The literature about the care givers of patients with Disorders of Consciousness (DOCs) has highlighted the impact on both mental and physical dimensions of quality of life. This study aimed to: (1) describe emotional burden, quality of life, and coping styles in care givers of hospitalized patients with DOCs, compared to Italian normative data; (2) explore the relationships between these variables and their associations with socio-demographic features; and (3) describe their changes over time.

Fifteen care givers of patients with DOCs, mostly middle-aged women, were assessed using the Family Strain Questionnaire, the SF-36 Health Survey, and the Coping Orientation to Problems Experienced – Nuova Versione Italiana. Eleven subjects were also assessed after 6 and 12 months. Data were analysed through descriptive statistics, correlations, and nonparametric tests of group differences.

Compared to the Italian normative data, our sample showed a worse outcome in mental health, social functioning, global mental component, and emotional role functioning. Furthermore, subjects with high emotional burden had more thoughts of death compared to subjects with low emotional burden. Follow-up analyses revealed no variables changed over time.

These results highlight the need for psychological interventions and support, since care givers represent an important part of an all-embracing support and care network for patients with DOCs.

Neuroimaging research has raised ethical concerns such as the management of unexpected findings and the classification and assessment of risks. Research ethics boards (REBs) bear responsibility for the oversight of these challenges but neuroimagers struggle with the practical aspects of ethics review and report that administrative load and inconsistency contribute to eroding confidence and trust in ethics review. Our goal was to discuss and propose strategies for institutional and educational change to improve ethics review. We used an iterative and deliberative workshop-based writing process involving multiple disciplines. We propose recommendations in three tension areas: (1) communication between researchers and REBs; (2) collaboration and sharing of expertise between REBs; and (3) practical considerations and the needs of neuroimagers engaged in the ethics review process. Our recommendations are intended as openings rather than endpoints. Researchers and research ethics governance communities should decide on the future uptake of these recommendations.

Karl Ludwig Kahlbaum originally described catatonia as a psychomotor disease that encompassed motor, affective, and behavioral symptoms. In the beginning of the 20th century, catatonia was considered to be the motoric manifestation of schizophrenia; therefore, neuropathologic research mostly focused on neuroanatomic substrates (ie, the basal ganglia underlying the generation of movements). Even though some alterations were found in basal ganglia, the findings in these subcortical structures are not consistent. Recently, there has been a reemergence of interest into researching catatonia. Brain imaging studies have shown major and specific alterations in a right hemispheric neural network that includes the medial and lateral orbitofrontal and posterior parietal cortex. This neural network may be abnormally modulated by altered functional interactions between γ-aminobutyric acid (GABA)-ergic and glutamatergic transmission. This may account for the interrelationship among motor, emotional, and behavioral alterations observed in both clinical phenomenology and the subjective experiences of patients with catatonia. Such functional interrelationships should be explored in further detail in catatonia, which may also serve as a paradigmatic model for the investigation of psychomotor and brain function in general.

Heinzel A, Northoff G, Boeker H, Boesiger P, Grimm S. Emotional processing and executive functions in major depressive disorder: dorsal prefrontal activity correlates with performance in the intra–extra dimensional set shift.

Susan Hurley's impressive article about the shared circuit model (SCM) raises two important issues. First, I suggest that the SCM presupposes relational coding rather than translational coding as neural code. Second, the SCM being the basis for self implies that the self may be characterized as format, relational, and embodied and embedded, rather than by specific and isolated higher-order cognitive contents.

Merker argues that subcortical regions are sufficient for the constitution of consciousness as “immediate, unreflective experience” as distinguished from self-consciousness. My point here is that Merker neglects the differentiation between pre-reflective self-awareness and reflective self-consciousness. Pre-reflective self-awareness allows us to immediately and unreflectively experience our self, which functionally may be mediated by what I call self-related processing in subcortical regions.

Lewis discusses the dynamic mechanisms of emotional-cognitive integration. I argue that he neglects the self and its neural correlate. The self can be characterized as an emotional-cognitive unity, which may be accounted for by the interplay between anterior and posterior medial cortical regions. I propose that these regions form an anatomical, physiological, and psychological unity, the cortical midline structures (CMSs).

Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called “conflict of paradigms.” Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting “horizontal modulation” of cortico-cortical relation. Furthermore, alteration in “top-down modulation” reflecting “vertical modulation” of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered “bottom-up modulation” between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation – “vertical” and “horizontal” modulation, respectively.

The excellent and highly interesting commentaries address the following concerns: (1) neuroanatomy and neurophysiology of catatonia; (2) cognitive-motor deficits in catatonia; (3) conceptual issues; (4) general methodology in neuropsychiatric research; and (5) neurophilosophical implications. The specific problems, issues, and aspects raised by the different commentators are grouped under these categories in Table R1 presented below. These five areas of concern are then discussed in the order listed in the five sections of the Response.