Author(s)

T. J. Reilly, R. T. Staff, T. S. Ahearn, P. Bentham, C. M. Wischik, A. D. Murray

ISBN

1872-7549 (Electronic) 0166-4328 (Linking)

Publication year

2011

Periodical

Behav Brain Res

Periodical Number

2

Volume

222

Pages

375-9

Author Address

Aberdeen Biomedical Imaging Centre, School of Medicine and Dentistry, University of Aberdeen, UK. t.j.reilly.06@aberdeen.ac.uk

Full version

Aberrant motor behaviour (AMB) in Alzheimer’s disease shares behavioural correlates with obsessive compulsive disorder (OCD). We investigated whether AMB was also comparable in terms of metabolic activity in the orbitofrontal cortex (OFC), an area shown to be hyperactive in OCD. In this study 135 patients meeting research criteria for Alzheimer’s disease were identified from a database of patients recruited as part of a phase II drug trial. These patients were assessed using the Neuropsychiatric Inventory, the Alzheimer’s disease assessment scale, cognitive subscale and perfusion SPECT performed with 99Tc(m) hexamethylpropyleneamine oxime. Regions of interest were created for orbitofrontal cortices and basal ganglia. In 35 patients with AMB, adjusted tracer uptake was greater in the OFC. This reached statistical significance in right superior, left superior, right medial and left medial orbital gyri (p < 0.05). The association between AMB and hyperactivity in the OFC remained significant after adjusting for the presence of anxiety. These results parallel the OFC hypermetabolism consistently seen in OCD. One model of OCD, proposes that dysfunctional interactions between frontal regions, including the OFC, produce the characteristic symptoms of OCD. The behaviour is though to be brought about by a perceived incompleteness of performing a task and is caused by an error in normal reward signals initiated upon task completion. These finding indicate that AMB in Alzheimer's disease are brought about by the same mechanistic failure.