A TC-99M-HMPAO SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY STUDY OF LEWY-BODY-DISEASE

Citation
Ar. Varma et al., A TC-99M-HMPAO SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY STUDY OF LEWY-BODY-DISEASE, Journal of neurology, 244(6), 1997, pp. 349-359
Citations number
57
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
03405354
Volume
244
Issue
6
Year of publication
1997
Pages
349 - 359
Database
ISI
SICI code
0340-5354(1997)244:6<349:ATSECS>2.0.ZU;2-Y
Abstract
The purpose of this study was to investigate patterns of Tc-99m-HMPAO single-photon emission computed tomography (SPECT) abnormality in Lewy body disease (LED) and to compare findings with those encountered in Alzheimer's disease (AD). The study group comprised 20 consecutive pat ient referrals fulfilling clinical criteria for LED. All patients had fluctuating cognitive impairment and 'subcortical' dysfunction with or without perceptuospatial and/or linguistic impairment. Six patients h ad asymmetrical signs of parkinsonism (three left-sided and three righ t-sided), and 14 patients had symmetrical features of extrapyramidal i nvolvement. Tc-99m-HMPAO SPECT imaging was performed on LED patients a nd findings compared with those of 57 patients with 'probable' AD and 11 normal age-matched controls. Within the LED and AD groups, patterns of cortical and subcortical blood-flow abnormality were compared with patterns of cognitive and neurological breakdown. LED was associated with bilateral posterior cortical blood flow abnormality, a pattern st rikingly similar to that found in AD. Within the LED group, cortical b lood-flow abnormality was found to reflect patterns of neurological dy sfunction (parkinsonism) indicative of subcortical involvement. In con trast, cortical blood-flow changes did not reflect patterns of neurops ychological impairment suggestive of cortical dysfunction. Within the AD group, cortical blood-flow changes were mirrored by the pattern of neuropsychological impairment. Findings support the notion that cortic al bloodflow abnormality in LED might reflect a combination of direct cortical pathology and cortical deafferentation secondary to subcortic al Lewy body pathology. It would appear that Tc-99m-HMPAO SPECT imagin g is of limited value in the clinical differentiation of LED and AD.