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Systematic analysis of mechanisms underlying deficits of stroke patients suffering from Constructional Apraxia

Final Activity Report Summary - CONSTRUCAPRAXIA (Systematic analysis of mechanisms underlying deficits of stroke patients suffering from Constructional Apraxia)

This fellowship constituted the first systematic research program specifically designed to discover the mechanisms underlying constructional problems after stroke. Constructional difficulties, termed constructional apraxia (CA), are a common and enduring result of brain injury to the right parietal lobe of the brain. Unfortunately, this type of brain injury is often found after a stroke. Some research efforts suggested that presence of these problems after stroke affecting the right brain hemisphere is found in as much as 95 % of patients (Hier et al., 1983). CA is commonly revealed through a failure of patients to copy two-dimensional drawings or three-dimensional models. These problems exist without the patient having any problems with making the individual movements involved in this type of skill. This body of work set out to understand the underlying mechanisms of the disorder. An advance in understanding a disorder is the first step towards discerning the best form of rehabilitation, thereby alleviating distress for the patients and their caretakers.

Our principal discovery was that constructional problems were a result of a failure in remapping spatial information over eye movements. In healthy individuals complicated computations were performed whenever the eyes moved. Individuals had to be able to maintain a stable mental representation of where things were in the world around them despite the fact that during eyes' motion the position of everything on the eyes' retina shifted. Individuals did not perceive the world as moving around with every eye movement because their brain 'remapped' the information about the position of things around them in line with their eye movements. These remapping computations principally took place in the right parietal part of the brain, and it was this part of the brain that was consistently damaged in CA, as our results from brain lesion mapping proved.

The behavioural experiments that confirmed a remapping impairment examined whether CA patients had a problem when judging whether a small pattern moved between the first and the second time they fixated it, which was after they had made an eye movement. Importantly, the CA patients were compared to a group of other stroke patients who had brain damage affecting the right brain hemisphere but not the parietal region. Furthermore, in order to assess whether the problem concerned specifically spatial remapping, i.e. remapping of the information about position, we also examined what happened when the patient groups were required to say whether a pattern had changed in terms of form and not position from one fixation to the next, with intervening eye movements between the fixations.

Results revealed that CA patients were specifically impaired when they had to move their eyes and judge whether a pattern had moved between fixations. In contrast, the other patients, without constructional impairments, found this task trivial and, instead, found judging whether the pattern changed in form more difficult. This double dissociation demonstrated the importance of spatial remapping impairment in CA. It occurred that when CA patients moved their eyes they failed to update the position of items with respect to the new position of eyes. This was likely to lead to the drawing performance which was observed when information gained in one fixation was correctly copied, but all correct spatial relationships were lost when the eyes had to move.