• J Neuroimaging · Jul 2000

    Regional cerebral distribution of [Tc-99m] hexylmethylpropylene amineoxine in patients with progressive aphasia.

    • A B Newberg, P D Mozley, A H Sadek, M Grossman, and A Alavi.
    • Division of Nuclear Medicine, University of Pennsylvania Medical Center, Philadelphia, USA.
    • J Neuroimaging. 2000 Jul 1; 10 (3): 162-8.

    AbstractProgressive aphasia is a prominent clinical feature of several neurodegenerative disorders. This study used hexylmethylpropylene amineoxine (HMPAO) single photon emission computed tomography (SPECT) to estimate blood flow in areas of the brain that mediate language in patients with progressive aphasia and matched control subjects. The patient population consisted of four men and 12 women with a mean +/- SD age of 69.1 +/- 7.6. Of these, eight were classified as having a nonfluent form of aphasia, whereas the other eight had a fluent form. The patients were compared to 16 healthy volunteers who were studied with an identical protocol. The SPECT images of the brain were acquired with 740 MBq (20 mCi) of Tc-99m-labeled HMPAO on a triple-headed gamma camera equipped with fan beam collimators. The images were analyzed with a set of standardized templates. Mean counts per pixel in 33 regions of interest were compared to the mean counts in the whole supratentorial brain. A laterality index was determined for homotopic regions using the equation 100 x (R - L)/(1/2 x (R - L)). Patients with progressive aphasia had several regions of significantly decreased HMPAO uptake in the left cortex when compared to the homotopic regions on the right. The most prominent deficit in the nonfluent group, as determined by the laterality index, were found in the left dorsolateral prefrontal region (p < 0.05), whereas the most prominent deficits in the group with fluent aphasia were found in the left temporal and parietal language centers (p < 0.05). The left subcortical nuclei were differentially affected, particularly in patients with nonfluent aphasia. The HMPAO SPECT indicates that multiple regions of the left hemisphere are dysfunctional in patients with progressive aphasia. The pattern of perfusion deficits in patients with fluent aphasia appears to be distinct from the pattern in patients with nonfluent aphasia.

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