Biological factors affecting motor, sensory, and integrative processing may predispose to functional neurological disorder (FND) and functional somatic symptoms. While early-life influences have traditionally been conceptualized within psychological frameworks, the contribution of early-life biological vulnerabilities to symptom expression remains unclear.

Using TriNetX, a large electronic health records database, we assessed proportions of inherited, congenital, perinatal, and neurodevelopmental diagnoses, capturing a range of early-life conditions. We compared 188,868 individuals with FND and 406,202 with functional somatic symptoms to demographically matched migraine and depression cohorts. Subgroup analyses contrasted motor FND with functional seizures and system-predominant functional somatic symptom clusters (e.g. bowel and bladder) with the general cluster.

Compared with migraine and depression, individuals with FND and functional somatic symptoms showed higher proportions of multiple inherited and early-life vulnerability factors. Congenital and inherited conditions, including Ehlers–Danlos syndrome (OR = 2.1–3.6 across comparisons), congenital musculoskeletal malformations (1.7–2.0), and chromosomal abnormalities (2.5–3.2), were more prevalent. Perinatal factors such as low birth weight (1.8–2.4) were enriched, alongside neurodevelopmental disorders, including intellectual disability (1.9–5.4) and autism spectrum disorder (1.2–3.5). Subgroup analyses revealed phenotype-specific patterns: joint hypermobility and musculoskeletal malformations were more common in functional motor disorder and musculoskeletal functional somatic symptoms, whereas neurodevelopmental disorders were enriched in functional seizures and the general functional somatic symptom cluster.

Inherited and early-life biological vulnerabilities were more common in FND and functional somatic symptom cohorts. Their prevalence differed among phenotypes. Our findings suggest that developmental variation in brain–body systems may influence the risk and clinical expression of functional symptoms.

There is evidence that the two most common subtypes of functional neurological disorder, functional seizures (FSs) and functional motor symptoms (FMDs), have differences between them beyond symptom type, creating debate as to whether they may best be considered distinct disorders. However, most research has studied FS or FMD separately, and the few studies that have directly compared them have been relatively small. We used the large TriNetX electronic health database to see whether the differences previously identified would be confirmed in a larger sample of both subtypes.

All cases of FMD without FS were compared with cases of FS without FMD, extracted from the TriNetX electronic health records database. Previously identified between-group differences in demographics, comorbidity, and antecedents were compared between groups.

Over 120,000 cases of FMD and FS were extracted. They confirmed that people with FS were significantly younger and had a younger onset than those with FMD, were more likely to be Black and less likely to be Asian, and had higher rates of all comorbid mental health diagnoses, other than somatoform diagnoses, which were more common in FMD. The onset of FS was more commonly preceded by psychological injury, as measured by preceding depression or stress reactions.

The differences between FMD and FS previously identified in small studies were confirmed in this much larger dataset. They provide indirect support for differences in etiology and mechanism, which may in turn support a nosological distinction between FMD and FS.

Despite extensive research on temporal lobe epilepsy (TLE), most work focuses on treatment outcomes and their determinants. Detailed evaluation of causal factors has not been adequately addressed in most published studies. This study aimed to explore potential etiologic risk factors for TLE through a chart review of prospectively collected data from a Canadian epilepsy clinic.

Consecutive patients diagnosed with TLE at a Canadian epilepsy clinic were included. Consecutive patients with genetic generalized epilepsy (GGE) served as a comparison group. The study database comprised prospectively collected demographic and epilepsy data, including birth history, development, antecedents, imaging and EEG findings. Statistical analysis compared antecedent factors between the TLE and GGE groups.

Eighty-nine TLE patients (mean age 42.3 ± 15.9 years, 45M), and 69 GGE patients (mean age 32.8 ± 14 years, 36M) were included. TLE was strongly associated with prior significant head trauma (p < 0.001) and seizure following major neurological insult (p = 0.044). MRI showed mesial temporal sclerosis in 13 TLE patients (14.6%) and was normal in 45 (50.5%). Among EEG abnormalities in TLE, 48% localized to the posterior temporal region.

Significant head trauma and early post-insult seizures were the strongest associated risk factors for TLE in this Canadian cohort.

This research aims to assess the prevalence, severity and underlying causes of hearing impairments.

This cross-sectional study used multistage stratified sampling to select 2148 individuals from Salyan and Surkhet, following the World Health Organization’s Ear and Hearing Survey Handbook.

Among 1946 participants, 38.9 per cent had hearing impairments, including 15.9 per cent with disabling hearing loss, with severity increasing with age. Ear diseases affected 34.3 per cent, including dull or retracted tympanic membranes (18 per cent), impacted wax (8 per cent), perforated tympanic membrane (6.1 per cent), and abnormal tympanometry (23.1 per cent). The major causes were age-related hearing loss (50.5 per cent), Eustachian tube dysfunction (23 per cent), chronic suppurative otitis media (10.8 per cent), and otitis media with effusion (4.7 per cent). Higher education and immunisation were associated with reduced risk, while chronic conditions, earaches, drainage and tinnitus increased the risk.

The high prevalence of hearing impairment, primarily from preventable causes, underscores the importance of early screening and strengthened primary health care.

Despite bold commitments to reduce anaemia, little change in prevalence was observed over the past decade. We aimed to generate subnational maps of anaemia among women of reproductive age (WRA), malaria transmission and hemoglobinopathies to identify priority areas but also explore their geographical overlap.

Using the most recent Demographic and Health Surveys (DHS), we first mapped anaemia clusters across sub-Saharan Africa and identified the West and Central Africa (WCA) as a major cluster. Geographic clusters with high anaemia and related aetiologic factors were identified using spatial statistics. Multilevel regression models were run to identify factors associated with any, moderate and severe anaemia.

West and Central African countries (n 17).

WRA (n 112 024) residing in seventeen WCA countries.

There was a significant overlap in geographical clusters of anaemia, malaria and hemoglobinopathies, particularly in the coastal areas of the WCA region. Low birth interval (0·86 (0·77, 0·97)), number of childbirth (1·12 (1·02, 1·23)) and being in the 15–19 age range (1·47 (1·09, 1·98)) were associated with increased odds of any anaemia. Unimproved toilet facility and open defecation were associated with any anaemia, whereas the use of unclean cooking fuel was associated with moderate/severe anaemia (P < 0·05). Access to healthcare facility, living in malaria-prone areas and hemoglobinopathies (HbC and HbS) were all associated with any, moderate or severe anaemia.

Interlinkages between infection, hemoglobinopathies and nutritional deficiencies complicate the aetiology of anaemia in the WCA region. Without renewed efforts to integrate activities and align various sectors in the prevention of anaemia, progress is likely to remain elusive.

Pre-diagnostic stages of psychotic illnesses, including ‘clinical high risk’ (CHR), are marked by sleep disturbances. These sleep disturbances appear to represent a key aspect in the etiology and maintenance of psychotic disorders. We aimed to examine the relationship between self-reported sleep dysfunction and attenuated psychotic symptoms (APS) on a day-to-day basis.

Seventy-six CHR young people completed the Experience Sampling Methodology (ESM) component of the European Union Gene-Environment Interaction Study, collected through PsyMate® devices, prompting sleep and symptom questionnaires 10 times daily for 6 days. Bayesian multilevel mixed linear regression analyses were performed on time-variant ESM data using the brms package in R. We investigated the day-to-day associations between sleep and psychotic experiences bidirectionally on an item level. Sleep items included sleep onset latency, fragmentation, and quality. Psychosis items assessed a range of perceptual, cognitive, and bizarre thought content common in the CHR population.

Two of the seven psychosis variables were unidirectionally predicted by previous night's number of awakenings: every unit increase in number of nightly awakenings predicted a 0.27 and 0.28 unit increase in feeling unreal or paranoid the next day, respectively. No other sleep variables credibly predicted next-day psychotic symptoms or vice-versa.

In this study, the relationship between sleep disturbance and APS appears specific to the item in question. However, some APS, including perceptual disturbances, had low levels of endorsement amongst this sample. Nonetheless, these results provide evidence for a unidirectional relationship between sleep and some APS in this population.

Some preliminary research suggests higher rates of gastrointestinal disease in individuals with eating disorders (EDs). However, research is limited, and it remains unknown what etiologic factors account for observed associations. This was the first study to examine how EDs and dimensional ED symptoms (e.g. body dissatisfaction, binge eating) are phenotypically and etiologically associated with gastrointestinal disease in a large, population-based twin sample.

Adult female (N = 2980) and male (N = 2903) twins from the Michigan State University Twin Registry reported whether they had a lifetime ED (anorexia nervosa, bulimia nervosa, or binge-eating disorder) and completed a measure of dimensional ED symptoms. We coded the presence/absence of lifetime gastrointestinal disease (e.g. inflammatory bowel disease) based on responses to questions regarding chronic illnesses and medications. We first examined whether twins with gastrointestinal disease had higher rates of EDs and ED symptoms, then used correlated factors twin models to investigate genetic and environmental contributions to the overlap between disorders.

Twins with gastrointestinal disease had significantly greater dimensional ED symptoms (β = 0.21, p < 0.001) and odds of a lifetime ED (OR 2.90, p = 0.001), regardless of sex. Shared genetic factors fully accounted for the overlap between disorders, with no significant sex differences in etiologic associations.

Comorbidity between EDs and gastrointestinal disease may be explained by overlap in genetic influences, potentially including inflammatory genes implicated in both types of disorders. Screening for gastrointestinal disease in people with EDs, and EDs in those with gastrointestinal disease, is warranted.

Cognitive control impairments are observed across several psychiatric conditions, highlighting their role as a transdiagnostic marker. Individuals with attention deficit hyperactivity disorder (ADHD) have difficulties with inhibition, working memory, processing speed, and attention regulation. These cognitive control impairments may either mediate or moderate the association between neurobiological vulnerabilities and phenotypic presentation in neurodevelopmental disorders. Alternately, neurocognitive vulnerabilities in ADHD may be additive, akin to a multiple deficit model. We tested the mediation, moderation, and additive models using neurocognitive data in youth with ADHD.

7–11 year-old children diagnosed with ADHD (n = 75) and control children (n = 29) completed EEG recordings and neuropsychological testing (full scale IQ; cognitive control). Caregivers provided ADHD symptom ratings. Correlations and linear regression analyses were completed to examine the associations among cortical functioning (aperiodic slope), cognitive control, and ADHD symptoms.

We found support for an additive model wherein vulnerabilities in aperiodic slope, event-related potentials, and cognitive control each explained unique variance in ADHD symptoms. There was some evidence that cognitive control moderates the effect of atypical cortical development on ADHD symptoms. There was no support for the mediation model.

The etiology of ADHD symptoms is multifaceted and involves multiple “hits” across neurological and cognitive-behavioral factors.

Acute facial palsy is a consequence of various diseases, with the number of patients increasing with advancing age. This study aimed to analyse the clinical characteristics of acute peripheral facial palsy in older adults.

A total of 30 patients with a mean age of 68.4 ± 9.1 years were included in the study. All patients received a standardised investigation and follow up. The hospital charts of the patients with acute facial palsy were reviewed retrospectively.

The predominant causes of acute facial palsy in older adults were: Bell's palsy, Ramsay Hunt syndrome, trauma, otitis media and malignancy. At baseline, complete and incomplete facial palsies were seen in 26.7 per cent and 73.3 per cent of patients, respectively. The overall rates of good recovery, partial recovery and no recovery were 66.7 per cent, 10 per cent and 23.3 per cent, respectively. Increased age led to a significantly lower level of recovery in older adults.

Bell's palsy and Ramsay Hunt syndrome were the most common aetiologies of acute facial palsy in older adults, and such patients are likely to have incomplete recovery. Active early treatment is necessary for achieving good outcomes in older adults.

Many studies report an ethnic density effect whereby psychosis incidence among ethnic minority groups is higher in low co-ethnic density areas. It is unclear whether an equivalent density effect applies with other types of socioeconomic disadvantages.

We followed a population cohort of 2 million native Danes comprising all those born on 1st January 1965, or later, living in Denmark on their 15th birthday. Socioeconomic disadvantage, based on parents' circumstances at age 15 (low income, manual occupation, single parent and unemployed), was measured alongside neighbourhood prevalence of these indices.

Each indicator was associated with a higher incidence of non-affective psychosis which remained the same, or was slightly reduced, if neighbourhood levels of disadvantage were lower. For example, for individuals from a low-income background there was no difference in incidence for those living in areas where a low-income was least common [incidence rate ratio (IRR) 1.01; 95% confidence interval (CI) 0.93–1.10 v. those in the quintile where a low income was most common. Typically, differences associated with area-level disadvantage were the same whether or not cohort members had a disadvantaged background; for instance, for those from a manual occupation background, incidence was lower in the quintile where this was least v. most common (IRR 0.83; 95% CI 0.71–0.97), as it was for those from a non-manual background (IRR 0.77; 95% CI 0.67–0.87).

We found little evidence for group density effects in contrast to previous ethnic density studies. Further research is needed with equivalent investigations in other countries to see if similar patterns are observed.