Psychoanalytic investigation of the inner life of neurological patients clearly has much to offer us. In each instance described above, it has been able to throw important light on a number of syndromes that neurocognitive theories cannot fully explain due to their failure to accommodate the psychological complexities of human emotional life. However, psychoanalytic hypotheses are no less prone to error than cognitive ones and therefore need to be subjected to the same rigorous empirical tests. Though detailed discussion of such investigations has been beyond the scope of this chapter, some progress has recently been made in investigating the various classes of disorder reported above with greater empirical rigor than is possible in the context of the conventional psychoanalytic setting. Where appropriate investigations have been performed, it appears that the data from the more highly controlled studies are consistent with the earlier, purely clinical, investigations (Turnbull, 2003; Turnbull et al., 2002; in press c).

It also seems appropriate to point out that our research has focused only on a few of the many psychiatric disorders that may follow from brain damage. To take the narrowest of examples, we have described the confabulatory states that are seen after bilateral medial frontal lesions. However, the depth psychological issues that follow from lesions in other frontal sites (such as disinhibition or adynamia) require far closer scrutiny than we have been able to offer thus far. On a broader scale, there are a range of disorders that follow from lesions (and excitatory states) involving limbic regions that clearly require further investigation. These include the personality changes seen after the viral encephalopathies (such as herpes simplex encephalitis) that target the medial temporal lobes. Similarly, there are fascinating issues related to the preictal experiences of those with epilepsies (especially complex partial epilepsy), not to mention modifications of interictal personality in those whose seizures are not fully controlled. A range of interesting changes to personality also occur after lesions to the diencephalon, not only in Korsakoff's syndrome, but also after disruption to the various hypothalamic emotion and motivation systems. We could easily extend this list of brain regions of interest to a depth psychology. Indeed, it is becoming apparent that an extraordinarily wide range of brain regions (perhaps even the majority) play some role in motivation, emotion, and personality.9

It is clear that we stand at the dawn of an exciting new era in psychological science. All sorts of possibilities are opening up. We appear, at last, to have within our grasp the possibility of studying the biological basis of a range of psychological and psychiatric phenomena that were poorly understood even a decade or two ago. In understanding the way in which focal brain disease/damage affects the mental apparatus, we appear to be gaining a much clearer understanding of the "psychiatric" presentation of many neurological patients. In addition, we now also appear to better understand how mental disorders in general arise. Perhaps the clearest example would be the fact that the con-fabulatory states of patients with ventromesial frontal lesions might be similar to those of traditionally psychiatric individuals with psychosis. With a better understanding of the biological basis of psychiatric disorder, we will be able to target our therapies to those who can benefit most, and in the ways that work best. We may even extend our clinical reach in previously undreamt of directions.

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