PhD ThesisBackground
Accurate diagnosis of dementia with Lewy bodies (DLB) has important implications for
treatment and prognosis, but it is not currently clear how frequently DLB is diagnosed in
routine clinical practice, nor how frequently they are assigned an alternative dementia
diagnosis.
123I-metaiodobenzylguanidine (MIBG) may be capable of improving DLB diagnostic accuracy
but it has not been investigated in clinically representative populations that include patients
with comorbidities or interfering medications.
Methods
We conducted a cross-sectional survey of 5 569 patients attending three Psychiatry of Old
Age services. From this cohort, 51 DLB and 51 matched non-DLB cases consented to
extraction of data relating to the diagnostic process from their clinical case notes.
We enrolled a clinically representative cohort of 17 patients with DLB and 16 with
Alzheimer’s disease (AD) to a MIBG utility study. Each patient underwent detailed clinical
examination, cardiac MIBG and FP-CIT SPECT imaging.
Results
DLB represented 5.6% of dementia cases but prevalence varied across services (3.5-5.9%).
DLB cases were often given a different dementia subtype diagnosis (39%) and experienced a
longer time from referral to diagnosis (265 days) than non-DLB patients (154 days).
MIBG had a sensitivity and specificity of 71% and 75% for differentiating DLB from AD, but a
lower HMR threshold enhanced specificity (100%) without compromising sensitivity. No
significant relationships between HMR and either myocardial infarction, or medication
prescription, were identified.
ii
Conclusions
Variation in DLB prevalence across services may suggest differences in detection rather than
in the true prevalence of the disease. The higher frequency of clinical contacts seen in DLB
may provide opportunities to improve both diagnostic accuracy and time to diagnosis.
Our findings support the use of representative cohorts in further MIBG research, particularly
in determining appropriate HMR cut-offs. Our finding that three DLB patients had normal
MIBG, but abnormal FP-CIT results challenges the Braak hypothesis of DLB pathogenesi
