Striatal and Hippocampal Atrophy in Idiopathic Parkinson’s Disease Patients without Dementia: A Morphometric Analysis

Jared J. Tanner, Nikolaus R. McFarland, and Catherine C. Price*

Background: Analyses of subcortical gray structure volumes in non-demented idiopathic
Parkinson’s disease (PD) often, but not always, show volume loss of the putamen,
caudate nucleus, nucleus accumbens, and hippocampus. There is building evidence
that structure morphometry might be more sensitive to disease-related processes than
volume.

Objective: To assess morphometric differences of subcortical structures (putamen,
caudate nucleus, thalamus, globus pallidus, nucleus accumbens, and amygdala) as well
as the hippocampus in non-demented individuals with PD relative to age and education
matched non-PD peers.

Methods: Prospective recruitment of idiopathic no-dementia PD and non-PD peers as
part of a federally funded investigation. T1-weighted isovoxel metrics acquired via 3-T
Siemens Verio for all individuals [PD n = 72 (left side onset n = 27, right side onset n = 45);
non-PD n = 48]. FIRST (FMRIB Software Library) applications provided volumetric and
vertex analyses on group differences for structure size and morphometry.

Results: Group volume differences were observed only for putamen and hippocampi
(PD < non-PD) with hippocampal volume significantly associating with disease duration.
Group shape differences were observed for bilateral putamen, caudate nucleus, and
hippocampus with greater striatal atrophy contralateral to side of motor symptom onset.
Hippocampal shape differences disappeared when removing the effects of volume.

Conclusion: The putamen was the primary structure to show both volume and shape
differences in PD, indicating that the putamen is the predominant site of basal ganglia
atrophy in early- to mid-stage PD. Side of PD symptom onset associates with contralateral
striatal atrophy. Left-onset PD might experience more extensive striatal atrophy than
right-onset PD. Hippocampus morphometric results suggest possible primary atrophy
of CA3/4 and dentate gyrus.

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