Typical Age Of Onset Research Articles

Knowledge of Narcolepsy Among Physicians in Makkah Region, Saudi Arabia: A Cross-Sectional Study.

Background Narcolepsy is a chronic sleep disorder that is characterized by excessive daytime sleepiness and cataplexy. It has been increasingly diagnosed over the years, impacting productivity and employment rates. Awareness of healthcare providers is crucial for the early identification and management of this condition. Objectives This study assessed physicians' knowledge of narcolepsy in the Makkah region of Saudi Arabia. Method This cross-sectional study was conducted from February to November 2023. An online self-administered questionnaire has been used to target physicians working in the Makkah region of Saudi Arabia. The utilized questionnaire assessed demographic and professional data as well as the participants' knowledge of narcolepsy. Statistical analysis was performed using RStudio (R version 4.3.1.). Statistical differences in knowledge were assessed using Pearson's chi-squared and Fisher's exact tests. Factors associated with knowledge of narcolepsy were investigated through univariable and multivariable regression analyses expressed using beta coefficients and 95% confidence intervals (95% CIs). Statistical significance was considered at p < 0.05. Results A total of 226 physicians participated in this study. Male physicians (54.4%, n = 123), practicing in governmental hospitals (77.9%, n = 176) and residing in Makkah City (43.4%, n = 98) were predominant. Non-surgical specialties represented 73.5% (n = 166) of the sample. Around 81% (n = 184) of the participants were aware of narcolepsy, with a significant difference according to professional status (p = 0.045). The majority of physicians have correctly identified narcolepsy as a sleep disorder (78.3%, n = 177), but only 32.3% (n = 73) have identified its typical onset age group and recognized that there are two types of narcolepsy. Almost half of the respondents indicated a lack of knowledge about the diagnostic criteria for narcolepsy in the DSM-5 (52.2%, n = 118). Only 27.4% (n = 62) recognized the correct diagnostic criteria. Half of the sample (51.3%, n = 116) recognized the use of multiple sleep latency tests for the diagnosis. For factors associated with higher participants' knowledge, non-surgical specialties showed significantly higher knowledge scores compared to surgical specialties (beta = 0.91, 95% CI, 0.13 to 1.7, p = 0.024). Conclusion This study has revealed a significant lack of knowledge about narcolepsy among physicians inMakkah region. This raises concerns about the timely identification, proper understanding, and accurate diagnosis of patients with narcolepsy. Adequate understanding of narcolepsy is crucial to avoid its misdiagnosis or delays in receiving appropriate treatment and support, ultimately impacting their quality of life.

Mitochondrial neurogastrointestinal encephalopathy: a case report

BackgroundMitochondrial neurogastrointestinal encephalopathy (MNGIE) is an autosomal recessive disease associated with alterations in mitochondrial DNA (mtDNA). The typical age of onset of MNGIE is between the first and second decade of life. Diagnosis requires the presence of several key clinical features: sensorimotor neuropathy, external ophthalmoplegia, ocular ptosis, leukoencephalopathy, and gastrointestinal (GI) dysmotility. Unfortunately, MNGIE diagnosis is very challenging, and patients often undergo multiple diagnostic and surgical operations that are unnecessary.Case presentationThis case is of a 51-year-old male presenting with a 2-year history of limb weakness, GI problems and cachexia. There was also a 1-year history of progressive ptosis and ophthalmoplegia. The patient’s uncle and brother had both died from GI-related issues prior to the age of 40. On physical examination, ocular motility was impaired in all directions and there was atrophy and reduction in power in both lower and upper extremities. FLAIR and T2-weighted sequences of brain MRI demonstrated diffuse cerebral white matter hyperintensity (leukoencephalopathy). On discharge, the patient was referred for genetic consultation for bone marrow transplantation and had regular follow-up with a gastroenterology specialist.ConclusionIn patients presenting with chronic progressive ophthalmoplegia, severe gastrointestinal complications, sensorimotor neuropathy and white matter lesions on MRI, it is important to consider investigating for MNGIE.

DNA Damage and Senescence in the Aging and Alzheimer's Disease Cortex Are Not Uniformly Distributed.

Alzheimer's disease (AD) is a neurodegenerative illness with a typical age of onset exceeding 65 years of age. The age dependency of the condition led us to track the appearance of DNA damage in the frontal cortex of individuals who died with a diagnosis of AD. The focus on DNA damage was motivated by evidence that increasing levels of irreparable DNA damage are a major driver of the aging process. The connection between aging and the loss of genomic integrity is compelling because DNA damage has also been identified as a possible cause of cellular senescence. The number of senescent cells has been reported to increase with age, and their senescence-associated secreted products are likely contributing factors to age-related illnesses. We tracked DNA damage with 53BP1 and cellular senescence with p16 immunostaining of human post-mortem brain samples. We found that DNA damage was significantly increased in the BA9 region of the AD cortex compared with the same region in unaffected controls (UCs). In the AD but not UC cases, the density of cells with DNA damage increased with distance from the pia mater up to approximately layer V and then decreased in deeper areas. This pattern of DNA damage was overlaid with the pattern of cellular senescence, which also increased with cortical depth. On a cell-by-cell basis, we found that the intensities of the two markers were tightly linked in the AD but not the UC brain. To test whether DNA damage was a causal factor in the emergence of the senescence program, we used etoposide treatment to damage the DNA of cultured mouse primary neurons. While DNA damage increased after treatment, after 24 h, no change in the expression of senescence-associated markers was observed. Our work suggests that DNA damage and cellular senescence are both increased in the AD brain and increasingly coupled. We propose that in vivo, the relationship between the two age-related processes is more complex than previously thought.

Investigating Post-Menopausal Characteristics and Perceptions of the Menopausal Transition

OBJECTIVES This study aimed to investigate the knowledge and perceptions of menopause among post-menopausal women.METHODOLOGYA descriptive cross-sectional study was conducted at Hayatabad Medical Complex, Medical, and Teaching Institute Peshawar from March 2022 to March 2023. Participants meeting the inclusion criteria were assessed using a semi-structured proforma covering demographic variables, knowledge, and attitudes toward menopause. Delving into knowledge and perceptions of menopause, the questionnaire probed participants about their awareness of menopause upon cessation of menstrual periods, knowledge of the age of menopause, understanding of menopausal symptoms, whether they perceived menopause as a disease, medical condition, or a natural process, and their opinions on the treatment of menopausal symptoms.RESULTSIn a survey assessing menopausal characteristics and perceptions, 81% of women experienced natural menopause and 19% underwent surgical menopause. 85% had prior knowledge of menopause, but only 45% knew its typical onset age. 56% held a positive perception of menopause. Hot flashes and mood swings were reported by 55% of women, while 48% experienced insomnia.CONCLUSIONMany post-menopausal women are not aware of menopausal symptoms. Tailored health education and comprehensive support are necessary to address knowledge disparities and provide holistic care for women in this transition.

Early-childhood linear growth faltering in low- and middle-income countries

Globally, 149 million children under 5 years of age are estimated to be stunted (length more than 2 standard deviations below international growth standards)1,2. Stunting, a form of linear growth faltering, increases the risk of illness, impaired cognitive development and mortality. Global stunting estimates rely on cross-sectional surveys, which cannot provide direct information about the timing of onset or persistence of growth faltering—a key consideration for defining critical windows to deliver preventive interventions. Here we completed a pooled analysis of longitudinal studies in low- and middle-income countries (n = 32 cohorts, 52,640 children, ages 0–24 months), allowing us to identify the typical age of onset of linear growth faltering and to investigate recurrent faltering in early life. The highest incidence of stunting onset occurred from birth to the age of 3 months, with substantially higher stunting at birth in South Asia. From 0 to 15 months, stunting reversal was rare; children who reversed their stunting status frequently relapsed, and relapse rates were substantially higher among children born stunted. Early onset and low reversal rates suggest that improving children’s linear growth will require life course interventions for women of childbearing age and a greater emphasis on interventions for children under 6 months of age.

Modified Atkins diet in children with epilepsy with eyelid myoclonia (Jeavons syndrome)

BackgroundEpilepsy with eyelid myoclonia(EEM) or Jeavons syndrome is considered a genetic generalized epilepsy with a typical age of onset in childhood. Many types of seizures can be observed, including eyelid myoclonia, absence, generalized tonic-clonic, and myoclonic seizures. Seizures tend to be difficult to control requiring polypharmacy treatment or become drug-resistant. Dietary therapy, particularly with Modified Atkins Diet (MAD), as a treatment of seizures in this syndrome has rarely been studied. We report efficacy and tolerability of MAD in children with epilepsy with eyelid myoclonia. MethodsWe reviewed medical records of children with EEM treated at the University of Chicago Ketogenic Diet program from 2017 to 2022. Patient’s demography, seizure characteristics, EEG findings, response to treatment, and adverse effects were reviewed. ResultSix patients with EEM were identified. Average age of seizure onset was 6 (2–11) years and an average age when the MAD started was 10.7 (6–15) years. All patients were started on MAD and completed at least 6 months on the diet at the time of report. An average of 4 (0–9) anti-seizure medications (ASM) had been tried prior to the MAD. All patients achieved ketosis with an average level of serum beta-hydroxybutyrate of 1.9 (1.03–3.61) mmol/L. At the 6-month follow-up visit, all patients (100%) experienced a greater than 50% seizure reduction, 3/6 patients (50%) had more than 90% seizure reduction, 1/6 patients (17%) became seizure-free. All seizure types demonstrated a greater than 80% reduction in frequency.Absence and myoclonic seizures showed the greatest reduction with 100% seizure reduction. Eyelid myoclonia and generalized tonic-clonic seizures showed more than 80% seizure reduction.Moreover, all patients reported improvement in alertness, mood, and concentration. Initial weight loss and mild gastrointestinal disturbances were reported in 2/6 patients (33%) and corrected with dietary adjustment. ConclusionThe Modified Atkins Diet has shown to be effective and welltolerated for children with EEM in our study. Cognitive improvement has also been subjectively reported in all patients. Adverse effects are tolerable and correctable. The MAD, therefore, may be considered as a treatment option for patients with epilepsy with eyelid myoclonia.

EPH38 Burden of Psychiatric Health in Elderly Myasthenia Gravis Patients: A Nationwide Medicare Perspective

Myasthenia gravis (MG) is a chronic autoimmune disease marked by heterogeneous presentations of progressive muscle weakness with a typical age of onset between 20-40 years. Treatment advancements have increased the lifespan of people with MG, but disease burden in older populations is not well-characterized. The objective of this analysis was to characterize the burden of MG among elderly Medicare beneficiaries in terms of the prevalence and association between muscle weakness and psychiatric health.

Abstract A38: Pediatric Germline CSF3R T618I mutation gives insight into disease progression and long-term therapy options of Chronic Neutrophilic Leukemia

Abstract Chronic Neutrophilic Leukemia (CNL) is a rare BCR-ABL negative myeloproliferative neoplasm that affects approximately 1 in a million individuals. The typical age of onset and disease presentation is in elderly patients with a median age of 63 and a range of 9-84. The oncogenic driver of CSF3R, the G-CSF receptor protein, in CNL has been classified over the last decade and has improved therapies for patients with targeted Tyrosine Kinase Inhibitors, such as Ruxolitinib (a potent JAK1/2 inhibitor). Currently, the only curative option is an allogeneic hemopoietic stem cell transplant with typical median overall survival of 2 years. Because of the low occurrence rate of CNL, there have only been 3 germline cases of CSF3R classified in literature. With these patients, they exhibit a lifelong skewing of the myeloid lineage causing gross neutrophilia. Our patient presented at 13 months with leukocytosis and neutrophilia, resulting in genetic testing revealing the diagnosis of the youngest documented case of CNL. A germline CSF3R T618I constitutive activating mutation was documented in our patient and in her father. Her father had documented lifelong leukocytosis of indeterminate origin and it was not until 33 that genetic testing was done, and he was diagnosed with CNL. He underwent an allogeneic stem cell transplant after being admitted with gross hepatosplenomegaly with a WBC of 322, the highest recorded in a germline CNL patient in literature. Our patient presented to clinic with leukocytosis ranging from 45-98 and hepatosplenomegaly. After a bone marrow aspirate and biopsy was taken to determine disease stage and severity, we immediately began Ruxolitinib therapy. We began 20 mg BID dosing based on platelets and monitored response to therapy while conducting targeted RNA-seq for myelodysplastic and myeloid leukemia genes on the bone marrow, which did not detect any secondary mutations. Ruxolitinib dosing was tapered down in a stepwise fashion, until the patient arrived at the current dose of 7.5 mg BID Ruxolitinib, resulting in stable leukocyte counts around 25. As part of monitoring, we are currently conducting 6-month BM procedures and NGS for AML/MDS genes and Ruxolitinib resistance mutations alongside monthly CBCs. Our patient has been on Ruxolitinib for 9 months and has not developed any secondary contributing mutations and remains sensitive to therapy. We continue to monitor our patient’s response to Ruxolitinib to determine if germline predisposition alters the transformative nature of the disease. Within T618I germline CNL cases, we are investigating the difference in phenotype and disease burden that we observe in our patient’s family compared to literature. Based on current cases, it seems that germline CNL does not transform during childhood and adolescence into AML without the influence of a secondary mutation. Retrospective studies into previous cases of CNL to determine if there is a higher frequency of germline origin could pave the way for potential early-stage therapies and detection of CNL prior to transformation. Citation Format: Kevin Zhang, Matthew Rees, Mahsa Khanlari, Laura Rooms, Raul Ribeiro, Marcin Wlodarski. Pediatric Germline CSF3R T618I mutation gives insight into disease progression and long-term therapy options of Chronic Neutrophilic Leukemia [abstract]. In: Proceedings of the AACR Special Conference: Acute Myeloid Leukemia and Myelodysplastic Syndrome; 2023 Jan 23-25; Austin, TX. Philadelphia (PA): AACR; Blood Cancer Discov 2023;4(3_Suppl):Abstract nr A38.

A Young Girl With Granulomatosis with Polyangiitis: A Rare Case Report

Granulomatosis with polyangiitis (GPA), formerly known as Wegener's granulomatosis is a necrotizing vasculitides that primarily affects small-sized arteries and manifests differently depending on the organ involved and the severity of the disease. Here we are reporting a case of a 15-year-old girl presented with purulent nasal discharge with epistaxis, cough, reduced hearing, fever &amp; rash. Tissue biopsy report, positive C-ANCA, imaging and clinical features were consistent with the diagnosis of GPA. After counseling the patient &amp; her parents and taking consent, she has been treated with intravenous methylprednisolone and cyclophosphamide. Despite being a rare disease with a typical age of onset around 40 years, it should be suspected in any aged patient exhibiting constitutional symptoms and other evidence of upper or lower respiratory tract involvement or glomerulonephritis. Bangladesh J Medicine 2023; 34(2): 151-154

The American Psychiatric Association Practice Guideline for the Treatment of Patients With Eating Disorders.

The American Psychiatric Association Practice Guideline for the Treatment of Patients With Eating Disorders.

Relating pathogenic loss-of-function mutations in humans to their evolutionary fitness costs.

Causal loss-of-function (LOF) variants for Mendelian and severe complex diseases are enriched in 'mutation intolerant' genes. We show how such observations can be interpreted in light of a model of mutation-selection balance and use the model to relate the pathogenic consequences of LOF mutations at present to their evolutionary fitness effects. To this end, we first infer posterior distributions for the fitness costs of LOF mutations in 17,318 autosomal and 679 X-linked genes from exome sequences in 56,855 individuals. Estimated fitness costs for the loss of a gene copy are typically above 1%; they tend to be largest for X-linked genes, whether or not they have a Y homolog, followed by autosomal genes and genes in the pseudoautosomal region. We compare inferred fitness effects for all possible de novo LOF mutations to those of de novo mutations identified in individuals diagnosed with one of six severe, complex diseases or developmental disorders. Probands carry an excess of mutations with estimated fitness effects above 10%; as we show by simulation, when sampled in the population, such highly deleterious mutations are typically only a couple of generations old. Moreover, the proportion of highly deleterious mutations carried by probands reflects the typical age of onset of the disease. The study design also has a discernible influence: a greater proportion of highly deleterious mutations is detected in pedigree than case-control studies, and for autism, in simplex than multiplex families and in female versus male probands. Thus, anchoring observations in human genetics to a population genetic model allows us to learn about the fitness effects of mutations identified by different mapping strategies and for different traits.

A Family Cluster of Inherited Ataxia: Case Report and Clinical Review

The hereditary ataxias are a highly heterogeneous group of disorders phenotypically characterised by gait ataxia, incoordination of eye movements, speech, and hand movements, and usually associated with atrophy of the cerebellum. Friedreich's ataxia is a genetic, progressive, neurodegenerative movement disorder with a typical age of onset of between 10 and 15 years. Initial symptoms may include unsteady posture, frequent falling, and progressive difficulty in walking due to an impaired ability to coordinate voluntary movements (ataxia). A family of six members was diagnosed clinically, electro-physiologically, and radiologically with having this type of inherited ataxia from Basrah, southern Iraq. This article aims to describe the clinical presentation and diagnostic approach of cerebellar ataxia, with a focus on inherited forms of ataxia.

Pathogenic Mechanisms of Autoimmune Thyroid Disease

Autoimmune thyroid illnesses are a category of disorders characterized by aberrant lymphocyte activity directed against self-tissues and are mostly represented by Hashimoto's thyroiditis and Graves' disease, which affect about 2% to 3% of the population, with a female predominance. Autoimmune thyroid disease is the most prevalent thyroid illness in children; the most typical age of onset is puberty, although the disease can strike at any age, including children as young as one-year-old. Autoantibodies to pendrin, an iodide transporter found at the apical pole of thyroid follicular cells, have recently been discovered in the majority of Hashimoto's thyroiditis and Graves' disease patients. Excessive iodine administration has been linked to an increased prevalence of thyroiditis in humans, according to recent epidemiologic research. People in North America consumed more than three times the recommended daily iodine intake. Antithyroglobulin antibody, anti-thyroperoxidase antibody, serum thyroid-stimulating hormone, and exacerbation of lymphocytic infiltration in the thyroid were all higher in these persons, indicating that iodine overconsumption could cause hypothyroidism and exacerbate the autoimmune response. However, the exact mechanism by which high iodine consumption causes autoimmune thyroid disease is yet unknown.

AZACITIDINE-INDUCED SWEET SYNDROME: A UNIQUE PRESENTATION

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Sweet's Syndrome (SS) or febrile neutrophilic dermatosis, was first described in 1964 by Robert Sweet and has a female predilection with a female to male ratio of 4:1, with the typical age of onset between 30 and 60 years of age [1]. SS can either be idiopathic, pregnancy, or drug-induced, associated with infections or with malignancies [2]. We describe a unique presentation of SS in an elderly male with myelodysplastic syndrome (MDS) receiving Azacytidine (AZA). CASE PRESENTATION: A 76-year-old Caucasian male with medical history pertinent for MDS reported a new rash and fever which started immediately after completing his second 7-day cycle of AZA. Vitals were significant for hypotension and tachycardia. Physical exam was remarkable for nodules and erythematous plaques diffusely spread across the trunk, back, upper and, lower extremities. CBC showed pancytopenia and elevated inflammatory markers. The patient was adequately resuscitated, however, required low dose pressors, transfused two units of packed red blood cells, and started on broad-spectrum antibiotics. He was admitted for sepsis and neutropenic fever. Histopathology from a punch biopsy of the right calf plaque showed mild spongiosis, acanthosis, and papillary dermal edema. The dermis contained patchy perivascular inflammation, which was lymphoplasmacytic and neutrophilic. Stains for infectious agents were negative. Tissue cultures were negative for any bacterial or fungal growth. A diagnosis of SS, secondary to AZA was made. The patient was started on systemic steroids with a slow taper and made a full recovery ten days after. DISCUSSION: All five diagnostic criteria for drug-induced Sweet's syndrome proposed by Walker and Cohen were met [3]. Including an abrupt onset of painful erythematous plaques or nodules, histopathological evidence, temperature > 38°C, a temporal relationship between administration of AZA and development of the syndrome, and the resolution of symptoms when corticosteroids were given and AZA was withheld [4]. AZA is an antineoplastic agent used in the treatment of MDS. Recently, there has been an uptick in reports on AZA-associated SS [5]. The average time to resolution of clinical symptoms in drug-induced SS is reported to be around 8 days, consistent with the patient presentation [6]. CONCLUSIONS: Our case is unique in that the patient developed diffuse lesions, differing from current literature, which supports skin manifestations at the sites of injections. Prognosis is poor in patients with MDS who have SS [7]. Hence, a timely diagnosis of this condition is critical. REFERENCE #1: Vashisht P, Bansal P, Goyal A, Hearth Holmes MP. Sweet Syndrome. 2020 Sep 14. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 28613704. DISCLOSURES: No relevant relationships by Rabia Anees, source=Web Response No relevant relationships by Rosa Arancibia, source=Web Response No relevant relationships by Andrew Doodnauth, source=Web Response No relevant relationships by Khawaja Omar, source=Web Response

A Commentary on “Eating Disorders and the Rorschach” (Guinzbourg de Braude et al., 2021)

A Commentary on “Eating Disorders and the Rorschach” (Guinzbourg de Braude et al., 2021)

Lepromatous leprosy mimicking systemic lupus erythematosus

We describe a case of a 36-year-old woman who presented with bilateral symmetrical polyarthritis of the hands, malar rash, and discoid rash over three months. She was initially diagnosed and treated as systemic lupus erythematosus but later proven to have lepromatous leprosy. The patient showed a remarkable improvement after the administration of steroids. Due to typical features of a connectivetissue disorder, a positive serological marker, photosensitivity, typical age of onset and initial response to treatment led to the confusion and delay in diagnosis of lepromatous leprosy. Further, this case emphasizes the importance of obtaining a detailed contact history and taking a skin biopsy even in a typical connective tissue lesion. Our case illustrates an unusual presentation of lepromatous leprosy mimicking systemic lupus erythematosus.

Massively Parallel Sequencing of 43 Arrhythmia Genes in a Selected SUDI Cohort from Cape Town.

Sudden unexpected death in infants (SUDI) is a devastating event, and unfortunately occurs frequently in developing countries. The emerging molecular autopsy has added value to post-mortem investigations, where genetic variants were able to explain the unexpected demise. Many of these variants have been found in genes involved in arrythmia pathways. The aim of this study was to sequence 43 genes previously associated with cardiac arrhythmia in a selected cohort of SUDI cases ( n = 19) in South Africa. A total of 335 variants were found among the 19 infants, of which four were novel. The variants were classified as "likely pathogenic" ( n = 1), "variant of unknown significance" ( n = 54), "likely benign" ( n = 56) or "benign" ( n = 224). The likely pathogenic variant was LMNA NM_170707.2:c.1279C > T (p.Arg427Cys) and was found in a 3-week-old male infant of African ancestry. Variants in LMNA have previously been associated with dilated cardiomyopathy, with a typical age of onset in adulthood; therefore, this may be the first report in an infant. The yield of pathogenic or likely pathogenic variants in the classic genes typically associated with channelopathies and sudden death, was less in this study compared with other settings. This finding highlights the importance of population-specific research to develop a molecular autopsy which is locally relevant.

Early Psychosis: Diagnosis and Treatment

Background: The typical age of onset for psychotic disorders is concurrent with the typical age of enrollment in higher education. College and graduate students often experience new academic and social demands that may leave them vulnerable to substance use and mental health problems, including the initial onset of a psychotic episode. Objective: To provide a current overview of the guidelines and literature for the diagnosis and treatment of early psychosis with special consideration for the college and graduate student population in the United States. To highlight areas of need and provide recommendations for clinicians who work at educational institutions and their health services, along with general psychiatrists and psychologists who work with post-secondary education populations, to help close the treatment gap. Method: A review of interventions and best practice for the treatment of early psychosis in college students was conducted, informed by the authors’ current experience as clinicians working with this population at a university in the United States. Results: Thorough psychiatric interviews and screening tools can help in the early identification of individuals at clinical high risk for, and at the first onset of, psychosis. Coordinated specialty care services are the gold standard for early psychosis and include psychotherapy interventions (such as cognitive behavioral therapy and individual resiliency training), as well as support for a student to return to school or work. Individuals experiencing a first episode of psychosis, in general, respond better to lower doses of antipsychotics and may also experience more adverse effects. Conclusion: Return to a high level of functioning is possible in many cases of early psychosis, with early identification and treatment essential.

Stigma and Treatment of Eating Disorders in School Counselors in Turkey (STED-SCIT)

Background: Eating disorders are severe and debilitating conditions, with a typical age of onset in adolescence, and carrying significant morbidity and mortality. To assess quality of school counselors' knowledge of and attitudes to eating disorders and discern extent to which knowledge gaps and stigma act as a barrier to service provision. Methods: Respondents were randomly allocated to one of five clinical vignettes, each depicting a young person with anorexia nervosa, bulimia nervosa, binge-eating disorder, depression, or type-1 Diabetes. A study-specific questionnaire examined school counselors' eating disorders attitudes, and knowledge. Results: Forty-nine counselors participated. School counselors correctly identified target case in over half of cases with anorexia nervosa being the most frequently correctly identified (75%) compared to depression or Diabetes. Diagnostic knowledge of anorexia nervosa was lower compared to other eating disorders, although not significant. The seminal role of the family in anorexia nervosa was also under-recognized. School counselors viewed eating disorders most often presenting in female youth, of long duration, and responsive to treatment. Conclusion: School counselors play a crucial role in the recognition and management of school-aged youth mental health difficulties, and eating disorders in particular, given the high rate among youth. This study is encouraging as it highlights reasonable knowledge levels and few stigmatizing attitudes.

Late onset multiple sclerosis - multiparametric MRI characteristics.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) with heterogenic character. Typical age of onset is between 20 and 35 years. Clinically definite multiple sclerosis (CDMS) can occur also in patients older than 50 years. This type of MS is called Late Onset Multiple Sclerosis (LOMS). Until now, the differences in clinical course, type of first symptoms, and prognosis of LOMS have not been well established. Also the MRI characteristics of patients with LOMS have not been determined. Neither conventional nor nonconventional MRI features are known to be typical for LOMS. To investigate the MRI characteristics of LOMS patients based on conventional and non-conventional techniques. Twenty patients with LOMS were included in the study and 17 patients with typical onset of MS (TOMS) served as a comparative group. The two groups were matched in terms of disease duration and EDSS score. Conventional (T1- and T2-weighted images) and non-conventional (magnetization transfer images, proton magnetic resonance spectroscopy) MRI techniques were performed in all participants. Parameters from both techniques were compared between LOMS and TOMS groups. Patients with late onset of MS had lower Brain Parenchyma Fraction (BPF) (p < 0.001) and Grey Matter Fraction (GMF) values (p = 0.008) than the TOMS group. There was no statistical differences in White Matter Fraction (WMF) values between the groups (p = 0.572). Patients with LOMS and TOMS statistically differed in the peak height (p = 0.018), peak location (p < 0.001), and MTR mean value (p < 0.001). Patients with LOMS manifested lower concentrations of NAA+NAAG and NAA+NAAG/Cr than patients with TOMS (p = 0.009 and p < 0.001 respectively). No statistical difference was found between the groups in terms of mean mIn (p = 0.346) and mean GPC+PCh (p = 0.563). We did not find a statistical difference in T1- and T2- lesion load (p = 0.1, p = 0.3 respectively) although T1/T2 lesion ratio was higher in the LOMS group. MRI parameters in patients with LOMS differed significantly from those obtained from the TOMS group. Our results, which indicate that in LOMS patients brain tissue damage is more advanced than in TOMS patients, may contribute to a better understanding of the heterogeneity of MS.