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At the interface between mind and body, psychiatry and neurology, functional neurological disorder (FND) remains poorly understood. Formerly dominant stress-related aetiological models have been increasingly challenged, in part due to cases without any history of past or recent trauma. In this perspective article, we review current evidence for such models, and how research into the role of traumatic stress in other disorders and the neurobiology of the stress response can inform our mechanistic understanding of FND. First, we discuss the association between stress and the onset or exacerbation of a variety of physical and mental health problems. Second, we review the role of hypothalamic-pituitary-adrenal axis dysfunction in the neurobiology of ill-health, alongside evidence for similar mechanisms in FND. Third, we advocate a stress-diathesis model, in which biological susceptibility interacts with early life adversity, where FND can be precipitated by traumatic events later in life and maintained by psychological responses. We hypothesise that greater biological susceptibility to FND is associated with less severe remote and recent stress, and that FND precipitated by more severe stress is associated with lower biological vulnerability. This would explain clinical experience of variable exposure to historical and recent traumatic stress among people with FND and requires empirical investigation. A testable, evidence-based stress-diathesis model can inform nuanced understanding of how biological and psychological factors interact at the individual level, with potential to inform personalised treatment pathways. Much-needed research to establish the aetiology of FND will enhance clinical care and communication, facilitate effective treatment and inform prevention strategies.

BackgroundFunctional movement disorders (FMDs), part of the wide spectrum of functional neurological disorders (conversion disorders), are common and often associated with a poor prognosis. Nevertheless, little is known about their neurobiological underpinnings, particularly with regard to the contribution of genetic factors. Because FMD and stress-related disorders share a common core of biobehavioural manifestations, we investigated whether variants in stress-related genes also contributed, directly and interactively with childhood trauma, to the clinical and circuit-level phenotypes of FMD.MethodsSixty-nine patients with a ‘clinically defined’ diagnosis of FMD were genotyped for 18 single-nucleotide polymorphisms (SNPs) from 14 candidate genes. FMD clinical characteristics, psychiatric comorbidity and symptomatology, and childhood trauma exposure were assessed. Resting-state functional connectivity data were obtained in a subgroup of 38 patients with FMD and 38 age-matched and sex-matched healthy controls. Amygdala–frontal connectivity was analysed using a whole-brain seed-based approach.ResultsAmong the SNPs analysed, a tryptophan hydroxylase 2 (TPH2) gene polymorphism—G703T—significantly predicted clinical and neurocircuitry manifestations of FMD. Relative to GG homozygotes, T carriers were characterised by earlier FMD age of onset and decreased connectivity between the right amygdala and the middle frontal gyrus. Furthermore, the TPH2 genotype showed a significant interaction with childhood trauma in predicting worse symptom severity.ConclusionsThis is, to our knowledge, the first study showing that the TPH2 genotype may modulate FMD both directly and interactively with childhood trauma. Because both this polymorphism and early-life stress alter serotonin levels, our findings support a potential molecular mechanism modulating FMD phenotype.

Background Dissociative disorders involve disruptions in memory, identity, sensory awareness, and motor control, often triggered by psychological distress. Dissociative amnesia may appear as either retrograde or anterograde memory loss, and dissociative stupor as well as conversion disorder are also considered part of the dissociative disorders spectrum. Cases presenting with generalized amnesia (both retrograde and anterograde), dissociative stupor, and conversion disorder are rare. Here, I report a unique case of a 17-year-old female exhibiting this combination of symptoms following her mother’s depressive relapse. Case presentation A 17-year-old Japanese female developed complete amnesia 3 weeks before presentation. Her mother, diagnosed with depression, had been hospitalized. The patient had a history of exposure to domestic violence and had taken on a caregiving role for her mother. She initially experienced episodic stupor, involuntary eye deviation, and transient unconsciousness, followed by generalized amnesia affecting personal, semantic, and procedural memory. Neurological and medical evaluations ruled out organic causes, leading to a psychiatric referral. As amnesia improved, she recalled witnessing her mother’s suicide attempt 2 years prior. Her symptoms were diagnosed as dissociative amnesia, dissociative stupor, and conversion disorder, attributed to psychological distress. Supportive psychotherapy, psychoeducation, and environmental stabilization led to symptom resolution without medication. Conclusion This case highlights a rare presentation of dissociative amnesia with stupor and conversion disorder. The diagnosis was initially challenging owing to amnesia masking the stressor. Careful exclusion of organic causes and thorough psychological assessment were key. This case underscores the importance of identifying underlying trauma in complex dissociative presentations.

Traumatic brain injury (TBI) is an important cause of death in young adults and children. Till now, the treatment of TBI in the short- and long-term complications is still a challenge. Our previous evidence implied aquaporin 4 (AQP4) and hypoxia inducible factor-1α (HIF-1α) might be potential targets for TBI. In this study, we explored the roles of AQP4 and HIF-1α on brain edema formation, neuronal damage and neurological functional deficits after TBI using the controlled cortical injury (CCI) model. The adult male Sprague Dawley rats were randomly divided into sham and TBI group, the latter group was further divided into neutralized-AQP4 antibody group, 2-methoxyestradiol (2-ME2) group, and their corresponding control, IgG and isotonic saline groups, respectively. Brain edema was examined by water content. Hippocampal neuronal injury was assessed by neuron loss and neuronal skeleton related protein expressions. Spatial learning and memory deficits were evaluated by Morris water maze test and memory-related proteins were detected by western blot. Our data showed that increased AQP4 protein level was closely correlated with severity of brain edema after TBI. Compared with that in the control group, both blockage of AQP4 with neutralized-AQP4 antibody and inhibition of HIF-1α with 2-ME2 for one-time treatment within 30–60 min post TBI significantly ameliorated brain edema on the 1st day post-TBI, and markedly alleviated hippocampal neuron loss and spatial learning and memory deficits on the 21st day post-TBI. In summary, our preliminary study revealed the short-term and long-term benefits of targeting HIF-1α-AQP4 axis after TBI, which may provide new clues for the selection of potential therapeutic targets for TBI in clinical practice.

The purpose of this review is to provide an update of the research regarding the etiology, diagnosis and management of psychogenic non-epileptic seizures (PNES). A literature search using Pubmed, Ovid MEDLINE and EMBASE database was performed from 2000 up to August 2017. We have evaluated the different factors leading to PNES as well as the diagnostic approach and management of this disorder which continue to be very difficult. The coexistence of epilepsy and PNES poses special challenges and requires the coordinated efforts of the family physicians, psychiatrists, psychologists and neurologists. Although this condition has an overall poor prognosis, a multidisciplinary approach in the diagnosis and management of this disorder would likely improve the outcomes. We have proposed a diagnostic and treatment algorithm for PNES and suggested a national registry of patients suffering from this condition. The registry would contain data regarding treatment and outcomes to aid in the understanding of this entity. Vue d’ensemble des crises psychogènes non-épileptiques: étiologie, diagnostic et prise en charge. L’objectif de cet article est de présenter une mise à jour des activités de recherche qui concernent l’étiologie, le diagnostic et la prise en charge des crises psychogènes non-épileptiques (CPNE). Pour ce faire, nous avons mené de 2000 à août 2017 une recherche bibliographique au moyen des bases de données suivantes : PubMed, Ovid MEDLINE et Embase. Nous avons procédé à l’évaluation des divers facteurs causant les CPNE, des approches diagnostiques et de la prise en charge de ce trouble, laquelle continue à être très difficile. La coexistence de l’épilepsie et des CPNE présente aussi des défis particuliers et exige des efforts coordonnés de la part des médecins de famille, des psychiatres, des psychologues et des neurologues traitants. Bien que les pronostics au sujet de cette condition soient généralement réservés, une approche multidisciplinaire dans l’établissement d’un diagnostic et la prise en charge des CPNE contribueraient probablement à améliorer l’évolution de l’état de santé des patients. À cet égard, nous avons proposé, en plus d’un registre national des patients atteints de ce trouble, un algorithme de diagnostic et de traitement pour les CPNE. À noter que ce registre contiendrait des données portant sur les modalités de traitement et leur résultat afin de favoriser la compréhension du cadre clinique des CPNE.

Conversion disorder may be broadly defined as the presence of neurologic symptoms in the absence of a neurologic diagnosis, or when a neurologic diagnosis exists, it does not fully account for all of the patient's symptoms. The purpose of this review is to examine the classification, epidemiology and theories as to the causes of conversion disorder, as well as the issues related to the condition's diagnosis and management. The paper will also focus on advances in magnetic resonance imaging (MRI) that complement long-held psychoanalytic beliefs concerning the notion of primary gain underpinning the pathogenesis of conversion symptoms, i.e., the \"conversion\" of emotional distress into a presentation of physical illness; in this case, neurologic symptoms. In a study of unilateral sensory loss thought to be a conversion symptom, patients had a vibratory stimulus applied first to their sensate region, then to their anesthetic side. Data from a functional MRI study showed contralateral somato sensory activation when the stimulus was applied to the sensate region, as expected, but no such activation when the stimulus was applied to the anesthetic side (Figure 1).18 Instead, the stimulus applied to the anaesthetic side activated regions in the patients' orbitofrontal and anterior cingulate regions. Similar results, including anciliary activation in the basal ganglia, have emerged from other studies using functional MRI and single-photon emission computed tomography (SPECT) scans to investigate motor conversion symptoms.19,20 The association between conversion symptoms and activity in the orbitofrontal and cingulate regions is informative because these regions are important components of the neural networks regulating emotion and the expression of that emotion, i.e., a person's affect. Patients with repressed (unwanted) emotional memories (what the DSM terms dissociative amnesia) have a functional MRI pattern of regional cerebral deactivation and ancillary activation that complements the data on conversion disorder. Neural activity in the hippocampus (a repository of memories) is suppressed by activation in a network rich in frontal (i.e., dorsolateral and ventrolateral prefrontal cortices and the anterior cingulate gyrus) connectivity.22 It is to be expected that regional brain specificity would differ between the data from functional MRI studies of patients with conversion disorder and patients with dissociative amnesia, given the differences in phenomenology. Of greater importance is that, in both conditions, the discrete neural networks involved in processing emotion and executive control can suppress regions associated with a plethora of other functions (e.g., motor, sensory, memory, vision). This bolsters the validity of the construct underpinning how atypical symptoms, irrespective of their phenotype, may arise. These explanations do not necessarily refute current psychological theories as outlined by the DSM-IV. Rather, they provide a complementary cerebral model to account for the development of symptoms using the notion of primary gain. What the imaging data cannot answer, however, is why a particular symptom manifests.

Conversion disorder is a psychiatric disorder in which psychological stress causes neurologic deficits. A 28-year-old female surgical patient had uneventful general anesthesia and emergence but developed conversion disorder 1 hour postoperatively. She reported difficulty speaking, right-hand numbness and weakness, and right-leg paralysis. Neurologic examination and imaging revealed no neuronal damage, herniation, hemorrhage, or stroke. The patient mentioned failing examinations the day before surgery and discontinuing her prescribed antidepressant medication, leading us to diagnose conversion disorder, with eventual confirmation by neuroimaging and follow-up examinations.

•Neurologists and psychiatrists do not consider FNS as a mere psychiatric disorder.•Disordered brain functioning together with psychogenic factors was considered responsible.•FNS should not be solely diagnosed and treated by psychiatrists. Functional neurological symptoms (FNS) were considered as a psychiatric disorder at the beginning of the 20th century (conversion disorder). Psychiatrists performed diagnosis and treatment throughout most of the past century in the Netherlands, but in the latest decades patients were usually firstly referred to neurologists. The aim of this study was to investigate the opinions of today’s neurologists, psychiatrists and rehabilitation physicians in the Netherlands, regarding pathogenesis, diagnosis and treatment of FNS. An electronic questionnaire was sent to all neurologists registered with the Dutch Society for Neurology and to the members of the Department for Consultation-liaison and General Hospital Psychiatry. 343 of 780 neurologists, 64 of 197 psychiatrists and 47 of 750 rehabilitation physicians completed the questionnaire. 60% of neurologists and 67% of psychiatrists considered disordered brain functioning together with psychogenic factors responsible for FNS. 29% of neurologists and 88% of psychiatrists felt a psychiatrist was needed for diagnosis. 55% of neurologists and 88% of psychiatrists preferred combined treatment consisting of explaining FNS to patients, psychotherapy and physiotherapy provided by a therapist trained in FNS. 15% of neurologists preferred only physiotherapy. Most neurologists and psychiatrists did not consider FNS as a mere psychiatric disorder, but counted disordered brain functioning together with psychogenic factors responsible for FNS. Subsequently, according to the majority of neurologists and psychiatrists FNS should not be solely diagnosed and treated by psychiatrists. These results can help to formulate treatment strategies.

Background The clenched fist syndrome/psycho-flexed hand, first described in the early 1980s, has not yet entered the major psychiatric textbooks. Curiously, the phenomenon has been illuminated mainly in journals and textbooks on hand surgery. There is a need to examine, describe, and understand this syndrome from a psychiatric perspective. Case presentation We present a case we encountered in an intensive care unit. A 60-year-old white man with schizophrenia, cerebrovascular disease, diabetes mellitus type 2, and peripheral neuropathy, developed rather acutely bilateral clenched fists in the aftermath of a traumatic dislocated hip fracture that was operated on. He later died due to complications from the surgical procedure. Conclusions While this was a complex case with some clinical uncertainty regarding the cause of our patient’s symptoms, we conclude that psychological processes were central to the development of his clenched fists. The phenomenon of clenched fists and our case are discussed with reference to the accumulated literature on psychogenic hand disorders and the International Statistical Classification of Diseases and Related Health Problems , 10th version. The nosological status appears to be obscure. This case presentation is a first step in increasing the understanding of this syndrome from a psychiatric perspective.

Detailed observation reveals a lump of translucent sticky mucus standing in the epipharynx of most globus patients, suggesting that the mucus adherent to the epipharynx causes a globus sensation. The epipharyngeal mucus of 70 consecutive globus patients was sampled via the nasal cavity. Fucose and sialic acid, the determinants of the viscoelasticity of mucus, were measured. Twenty-three patients were also asked to complete the Throat Questionnaire so we could evaluate the correlation between the degree of globus sensation and the viscoelasticity of the mucus. The mucus of 10 healthy subjects was sampled, analyzed, and compared with the data of the patients. The fucose and sialic acid concentrations found in the patients with globus pharyngis were significantly higher than those in the control subjects (Mann-Whitney U test, p < .01). The fucose concentrations correlated significantly with the globus pharyngis scores (Spearman correlation, p < .05). We conclude that there is a close association between stagnant mucus in the epipharynx and globus sensation.