Although patients may be available, their deficits are often transient. It is here that TMS can be used to formally reproduce the basis of the deficit of interest. For example, Fierro et al.applied rTMS (25 Hz for 400 ms) over the right parietal cortex to induce a transient neglect syndrome.
Subjects were asked to judge whether a briefly presented line was bisected centrally, or to the left or the right of centre. Patients with right parietal damage and left hemineglect typically underestimated the length of the left side of the line. Normal subjects, without TMS, tend to overestimate the length of the left side of the line (known as a ‘pseudo-neglect’). Right-sided TMS reduced this pseudo-neglect, that is, it caused subjects to underestimate the left side of the line relative to their own normal judgment. Here, then, is a transient, but formal and reproducible recreation of an effect associated with neglect that can be used to test the theories resulting from classical neuropsychological studies. The protocol adopted by Fierro et al. might also be more powerful if it could be developed in a reaction-time paradigm, which might allow the application of single pulse TMS and therefore chronometric analysis of the neglect syndrome. This study illustrates how TMS can be used to advance neuropsychology. First, Fierro et al. addressed a robust and widely studied phenomenon, the first step in any convincing extensions of neuropsychological findings. Second, they observed a surface difference between the TMS-induced deficits and the deficits seen in patients. This latter point is a feature of many TMS studies and far from driving a wedge between real and virtual neuropsychology, it demands that each approach take note of the differences observed with permanent and transient lesions. From the standpoint of making inferences about normal brain function, a dialogue between the results of these two disciplines is not an optional extra — it is an absolute necessity. The differences between real and virtual lesions may be accounted for by the effects of diaschisis (changes in activity acquired a wide repertoire of compensatory strategies to cope with the deficit. As Lomber pithily, but accurately, observes, this “spectre of compensation” means that lesion studies may “examine the capability of other cortical circuits in the absence of the removed cortical tissue and not the true functions of the vision and some aspects of functional specialization of vision. However, in the study of patients with brain damage or monkeys with specific brain lesions, one is studying an abnormal brain.