MR features of the substantia innominata and therapeutic implications in dementias

Hanyu, Haruo; Shimizu, Soichiro; Tanaka, Yuriko; Hirao, Kentaro; Iwamoto, Toshihiko; Abe, Kimihiko

doi:10.1016/j.neurobiolaging.2006.02.009

« Previous Next »Neurobiology of Aging
Volume 28, Issue 4 , Pages 548-554, April 2007

MR features of the substantia innominata and therapeutic implications in dementias

Haruo Hanyu
- Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku Shinjuku-ku, Tokyo 160-0023, Japan
- Corresponding author. Tel.: +81 3 3342 6111; fax: +81 3 3342 2305.
Soichiro Shimizu
- Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku Shinjuku-ku, Tokyo 160-0023, Japan
Yuriko Tanaka
- Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku Shinjuku-ku, Tokyo 160-0023, Japan
Kentaro Hirao
- Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku Shinjuku-ku, Tokyo 160-0023, Japan
Toshihiko Iwamoto
- Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku Shinjuku-ku, Tokyo 160-0023, Japan
Kimihiko Abe
- Department of Radiology, Tokyo Medical University, Tokyo, Japan

Received 29 July 2005; received in revised form 5 December 2005; accepted 11 February 2006. published online 27 March 2006.

Abstract

We measured the thickness of the substantia innominata using magnetic resonance imaging in 122 patients with Alzheimer's disease (AD), 31 patients with dementia with Lewy bodies (DLB) and 34 patients with vascular dementia (VaD), and examined the correlates of cognitive response to donepezil. Although all dementia groups showed significant atrophy of the substantia innominata compared to 28 age-matched controls, atrophy was greater in the DLB group, but less in the VaD group than the AD group. Mini-Mental State Examination score changes at 12 weeks after donepezil administration inversely and significantly correlated with the thickness of the substantia innominata in patients with AD (n=103, r=−0.43, p<0.0001) and in patients with DLB (n=24, r=−0.57, p<0.01), but not in patients with VaD (n=12, r=−0.22, p>0.1). There may be some differences in cholinergic impairment among AD, DLB and VaD, reflecting cholinergic neuropathology. Clinical response to cholinergic therapy may be partly attributable to damaged cholinergic neurons in AD and DLB, but not in VaD, suggesting differences in the therapeutic implication of cholinergic system degeneration.