Middlekoop et al. [1] examined whether occipital lobe hypoperfusion
and hypometabolism observed in dementia with Lewy bodies (DLB) and
sometimes in Alzheimer’s disease (AD) is associated with occipital lobe
atrophy. They found normal occipital lobe volumes in both diseases.
We studied 15 patients with probable AD, 15 patients with probable AD
(14 DLB and 1AD patient with visual hallucinations) and 12 controls using
a similar protocol. The groups had comparable ages (70.4+8, 70.1+9.1,
66+5.9; means + SD; p=0.23, Kruskal-Wallis ANOVA). Length of history of
dementia (DLP 2.9+2.5, AD 2.4+1.4 years; p=0.22) and Mini-Mental State
Examination scores (DLP 21.0+4.8, AD 18.1+5.2; p=0.85, Mann-Whitney U
test) were comparable. The study was performed on a Siemens Magnetom
Vision plus 1.5 Tesla MRI unit using T1-weighted, three-dimensional MPRAGE
sagittal sequences (slice thickness 1.2 mm, TR 9.7 msec, TE 4 msec, flip
angle 12 deg. Matrix 200 x 256 mm, pixel size 1.2 x 0.94mm) and a Allegro
work station (ISG Technologies, Canada). Forebrain, occipital lobe and
supratentorial subarachnoid space volumes were measured by one experienced
person blinded to the diagnosis using a semiautomated segmentation
process.
Because of different intracranial volumes (DLB 1262.2+95.9, DAT
1154.2+149.7, controls 1136.1+87.2 cm3; p=.009), occipital lobe (DLB
120.2+12.7, DAT 111.1+13.1, controls 121.6+9.6 cm3) and forebrain volumes
(925.8+101.9, DAT 817.6+110.3, controls 897.6+93.86 cm3 were normalized
(divided by intracranial volumes). Normalized forebrain volumes (NFV) were
significantly smaller in AD (0.71+0.1, p=0.003) and insignificantly
smaller in DLB (0.73+0.09, p=0.0.57) than in controls (0.79+0.09), and
similar in DLB and AD (p=0.039). Normalized occipital lobe volumes (NOV)
were smaller in DLB (0.095+0.01) and AD (0.096+0.01), p=0.02 than in
controls (0.107+0.01), p=0.07 and similar in DLB and DAT (p=0.085). NFV
minus NOV (DLB 0.64+0.1, AD 0.61+0.1, control 0.68+0.05) were
significantly smaller in AD (p-0.0031) and insignificantly smaller in DLB
(p=0.072) than in controls, and similar in DLB and AD (p=0.37). NOV
divided by NFV minus NOV were similar in all groups (DLB 0.149+0.02, AD
0.155+0.01, controls 0.156+0.02; p=0.39).
Our study, performed in smaller collectives than those of Middlekoop
et al. [1], corresponds to previous publications demonstrating forebrain
atrophy in AD and mild atrophy also in DLB. [2, 3, 4] In contrast to
Middlekoop et al. [1] occipital lobe atrophy was found, which was similar
in DLB and AD, and does therefore not explain occipital hypometabolism and
hallucinations in DLB.
References:
1) Middlekoop HAM, van der Flier WM, Burton EJ, et al. Dementia with
Lewy bodies and AD are not associated with occipital lobe atrophy on MRI.
Neurology 2001;57:2117-2120.
2) Mann DM, Snowdon JS. The topographic distribution of brain atrophy
in cortical Lewy body disease: Comparison with Alzheimer’s disease. Acta
Neuropathol 1995;89:178-183.
3) Hashimoto M, Kitagaki H, Imamura T, et al. Medial temporal and
whole brain atrophy in dementia with Lewy bodies: A volumetric MRI study.
Neurology 1998;51:357-362.
4) Barber R, Ballard C, McKeith IG, Gholkar A, O’Brien JT. MRI
volumetric study of dementia with Lewy bodies: A comparison with AD and
vascular dementia. Neurology 2000;54:1304-1309.