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Behavioural disturbances in attention deficit hyperactivity disorder (ADHD) are thought to be due to dysfunction of spatially distributed, interconnected neural systems. While there is a fast-growing literature on functional dysconnectivity in ADHD, far less is known about the structural architecture underpinning these disturbances and how it may contribute to ADHD symptomology and treatment prognosis. We applied graph theoretical analyses on diffusion MRI tractography data to produce quantitative measures of global network organisation and local efficiency of network nodes. Support vector machines (SVMs) were used for comparison of multivariate graph measures of 37 children and adolescents with ADHD relative to 26 age and gender matched typically developing children (TDC). We also explored associations between graph measures and functionally-relevant outcomes such as symptom severity and prediction of methylphenidate (MPH) treatment response. We found that multivariate patterns of reduced local efficiency, predominantly in subcortical regions (SC), were able to distinguish between ADHD and TDC groups with 76% accuracy. For treatment prognosis, higher global efficiency, higher local efficiency of the right supramarginal gyrus and multivariate patterns of increased local efficiency across multiple networks at baseline also predicted greater symptom reduction after 6 weeks of MPH treatment. Our findings demonstrate that graph measures of structural topology provide valuable diagnostic and prognostic markers of ADHD, which may aid in mechanistic understanding of this complex disorder.

Background Impaired renal function may be observed in individuals with a restrictive eating disorder, yet its prevalence and underlying pathophysiological mechanisms are inadequately characterised. The impact of elevated protein intake on estimated glomerular filtration rate (eGFR) in this demographic remains unclear, leading to a lack of specific guidelines regarding protein prescriptions during inpatient treatment. This study describes changes in eGFR as a marker of renal function among adolescents and young adults receiving inpatient care for restrictive eating disorders and evaluates protein prescriptions during nutritional rehabilitation. Methods A retrospective audit of adolescent and young adults hospitalised with restrictive eating disorders (2016–2020) on a specialised medical ward was conducted. Data collected included anthropometric measurements, age, serum creatinine, blood urea, energy and protein prescriptions, medical stability upon admission, and hospital length-of-stay. The eGFR was calculated using the CKiDU25 equation. A random intercepts model was employed to assess the relationship between protein intake and eGFR changes during hospitalisation, controlling for confounding variables including age, sex, %mBMI, medical instability, and purging history. Results Among the 187 admissions that met inclusion criteria, the mean age was 17.0 ± 1.2 years, 90.9% ( n  = 170) were females, and mean %mBMI was 80.1 ± 9.5% at admission. Impaired renal function (eGFR < 90 mL/min/1.73 m²) was observed in 35.3% of patients at admission, and 3.2% of patients at discharge. Protein intake increased from 1.9 ± 0.4 g/kg/day on admission to 2.7 ± 0.6 g/kg/day at discharge. Conclusions Impaired renal function was observed in approximately one third of this sample of adolescents and young adults hospitalised with restrictive eating disorders and typically resolves during the admission. A high protein prescription of 1.9–2.7 g/kg/day did not deleteriously affect renal function, with eGFR levels improving with nutritional rehabilitation. Prospective studies are needed to confirm the optimal protein prescription during nutritional rehabilitation in patients hospitalised with restrictive eating disorders, and to further explore outcomes in the small subgroup of patients who remain with renal impairment at discharge. Plain language summary Impaired kidney function is a potential complication of malnutrition in individuals with restrictive eating disorders, although its prevalence is poorly characterised. During refeeding, increased energy intake may lead to high protein consumption, but the impact of this on kidney function, as measured by estimated glomerular filtration rate (eGFR), remains unclear in this population. This study describes changes in eGFR as a marker of kidney function among adolescents and young adults receiving inpatient care for restrictive eating disorders and evaluates protein prescriptions during nutritional rehabilitation. Over a five-year period, 187 patients met the inclusion criteria for this study and were included in the analysis. Of these, 35.3% presented with impaired kidney function at admission, and 3.2% of cases remained with impaired kidney function at discharge. Protein intake increased from 1.9 ± 0.4 g/kg/day at admission to 2.7 ± 0.6 g/kg/day at discharge. Overall, the study suggests that a high protein prescription did not negatively affect kidney function, with eGFR normalised for the majority of patients by discharge. Further prospective studies are needed to determine the optimal protein prescription for patients with restrictive eating disorders during medical refeeding.

Neuroimaging studies have revealed neurobiological differences in ADHD, particularly studies examining connectivity disruption and anatomical network organization. However, the underlying pathophysiology of ADHD types remains elusive as it is unclear whether dysfunctional network connections characterize the underlying clinical symptoms distinguishing ADHD types. Here, we investigated intrinsic functional network connectivity to identify neural signatures that differentiate the combined (ADHD-C) and inattentive (ADHD-I) presentation types. Applying network-based statistical (NBS) and graph theoretical analysis to task-derived intrinsic connectivity data from completed fMRI scans, we evaluated default mode network (DMN) and whole-brain functional network topology in a cohort of 34 ADHD participants (aged 8–17 years) defined using DSM-IV criteria as predominantly inattentive (ADHD-I) type (n = 15) or combined (ADHD-C) type (n = 19), and 39 age and gender-matched typically developing controls. ADHD-C were characterized from ADHD-I by reduced network connectivity differences within the DMN. Additionally, reduced connectivity within the DMN was negatively associated with ADHD-RS hyperactivity-impulsivity subscale score. Compared with controls, ADHD-C but not ADHD-I differed by reduced connectivity within the DMN; inter-network connectivity between the DMN and somatomotor networks; the DMN and limbic networks; and between the somatomotor and cingulo-frontoparietal, with ventral attention and dorsal attention networks. However, graph-theoretical measures did not significantly differ between groups. These findings provide insight into the intrinsic networks underlying phenotypic differences between ADHD types. Furthermore, these intrinsic functional connectomic signatures support neurobiological differences underlying clinical variations in ADHD presentations, specifically reduced within and between functional connectivity of the DMN in the ADHD-C type.

Evidence from functional neuroimaging studies support neural differences between the Attention Deficit Hyperactivity Disorder (ADHD) presentation types. It remains unclear if these neural deficits also manifest at the structural level. We have previously shown that the ADHD combined, and ADHD inattentive types demonstrate differences in graph properties of structural covariance suggesting an underlying difference in neuroanatomical organization. The goal of this study was to examine and validate white matter brain organization between the two subtypes using both scalar and connectivity measures of brain white matter. We used both tract-based spatial statistical (TBSS) and tractography analyses with network-based Statistics (NBS) and graph-theoretical analyses in a cohort of 35 ADHD participants (aged 8–17 years) defined using DSM-IV criteria as combined (ADHD-C) type (n = 19) or as predominantly inattentive (ADHD-I) type (n = 16), and 28 matched neurotypical controls. We performed TBSS analyses on scalar measures of fractional anisotropy (FA), mean (MD), radial (RD), and axial (AD) diffusivity to assess differences in WM between ADHD types and controls. NBS and graph theoretical analysis of whole brain inter-regional tractography examined connectomic differences and brain network organization, respectively. None of the scalar measures significantly differed between ADHD types or relative to controls. Similarly, there were no tractography connectivity differences between the two subtypes and relative to controls using NBS. Global and regional graph measures were also similar between the groups. A single significant finding was observed for nodal degree between the ADHD-C and controls, in the right insula (corrected p = .029). Our result of no white matter differences between the subtypes is consistent with most previous findings. These findings together might suggest that the white matter structural architecture is largely similar between the DSM-based ADHD presentations is similar to the extent of being undetectable with the current cohort size.

Background Lisdexamfetamine dimesylate (LDX) has demonstrated safety and efficacy for treatment of Binge Eating Disorder (BED). However, to date, trials have not included participants with co-occurring psychiatric disorders. This study explores how LDX affects eating disorder psychopathology, symptoms of common psychiatric comorbidities of BED (ADHD, depression, anxiety), and psychological quality of life, in people with moderate to severe BED. Methods These are secondary analyses of an open-label LDX trial conducted in 41 adults (18–40 years) over eight-weeks. Participants received LDX titrated to 50 or 70 mg. Clinical assessments and self-report questionnaires were conducted at baseline and 8-week follow-up. Results Eating disorder psychopathology and psychological quality of life improved after 8-weeks of LDX. No significant group-level changes in depression, anxiety or ADHD severity scores were observed. However, the majority within the small subsets with elevated depression and ADHD symptoms experienced reduced depressive and inattentive symptom severity, respectively. Conclusions We provide proof-of-concept evidence that LDX may provide broader psychological benefits to individuals with BED, beyond reducing their BE frequency. Effects of LDX on anxiety should be monitored closely by clinicians. Early indications suggest that LDX may be effectively used in people with BED, with and without co-occurring psychiatric conditions, however tolerability may be lower in highly complex cases. Trial registration : Australian and New Zealand Clinical Trials Registry (anzctr.org.au) #ACTRN12618000623291. Plain English summary Lisdexamfetamine dimesylate (LDX) has been shown to reduce binge eating frequency among those with Binge Eating Disorder (BED). However, little is known about how LDX affects symptoms of common co-occurring conditions (ADHD, depression, anxiety) and mental health more broadly. In this study, 41 people with BED received an 8-week course of LDX and their symptoms were monitored before and after treatment. Overall, people experienced a robust improvement in eating disorder psychopathology and psychological quality of life. For those with higher levels of depression and ADHD, LDX had the additional benefit of improving depressive symptoms and inattentive symptom severity, respectively. The effect of LDX on anxiety symptoms appears to be more complex, with an equal proportion of people experiencing a decrease or an increase in anxiety over the course of treatment. Those who experienced reductions in anxiety during treatment tended to have greater concurrent reductions in binge eating frequency. This study provides preliminary evidence that for people with BED, LDX may be effective at improving co-occurring symptoms of eating disorder psychopathology and psychological well-being, and potentially ADHD and depression symptoms when present at an elevated level. More research is needed among a larger sample to verify these findings.

Purpose Carotid–femoral pulse wave velocity (cfPWV), an index of arterial stiffness, is one of the earliest indicators of cardiovascular risk. Studies of adolescents with anorexia nervosa have demonstrated increased arterial stiffness compared to healthy controls. Little information is available on the effect of weight restoration on arterial stiffness in adolescents with anorexia nervosa. Methods This pilot longitudinal study examined changes in arterial stiffness during weight restoration in adolescent females admitted to an inpatient eating disorder unit. Female adolescents aged 15–19 years with a diagnosis of anorexia nervosa and a body mass index (BMI) < 85% of median BMI for age and sex, were recruited from consecutive eating disorder admissions at Westmead Hospital, Australia. Weekly measurements of cfPWV were performed for up to 4 consecutive weeks. Results 12 participants were included, with an average follow-up of 3.2 ± 1.1 weeks. Using mixed-effects models, we observed a significant increase in BMI (95% CI 0.60, 0.80; p  < 0.01) along with a modest but statistically significant decrease in cfPWV. The rate of change in cfPWV observed was − 0.2 m/s per week (95% CI − 0.37, − 0.03; p  = 0.03). Mean arterial pressure (MAP) was significantly associated with cfPWV ( p  < 0.01). There was a borderline association between cfPWV and BMI ( p  = 0.05). Conclusions Our findings suggest a possible reduction in arterial stiffness with weight restoration, although results must be interpreted with caution due to the small sample. Nevertheless, serial measurements of cfPWV in this population are feasible, supporting the need for larger longitudinal studies in this population. Level of evidence : Level III.

The Society for Adolescent Health and Medicine (SAHM) has expanded the definition of severe malnutrition in adolescents and young adults to include not only a low BMI, but also includes those who have lost > 20% of body mass over a period of one year or > 10% body mass over six months, in recognition of the effect of weight suppression on severity of medical complications [10]. In this pilot study, 23 adolescent patients with anorexia nervosa were randomised to receive an isocaloric oral feeding regime of either high carbohydrate (50–60% energy content) or low carbohydrate (< 40% energy content). In this double blind randomised controlled trial there was no significant difference in weight gain between the two groups over the first two weeks of refeeding, but a significantly lower rate of hypophosphatemia was found in patients who received the enteral feed with lower carbohydrate/high fat compared to standard formula. Position Paper of the Society for Adolescent Health and Medicine: medical management of restrictive eating disorders in adolescents and young adults.

Introduction. This study examines weight gain and assesses complications associated with refeeding hospitalised adolescents with restrictive eating disorders (EDs) prescribed initial calories above current recommendations. Methods. Patients admitted to an adolescent ED structured “rapid refeeding” program for >48 hours and receiving ≥2400 kcal/day were included in a 3-year retrospective chart review. Results. The mean (SD) age of the 162 adolescents was 16.7 years (0.9), admission % median BMI was 80.1% (10.2), and discharge % median BMI was 93.1% (7.0). The mean (SD) starting caloric intake was 2611.7 kcal/day (261.5) equating to 58.4 kcal/kg (10.2). Most patients (92.6%) were treated with nasogastric tube feeding. The mean (SD) length of stay was 3.6 weeks (1.9), and average weekly weight gain was 2.1 kg (0.8). No patients developed cardiac signs of RFS or delirium; complications included 4% peripheral oedema, 1% hypophosphatemia (<0.75 mmol/L), 7% hypomagnesaemia (<0.70 mmol/L), and 2% hypokalaemia (<3.2 mmol/L). Caloric prescription on admission was associated with developing oedema (95% CI 1.001 to 1.047; p = 0.039 ). No statistical significance was found between electrolytes and calories provided during refeeding. Conclusion. A rapid refeeding protocol with the inclusion of phosphate supplementation can safely achieve rapid weight restoration without increased complications associated with refeeding syndrome.

Background The efficacy and safety of Lisdexamfetamine dimesylate (LDX) in the treatment of moderate to severe binge eating disorder (BED) has been demonstrated in multiple randomised clinical trials. Despite this, little is known about how LDX acts to improve binge eating symptoms. This study aims to provide a comprehensive understanding of the neural mechanisms by which LDX improves symptoms of BED. We hypothesise that LDX will act by normalising connectivity within neural circuits responsible for reward and impulse control, and that this normalisation will correlate with reduced binge eating episodes. Methods This is an open-label Phase 4 clinical trial of LDX in adults with moderate to severe BED. Enrolment will include 40 adults with moderate to severe BED aged 18–40 years and Body Mass Index (BMI) of 20–45 kg/m 2 , and 22 healthy controls matched for age, gender and BMI. Clinical interview and validated scales are used to confirm diagnosis and screen for exclusion criteria, which include comorbid anorexia nervosa or bulimia nervosa, use of psychostimulants within the past 6 months, and current use of antipsychotics or noradrenaline reuptake inhibitors. Baseline assessments include clinical symptoms, multimodal neuroimaging, cognitive assessment of reward sensitivity and behavioural inhibition, and an (optional) genetic sample. A subset of these assessments are repeated after eight weeks of treatment with LDX titrated to either 50 or 70 mg. The primary outcome measures are resting-state intrinsic connectivity and the number of binge eating episodes. Analyses will be applied to resting-state fMRI data to characterise pharmacological effects across the functional connectome, and assess correlations with symptom measure changes. Comparison of neural measures between controls and those with BED post-treatment will also be performed to determine whether LDX normalises brain function. Discussion First enrolment was in May 2018, and is ongoing. This study is the first comprehensive investigation of the neurobiological changes that occur with LDX treatment in adults with moderate to severe BED. Trial registration ACTRN12618000623291, Australian and New Zealand Clinical Trials Registry URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=374913&isReview=true . Date of Registration: 20 April 2018.

Research on children and parents’ experiences of ADHD has grown in recent years, attracting attention to their subjective perception of ADHD as a disorder. Theoretical accounts of illness perception suggest that it is multi-dimensional, consisting of at least five core constructs (see the common-sense model of illness representations or CSM: Leventhal et al., in: Rachman (ed) Medical psychology, Pergamon, New York, vol 2, pp 7–30, 1980, in: Baum, Taylor, Singer (eds) Handbook of psychology and health: social psychological aspects of health, Earlbaum, Hillsdale, vol 4, pp 219–252, 1984). We suggest that the application of CSM in children/adolescents with ADHD and their parents may play an important role in understanding their coping behavior, treatment adherence, and emotional well-being. A systematic search identified 101 eligible studies that investigated the perception of ADHD among diagnosed children/adolescents and their parents. In general, these studies support the existence of the multiple facets of illness representations proposed by the CSM in both diagnosed youngsters and parents indicating substantial variability among both parents and youngsters on each of these facets. The comprehensive assessment of the representations of ADHD indicates imbalance attention to the different representations of ADHD in the literature; disproportional research attention has been paid to the perceived effectiveness of treatment (i.e., treatment control dimension) compared to other illness representations (e.g., timeline, consequence, and coherence), despite research showing their relevance to treatment adherence among other implications. The review identifies the limitation of existing relevant research, needed foci for future studies, specific testable hypotheses, and potential clinical implications of the multifaceted representations of ADHD among youngsters and carers alike.