Suicide in later life: A comparison between cases with early-onset and late-onset depression

2011 ◽  
Vol 132 (1-2) ◽  
pp. 185-191 ◽  
Author(s):  
Richard C. Oude Voshaar ◽  
Nav Kapur ◽  
Harriet Bickley ◽  
Alyson Williams ◽  
Nitin Purandare
Keyword(s):  
2020 ◽  
Vol 80 (10) ◽  
pp. 1016-1025 ◽  
Author(s):  
Dietmar Schlembach

AbstractFetal or intrauterine growth restriction (FGR/IUGR) affects approximately 5 – 8% of all pregnancies and refers to a fetus not exploiting its genetically determined growth potential. Not only a major cause of perinatal morbidity and mortality, it also predisposes these fetuses to the development of chronic disorders in later life. Apart from the timely diagnosis and identification of the causes of FGR, the obstetric challenge primarily entails continued antenatal management with optimum timing of delivery. In order to minimise premature birth morbidity, intensive fetal monitoring aims to prolong the pregnancy and at the same time intervene, i.e. deliver, before the fetus is threatened or harmed. It is important to note that early-onset FGR (< 32 + 0 weeks of gestation [wks]) should be assessed differently than late-onset FGR (≥ 32 + 0 wks). In early-onset FGR progressive deterioration is reflected in abnormal venous Doppler parameters, while in late-onset FGR this manifests primarily in abnormal cerebral Doppler ultrasound. According to our current understanding, the “optimum” approach for monitoring and timing of delivery in early-onset FGR combines computerized CTG with the ductus venosus Doppler, while in late-onset FGR assessment of the cerebral Doppler parameters becomes more important.


2008 ◽  
Vol 14 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Hannele Variend ◽  
Y. Vishnu Gopal

A growing body of evidence suggests that late-onset depression (depression occurring for the first time in later life) differs from early-onset (recurrent) depression in terms of clinical features, aetiology, neuroanatomical substrates and prognosis. Some evidence suggests that late-onset depression is more associated with somatic symptoms, cognitive deficits, cerebral structural abnormalities, vascular disease (‘vascular depression’) and poorer treatment outcomes than is early-onset depression. Both general adult and old age psychiatrists face the challenges of managing late-onset depression. In this article we attempt to clarify specific issues relating to late-onset depression in terms of clinical features, aetiology, treatment response and prognosis.


1995 ◽  
Vol 167 (5) ◽  
pp. 649-652 ◽  
Author(s):  
R. C. Baldwin ◽  
Barbara Tomenson

BackgroundDepression in later life is often thought to differ from that at other times of adulthood. The evidence for this is controversial but is important to any proposed organic model of depression in the elderly. Here, early- and late-onset depressions in later life are compared.MethodFifty-seven depressed patients with a mean age of 74 were studied, 21 with an early onset (aged 59 or less) and 36 with a late onset. All were suffering from major depression according to DSM–III–R. The measures at entry included severity and symptoms, cognitive function, antecedent life events, physical health and vascular risk factors and/or vascular disease. We also recorded any family history of mood disorders, as well as the course of illness.ResultsThe anxiety item scores of the Hamilton Depression Rating Scale were significantly higher in those with an early onset, but otherwise symptoms differed little. Heritability was greater in the early-onset group. There was a striking association of vascular disease and/or risk with late-onset patients.ConclusionsVascular disease is associated with late-onset depression. This is consistent with the hypothesis that depression in later life is a more ‘biological’ disorder.


Author(s):  
Pramod P. Singhavi

Introduction: India has the highest incidence of clinical sepsis i.e.17,000/ 1,00,000 live births. In Neonatal sepsis septicaemia, pneumonia, meningitis, osteomyelitis, arthritis and urinary tract infections can be included. Mortality in the neonatal period each year account for 41% (3.6 million) of all deaths in children under 5 years and most of these deaths occur in low income countries and about one million of these deaths are due to infectious causes including neonatal sepsis, meningitis, and pneumonia. In early onset neonatal sepsis (EOS) Clinical features are non-specific and are inefficient for identifying neonates with early-onset sepsis. Culture results take up to 48 hours and may give false-positive or low-yield results because of the antenatal antibiotic exposure. Reviews of risk factors has been used globally to guide the development of management guidelines for neonatal sepsis, and it is similarly recommended that such evidence be used to inform guideline development for management of neonatal sepsis. Material and Methods: This study was carried out using institution based cross section study . The total number neonates admitted in the hospital in given study period was 644, of which 234 were diagnosed for neonatal sepsis by the treating pediatrician based on the signs and symptoms during admission. The data was collected: Sociodemographic characteristics; maternal information; and neonatal information for neonatal sepsis like neonatal age on admission, sex, gestational age, birth weight, crying immediately at birth, and resuscitation at birth. Results: Out of 644 neonates admitted 234 (36.34%) were diagnosed for neonatal sepsis by the paediatrician based on the signs and symptoms during admission. Of the 234 neonates, 189 (80.77%) infants were in the age range of 0 to 7 days (Early onset sepsis) while 45 (19.23%) were aged between 8 and 28 days (Late onset sepsis). Male to female ratio in our study was 53.8% and 46% respectively. Out of total 126 male neonates 91(72.2%) were having early onset sepsis while 35 (27.8%) were late onset type. Out of total 108 female neonates 89(82.4%) were having early onset sepsis while 19 (17.6%) were late onset type. Maternal risk factors were identified in 103(57.2%) of early onset sepsis cases while in late onset sepsis cases were 11(20.4%). Foul smelling liquor in early onset sepsis and in late onset sepsis was 10(5.56%) and 2 (3.70%) respectively. In early onset sepsis cases maternal UTI, Meconium stained amniotic fluid, Multipara and Premature rupture of membrane was seen in 21(11.67%), 19 (10.56%), 20(11.11%) and 33 (18.33%) cases respectively. In late onset sepsis cases maternal UTI, Meconium stained amniotic fluid, Multipara and Premature rupture of membrane was seen in 2 (3.70%), 1(1.85%), 3 (5.56%) and 3 (5.56%) cases respectively. Conclusion: Maternal risk identification may help in the early identification and empirical antibiotic treatment in neonatal sepsis and thus mortality and morbidity can be reduced.


2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.


PEDIATRICS ◽  
2000 ◽  
Vol 106 (1) ◽  
pp. e14-e14 ◽  
Author(s):  
Wayne Wisemandle ◽  
L. Michele Maynard ◽  
Shumei S. Guo ◽  
Roger M. Siervogel

2020 ◽  
Vol 31 ◽  
pp. S52-S53
Author(s):  
W.R. Chae ◽  
M. Fuentes Casan ◽  
F. Gutknecht ◽  
A. Ljubez ◽  
S.M. Gold ◽  
...  

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