Productive symptoms in right brain damage: behavioural and anatomical observations

This thesis describes behavioural observations and anatomical investigations concerning productive symptoms observable in right brain damaged patients with spatial neglect. A "productive" symptom is defined here as a behavioural manifestation that, contrary to what observed when performance is lacking or its failure is acknowledged by patients, is characterized by the active generation of acts or verbal reports reflecting a distorted mental representation of reality. A first classification of productive symptoms in neglect patients pertains the spatial frame of their manifestation, extrapersonal or personal. Following this classification, I examine these manifestations in separate sections of the thesis. Section 1 is dedicated to the peri/extrapersonal space, while, in Section 2, I focus on symptoms manifesting in the own bodily space. In chapter 2, I concentrate on graphic perseveration in cancellation tasks, the main productive symptom observable for the extrapersonal space in neglect patients. Together with omission of left-sided targets, a variety of irrelevant marks over already cancelled targets on the ipsilesional side can be observed. It is not clear whether these perseverative behaviours are functionally and anatomically connected, nor whether they correlate with the severity of spatial neglect. We retrospectively identified two well-distinct forms of perseveration on cancellation tasks ("additional marks" and "inkblot") in 33 neglect patients, and we investigated their relationship with neglect severity and their anatomical correlates. We show, on both a behavioural and anatomical level, that different kinds of perseverative behaviours are differently related with neglect. From chapter 3 onwards I concentrate on productive manifestations in personal space. One main such productive symptom is somatoparaphrenia, the delusional belief whereby a patient feels that a paralyzed limb does not belong to his body; the symptom is typically associated with unilateral neglect and most frequently with anosognosia for hemiplegia. In chapter 3, I describe the anatomical pattern associated with somatoparaphrenia in a wide sample of patients, and I propose that somatoparaphrenia occurs providing that a distributed cortical lesion pattern is present together with a subcortical lesion load that prevents most sensory input from being processed in neocortical structures. In chapter 4, I also show how somatoparaphrenia, that, so far, has been often considered simply the most severe and delusional manifestation along a continuum of body disorders also including anosognosia for hemiplegia, can be also observed in isolation from this symptom. I report anatomical observations on a small group of pure somatoparaphrenic patients and discuss the implications of this uncommon symptomatological dissociation. The experiments mentioned so far were based on classical anatomoclinical correlation inference. The study of productive/positive symptoms, however, would ideally need functional methods as well, in order to capture the neural correlates of the "active" component implied by the symptoms under investigation. I present an initial attempt along these lines. I considered the delusional behaviour of patients with anosognosia for hemiplegia (AHP): this has been often classified as a “negative” symptom as patients crucially “lack” the awareness of the motor deficit. However, beyond this defective aspect, AHP is usually characterized by an active delusional component that manifests in the patients’ firm assertion of having performed a movement with the paralyzed limb, in spite of any clear evidence that no movement has actually occurred. In this case, one has to postulate the presence of a residual, and maybe misinterpreted, motor brain activity to account for this delusional component. Here I illustrate, for the first time, the missing direct imaging evidence that the illusory movement of the left plegic hand is associated with brain activation of intact cortical motor regions implicated in motor control and intention (see chapter 5). It is suggested that motor delusions observed in AHP depend on a combination of well placed lesions and the presence of some motor intentionality represented by residual activity within the spared motor cortices. The diversity of the phenomena considered in this thesis makes it difficult to generalize anatomical considerations about productive manifestations associated with spatial neglect; yet, it is worth of notice the fact that all these disorders can be also conceptualized as self-monitoring disorders particularly related to motor/sensory control aspects in which the opercular part of the inferior frontal gyrus seems to play an important role. Indeed, we found it constantly involved in all the productive disorders considered, irrespective of whether defective monitoring was about the left plegic limb or the right intact one. In addition, we find it promising the adoption of functional methods to gather a more complete description of the neural underpinnings of symptoms of great complexity like the productive ones.