Dissociation between intentional and incidental sequence learning in Huntington's disease.

The ability to acquire and act upon serial order information is fundamental to almost all forms of adaptive behaviour. There is growing evidence that such knowledge may be acquired through a number of different means, each perhaps with its own neuronal substrate. One major distinction is between serial order information acquired intentionally and leading to explicit conscious knowledge of the sequence structure, and information acquired incidentally through experience. While this latter form of knowledge influences behaviour, it may do so without the participant being aware of the sequential information, i.e. it is acquired implicitly. Evidence from physiological and lesion studies in animals and imaging studies in humans suggests that these two forms of learning may have dissociable neuronal substrates. Specifically, the striato-thalamo-cortical circuit centred on the caudate nucleus is proposed to be involved in intentional sequence learning and that based on the putamen on incidental learning. The present study tested one part of this proposed dissociation by assessing patients with Huntington's disease on tasks of the two forms of learning. On the test of trial-and-error intentional learning there were marked deficits, which were closely related to disease progression and to measures of executive cognitive dysfunction. This finding was in contrast to the finding from the incidental learning task. Performance of the Huntington's disease group was essentially normal and unrelated to measures of disease progression and cognitive status. The results, although supportive of the proposed dual-system hypothesis, offer only partial confirmation. Further direct study is required using similar tasks in patients with putamenal disorder or lesions within the skeletomotor striato-thalamo-cortical circuit.