pikus, and Robert M. Cohen A prior study documented the failure of dyslexic men to activate left temporoparietal cortex during phonologic processing. Because of reports of an anomalous right planum temporale in developmental dyslexia, the functional implications of which are unknown, this study examined the ability of dyslexics to activate right temporal cortex. Regional cerebral blood flow was measured in 15 right-handed dyslexic men during rest and during a tonal memory task expected to activate right-sided cortex in controls. A matched control sample (n = 18) showed significant activation of several rightfrontotemporal regions as well as of left temporal cortex. In contrast, severely dyslexic men activated fewer right frontotemporal regions, while making many more errors than controls, but showed normal activation of left mid to anterior temporal cortex. These results support hypothesized underlying deficits in rapid temporal processing and possible involvement of right (in addition to left) temporal cortex in severe dyslexia. Key Words: Dyslexia, cerebral bloodflow, positron emission tomography, cognitive activa- tion, tonal memory Introduction Although dyslexia is hypothesized to be a form of develop- mental language disorder(Mann and Brady 1988) involving the left hemisphere, recent neuroanatomic data suggest al- terations in the right hemisphere as well. Postmortem stud- ies of dyslexic brains (4 men, 3 women) have reported a lack of the usual left > right asymmetry of the planum temporale (seen in 67%-75% of the general population) (Galaburda et From the Child Psychiatry Branch (JMR, ACK, SDH, TA. APH) and the Section on Clinical Brain Imaging, Laboratory of Cerebral Metabolism (PA, AJZ, RMC) National Institute of Mental Health, and Clinical Audiology Branch, Hearing Section, National Institute on Deafness and Communication Disorders (AP), Bethesda, MA. Address reprint mtuests to Dr. Judith M. Rumsey, Child Psychiatry Branch, National Institute of Mental Health, Buildiog I0, Room 6N240. Bethesda, MA 20892. Received Febma~ 17, 1993; revised September22,1993. al 1985; Geschwind and Levitsky 1968; Humphreys et al 1990). Rather, the dyslexic brains were more symmetricas a result of an increase in size on the right, possibly because of a reduction in cell death on the right, leaving an excess of neurons in this region. As in the postmortem studies cited above, neuroanatomic imaging with both computed tomography (CT) and mag- netic resonance imaging (MR!) indicate alterations of nor- real posterior hemispheric asymmetries in dyslexia (Hynd and Semrud-Clikeman 1989). Recent MRI studies have, however, reported both increased symmetry, as well as re- versals of normal asymmetry in the region of the planum, although this structure is difficult to measure and handed- hess was not always well controlled (Duara et al 1991; Hynd and Semrud-Clikeman 1989; Hynd et al 1990; Larsen et al © 1994 Society of Biological Psychiatry 0006-3223/94/$07.00