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Funding Acknowledgements Type of funding sources: None. Background/Introduction Few studies have examined the relationship between exercise and adherence to antihypertensive medication, examining all possible factors contributing to blood pressure control. Purpose The purpose of our study was to access the possible dependence relationship among hypertensive patients visiting the Behavioral Cardiology Unit in a Tertiary Hospital. Methods The study population consisted of patients reporting to the Behavioral Cardiology Unit in a Tertiary Hospital during a period of 6 months in 2021. In terms of holistic approach, all patients underwent a thorough clinical in-depth interview, using the Morisky Medication Adherence Scale (MMAS8), the Frail Questionnaire Screening Tool (Frailty Score) and the Patient Health Questionnaire-4 (PHQ-4). All patients also provided full history of exercise (at least 150 minutes of physical activity or 75 minutes of intense activity per week), while completing the Duke Activity Status Index (DASI). Results The population consisted of 42 hypertensive patients, 54.8% of them were females, with a mean age of all patients at 55.8±15.2 years. Body Mass Index was averaging at 27.6 kg/m2. Salt consumption above the daily suggested amount (>5gr/day) was reported by 60% of patients, binge drinking by 43% of them, while 43% had a history of active smoking. High adherence was reported by 17 patients (46%), medium adherence by 14 (37.8%) and low adherence by 6 (16.2%). Results indicate a relationship between exercise and adherence to medication. More specifically, Chi-Square test showed statistical significance between exercise and medium medication adherence in MMAS8 (MMAS8: 6-7, p=0.033). Moreover, statistical analysis showed significant relationship between exercise, frailty and PHQ-4 score. Particularly, patients with absence of exercise showed higher level of PHQ-4 score (F=7.07, p=0.011). Conclusions Our study highlights the possible dependency relationship of exercise and adherence to medication. Results indicate that patients with good adherence to medication have better behavioral activation. There is need for further research in this domain, to confirm the findings.

BackgroundThe role of blood uric acid and more recently bilirubin as biomarkers in symptomatic motor PD has been increasingly established in the literature.ObjectiveOur present study assessed the role of serum uric acid and total bilirubin as putative biomarkers in a prodromal PD cohort followed longitudinally.MethodsLongitudinal 5-year serum uric acid and total bilirubin measurement data of 65 Prodromal PD patients (including REM Sleep Behavior disorder (RBD), N=39 and Hyposmia, N=26) with an abnormal DATSCAN imaging were downloaded from the Parkinson’s Progression Markers Initiative (PPMI) database. This cohort was compared with 423 de novo sporadic PD patients and 196 healthy controls enrolled in the same study.ResultsAfter adjusting for age, sex and Body Mass Index (BMI), baseline and 5-year longitudinal serum uric acid levels were higher in the Prodromal cohort and RBD subgroup as compared to the motor PD cohort. This was also true for longitudinal measurements in the Hyposmic subgroup. In contrast, baseline and longitudinal serum total bilirubin did not differ between each prodromal group and the PD cohort.ConclusionsOur results are indicative of a role of serum uric acid (but probably not of total bilirubin) as a marker of neuroprotection, in a certain subgroup of premotor patients exhibiting exclusively non motor features (hyposmia or RBD). It is possible that an inherent antioxidant resistance of a subset of RBD or hyposmia patients with high serum uric acid level delayed or precluded the emergence of a motor PD phenotype as opposed to the PD cohort.

BackgroundHigher prevalence of motor and non-motor features has been observed in non-manifesting mutation carriers of Parkinson’s Disease (PD) compared to Healthy Controls (HC).ObjectivesThe aim was to detect the differences between GBA and LRRK2 mutation carriers without PD and HC on neuropsychiatric symptoms.MethodsThis is a cross-sectional retrospective study of non-manifesting GBA and LRRK2 mutation carriers and HC enrolled into Parkinson’s Progression Markers Initiative (PPMI). Data extracted from the PPMI database contained: demographics and performance in MoCA scale and MDS-UPDRS scale part 1A (neuropsychiatric symptoms). All six features were treated as both continuous (MDS-UPDRS individual scores) and categorical variables (MDS-UPDRS individual score>0 and MDS-UPDRS individual score=0). Logistic regression analyses were applied to evaluate the association between mutation carrying status and neuropsychiatric symptoms.ResultsWe found that non-manifesting mutation carriers as a whole (total N=654, GBA: n=285, LRRK2: n=369) were 2.3 times more likely to present apathy compared to HC, even after adjustment for covariates (adjusted OR=2.3, 95% CI=1.1-5.0, p-value=0.027). The effect was mainly driven by GBA mutation carriers (adjusted OR= 2.6, 95% CI=1.1-6.3, p=0.031), while the higher percentage of apathy for LRRK2 carriers compared to HC was marginally non-significant. Other neuropsychiatric symptoms, such as psychotic or depressive manifestations, did not differ between groups.ConclusionsSymptoms of apathy could be present in the premotor period of LRRK2 and, especially, GBA mutation carriers. Longitudinal data, including detailed neuropsychiatric evaluation and neuroimaging, would be essential to further investigate the pathophysiological basis of this finding.

Background: Previous studies have highlighted serum uric acid as a putative idiopathic Parkinson’s disease (iPD) biomarker. Only one study, so far, showed higher levels of serum uric acid in leucine-rich repeat kinase 2 (LRRK + 2) carriers compared to those who developed PD, however a longitudinal comparison between LRRK2 + PD and healthy controls (HC) has not been performed. Objective: The aim of this study was to determine whether there are longitudinal differences in serum uric acid between iPD, LRRK2 + PD and HC and their association with motor and non-motor features. Methods: Longitudinal data of uric acid of 282 de novo iPD, 144 LRRK2 + PD patients, and 195 age-matched HC were obtained from the Parkinson’s Progression Markers Initiative (PPMI) database. We also used longitudinal Montreal Cognitive Assessment (MoCA), Movement Disorder Society–Unified Parkinson’s Disease Rating Scale part III (MDS-UPDRS-III), Geriatric Depression Scale (GDS) scores, and DaTSCAN striatal binding ratios (SBRs). Results: Longitudinal uric acid measurements were significantly lower in LRRK2 + PD patients compared to HC up to 5 years follow-up. There was no significant impact or correlation of adjusted or unadjusted uric acid levels with MoCA, MDS-UPDRS III, or GDS scores, the presence of RBD or DAT-SCAN SBRs. Conclusion: LRRK2 + PD group had significantly lower uric acid concentrations compared to HC after adjusting for age, sex and baseline BMI up to 5 years follow-up. There were no significant associations between uric acid levels and indices of disease severity. These findings identify serum uric acid as a marker linked to LRRK2 + PD.

Background: Previous studies have highlighted serum uric acid as a putative idiopathic Parkinson's disease (iPD) biomarker. Only one study, so far, showed higher levels of serum uric acid in leucine-rich repeat kinase 2 (LRRK+2) carriers compared to those who developed PD, however a longitudinal comparison between LRRK2+PD and healthy controls (HC) has not been performed. Objective: The aim of this study was to determine whether there are longitudinal differences in serum uric acid between iPD, LRRK2+PD and HC and their association with motor and non-motor features. Methods: Longitudinal data of uric acid of 282 de novo iPD, 144 LRRK2+PD patients, and 195 age-matched HC were obtained from the Parkinson's Progression Markers Initiative (PPMI) database. We also used longitudinal Montreal Cognitive Assessment (MoCA), Movement Disorder Society-Unified Parkinson's Disease Rating Scale part III (MDS-UPDRS-III), Geriatric Depression Scale (GDS) scores, and DaTSCAN striatal binding ratios (SBRs). Results: Longitudinal uric acid measurements were significantly lower in LRRK2+PD patients compared to HC up to 5 years follow-up. There was no significant impact or correlation of adjusted or unadjusted uric acid levels with MoCA, MDS-UPDRS III, or GDS scores, the presence of RBD or DAT-SCAN SBRs. Conclusion: LRRK2+PD group had significantly lower uric acid concentrations compared to HC after adjusting for age, sex and baseline BMI up to 5 years follow-up. There were no significant associations between uric acid levels and indices of disease severity. These findings identify serum uric acid as a marker linked to LRRK2+PD. © 2021 - IOS Press. All rights reserved.

Introduction: Higher prevalence of motor and non-motor features has been observed in non-manifesting mutation carriers of Parkinson's Disease (PD) compared to Healthy Controls (HC). The aim was to detect the differences between GBA and LRRK2 mutation carriers without PD and HC on neuropsychiatric symptoms. Methods: This is a cross-sectional retrospective study of non-manifesting GBA and LRRK2 mutation carriers and HC enrolled into Parkinson's Progression Markers Initiative (PPMI). Data extracted from the PPMI database contained: demographics and performance in MoCA scale and MDS-UPDRS scale part 1A (neuropsychiatric symptoms). All six features were treated as both continuous (MDS-UPDRS individual scores) and categorical variables (MDS-UPDRS individual score>0 and MDS-UPDRS individual score = 0). Logistic regression analyses were applied to evaluate the association between mutation carrying status and neuropsychiatric symptoms. Results: In this study, the neuropsychiatric evaluation was performed in 285 GBA non-manifesting carriers, 369 LRRK2 non-manifesting carriers and 195 HC. We found that GBA non-manifesting mutation carriers were 2.6 times more likely to present apathy compared to HC, even after adjustment for covariates (adjusted OR = 2.6, 95% CI = 1.1–6.3, p = 0.031). The higher percentage of apathy for LRRK2 carriers compared to HC was marginally non-significant. GBA carriers were 1.5 times more likely to develop features of anxiety compared to LRRK2 carriers (adjusted OR = 1.5, 95% CI = 1.1–2.2, p = 0.015). Other neuropsychiatric symptoms, such as psychotic or depressive manifestations, did not differ between groups. Conclusion: Symptoms of apathy could be present in the prediagnostic period of non-manifesting mutation carriers, especially, GBA. Longitudinal data, including detailed neuropsychiatric evaluation and neuroimaging, would be essential to further investigate the pathophysiological basis of this finding. © 2021

Blood uric acid represents an important biomarker in sporadic Parkinson's disease (PD). Whether uric acid levels change in genetic forms of PD is beginning to be assessed. The aim of the present study was to evaluate differences in serum uric acid level among PD patients harboring mutations in the glucocerebrosidase (GBA1) gene, sporadic PD, and healthy controls followed longitudinally.Longitudinal 2-year serum uric acid measurement data of 120 GBA-PD patients have been downloaded from the Parkinson's Progression Markers Initiative (PPMI) database. This cohort was compared with 369 de novo sporadic PD patients and 195 healthy controls enrolled in the same study.Following adjustment for age, sex and BMI the GBA-PD cohort exhibited lower 2-year longitudinal uric acid level as compared to the controls (p = 0.016). Baseline uric acid measurements showed only a marginal difference (p = 0.119), but year 2 uric acid levels were lower in the GBA-PD cohort (p 0.001). There was no difference in baseline, year 2 and 2-year longitudinal serum uric acid in the GBA-PD cohort as compared to sporadic PD (p = 0.664, p = 0.117 and p = 0.315).This is the first study to assess serum uric acid in a GBA-PD cohort. Our findings suggest that low serum uric acid might be a progression biomarker in GBA-PD. However, more studies (ideally longitudinal) on the association between low serum uric acid and clinical data in GBA-PD are needed. These results are consistent with data from previous reports assessing uric acid as a biomarker in other genetic forms of PD.

Background Blood uric acid level represents an emerging biomarker in Parkinson's disease (PD). Whether uric acid levels change in genetic forms of PD is just beginning to be explored. Objective The aim of the present study was to assess differences in serum uric acid level among PD patients harboring the p.A53T mutation in the alpha-synuclein gene, idiopathic PD, and healthy controls. Methods Longitudinal 5-year serum uric acid measurement data of 369 de novo idiopathic PD patients and 174 age- and gender-matched healthy controls have been downloaded from the Parkinson's Progression Markers Initiative (PPMI) database. Furthermore, we assessed baseline serum uric acid measurements of 24 p.A53T alpha-synuclein PD patients enrolled in PPMI and followed in our site as compared to 24 age-, gender- and disease duration-matched sporadic PD patients and 24 healthy controls. Results Longitudinal serum uric acid measurements did not differ statistically between idiopathic PD patients and healthy controls (despite a trend for lower uric acid in the PD group) (p = 0.879). This was also true when male and female subgroups were assessed separately. The p.A53T SNCA mutation carrier PD group exhibited lower baseline serum uric acid level as compared to their matched healthy controls (p = 0.025). Conclusion In the present study we did not replicate the established lower serum uric acid measurements in PD patients as compared to controls using PPMI data, possibly due to the fact that PD patients in baseline visit were de novo and the average disease duration was shorter than that observed in most epidemiological PD studies. The faster progression rate and increased disease severity in p.A53T PD possibly correlate with the lower serum uric acid observed in this subgroup.

Introduction: It has been reported that early onset Parkinson’s Disease (PD) patients have a less profound dopaminergic degeneration. The aim of the current study was to determine whether there are longitudinal differences in dopaminergic denervation [signal reduction in 123I-FP-CIT SPECT] in early versus mid and late onset PD. Methods: DaTSCAN (123I-FP-CIT SPECT) imaging was acquired at Parkinson’s Progression Markers Initiative (PPMI) imaging centers and sent to the imaging core for calculation of striatal binding ratios. Data from the PPMI database of 58 early de novo PD patients (age 50 years). Results: Although raw striatal binding ratios were higher in early onset versus mid/late onset PD, especially on the ipsilateral side, such differences were not observed, and were in fact reversed in the contralateral putamen, after age correction. The rate of signal decline was similar between the two groups. Interestingly, based on both raw and age-adjusted data, caudate nucleus and putamen asymmetry (contralateral/ipsilateral ratio) was more pronounced in early onset PD. Striatal asymmetry also significantly correlated with age at onset as a continuous variable. Conclusion: Early onset PD patients exhibited similar rates of decline of dopaminergic denervation compared to mid/late onset PD. These results are not supportive of a more benign disease in this subgroup. The more pronounced asymmetry in early onset PD may however signify a qualitatively different pattern of neurodegeneration compared to mid/late onset PD.

Background: Blood uric acid level represents an emerging biomarker in Parkinson's disease (PD). Whether uric acid levels change in genetic forms of PD is just beginning to be explored. Objective: The aim of the present study was to assess differences in serum uric acid level among PD patients harboring the p.A53T mutation in the alpha-synuclein gene, idiopathic PD, and healthy controls. Methods: Longitudinal 5-year serum uric acid measurement data of 369 de novo idiopathic PD patients and 174 age- and gender-matched healthy controls have been downloaded from the Parkinson's Progression Markers Initiative (PPMI) database. Furthermore, we assessed baseline serum uric acid measurements of 24 p.A53T alpha-synuclein PD patients enrolled in PPMI and followed in our site as compared to 24 age-, gender- and disease duration-matched sporadic PD patients and 24 healthy controls. Results: Longitudinal serum uric acid measurements did not differ statistically between idiopathic PD patients and healthy controls (despite a trend for lower uric acid in the PD group) (p = 0.879). This was also true when male and female subgroups were assessed separately. The p.A53T SNCA mutation carrier PD group exhibited lower baseline serum uric acid level as compared to their matched healthy controls (p = 0.025). Conclusion: In the present study we did not replicate the established lower serum uric acid measurements in PD patients as compared to controls using PPMI data, possibly due to the fact that PD patients in baseline visit were de novo and the average disease duration was shorter than that observed in most epidemiological PD studies. The faster progression rate and increased disease severity in p.A53T PD possibly correlate with the lower serum uric acid observed in this subgroup.

Background The p.A53T point mutation in the α-synuclein gene (SNCA) is a rare but highly relevant cause of autosomal dominant Parkinson's disease (PD). Objectives The objective of this study was to assess striatal dopaminergic denervation in a cohort of symptomatic carriers of the p.A53T SNCA mutation as compared to PD patients. Methods Data from the Parkinson's Progression Markers Initiative database of 11 symptomatic p.A53T SNCA mutation carriers who underwent 123I-FP-CIT SPECT [(123) I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl) nortropane single photon emission computed tomography] imaging at our site were compared with those of 33 age-, sex-, and disease duration-matched PD patients. Results The p.A53T mutation carriers had significantly lower caudate nucleus binding ratio both contralaterally and ipsilaterally to the most affected side (P = .002 and P = .006) and a decreased contralateral caudate/putamen signal ratio (P = .007) as compared to PD. A similar degree of striatal asymmetry was observed in both subgroups. No correlation between scores in neuropsychological tests and caudate nucleus dopaminergic denervation could be demonstrated. Conclusions PD patients harboring the p.A53T SNCA mutation show evidence of a more severe nigrostriatal denervation, especially evident in the caudate nucleus. The lack of significant differences in the putaminal binding ratios may reflect a floor effect or a true preferential targeting of the caudate terminals in p.A53T SNCA-associated PD. © 2018 International Parkinson and Movement Disorder Society.

Introduction It has been reported that early onset Parkinson's Disease (PD) patients have a less profound dopaminergic degeneration. The aim of the current study was to determine whether there are longitudinal differences in dopaminergic denervation [signal reduction in 123I-FP-CIT SPECT] in early versus mid and late onset PD. Methods DaTSCAN (123I-FP-CIT SPECT) imaging was acquired at Parkinson's Progression Markers Initiative (PPMI) imaging centers and sent to the imaging core for calculation of striatal binding ratios. Data from the PPMI database of 58 early de novo PD patients (age ≤ 50 years) were compared to those of 362 mid and late onset PD patients (age > 50 years). Results Although raw striatal binding ratios were higher in early onset versus mid/late onset PD, especially on the ipsilateral side, such differences were not observed, and were in fact reversed in the contralateral putamen, after age correction. The rate of signal decline was similar between the two groups. Interestingly, based on both raw and age-adjusted data, caudate nucleus and putamen asymmetry (contralateral/ipsilateral ratio) was more pronounced in early onset PD. Striatal asymmetry also significantly correlated with age at onset as a continuous variable. Conclusion Early onset PD patients exhibited similar rates of decline of dopaminergic denervation compared to mid/late onset PD. These results are not supportive of a more benign disease in this subgroup. The more pronounced asymmetry in early onset PD may however signify a qualitatively different pattern of neurodegeneration compared to mid/late onset PD.

Background: The p.A53T point mutation in the alpha-synuclein gene (SNCA) is a rare but highly relevant cause of autosomal dominant Parkinson’s disease (PD). Objectives: The objective of this study was to assess striatal dopaminergic denervation in a cohort of symptomatic carriers of the p.A53T SNCA mutation as compared to PD patients. Methods: Data from the Parkinson’s Progression Markers Initiative database of 11 symptomatic p.A53T SNCA mutation carriers who underwent 123I-FP-CIT SPECT [(123) I-2 beta-carbomethoxy-3 beta-(4-iodophenyl)-N-(3-fluoropropyl) nortropane single photon emission computed tomography] imaging at our site were compared with those of 33 age-, sex-, and disease duration-matched PD patients. Results: The p.A53T mutation carriers had significantly lower caudate nucleus binding ratio both contralaterally and ipsilaterally to the most affected side (P = .002 and P = .006) and a decreased contralateral caudate/putamen signal ratio (P = .007) as compared to PD. A similar degree of striatal asymmetry was observed in both subgroups. No correlation between scores in neuropsychological tests and caudate nucleus dopaminergic denervation could be demonstrated. Conclusions: PD patients harboring the p.A53T SNCA mutation show evidence of a more severe nigrostriatal denervation, especially evident in the caudate nucleus. The lack of significant differences in the putaminal binding ratios may reflect a floor effect or a true preferential targeting of the caudate terminals in p.A53T SNCA-associated PD. (c) 2018 International Parkinson and Movement Disorder Society

The p.A53T point mutation in the α-synuclein gene (SNCA) is a rare but highly relevant cause of autosomal dominant Parkinson's disease (PD).The objective of this study was to assess striatal dopaminergic denervation in a cohort of symptomatic carriers of the p.A53T SNCA mutation as compared to PD patients.Data from the Parkinson's Progression Markers Initiative database of 11 symptomatic p.A53T SNCA mutation carriers who underwent 123I-FP-CIT SPECT [(123) I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl) nortropane single photon emission computed tomography] imaging at our site were compared with those of 33 age-, sex-, and disease duration-matched PD patients.The p.A53T mutation carriers had significantly lower caudate nucleus binding ratio both contralaterally and ipsilaterally to the most affected side (P = .002 and P = .006) and a decreased contralateral caudate/putamen signal ratio (P = .007) as compared to PD. A similar degree of striatal asymmetry was observed in both subgroups. No correlation between scores in neuropsychological tests and caudate nucleus dopaminergic denervation could be demonstrated.PD patients harboring the p.A53T SNCA mutation show evidence of a more severe nigrostriatal denervation, especially evident in the caudate nucleus. The lack of significant differences in the putaminal binding ratios may reflect a floor effect or a true preferential targeting of the caudate terminals in p.A53T SNCA-associated PD. © 2018 International Parkinson and Movement Disorder Society.

In this paper, we present a fuzzy-logic based model for the diagnosis of the so-called students' learning profile. The fuzzy logic module is coupled with an interactive open learning environment (StuDiAsE) that incorporates the text comprehension theory by Denhiere and Baudet, the dialogue theory of Collins and Beranek, and the learning styles theory of Felder and Silverman. This intelligent learning environment is used for diagnosis, assistance and evaluation of engineering students. Preliminary tests for student assessment displayed high influence on the performance and motivation of its users.

Radiographers constitute an important part of a multidisciplinary radiation-based imaging and therapy chain. However, is there a common framework for assuring high education, training, and subsequent practice of profession among European countries? A study was conducted, based on a questionnaire that consisted of three parts, concerning education and training (Part A), national registry (Part B), and professional issues (Part C). Analysis of the collected data suggested that a common policy is generally followed in the countries investigated; however, differences were not negligible. A common framework of educational programmes among European countries could form the basis for overall standardisation at national and international level.Keywords: radiographer, education, training, practice, continuing professional development(Published: 5 April 2016)Citation: Journal of European CME 2016, 5: 31092 - http://dx.doi.org/10.3402/jecme.v5.31092

Purpose The clinical medical physicist is part of a team responsible for safe and competent provision of radiation-based diagnostic examinations and therapeutic practices. To ensure that the physicist can provide an adequate service, sufficient education and training is indispensable. The aim of this study is to provide a structured description of the present status of the clinical medical physicist education and training framework in 25 European, 2 North American and 2 Australasian countries. Methods For this study, data collection was based on a questionnaire prepared by the European Federation of Organizations in Medical Physics (EFOMP) and filled-in either by the corresponding scientific societies-organizations or by the authors. Results In the majority of cases, a qualified medical physicist should have an MSc in medical physics and 1–3 years of clinical experience. Education and training takes place in both universities and hospitals and the total duration of the programs ranges from 2.5 to 9 years. In 56% of all European countries, it is mandatory to hold a diploma or license to work as a medical physicist, the situation being similar in Australasian and 4 states of USA. Generally, there are national registers of medical physicists with inclusion on the register being voluntary. There are renewal mechanisms in the registers usually based on a Continuing Professional Development (CPD) system. Conclusions In conclusion, a common policy is followed in general, on topics concerning education and training as well as the practice of the medical physicist profession, notwithstanding the presence of a few differences.

Brain perfusion imaging by means of 99mTc-labeled hexamethyl propylene amine oxime (HMPAO) is a well-established Nuclear Medicine diagnostic procedure. The administered dose range recommended by the supplying company and reported in bibliography is rather wide (approximately 9.5-27 mCi). This fact necessitates further quantitative analysis of the technique, so as to minimise patient absorbed dose without compromising the examination diagnostic value. In this study, a quantitative evaluation of the radiopharmaceutical performance for different values of administered dose (10, 15, 20 mCi) was carried out. Subsequently, a generic image quality index was correlated with the administered dose, to produce an overall performance indicator. Through this cost-to-benefit type analysis, the necessity of administration of higher radioactive dose levels in order to perform the specific diagnostic procedure was examined.Materials & methods: The study was based on a sample of 78 patients (56 administered with 10 mCi, 10 with 15 mCi and 12 with 20 mCi). Some patients were classified as normal, while others presented various forms of pathology. Evaluation of image quality was based on contrast, noise and contrast-to-noise ratio indicators, denoted CI, NI and CNR respectively. Calculation of all indicators was based on wavelet transform. An overall performance indicator (denoted PI), produced by the ratio of CNR by administered dose, was also calculated.Results: Calculation of skewness parameter revealed the normality of CI, NI and non-normality of CNR, PI populations. Application of appropriate statistical tests (analysis of variance for normal and Kruskal-Wallis test for non-normal populations) showed that there is a statistically significant difference in CI (p0.05) values. Application of Tukey test for normal populations CI, NI led to the conclusion that CI(10 mCi) = CI(20 mCi)NI(20 mCi), while NI(15 mCi) can not be characterised. Finally, application of non-parametric multiple comparisons showed that CNR(20 mCi)>CNR(10 mCi), while CNR(15 mCi) can not be characterised.Conclusion: Brain perfusion imaging by means of 99mTc- HMPAO utilising an administered dose of 20 mCi results in improved image quality, on the basis of the estimated indicators and for the range of radioactive dose levels examined. Additionally, this image quality improvement is sufficient to justify the increased radiation burden for the patient.