scholarly journals Gangguan Depresi Mayor: Mini Review

2017 ◽  
Vol 9 (1) ◽  
pp. 34-49 ◽  
Author(s):  
Indriono Hadi ◽  
Fitri Wijayanti ◽  
Reni Devianti Usman ◽  
Lilin Rosyanti

Depression is a condition of a person feeling sad, disappointed when experiencing a change, loss, failure and becoming pathological when unable to adapt. Depression is a condition that affects a person affectively, physiologically, cognitively and behaviorally thus changing the usual patterns and responses. Major Depressive Disorder is a heterogeneous disease characterized by feelings of depression, anhedonia, changes in cognitive function, changes in sleep, changes in appetite, guilt that occur over two weeks, described with a loss of interest or pleasure in the usual activity and is a disease with neurobiological consequences involving structural, functional and molecular changes in some areas of the brain. Maladaptive neural responses, social, psychological, and physiological rejections interact with each other with other susceptibility factors, such as a history of depression, life stress levels, genetic factors, will increase a person's susceptibility to depression. Catatan PenerbitPolekkes Kemenkes Kendari menyatakan tetap netral sehubungan dengan klaim dari perspektif atau buah pikiran yang diterbitkan dan dari afiliasi institusional manapun.

2020 ◽  
pp. 1-9 ◽  
Author(s):  
Richard A. Bryant ◽  
Elpiniki Andrew ◽  
Mayuresh S. Korgaonkar

Abstract Background Prolonged grief disorder (PGD) has recently been recognized as a separate psychiatric diagnosis, despite controversy over the extent to which it is distinctive from posttraumatic stress disorder (PTSD) and major depressive disorder (MDD). Methods This study investigated distinctive neural processes underpinning emotion processing in participants with PGD, PTSD, and MDD with functional magnetic resonance study of 117 participants that included PGD (n = 21), PTSD (n = 45), MDD (n = 26), and bereaved controls (BC) (n = 25). Neural responses were measured across the brain while sad, happy, or neutral faces were presented at both supraliminal and subliminal levels. Results PGD had greater activation in the pregenual anterior cingulate cortex (pgACC), bilateral insula, bilateral dorsolateral prefrontal cortices and right caudate and also greater pgACC–right pallidum connectivity relative to BC during subliminal processing of happy faces. PGD was distinct relative to both PTSD and MDD groups with greater recruitment of the medial orbitofrontal cortex during supraliminal processing of sad faces. PGD were also distinct relative to MDD (but not PTSD) with greater activation in the left amygdala, caudate, and putamen during subliminal presentation of sad faces. There was no distinction between PGD, PTSD, and MDD during processing of happy faces. Conclusions These results provide initial evidence of distinct neural profiles of PGD relative to related psychopathological conditions, and highlight activation of neural regions implicated in reward networks. This pattern of findings validates current models of PGD that emphasize the roles of yearning and appetitive processes in PGD.


2021 ◽  
Author(s):  
Maria Eduarda M. Botelho ◽  
Anelise S. Carlessi ◽  
Luana M. Manosso ◽  
Laura A. Borba ◽  
Airam B. de Moura ◽  
...  

Abstract Major depressive disorder is a debilitating mental disorder. Although the etiology is not fully understood, the impairment to the blood-brain barrier (BBB) integrity may be involved. Maternal deprivation was performed in the first 10 postnatal days for 3h/day. Male and female rats were divided into control and maternal deprivation. Maternal deprivation animals were subdivided and received treatment with saline, escitalopram, ketamine, or probiotic. The integrity of BBB was evaluated in the prefrontal cortex and hippocampus at postnatal days 11, 21, 41, and 61. Maternal deprivation caused BBB breakdown in the prefrontal cortex and hippocampus in female and male rats in all ages evaluated, except in the prefrontal cortex of females at postnatal day 41. In females, escitalopram, ketamine, and probiotic reversed BBB breakdown in all ages evaluated, except probiotic at postnatal day 21 (prefrontal cortex), and ketamine at postnatal days 21 and 41 (hippocampus). In males, escitalopram, ketamine, and probiotic reversed BBB breakdown in the prefrontal cortex in all ages evaluated, except escitalopram at postnatal days 41 and 61. In the hippocampus of males, BBB damage was reversed by escitalopram at postnatal day 21 and ketamine at postnatal day 41. Treatment with escitalopram, ketamine, or probiotics can prevent changes in the BBB integrity, depending on the age and sex of the animal. Clinically it is important to evaluate different treatments depending on age and sex.


2010 ◽  
Vol 41 (7) ◽  
pp. 1385-1395 ◽  
Author(s):  
A. L. Singh ◽  
B. M. D'Onofrio ◽  
W. S. Slutske ◽  
E. Turkheimer ◽  
R. E. Emery ◽  
...  

BackgroundAssociations between parental depression and offspring affective and disruptive disorders are well documented. Few genetically informed studies have explored the processes underlying intergenerational associations.MethodA semi-structured interview assessing DSM-III-R psychiatric disorders was administered to twins (n=1296) from the Australian Twin Register (ATR), their spouses (n=1046) and offspring (n=2555). We used the Children of Twins (CoT) design to delineate the extent to which intergenerational associations were consistent with a causal influence or due to genetic confounds.ResultsIn between-family analyses, parental depression was associated significantly with offspring depression [hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.20–1.93] and conduct disorder (CD; HR 2.27, CI 1.31–3.93). Survival analysis indicated that the intergenerational transmission of depression is consistent with a causal (environmental) inference, with a significant intergenerational association in offspring of discordant monozygotic (MZ) twin pairs (HR 1.39, CI 1.00–1.94). Logistic regression analysis suggested that the parental depression–offspring CD association was due to shared genetic liability in the parents and offspring. No intergenerational association was found when comparing the offspring of discordant MZ twins [odds ratio (OR) 1.41, CI 0.63–3.14], but offspring of discordant dizygotic (DZ) twins differed in their rates of CD (OR 2.53, CI 0.95–6.76). All findings remained after controlling for several measured covariates, including history of depression and CD in the twins' spouses.ConclusionsThe mechanisms underlying associations between parental depression and offspring psychopathology seem to differ depending on the outcome. The results are consistent with a causal environmental role of parental depression in offspring depression whereas common genetic factors account for the association of parental depression and offspring CD.


2011 ◽  
Vol 41 (9) ◽  
pp. 1845-1855 ◽  
Author(s):  
E. J. Thomas ◽  
R. Elliott ◽  
S. McKie ◽  
D. Arnone ◽  
D. Downey ◽  
...  

BackgroundBoth past depressive episodes and the personality trait of depressive rumination are strong risk factors for future depression. Depression is associated with abnormal emotional processing, which may be a neurobiological marker for vulnerability to depression. A consistent picture has yet to emerge as to how a history of depression and the tendency to ruminate influence emotional processing. The aim of this study was to investigate the relationship between rumination, past depression and neural responses when processing face emotions.MethodThe Ruminative Responses Scale (RRS) was completed by 30 remitted depressives and 37 controls who underwent functional magnetic resonance imaging (fMRI) scanning while viewing happy, sad, fearful and neutral faces.ResultsThe remitted depressives showed overall reductions in neural responses to negative emotions relative to the controls. However, in the remitted depressives, but not the controls, RRS scores were correlated with increased neural responses to negative emotions and decreased responses to happiness in limbic regions.ConclusionsAutomatic emotion processing biases and rumination seem to be correlated to aspects of vulnerability to depression. However, remission from depression may be maintained by a general suppression of limbic responsiveness to negative emotion.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
M.A. Rapp ◽  
V. Haroutunian ◽  
A. Heinz

Aims:We have recently shown both increases in the number of neuropathological changes in Alzheimer's disease patients with a history of recurrent major depression, and evidence for Alzheimer's disease-related neuropathological changes in patients with geriatric major depression. However, the correlates and possible underlying mechanisms for these neuropathological changes in Alzheimer's disease patients as a function of depression remains to be studied.Method:Levels of several neurotrophic factors, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) were measured in a sample of Alzheimer's disease patients with and without a lifetime history of major depressive disorder.Results:Alzheimer's disease patients with co-morbid depression showed lower levels BDNF (P < .001) and NGF (P < .001) than Alzheimer's disease patients without co-morbid depression. Results remained stable when controlling for age, gender, level of education, and other medical co-morbidities.Conclusion:In Alzheimer's disease, the presence of depression co-morbidity corresponds to decreases in neurotrophic factors beyond effects of age, education, and medical co-morbidities, suggesting that the previously described link between major depression and the neuropathological processes in Alzheimer's disease may be related to changes in neuronal survival mediated by neurotrophic factors.Funded by the National Institute on Aging (U01 AG016976 and NIA P01-AG05138) and NARSAD.


2010 ◽  
Vol 197 (3) ◽  
pp. 180-185 ◽  
Author(s):  
Sophie A. Vreeburg ◽  
Catharina A. Hartman ◽  
Witte J. G. Hoogendijk ◽  
Richard van Dyck ◽  
Frans G. Zitman ◽  
...  

BackgroundIt is unclear whether altered hypothalamic–pituitary–adrenal (HPA) axis regulation, which frequently accompanies depression and anxiety disorders, represents a trait rather than a state factor.AimsTo examine whether HPA axis dysregulation represents a biological vulnerability for these disorders, we compared cortisol levels in unaffected people with and without a parental history of depressive or anxiety disorders. We additionally examined whether possible HPA axis dysregulations resemble those observed in participants with depression or anxiety disorders.MethodData were from the Netherlands Study of Depression and Anxiety. Within the participants without a lifetime diagnoses of depression or anxiety disorders, three groups were distinguished: 180 people without parental history, 114 with self-reported parental history and 74 with CIDI-diagnosed parental history. These groups were additionally compared with people with major depressive disorder or panic disorder with agoraphobia (n = 1262). Salivary cortisol samples were obtained upon awakening, and 30, 45 and 60 min later.ResultsAs compared with unaffected participants without parental history, unaffected individuals with diagnosed parental history of depression or anxiety showed a significantly higher cortisol awakening curve (effect size (d) = 0.50), which was similar to that observed in the participants with depression or anxiety disorders. Unaffected people with self-reported parental history did not differ in awakening cortisol levels from unaffected people without parental history.ConclusionsUnaffected individuals with parental history of depression or anxiety showed a higher cortisol awakening curve, similar to that of the participants with depression or anxiety disorders. This suggests that a higher cortisol awakening curve reflects a trait marker, indicating an underlying biological vulnerability for the development of depressive and anxiety disorders.


Author(s):  
Noor Suryani Mohd Ashari ◽  
Siti Nor Fairus Mohamed Sanusi ◽  
Mohd Azhar Mohd Yasin ◽  
Rohimah Mohamud ◽  
Che Maraina Che Hussin

Introduction: Major Depressive Disorder (MDD) isexpected to become the second leading cause of worldwide disability by the year 2020 and the major contributor to the overall global burden of disease.Objective: This study was done to compare sociodemographicpredisposingfactors in MDD patients and controls in Kelantan, Malaysia.Methods: A total of 47 MDD patients and 47 healthy controls participated in this study. MDD patients were recruited from Psychiatric Clinic, HUSM and they were diagnosed according to DSM-V criteria. Patients’ biodata, medical and psychiatric history were taken by physician. Data were analysed using Pearson Chi-square and multiple logistic regression.Results: In MDD group, 61.7% were females and 38.3% were males. Forty two percent of MDD were in the age group of 45 to 65 years old and almost 12.8% of MDD patients had family history of depression, while all healthy controls were in good general health and had no family history of depression. Pearson Chi-square revealed that there were significant associations between smoking status (P=0.027), marital status (P=0.007) educational level (P=0.022) and area of living (P=0.0.036) with MDD. The results showed that unmarried person were less likely to have MDD compared to those married with adjusted odds ratio (OR) of 0.31. Smoker were 5.16 at odds of having MDD as compared to non-smoker, while individuals with a low education were more likely to have MDD compared to those highly educated with adjusted OR of 2.04. The result also showed those living in urban area were less likely to have MDD compared to those living in rural area with adjusted OR of 0.48.Conclusion: Higher age, female and positive family history possess a higher tendency of having MDD. In addition, smokers, married, less educated and living in rural area were more likely to have MDD compared to healthy controls.International Journal of Human and Health Sciences Vol. 03 No. 02 April’19. Page: 80-87


2021 ◽  
Vol 22 (4) ◽  
pp. 86-87
Author(s):  
Sooraj Kumar ◽  
Sharanyah Srinivasan ◽  
Tammer El-Aini

No abstract available. Article truncated after 150 words. A 35-year-old lady with a history of depression and anxiety presented to the emergency room with worsening shortness of breath after receiving polymethylmethacrylate (PMMA) injections in her buttock for cosmetic purposes in Mexico. Immediately after the injection in the outpatient office, she became acutely short of breath, tachypneic, and tachycardic. She was brought to the emergency room where she was hypoxic with oxygen saturations in the low 80s on a non-rebreather, tachypneic with a respiratory rate in the 40s, and tachycardic with heart rates in 140s. She was emergently intubated. A CTA of the chest demonstrated bilateral ground glass opacities throughout, most pronounced in the upper lobes which progressed to significant bilateral airspace disease consistent with acute respiratory distress syndrome (Figure 1). Her neurological examination declined over the course of her hospitalization. An MRI of the brain with contrast demonstrated bilateral foci of susceptibility artifact throughout the entirety of the …


Author(s):  
Jennifer Gillies

An important causal factor of depression is family history ¾ there is compelling evidence that Major Depressive Disorder (MDD) is familial. Although the connection between a maternal history of depression and offspring risk is well established, paternal history has been largely ignored in research thus far. The first goal of this study is to examine differences in the clinical profile of MDD across parental depression history groups (i.e., both-parent history versus maternal history only versus paternal history only versus no parental history).  Based on previous findings, I predict that the severity of the clinical course of MDD (as operationalized by a higher severity of depression and anxiety symptoms, an increased likelihood of recurrence, and a greater likelihood of a comorbid anxiety disorder) will be highest for offspring with a both-parent history of depression, followed by those with a maternal history only, followed by individuals with a paternal history only, and lastly by offspring with no parental history of depression. The second goal is to determine if the group differences hypothesized above are further moderated by offspring sex. To date, very little is known about how parental history influences the clinical presentation of MDD in depressed offspring. This study will contribute to a limited body of research, and is unique in that it will include four parental history groups as well as offspring sex in its analyses. The study will use a quasi-archival sample of approximately 250 participants between 12 and 29 years of age, who have been diagnosed with MDD.


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