Jesus Ramirez-Bermudez

Introduction: Cotard syndrome is a neuropsychiatric entity recognised by the presence of nihilistic delusions. Although different models have been proposed for the development of monothematic delusions, including Cotard syndrome, functional neuroanatomical models are lacking. Methods: A case report of a 19-year old male with autoimmune encephalitis and Cotard syndrome, in whom Positron Emission Tomography (18F-FDG-PET) scans were performed before and after successful treatment with electroconvulsive therapy (ECT), is presented. Literature review on brain imaging is provided to discuss a functional neuroanatomical model of Cotard syndrome, in accordance with the two-factor theory of delusions. Results: The patient’s 18F-FDG-PET showed marked insular and prefrontal metabolic abnormalities. Except for insular hypometabolism, metabolic abnormalities improved after ECT. Previously reported structural neuroimaging studies in Cotard syndrome showed a predominance of right hemisphere lesions, in which frontal lobes were more frequently involved, followed by parietal and temporal lesions. Functional neuroimaging studies reported abnormalities in frontoparietal circuits as well as midline structures included in the “default mode network”. Conclusions: Abnormalities in the functioning of the insular cortex and the prefrontal cortex could be related to the development of nihilistic delusions when a two-factor theory of delusions is considered.

Introduction: We report an epileptic patient who experienced hallucinatory visual experiences of autobiographical memories from her past. These visual experiences were confined to the lower left quadrant of her visual field. Methods: We carried out a single-case study that used brain-imaging, EEG and behavioural methods to study this patient. Results: We found that this patient had an incomplete left inferior homonymous quadrantanopia due to a lesion of right occipital cortex, and also that she showed neurological abnormalities in right temporal cortex, a region that is part of the brain’s autobiographical-memory circuit. Conclusion: We attribute the occurrence of this patient’s autobiographical-memory hallucinations to the combination of degraded visual input to right temporal cortex plus hyperexcitability of that region.

This article explores a literary tradition situated at the intersection of scientific reports, memoirs, and creative writing, termed “clinical narrative.” This genre offers a profound approach to the painful aspects of conscious experience, particularly the phenomenological states associated with mental illness and brain disease, seen as unsettling landscapes of phenomenal experience. Through case studies providing multifaceted viewpoints – first-person, second-person, and third-person perspectives – we argue that clinical narratives are valuable resources for a transepistemic study of consciousness. By examining clinical conundrums such as somatic and nihilistic delusions, and anosognosia, we highlight the importance of detailed phenomenological, hermeneutic, and narrative accounts while acknowledging the significance of subpersonal, mechanistic models from cognitive and affective neuroscience. The tradition embodies the tension between the diverse perspectives in the field of mental health, including stories that directly challenge the medical discourse. However, the narrative arts can act as mediators or even peacemakers, by fostering an understanding between the opposing views. Stories are open to multiple interpretations, preserving the diversity of discourses on human meaning and avoiding the imposition of monolithic versions of our humanness.

Cotard syndrome is a clinical condition defined by the presence of nihilistic delusions. We report two patients with Cotard syndrome in whom anti-NMDAR encephalitis (ANMDARE) was confirmed. Both cases showed features of affective psychosis, developed catatonic syndrome, and worsened after the use of antipsychotics. 18F-FDG PET brain studies showed a bilateral hemispheric pattern of hypometabolism in posterior regions, mainly in the cingulate cortex and in the medial aspects of parietal and occipital lobes. A more severe hypometabolism was observed in the right hemisphere of both patients. Both cases remitted with the use of specific immunotherapy for ANMDARE.

This essay provides an analysis of the clinical problems that arise at the borderline between neurology and psychiatry. We postulate that psychopathological and neuropathological constructs have distinct referents and conceptual fields, but they are not mutually exclusive categories. After establishing criteria for defining neuropsychiatric constructs, we outline rules for identifying cases where a significant relationship exists between neuropathological and psychopathological patterns. We propose three approaches to establishing this relationship: a clinical epidemiology approach, a clinical neuroscience approach offering a mechanistic model, and a longitudinal study of individual cases incorporating idiographic perspectives. We discuss the logic of brain-behavior relationships and emphasize the need for closer academic feedback between neuroscientific research and clinical practice to better understand the causality of psychopathological phenomena in the context of neuropsychiatry. While precise demarcation may be challenging in some cases, we provide two types of examples: first, straightforward cases where neuropathology explains psychopathological patterns; second, complex cases that require studying the causal interactions between neuropathological factors, psychological factors, and sociocultural contexts, leading to intricate clinical patterns that demand cognitive neuropsychiatry resources, and a multidisciplinary approach to clinical care.