Pregnancy and birth complications associations with long-term adverse maternal mental health outcomes: a systematic review and meta-analysis protocol.

Background: Existing studies have established an association between pregnancy, birth complications, and mental health in the first few weeks postpartum. However, there is no clear understanding of whether pregnancy and birth complications increase the risk of adverse maternal mental outcomes in the longer term. Research on maternal adverse mental health outcomes following pregnancy and birth complications beyond 12 months postpartum is scarce, and findings are inconsistent. Objective: This systematic review and meta-analysis will examine the available evidence on the association between pregnancy and birth complications and long-term adverse maternal mental health outcomes. Methods and analysis: We will include cohort, cross-sectional, and case-control studies in which a diagnosis of pregnancy and/or birth complication (preeclampsia, pregnancy loss, caesarean section, preterm birth, perineal laceration, neonatal intensive care unit admission, major obstetric haemorrhage, and birth injury/trauma) was reported and maternal mental disorders (depression, anxiety disorders, bipolar disorders, psychosis, and schizophrenia) after 12 months postpartum were the outcomes. A systematic search of PubMed, Embase, CINAHL, PsycINFO, and Web of Science will be conducted following a detailed search strategy until August 2022. Three authors will independently review titles and abstracts of all eligible studies, extract data using pre-defined standardised data extraction and assess the quality of each study using the Newcastle-Ottawa Scale. We will use random-effects meta-analysis for each exposure and outcome variable to calculate overall pooled estimates using the generic inverse variance method. This systematic review will follow the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines. Ethical consideration: The proposed systematic review and meta-analysis is based on published data; ethics approval is not required. The results will be presented at scientific meetings and publish in a peer-reviewed journal. PROSPERO registration: CRD42022359017.

Case series: Psychosocial challenges of female youth within the Irish Travelling community.

BACKGROUND: The Irish Travelling community are an ethnic minority group known for their distinct identity, traditions and language. Although this group has its roots in Ireland, they are marginalised and discriminated against by every part of Irish society. Irish Travellers are a group who are vulnerable to exclusion and experience health, economic and educational inequalities. Young female Irish Travellers in Ireland are highly susceptible to mental illnesses which makes the engagement of this ethnic group by healthcare services important. AIMS: To review the cases of three female adolescents from the Irish Travelling community living in Ireland with a focus on their psycho-social difficulties. Complete a literature review, to complement and inform the three cases reviewed, on the socio-cultural and mental health challenges which effect adolescent females in the Irish Travelling community. METHODS: Case series with literature search and review of relevant published articles using a keyword search of databases PubMed, PsycINFO and HSE protocols and reports. Hand searching of relevant references utilised. Informed signed consent obtained from each patient attending child and adolescent services in Ireland. Signed parental consent also obtained. Written consent obtained due to the use of patient history and assessments in the case series. RESULTS: Adolescent females within the Irish Travelling community encounter particular difficulties within the moral constraints and expectations of this community. They encounter specific issues including mental illness, sexual stigma, domestic violence and limitations to the role of women. The three cases outlined give representative examples of the challenges faced by adolescent females within the Travelling community. CONCLUSIONS: Psychiatric services need to be aware of this vulnerable group and focus on the recognition of their needs within the context of their community.

Late-Onset Neutropenia in Long-Term Clozapine Use and Its Management Utilizing Prophylactic G-CSF.

This case outlines recurrent neutropenia after fourteen years of successful clozapine use. The patient has a diagnosis of treatment-resistant schizophrenia which has been complicated by sensitivity to side effects of haloperidol and past failure of antipsychotics to manage her symptoms. It was necessary for our patient to follow a complicated treatment path involving close monitoring of blood levels, admissions, the initiation of lithium and the regular use of filgrastim (Neupogen), granulocyte colony stimulating factor (G-CSF). Following a failure of rescue filgrastim to increase her neutrophil levels, a management protocol was designed with input from the on-site hematology team. This protocol involved the use of filgrastim on a regular prophylactic basis. This management plan has worked for the patient who has been able to continue use of clozapine and has not suffered from any neutropenic episodes in over six months.

An analysis of childhood consultations in general practice: a multi-practice study.

BACKGROUND: The majority of illnesses in children are managed by general practitioners (GPs) and there is a need for up to date data on consultations with children in order to improve healthcare service planning and allocation of resources. AIMS: To investigate the presenting symptoms, diagnoses and actions taken by the GP at consultations with children in general practice. METHODS: Senior medical students on general practice placement and their GP supervisors used practice management software to collect data on 100 randomly selected patients aged between 12 months and 14 years of age in each practice. Presenting symptoms, diagnoses and actions taken by the GP for the most recent attendance in the previous 12 months were summarised by age group (1-4 years; 5-10 years; 11-14 years). RESULTS: Data were collected from 5959 patients at 64 practices. During the 12-month study, 3241 (54%) of children had a consultation with their GP. The most common presenting symptoms were respiratory (1-4 yrs, 28%; 5-10 yrs, 39%; 11-14 yrs, 32%) and skin complaint (1-4 yrs, 13%; 5-10 yrs, 16%; 11-14 yrs, 21%). The most common actions for all age groups were prescribing (1-4 yrs, 55%; 5-10 yrs, 58%; 11-14 yrs, 56%) and providing reassurance (1-4 yrs, 53%; 5-10 yrs, 51%; 11-14 yrs, 48%). Rates of referral and requiring further investigation increased with age. CONCLUSION: This study provides a comprehensive snapshot of what children commonly present with in general practice, common diagnoses and the actions taken by GPs. The findings will help GPs to organise their practice systems and will inform healthcare service planners.

What effect do point of care fees have on childhood consultations in general practice?

BACKGROUND: General practice (GP) has historically been central to the prevention and treatment of childhood illnesses. In Ireland, this role has recently expanded with the introduction of free GP care for children aged under six years in 2015. The Republic of Ireland has the only health system in the European Union which does not offer universal coverage for primary care. This study aims to analyse general practice records to investigate the effect of point of care consultation fees on childhood attendances. METHODS: GPs affiliated to the medical school (n = 72) were invited to participate. 100 children aged 1 to 14 years were randomly sampled from each. Data was collected on service utilisation in the previous 12 months, specifically: age, gender, eligibility for free care and whether they had consulted their GP in the 12 month period. RESULTS: Sixty-four practices participated, producing data on 6007 eligible children. The median age of children was seven years; 3688(62%) were 'fee-paying'. GMS patients aged under six years had a median of three consultations/year, with a quarter attending six times a year or more, while fee paying patients had a median of two consultations/year with a quarter attending four times a year or more. CONCLUSIONS: Children eligible for free care attend more often with a subgroup attending very frequently. This study provides important information on the possible impact of fees on healthcare utilisation for countries considering co-payment.

Amitriptyline protects against TNF-α-induced atrophy and reduction in synaptic markers via a Trk-dependent mechanism.

Neuritic degeneration and synaptic loss are features of both neuroinflammation and neurodegenerative disease. The tricyclic antidepressant amitriptyline has neurotrophic and anti-inflammatory properties and acts as a novel agonist of the neurotrophin Trk receptors. Primary cortical neurons were treated with amitriptyline, nortriptyline and NGF and tested for neuronal complexity by Sholl analysis, protein expression by Western immunoblotting, and synapse number by colocalization of pre and postsynaptic makers. Amitriptyline (500 nmol/L) and its active metabolite nortriptyline (50 nmol/L) are found to induce neurite outgrowth in rat primary cortical neurons. Amitriptyline-induced neurite outgrowth is blocked by inhibition of Trk signaling using Trk antagonist K252a (200 nmol/L) but not by the neurotrophin inhibitor Y1036 (40 µmol/L), indicating that amitriptyline binds directly to the Trk receptor to initiate neurite outgrowth. MEK inhibitor PD98059 (10 µmol/L) also blocks amitriptyline-induced neurite outgrowth, implicating activation of the MAPK signaling pathway downstream of Trk receptor activation. Furthermore, pretreatment of primary cortical neurons with amitriptyline and nortriptyline prevents the effects of the proinflammatory cytokine TNF-α (10 ng/mL) on neurite outgrowth and colocalization of synaptic proteins. These findings suggest that amitriptyline and nortriptyline can exert neurotrophic effects in primary cortical neurons via activation of a Trk/MAPK signaling pathway. These compounds therefore have significant potential to be used in the treatment of neurodegenerative conditions where atrophy and loss of synaptic connections contribute to progression of disease.

Noradrenaline acting on astrocytic ß2-adrenoceptors induces neurite outgrowth in primary cortical neurons.

The neurotransmitter noradrenaline (NA) has anti-inflammatory properties and promotes expression of neurotrophic factors in the central nervous system (CNS) via activation of glial adrenoceptors. Here we examined the ability of conditioned media (CM) from NA-treated glial cells to impact upon neuronal complexity. Primary rat cortical neurons were treated either directly with NA (1-10 µM), or treated with CM from NA-stimulated primary mixed glial cells. Neuronal complexity was assessed using Sholl analysis. Exposure of neurons to CM from NA-stimulated glial cells increased all indices of neuronal complexity, whereas direct exposure of neurons to NA did not. CM from NA-stimulated astrocytes, but not microglia, also increased neuronal complexity indicating a key role for astrocytes. The ß-adrenergic subtype was implicated in this response as the increase was blocked by the ß-adrenoceptor antagonist propanolol, but not by the α-adrenoceptor antagonist phentolamine. CM from glial cells treated with the ß2-adrenoceptor agonists salmeterol and clenbuterol, but not the ß1-adrenoceptor agonist xamoterol, mimicked the ability of NA to increase neuronal complexity. NA induced expression of a range of growth factors (BDNF, NGF-ß, GDNF, FGF-2 and IL-6) in glial cells. In addition to this, the phosphatidylinositol 3-kinase (PI3K), mitogen activated protein kinase (MAPK) and JAK-STAT signalling pathways are implicated in NA CM-induced neuritic growth as inhibition of these pathways attenuated NA CM-induced neuritic growth. In conclusion, this study indicates a novel role for NA acting at glial ß2-adrenoceptors to induce neuritic growth through the expression of soluble factors that elicit a neurotrophic action and increase neuronal complexity.