Brain SPECT artifacts in patients having metallic cranioplasty.

OBJECTIVE: Over the past few years, we have performed several brain SPECT studies on patients who have had previous head trauma that required metallic cranioplasty. Transaxial images showed clearly defined photon-deficient areas extending from the brain tissue into the area of the scalp. To investigate the extent and pattern of this type of artifact, SPECT brain phantom studies were performed and compared with the patient studies. METHODS: SPECT brain phantom studies were performed using various metallic sheets to simulate metallic plates that were used for cranioplasty. RESULTS: Phantom studies using lead to represent tantalum plates were similar to our patient studies; that is, the photon-deficient area in normal brain tissue extended into the area where normal scalp activity would be. There was also increased tracer activity at the periphery of the photon-deficient area that extended to where normal scalp activity would be. This was similar to the patient studies and was not present on the phantom studies done without any metallic sheets present. CONCLUSION: One would expect photon-deficient artifacts caused by radiopaque metallic plates in brain SPECT studies. The patient and phantom studies demonstrate that an increased tracer activity artifact is also present at the periphery of the photon-deficient area that extends into the area of the scalp. Knowing the appearance of this type of artifact caused by radiopaque metallic plates in brain SPECT studies could be beneficial, especially in cases with poor patient history and lacking radiographic correlation.

Single SPECT measures of cerebral cortical perfusion reflect time-index estimation of dementia severity in Alzheimer's disease.

UNLABELLED: To determine the relationship between cerebral cortical blood flow loss and the temporal development of the dementia in Alzheimer's disease (AD), SPECT was studied in a cross section of AD patients with a broad range of impairment. METHODS: Thirty patients with a diagnosis of probable AD had their mini-mental state examination scores transformed into time-index values to give an estimation of dementia severity relative to the developmental time course. SPECT images were obtained using 99mTc-ethyl cysteinate dimer and a 3-head camera. Cortical surface perfusion was analyzed, including modified Talairach standardization, to obtain cortical elements from the convexity (each representing about 0.25 cm2 at the surface, 6.6-mm cortical depth) referenced to the mean perfusion of the full greater cerebellar hemisphere. These element ratios were analyzed (individually and by averages of estimated Brodmann's areas and brain regions) using linear regression with the time-index value. RESULTS: For individual posterotemporal and inferoparietal Brodmann's areas (21, 22 and 39, 40, respectively) the correlation coefficients between cortical perfusion ratios and dementia severity ranged between -0.67 and -0.78 (P < 0.001). Perfusion ratios from these regions declined 2.5%-4.2% for each estimated year of progression. Prefrontal area perfusion showed less association with severity. Perfusion in primary cortical regions had no significant association with dementia severity. CONCLUSION: Cerebral cortical perfusion loss is temporally related to development of dementia. The spatial pattern of high, significant correlations between cortical perfusion and dementia severity shows a regional distribution that corresponds closely to the distribution of AD pathology described in autopsy studies.