Abstract
We write to raise a number of questions regarding this study [1]. There is a paucity of data on the acquisition methodology of the cerebral perfusion studies. As 99m Tc HMPAO is an unstable agent, what was the level of quality assurance on the radiopharmaceutical prior to injection? Were these patients injected with eyes patched and ears plugged? If this was not done, it would make calculations of occipital and temporal uptake difficult to interpret. What type of camera were the studies acquired on and with what type of collimation? Such patients are difficult to image as they rarely comply with lying still for the duration of the study. How was this achieved and were images routinely checked for patient motion? Was this performed on MRI studies for each patient and then transferred to coregistered 99m Tc HMPAO images? What was the variability of count statistics in the regions of interest? How reproducible were regions of interest and the counting statistics for these regions of interest as ascribed or interpreted by each nuclear medicine observer?
One of the problems with the use of 99m Tc HMPAO in assessment of cerebral blood flow is that the rate of first-pass extraction falls with increases in cerebral blood flow [2]. This may have been an issue in patients who were anxious or agitated, particularly if injected without eyes patched and ears plugged. Was any correction or allowance given to this possibility? What other medications were the patients on at the time of the cerebral perfusion studies?
In the normal group, only three volunteers underwent neuropsychological assessment. Was the cerebral perfusion data for the normal population therefore only based on the results of these three volunteers or drawn from the five patients who underwent cerebral perfusion studies? Was there any attempt to age-match the normal to the patient population as there is variability in cerebral perfusion with increasing age? What was the variability of the regional data in the normal patients? Did this change between the three normals who underwent neuropsychological assessment versus that data from the addition of the other two patients?
What is the significance of cerebellar hyperperfusion? Is this a marker of relatively reduced blood flow to the cerebral hemispheres or a primary manifestation of the disease process? Was any attempt made to absolutely quantify cerebral blood flow in the patient population to correct for such possibilities?
The study appears to be methodologically flawed by virtue of the small number of patients and more importantly the tiny number of normal volunteers with no attempt at age-matching. Such variables would have significantly degraded the veracity of the results and rendered the conclusions questionable.