Delirium is a condition which impacts nearly half of older adults during hospital admission. It presents with a wide range of neuropsychiatric symptoms leading to increased morbidity and mortality. Despite this, specialised knowledge and ownership of the condition remain unclear.

To compare evidence surrounding the roles of neuronal and non-neuronal cells in the overall pathophysiology of delirium and consider the impact this could have in practice.

Using PRISMA systematic review guidelines, five medical research databases were screened for papers discussing the role of neuronal and/or non-neuronal cells in the pathophysiology of delirium between 2011 and 2021.

Fifteen papers which met the inclusion criteria were then categorised into discussing neuronal (n=2), non-neuronal (n=4) or both (n=9) types of cells’ roles in the pathophysiology of delirium. Delirium was often caused by a homeostatic imbalance secondary to acute illness leading to deterioration of neural synapses and therefore signal transmission. However, it was also argued that activated non-neuronal cells, particularly microglia and astrocytes, played a significant role through disruption of the blood brain barrier. This was likely to play a role in the more severe clinical presentations of delirium.

The pathophysiology of delirium is multifactorial with neuronal and non-neuronal cells implicated in neurological disruption. There is no clear agreement on how these mechanisms vary according to aetiology and, ultimately, the severity of delirium. Further research will help refine these theories, which will support the pharmacological and clinical management of the condition.

No significant relationships.

Employee of Gedeon Richter Plc.

Psychopathy is a personality disorder characterized by lack of empathy, grandiosity, an impulsive lifestyle and antisociality. Anti-social personality disorder (ASPD) and psychopathy are distinct concepts presenting different criteria. Most people with a diagnosis of psychopathy also meet criteria for ASPD while the reverse is not true. Along the years there has been an increasing interest in investigating genetic and neurobiological factors.

To analyze the neurobiological factors involved in psychopathy and anti-social personality disorder according to the scientific knowledge available.

Review of scientific literature via PubMed search, using the terms “anti-social personality disorder”, “biology or etiology or pathophysiology and psychopathy”.

The strongest evidence base for a genetic pathway is associated with the low-expression variant of the Monoamine Oxidase-A (MAO-A) which is linked to the X chromosome. Other genetic factors involve the 5-HTT gene, dopamine receptor genes (DRD4 and DRD2) and genetic polimorfisms at SNAP25 t-snare protein, OXT gene and the CNR1 and FAAH cannabinoid receptor gene. Structural differences in the brain have been noticed such as reduced gray matter volume in the orbitofrontal cortex, gray matter volume reductions in the mid-anterior insula and left anterior temporal cortex, subtle reductions in gray matter volume across several paralimbic and limbic areas.

There is considerable evidence regarding various possible underlying neurobiological processes in psychopathy although it is insufficient to suggest a single biological etiology and environmental influences cannot be excluded from a complete understanding of this disorder. The neurobiological correlates found hold promise for new research and treatment.

Nightmares are a hallmark symptom of posttraumatic stress disorder (PTSD). This strong association may reflect a shared pathophysiology in the form of altered autonomic activity and increased reactivity. Using an acoustic startle paradigm, we investigated the interrelationships of psychophysiological measures during wakefulness and PTSD diagnosis, posttraumatic nightmares, and nontraumatic nightmares.

A community sample of 122 trauma survivors were presented with a series of brief loud tones, while heart rate (HRR), skin conductance (SCR), and orbicularis oculi electromyogram (EMGR) responses were measured. Prior to the tone presentations, resting heart rate variability (HRV) was assessed. Nightmares were measured using nightmare logs. Three dichotomous groupings of participants were compared: (1) current PTSD diagnosis (n = 59), no PTSD diagnosis (n = 63), (2) those with (n = 26) or without (n = 96) frequent posttraumatic nightmares, and (3) those with (n = 22) or without (n = 100) frequent nontraumatic nightmares.

PTSD diagnosis was associated with posttraumatic but not with nontraumatic nightmares. Both PTSD and posttraumatic nightmares were associated with a larger mean HRR to loud tones, whereas nontraumatic nightmare frequency was associated with a larger SCR. EMGR and resting HRV were not associated with PTSD diagnosis or nightmares.

Our findings suggest a shared pathophysiology between PTSD and posttraumatic nightmares in the form of increased HR reactivity to startling tones, which might reflect reduced parasympathetic tone. This shared pathophysiology could explain why PTSD is more strongly related to posttraumatic than nontraumatic nightmares, which could have important clinical implications.

Pulmonary vascular disease resulting from CHDs may be the most preventable cause of pulmonary artery hypertension worldwide. Many children in developing countries still do not have access to early closure of clinically significant defects, and the long-term outcomes after corrective surgery remain unclear. Focused on long-term results after isolated ventricular septal defect repair, our review sought to determine the most effective medical therapy for the pre-operative management of elevated left-to-right shunts in patients with an isolated ventricular septal defect.

We identified articles specific to the surgical repair of isolated ventricular septal defects. Specific parameters included the pathophysiology and pre-operative medical management of pulmonary over-circulation and outcomes.

Studies most commonly focused on histologic changes to the pulmonary vasculature and levels of thromboxanes, prostaglandins, nitric oxide, endothelin, and matrix metalloproteinases. Only 2/44 studies mentioned targeted pharmacologic management to any of these systems related to ventricular septal defect repair; no study offered evidence-based guidelines to manage pulmonary over-circulation with ventricular septal defects. Most studies with long-term data indicated a measurable frequency of pulmonary artery hypertension or diminished exercise capacity late after ventricular septal defect repair.

Long-term pulmonary vascular and respiratory changes can occur in children after ventricular septal defect repair. Research should be directed at providing an evidenced-based approach to the medical management of infants and children with ventricular septal defects (and naturally all CHDs) to minimise consequences of pulmonary artery hypertension, particularly as defect repair may occur late in underprivileged societies.

Dissociative seizures (DS) are brief episodes of disrupted awareness and behavioural control that may resemble epileptic seizures. They are thought to arise in the context of impaired emotion processing and disinhibition. In a multi-perspective neuropsychological study, we aim to assess specific metacognitive traits and behavioural features involved in the affective and cognitive underpinnings of DS (emotion recognition and regulation, inhibition, interoception and sense of agency).

Twenty prospectively recruited patients with video-EEG-confirmed DS and 20 healthy controls underwent comprehensive neuropsychological and psychiatric testing using validated questionnaires and structured interviews. Behavioural experimental data was obtained using a custom-made emotional go/no-go task, a digital Libet clock setup and a heartbeat counting paradigm.

Emotion recognition, as quantified in the emotional go/no-go task, was impaired in the DS group, and correlated with alexithymic traits. Behavioural inhibition, especially under conditions that would require emotion regulation, was also reduced in the emotional go/no-go task compared to controls and was correlated with neuropsychometric measures of emotion regulation. Data from the Libet clock experiment suggested impaired behavioural awareness in DS patients. No evidence of impaired interoceptive awareness was found in the heartbeat counting task.

These results represent comprehensive experimental evidence for alterations in emotional and behavioural awareness and control in patients with DS that yield empirical evidence for current psychopathological models. Our findings offer a more detailed understanding of key pathogenic factors in DS and provide theoretical support for recently developed cognitive-behavioural therapies for DS.