The article reviewed here is ‘Implicit and Explicit Aspects of Sequence Learning in Presymptomatic Huntington’s Disease’ by Ghilardi and colleagues and freely available here. In the abstract, the authors conclude
‘These results suggest that both explicit and implicit aspects of sequence learning may be impaired before the onset of motor symptoms. However, when attentional demands decrease, explicit, but not implicit, learning may improve‘
Thus the authors compare and contrast implict and explicit learning in Huntington’s Disease (HD) for a very specific task. The study revolves around a sequencing task and some assumptions. The assumptions are that in this case, implicit and explicit learning can be demarcated according to different elements of the response to the task. Thus for instance they argue that as learning proceeds, the movements become more efficient, saving energy and that this occurs implicitly. They also argue that the number of anticipatory movements in the task is a proxy for explicit learning. However it could be argued that there can be an overlap. Thus the subject could tire of the movements involved in the task and consciously seek to perform these actions more efficiently. Further these actions could be accompanied by an internal dialogue which could almost certainly be considered an explicit form of learning or it could occur non-verbally where the subject nevertheless attends to this goal. Similarly for the initial period of learning the task involves consideration of the sequence of events but here too it could be asked ‘does the learning take place consciously’ (the same could, I think, be asked of this example where the question could be asked ‘is this chimp consciously or explicitly aware of what he is doing?’). In effect then, it might be reasonable to ask if implicit or explict learning are continuous rather than discrete functions or even if this characterisation is task specific such that it might not be possible to generalise from single tasks.
The researchers have considered a large number of variables which are given in tables 2 and 3. Interestingly they mention that there is a ‘post-hoc analysis’ and a null hypothesis is not clearly stated although the authors do discuss their interpretation of the different components of the task response. The researchers have corrected for the multiple comparisons by using Bonferrini corrections. On the tasks, the subjects with presymptomatic HD (the number of CAG repeats averaged 41. The greater the number the greater is the risk of conversion) performed significantly worse on the implicit and explicit learning components of the tasks as interpreted by the researchers. My initial impression was that the explicit task involved sequencing and might under Baddeley’s model of working memory be attributed to the central executive. There would be expected to be executive dysfunction if the frontal-subcortical loops are affected by the disease process which is seen in HD. The only question here is whether or not there is interruption of the frontal-subcortical loops as this is prefmanifest HD. The researchers also found that if they reduced the complexity of the task there was no significant difference between the premanifest HD subjects and the controls on the ‘explicit learning’ but there was a significant difference on the ‘implicit learning’ task.
The researchers discuss their results and comment on the possible involvement of the dorsolateral prefrontal cortex and a number of other pathways. They also suggest that implicit memory involves primary motor cortex and supplementary motor areas but it is also interesting to note that the cerebellum is thought to play a significant role in this type of learning for motor tasks. I would be interested to see a larger replication study with clearly delineated primary outcome measures and a range of tasks examining both implicit and explicit memory.
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