Depression and low mood الاكتئاب

وَتَوَلَّىٰ عَنۡهُمۡ وَقَالَ يَٰٓأَسَفَىٰ عَلَىٰ يُوسُفَ وَٱبۡيَضَّتۡ عَيۡنَاهُ مِنَ ٱلۡحُزۡنِ فَهُوَ كَظِيمࣱ‏

and he turned away from them, saying, ‘Alas for Joseph!’ His eyes went white with grief and he was filled with sorrow

وَقَالُواْ ٱلۡحَمۡدُ لِلَّهِ ٱلَّذِيٓ أَذۡهَبَ عَنَّا ٱلۡحَزَنَۖ إِنَّ رَبَّنَا لَغَفُورࣱ شَكُورٌ

They will say, ‘Praise be to God, who has separated us from all sorrow! Our Lord is truly most forgiving, most appreciative

إِذۡ تَمۡشِيٓ أُخۡتُكَ فَتَقُولُ هَلۡ أَدُلُّكُمۡ عَلَىٰ مَن يَكۡفُلُهُۥۖ فَرَجَعۡنَٰكَ إِلَىٰٓ أُمِّكَ كَيۡ تَقَرَّ عَيۡنُهَا وَلَا تَحۡزَنَۚ وَقَتَلۡتَ نَفۡسࣰ ا فَنَجَّيۡنَٰكَ مِنَ ٱلۡغَمِّ وَفَتَنَّٰكَ فُتُونࣰ اۚ فَلَبِثۡتَ سِنِينَ فِيٓ أَهۡلِ مَدۡيَنَ ثُمَّ جِئۡتَ عَلَىٰ قَدَرࣲ يَٰمُوسَىٰ

Your sister went out, saying, “I will tell you someone who will nurse him,” then We returned you to your mother so that she could rejoice and not grieve. Later you killed a man, but We saved you from distress and tried you with other tests. You stayed among the people of Midian for years, then you came here as I ordained

أَهَٰٓؤُلَآءِ ٱلَّذِينَ أَقۡسَمۡتُمۡ لَا يَنَالُهُمُ ٱللَّهُ بِرَحۡمَةٍۚ ٱدۡخُلُواْ ٱلۡجَنَّةَ لَا خَوۡفٌ عَلَيۡكُمۡ وَلَآ أَنتُمۡ تَحۡزَنُونَ

And are these the people you swore God would never bless? [Now these people are being told], “Enter the Garden! No fear for you, nor shall you grieve.”’

۞إِذۡ تُصۡعِدُونَ وَلَا تَلۡوُۥنَ عَلَىٰٓ أَحَدࣲ وَٱلرَّسُولُ يَدۡعُوكُمۡ فِيٓ أُخۡرَىٰكُمۡ فَأَثَٰبَكُمۡ غَمَّۢا بِغَمࣲّ لِّكَيۡلَا تَحۡزَنُواْ عَلَىٰ مَا فَاتَكُمۡ وَلَا مَآ أَصَٰبَكُمۡۗ وَٱللَّهُ خَبِيرُۢ بِمَا تَعۡمَلُونَ

You fled without looking back while the Messenger was calling out to you from behind, and God rewarded you with sorrow for sorrow. [He has now forgiven you] so that you may not grieve for what you missed or for what happened to you. God is well aware of everything you do

ثُمَّ أَنزَلَ عَلَيۡكُم مِّنۢ بَعۡدِ ٱلۡغَمِّ أَمَنَةࣰ نُّعَاسࣰ ا يَغۡشَىٰ طَآئِفَةࣰ مِّنكُمۡۖ وَطَآئِفَةࣱ قَدۡ أَهَمَّتۡهُمۡ أَنفُسُهُمۡ يَظُنُّونَ بِٱللَّهِ غَيۡرَ ٱلۡحَقِّ ظَنَّ ٱلۡجَٰهِلِيَّةِۖ يَقُولُونَ هَل لَّنَا مِنَ ٱلۡأَمۡرِ مِن شَيۡءࣲۗ قُلۡ إِنَّ ٱلۡأَمۡرَ كُلَّهُۥ لِلَّهِۗ يُخۡفُونَ فِيٓ أَنفُسِهِم مَّا لَا يُبۡدُونَ لَكَۖ يَقُولُونَ لَوۡ كَانَ لَنَا مِنَ ٱلۡأَمۡرِ شَيۡءࣱ مَّا قُتِلۡنَا هَٰهُنَاۗ قُل لَّوۡ كُنتُمۡ فِي بُيُوتِكُمۡ لَبَرَزَ ٱلَّذِينَ كُتِبَ عَلَيۡهِمُ ٱلۡقَتۡلُ إِلَىٰ مَضَاجِعِهِمۡۖ وَلِيَبۡتَلِيَ ٱللَّهُ مَا فِي صُدُورِكُمۡ وَلِيُمَحِّصَ مَا فِي قُلُوبِكُمۡۚ وَٱللَّهُ عَلِيمُۢ بِذَاتِ ٱلصُّدُورِ

After sorrow, He caused calm to descend upon you, a sleep that overtook some of you. Another group, caring only for themselves, entertained false thoughts about God, thoughts more appropriate to pagan ignorance, and said, ‘Do we get a say in any of this?’ [Prophet], tell them, ‘Everything to do with this affair is in God’s hands.’ They conceal in their hearts things they will not reveal to you. They say, ‘If we had had our say in this, none of us would have been killed here.’ Tell them, ‘Even if you had resolved to stay at home, those who were destined to be killed would still have gone out to meet their deaths.’ God did this in order to test everything within you and in order to prove what is in your hearts. God knows your innermost thoughts very well

" Oh, my grief for Joseph! " And his eyes turned white because of the sorrow that he was suppressing. Revelation came from the Compeller of all engendered beings: " O Jacob! You grieve so much for him, but you do not grieve for what you are missing of Me by being busy with grief for him! " O Jacob, how long this sorrow and regret at separation from Joseph? How long will you suffer grief and coldly sigh? Do you not suffer grief that you are held back from Me while busy with him? " With two kiblahs you can't walk straight on the road of tawḤīd- either the Friend's approval, or your own caprice. [DS 488] " O Jacob! Be careful not to pass Joseph's name over your tongue any more, or I will remove your name from the register of the prophets. " The Pir of the Tariqah said, " Jacob's remembrance of Joseph was the seed of heartache, and Joseph's remembrance of Jacob was the seed of ease. Since Ja

And they shall say, “Praise belongs to God, who has put away sorrow from us.” O chevalier! The worth of the antidote is known by the snake-bitten, the worth of burning fire is known by the moth, the worth of Joseph's shirt is known by grieving Jacob. When someone is de- luded by his own safety and is given the antidote, how will he know its worth? If you want some- one to know the worth and gravity of the antidote, you need him whose spirit has reached his lips. A poor man is needed, broken-hearted, suffering pain, and burdened with grief to know the worth of this caress and the exaltedness of this address: “Praise belongs to God, who has put away sorrow from us.” Wait until tomorrow when that wounded-hearted poor man is placed on the throne of joy in the palisade of holiness while the serving boys and servants act like his slaves to spread the carpet before the seat of his good fortune.

And We tried thee with trials. In other words, “We cooked you well with trial until you became limpid and immaculate, then We took you totally to Ourselves, so that you would not belong to any other.” “O Moses, We took you to the oven of trial and put you into self-purification so that nothing would remain in your heart but My love and nothing on your tongue but My remembrance.” What were those trials and troubles that sat on his head? When he was first born he was born in secrecy, in a house without lamp, poor, without pleasures. His mother could not have a son be- cause of fear of Pharaoh, who was killing sons. She put him into the casket and threw it in the river. His first home was the river. His second home was the sword, the execution ground, and seeing the enemy. His third home was fear of the Egyptians, because he had killed one of them. Then he fled looking back at them, his hea

And he turned away from them no longer addressing them and said ‘Alas my grief for Joseph!’ yā asafā the final alif of asafā has taken the place of the possessive yā’ of genitive annexation sc. yā asafī in other words it means yā huznī ‘O my sorrow’. And his eyes turned white their dark colour was effaced and became white on account of his tears with grief for him such that he was filled with suppressed agony anguished and grief-stricken but not manifesting his grief.

And they will say ‘Praise be to God Who has removed all grief from us. Truly our Lord is Forgiving of sins Appreciative of obedience

Are these the ones of whom you swore that God would never grant them mercy?’ it has already been said to them ‘Enter Paradise; no fear shall come upon you nor shall you grieve’ a variant reading for udkhulū ‘enter’ imperative second person plural has the passive udkhilū ‘they have been admitted’ or dakhalū ‘they entered’; the negation clause ‘no fear shall come upon you nor shall you grieve’ is a circumstantial qualifier in other words they enter Paradise while this is being said to them.

حَدَّثَنَا هَدَّابُ بْنُ خَالِدٍ، حَدَّثَنَا حَمَّادُ بْنُ سَلَمَةَ، ح وَحَدَّثَنِي زُهَيْرُ بْنُ حَرْبٍ، حَدَّثَنَا مُعَاذُ بْنُ مُعَاذٍ الْعَنْبَرِيُّ، ح وَحَدَّثَنِي مُحَمَّدُ بْنُ عَبْدِ الأَعْلَى، حَدَّثَنَا الْمُعْتَمِرُ، ح وَحَدَّثَنَا إِسْحَاقُ، بْنُ إِبْرَاهِيمَ أَخْبَرَنَا جَرِيرٌ، كُلُّهُمْ عَنْ سُلَيْمَانَ التَّيْمِيِّ، ح وَحَدَّثَنَا أَبُو كَامِلٍ، فُضَيْلُ بْنُ حُسَيْنٍ - وَاللَّفْظُ لَهُ - حَدَّثَنَا يَزِيدُ بْنُ زُرَيْعٍ، حَدَّثَنَا التَّيْمِيُّ، عَنْ أَبِي عُثْمَانَ، عَنْ أُسَامَةَ بْنِ زَيْدٍ، قَالَ قَالَ رَسُولُ اللَّهِ صلى الله عليه وسلم ‏ "‏ قُمْتُ عَلَى بَابِ الْجَنَّةِ فَإِذَا عَامَّةُ مَنْ دَخَلَهَا الْمَسَاكِينُ وَإِذَا أَصْحَابُ الْجَدِّ مَحْبُوسُونَ إِلاَّ أَصْحَابَ النَّارِ فَقَدْ أُمِرَ بِهِمْ إِلَى النَّارِ وَقُمْتُ عَلَى بَابِ النَّارِ فَإِذَا عَامَّةُ مَنْ دَخَلَهَا النِّسَاءُ ‏"‏ ‏.‏

Usama b. Zaid reported that Allah's Messenger (way peace be upon him) said:I stood at the door of Paradise and I found that the overwhelming majority of those who entered therein was that of poor persons and the wealthy persons were detained to get into that. The denizens of Hell were commanded to get into Hell, and I stood upon the door of Fire and the majority amongst them who entered there was that of women

حَدَّثَنَا أَبُو كُرَيْبٍ، حَدَّثَنَا أَبُو أُسَامَةَ، عَنْ سَعِيدِ بْنِ أَبِي عَرُوبَةَ، سَمِعَ أَبَا رَجَاءٍ، عَنِ ابْنِ عَبَّاسٍ، قَالَ قَالَ رَسُولُ اللَّهِ صلى الله عليه وسلم فَذَكَرَ مِثْلَهُ ‏.‏

This hadith is narrated likewise through another chain of transmitters

حَدَّثَنِي عَبْدُ اللَّهِ بْنُ مُحَمَّدٍ، حَدَّثَنَا عَبْدُ الْمَلِكِ بْنُ عَمْرٍو، حَدَّثَنَا زُهَيْرُ بْنُ مُحَمَّدٍ، عَنْ مُحَمَّدِ بْنِ عَمْرِو بْنِ حَلْحَلَةَ، عَنْ عَطَاءِ بْنِ يَسَارٍ، عَنْ أَبِي سَعِيدٍ الْخُدْرِيِّ، وَعَنْ أَبِي هُرَيْرَةَ، عَنِ النَّبِيِّ صلى الله عليه وسلم قَالَ ‏ "‏ مَا يُصِيبُ الْمُسْلِمَ مِنْ نَصَبٍ وَلاَ وَصَبٍ وَلاَ هَمٍّ وَلاَ حُزْنٍ وَلاَ أَذًى وَلاَ غَمٍّ حَتَّى الشَّوْكَةِ يُشَاكُهَا، إِلاَّ كَفَّرَ اللَّهُ بِهَا مِنْ خَطَايَاهُ ‏"‏‏.‏

Narrated Abu Sa`id Al-Khudri and Abu Huraira:The Prophet (ﷺ) said, "No fatigue, nor disease, nor sorrow, nor sadness, nor hurt, nor distress befalls a Muslim, even if it were the prick he receives from a thorn, but that Allah expiates some of his sins for that

حَدَّثَنَا إِبْرَاهِيمُ بْنُ الْمُنْذِرِ، قَالَ حَدَّثَنِي مُحَمَّدُ بْنُ فُلَيْحٍ، قَالَ حَدَّثَنِي أَبِي، عَنْ هِلاَلِ بْنِ عَلِيٍّ، مِنْ بَنِي عَامِرِ بْنِ لُؤَىٍّ عَنْ عَطَاءِ بْنِ يَسَارٍ، عَنْ أَبِي هُرَيْرَةَ ـ رضى الله عنه ـ قَالَ قَالَ رَسُولُ اللَّهِ صلى الله عليه وسلم ‏ "‏ مَثَلُ الْمُؤْمِنِ كَمَثَلِ الْخَامَةِ مِنَ الزَّرْعِ مِنْ حَيْثُ أَتَتْهَا الرِّيحُ كَفَأَتْهَا، فَإِذَا اعْتَدَلَتْ تَكَفَّأُ بِالْبَلاَءِ، وَالْفَاجِرُ كَالأَرْزَةِ صَمَّاءَ مُعْتَدِلَةً حَتَّى يَقْصِمَهَا اللَّهُ إِذَا شَاءَ ‏"‏‏.‏

Narrated Abu Huraira:Allah's Messenger (ﷺ) said, "The example of a believer is that of a fresh tender plant; from whatever direction the wind comes, it bends it, but when the wind becomes quiet, it becomes straight again. Similarly, a believer is afflicted with calamities (but he remains patient till Allah removes his difficulties.) And an impious wicked person is like a pine tree which keeps hard and straight till Allah cuts (breaks) it down when He wishes." (See Hadith No. 558, Vol)

حَدَّثَنَا عَبْدُ اللَّهِ بْنُ مَسْلَمَةَ بْنِ قَعْنَبٍ، حَدَّثَنَا سُلَيْمَانُ، - يَعْنِي ابْنَ بِلاَلٍ - عَنْ جَعْفَرٍ، عَنْ أَبِيهِ، عَنْ جَابِرِ بْنِ عَبْدِ اللَّهِ، أَنَّ رَسُولَ اللَّهِ صلى الله عليه وسلم مَرَّ بِالسُّوقِ دَاخِلاً مِنْ بَعْضِ الْعَالِيَةِ وَالنَّاسُ كَنَفَتَهُ فَمَرَّ بِجَدْىٍ أَسَكَّ مَيِّتٍ فَتَنَاوَلَهُ فَأَخَذَ بِأُذُنِهِ ثُمَّ قَالَ ‏"‏ أَيُّكُمْ يُحِبُّ أَنَّ هَذَا لَهُ بِدِرْهَمٍ ‏"‏ ‏.‏ فَقَالُوا مَا نُحِبُّ أَنَّهُ لَنَا بِشَىْءٍ وَمَا نَصْنَعُ بِهِ قَالَ ‏"‏ أَتُحِبُّونَ أَنَّهُ لَكُمْ ‏"‏ ‏.‏ قَالُوا وَاللَّهِ لَوْ كَانَ حَيًّا كَانَ عَيْبًا فِيهِ لأَنَّهُ أَسَكُّ فَكَيْفَ وَهُوَ مَيِّتٌ فَقَالَ ‏"‏ فَوَاللَّهِ لَلدُّنْيَا أَهْوَنُ عَلَى اللَّهِ مِنْ هَذَا عَلَيْكُمْ ‏"‏ ‏.‏

Jabir b. Abdullah reported that Allah's Apostle (ﷺ) happened to walk through the bazar coming from the side of 'Aliya and the people were on both his sides. There he found a dead lamb with very short ears. He took hold of his ear and said:Who amongst you would like to have this for a dirham? They said: We do not like to have it even for less than that as it is of no use to us. He said: Do you wish to have it (free of any cost)? They said: By Allah, even if it were alive (we would not have liked to possess that), for there is defect in it as its ear is very short; now it is dead also. Thereupon Allah's Messenger (ﷺ) said: By Allah, this world is more insignificant in the eye of Allah than it (this dead lamb) is in your eye

حَدَّثَنِي مُحَمَّدُ بْنُ الْمُثَنَّى الْعَنَزِيُّ، وَإِبْرَاهِيمُ بْنُ مُحَمَّدِ بْنِ عَرْعَرَةَ السَّامِيُّ، قَالاَ حَدَّثَنَا عَبْدُ الْوَهَّابِ، - يَعْنِيَانِ الثَّقَفِيَّ - عَنْ جَعْفَرٍ، عَنْ أَبِيهِ، عَنْ جَابِرٍ، عَنِ النَّبِيِّ صلى الله عليه وسلم ‏.‏ بِمِثْلِهِ غَيْرَ أَنَّ فِي حَدِيثِ الثَّقَفِيِّ فَلَوْ كَانَ حَيًّا كَانَ هَذَا السَّكَكُ بِهِ عَيْبًا ‏.‏

Jabir reported Allah's Apostle (ﷺ) narrating a hadith like this with a slight variation of wording

الرابع أصوات النياحة ونغماتها وتأثيرها في تهييج الحزن والبكاء وملازمة الكآبة والحزن قسمان محمود ومذموم

ومن له قوت يوم بيوم فهو في سلامة من جميع ذلك، وهذا سوى ما يقاسيه أرباب الأموال في الدنيا، من الخوف والحزن والهم والغم والتعب.

وأما الاكتئاب فهو افتعال من الكآبة وهي سوء الحال والانكسار من الحزن وقد كئب الرجل يكأب كأبة وكآبة كرأفة ورآفة ونشأة ونشاءة فهو كئيب وامرأة كئيبة وكأباء أيضا قال الراجز

| الفصل السابع عشر في اذكار الكرب والغم والحزن والهم

وكان بعض السلف يقول: الزهد في الدنيا يريح القلب والبدن، والرغبة فيها تكثر الهم والحزن. ### | 7 فصل في درجات الزهد وأقسامه

وقال ابن مسعود رضى الله عنه: إن الله تعالى بقسطه وعمله جعل الروح والفرح في اليقين والرضى، وجعل الهم والحزن في الشك والسخط.

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Identification of depression and anxiety during pregnancy: A systematic review and meta-analysis of test accuracy.: Introduction: Depression and anxiety are significant contributors to maternal perinatal morbidity and a range of negative child outcomes. This systematic review and meta-analysis aimed to review and assess the diagnostic test accuracy of selected screening tools (Edinburgh Postnatal Depression Scale [EPDS], EPDS-3A, Patient Health Questionnaire [PHQ-9]-, PHQ-2, Matthey Generic Mood Question [MGMQ], Generalized Anxiety Disorder scale [GAD-7], GAD-2, and the Whooley questions) used to identify wom

Glucocorticoids, cytokines and brain abnormalities in depression.

Major depression (MD) is a common psychiatric disorder with a complex and multifactor aetiology. Potential mechanisms associated with the pathogenesis of this disorder include monoamine deficits, hypothalamic-pituitary-adrenal (HPA) axis dysfunctions, inflammatory and/or neurodegenerative alterations. An increased secretion and reactivity of cortisol together with an altered feedback inhibition are the most widely observed HPA abnormalities in MD patients. Glucocorticoids, such as cortisol, are vital hormones that are released in response to stress, and regulate metabolism and immunity but also neuronal survival and neurogenesis. Interestingly depression is highly prevalent in infectious, autoimmune and neurodegenerative diseases and at the same time, depressed patients show higher levels of pro-inflammatory cytokines. Since communication occurs between the endocrine, immune and central …

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A biobehavioral perspective on depressive symptoms in patients with cerebral astrocytoma.

More than 51,000 individuals are diagnosed with a primary brain tumor in the United States each year, and for those with the most common type of malignant tumor, an astrocytoma, almost 75% will die within 5 years of diagnosis. Although surgery, radiation, and chemotherapy have improved length of survival, mortality remains high, which underscores the need to understand how other factors affect the disease trajectory. Several recent studies have shown that depressive symptoms are independently associated with reduced quality of life and survival time after controlling for other variables in patients with an astrocytoma. Thus, depressive symptoms represent a significant risk factor for adverse outcomes in this patient population. A growing body of evidence indicates that depressive symptoms are linked to underlying biological phenomena, particularly inflammatory activation modulated throug…

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Depression and risk of developing dementia.

Depression is highly common throughout the life course and dementia is common in late life. Depression has been linked with dementia, and growing evidence implies that the timing of depression may be important in defining the nature of this association. In particular, earlier-life depression (or depressive symptoms) has consistently been associated with a more than twofold increase in dementia risk. By contrast, studies of late-life depression and dementia risk have been conflicting; most support an association, yet the nature of this association (for example, if depression is a prodrome or consequence of, or risk factor for dementia) remains unclear. The likely biological mechanisms linking depression to dementia include vascular disease, alterations in glucocorticoid steroid levels and hippocampal atrophy, increased deposition of amyloid-β plaques, inflammatory changes, and deficits of…

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Sleep and inflammation: psychoneuroimmunology in the context of cardiovascular disease.

Background: Poor sleep is prospectively linked to all-cause and cardiovascular mortality. Inflammatory processes may be an important biological mechanism linking poor sleep to cardiovascular disease. Such processes involve active participation of signaling molecules called cytokines in development of atherosclerotic plaques. Purpose: I review evidence from experimental sleep deprivation and clinical observational studies suggesting a bidirectional relationship between sleep and inflammatory cytokines. Results: Findings from sleep deprivation studies indicate that sleep loss is associated with increases in these cytokines. Similarly, studies in clinical populations with sleep problems, such as primary insomnia patients and those diagnosed with major depression, also show elevations in these same cytokines. Conclusions: Bidirectional communication between the brain and the immune system is…

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Complicated grief and related bereavement issues for DSM-5.

Bereavement is a severe stressor that typically incites painful and debilitating symptoms of acute grief that commonly progresses to restoration of a satisfactory, if changed, life. Normally, grief does not need clinical intervention. However, sometimes acute grief can gain a foothold and become a chronic debilitating condition called complicated grief. Moreover, the stress caused by bereavement, like other stressors, can increase the likelihood of onset or worsening of other physical or mental disorders. Hence, some bereaved people need to be diagnosed and treated. A clinician evaluating a bereaved person is at risk for both over-and under-diagnosis, either pathologizing a normal condition or neglecting to treat an impairing disorder. The authors of DSM IV focused primarily on the problem of over-diagnosis, and omitted complicated grief because of insufficient evidence. We revisit berea…

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Is depression an inflammatory disorder?

Studies consistently report that groups of individuals with major depressive disorder (MDD) demonstrate increased levels of a variety of peripheral inflammatory biomarkers when compared with groups of nondepressed individuals. These findings are often interpreted as meaning that MDD, even in medically healthy individuals, may be an inflammatory condition. In this article, we examine evidence for and against this idea by looking more closely into what the actual patterns of inflammatory findings indicate in terms of the relationship between MDD and the immune system. Data are presented in support of the idea that inflammation only contributes to depression in a subset of patients versus the possibility that the depressogenic effect of inflammatory activation is more widespread and varies depending on the degree of vulnerability any given individual evinces in interconnected physiologic sy…

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Reconsidering anhedonia in depression: lessons from translational neuroscience.

Anhedonia is a core symptom of major depressive disorder (MDD), the neurobiological mechanisms of which remain poorly understood. Despite decades of speculation regarding the role of dopamine (DA) in anhedonic symptoms, empirical evidence has remained elusive, with frequent reports of contradictory findings. In the present review, we argue that this has resulted from an underspecified definition of anhedonia, which has failed to dissociate between consummatory and motivational aspects of reward behavior. Given substantial preclinical evidence that DA is involved primarily in motivational aspects of reward, we suggest that a refined definition of anhedonia that distinguishes between deficits in pleasure and motivation is essential for the purposes of identifying its neurobiological substrates. Moreover, bridging the gap between preclinical and clinical models of anhedonia may require movi…

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Clinical considerations for the diagnosis of major depression after moderate to severe TBI.

Major depression (MD) is the most common psychiatric disorder after traumatic brain injury (TBI). Yet, diagnosing MD is often challenging because of cognitive, emotional, and somatic symptoms that overlap with TBI and other psychiatric disorders. Best current evidence suggests that depressed mood is characterized more by irritability, anger, and aggression than by sadness and tearfulness in persons with TBI. Rumination, self-criticism, and guilt may best differentiate depressed persons from nondepressed persons. Anxiety, aggression, sleep problems, alcohol use, lower-income levels, and poor social functioning appear to be primary associated factors to MD. Objective levels of injury severity, impairment, and functioning do not appear to be related to developing MD. The presence of "organic" TBI sequelae that overlap with the Diagnostic and Statistical Manual of Mental Disorders-Version IV…

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Depression and immunity: a role for T cells?

Much attention has been paid to the potential role of the immune system in the pathophysiology of major depression in humans. While activation of innate immune responses currently dominates the research landscape, early studies in depressed patients demonstrating impairment in acquired immune responses, in particular T cell responses, may warrant further consideration. Intriguing data suggest that activated T cells may play an important neuroprotective role in the context of both stress and inflammation. For example, generation of autoreactive T cells through immunization with central nervous system (CNS) specific antigens has been shown to reverse stress-induced decreases in hippocampal neurogenesis as well as depressive-like behavior in rodents. In addition, trafficking of T cells to the brain following stress, in part related to glucocorticoids, has been found to reduce stress-induced…

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Jet lag, circadian rhythm sleep disturbances, and depression: the role of melatonin and its analogs.

Traveling through several time zones results in a constellation of symptoms known as jet lag. These include reduced alertness, daytime fatigue, loss of appetite, reduced cognitive skills, and disruption of the sleep/wake cycle. In susceptible air travel passengers, jet lag may exacerbate affective illness and result in psychiatric morbidity. Dysregulation of circadian rhythms and melatonin secretion represent the common underlying factor in jet lag and other circadian disorders. Recent studies have established the effectiveness of strategically timed administration of melatonin and appropriate timed exposure to environmental schedules including light in counteracting the dysregulation (chronobiologic actions). With the introduction of melatonergic agonists such as ramelteon and tasimelteon, which have both a stronger affinity for MT₁ and MT₂ melatonin receptors and a longer half-life, ne…

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Women's mental health: depression and anxiety.

Sex ratios for selected mental disorders such as major depressive disorder and anxiety disorder are much higher in women than men. Anxiety disorders constitute the most prevalent mental disorder in adults, and affect twice as many women as men. Depression and anxiety exist comorbidly and along with other mental disorders. This article focuses on depression and anxiety in women, and other conditions comorbid with depression or anxiety: cardiac disease, obesity, vitamin D deficiency, and irritable bowel syndrome.

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Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression.

Recognition that inflammation may represent a common mechanism of disease has been extended to include neuropsychiatric disorders including major depression. Patients with major depression have been found to exhibit increased peripheral blood inflammatory biomarkers, including inflammatory cytokines, which have been shown to access the brain and interact with virtually every pathophysiologic domain known to be involved in depression, including neurotransmitter metabolism, neuroendocrine function, and neural plasticity. Indeed, activation of inflammatory pathways within the brain is believed to contribute to a confluence of decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of glial elements, consistent with neuropathologic findings that characterize depressive disorders. Further instantiating the link bet…

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Physical activity, exercise, depression and anxiety disorders.

There is a general belief that physical activity and exercise have positive effects on mood and anxiety and a great number of studies describe an association of physical activity and general well-being, mood and anxiety. In line, intervention studies describe an anxiolytic and antidepressive activity of exercise in healthy subjects and patients. However, the majority of published studies have substantial methodological shortcomings. The aim of this paper is to critically review the currently available literature with respect to (1) the association of physical activity, exercise and the prevalence and incidence of depression and anxiety disorders and (2) the potential therapeutic activity of exercise training in patients with depression or anxiety disorders. Although the association of physical activity and the prevalence of mental disorders, including depression and anxiety disorders hav…

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Does effective management of sleep disorders reduce depressive symptoms and the risk of depression?

The link between co-morbid insomnia and depression has been demonstrated in numerous groups. Insomnia has been associated with: (1) an increased risk of developing subsequent depression; (2) an increased duration of established depression; and (3) relapse following treatment for depression. In addition, specific insomnia symptoms, such as nocturnal awakening with difficulty resuming sleep, are more strongly associated with depression than classic symptoms of insomnia. Participants of a workshop, held at the 6th annual meeting of The International Sleep Disorders Forum: The Art of Good Sleep in 2008, evaluated whether the effective management of sleep disorders could reduce both concurrent depressive symptoms and the risk of developing subsequent depression. Following the workshop, a targeted literature review was conducted. Initial evidence demonstrated that in patients with insomnia and…

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The stress system in depression and neurodegeneration: focus on the human hypothalamus.

The stress response is mediated by the hypothalamo-pituitary-adrenal (HPA) system. Activity of the corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus (PVN) forms the basis of the activity of the HPA-axis. The CRH neurons induce adrenocorticotropin (ACTH) release from the pituitary, which subsequently causes cortisol release from the adrenal cortex. The CRH neurons co-express vasopressin (AVP) which potentiates the CRH effects. CRH neurons project not only to the median eminence but also into brain areas where they, e.g., regulate the adrenal innervation of the autonomic system and affect mood. The hypothalamo-neurohypophysial system is also involved in stress response. It releases AVP from the PVN and the supraoptic nucleus (SON) and oxytocin (OXT) from the PVN via the neurohypophysis into the bloodstream. The suprachiasmatic nucleus (SCN), the hypo…

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Depression and Korean American immigrants.

Koreans are a relatively new and fast-growing immigrant group in the United States. Research has shown that immigration experiences are associated with depression, whereas acculturation and social support are moderating factors. Korean culture is informed by Confucianism, which emphasizes family integrity, group conformity, and traditional gender roles, and has influenced how Korean immigrants conceptualize depression, express depressive symptoms, and demonstrate help-seeking behavior. An understanding of Korean patterns of manifesting and expressing depression will be helpful to provide culturally appropriate mental health services to Korean American immigrants.

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The dorsal raphe nucleus and serotonin: implications for neuroplasticity linked to major depression and Alzheimer's disease.

The dorsal raphe nucleus (DRN) is a heterogeneous brainstem nucleus located in the midbrain and pons. Via widespread projections, which target a multitude of brain areas, its neurons utilize many transmitters to control various physiological functions, including learning, memory and affect. Accordingly, the DRN has been strongly associated with brain dysfunction, especially mood disorders such as depression, but also Alzheimer's disease. The DRN's most abundant transmitter, serotonin, has received the most attention in studies on both normal brain function and disease, and lately its involvement in the regulation of neuroplasticity has been under particular scrutiny. This chapter begins with a systematic overview of what we currently know about the anatomy of the DRN and its neurons, including their ascending projections. It continues with a review of the transmitters of the DRN, followe…

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A psychoneuroimmunological perspective to Emil Kraepelins dichotomy: schizophrenia and major depression as inflammatory CNS disorders.

The Kraepelinian classification of psychiatric disorders, in particular the dichotomy of dementia praecox and manic-depressive psychosis is under discussion since a long time. In recent years, not only new research in the fields of psychopathology and clinical outcome, but also findings of biological markers in the areas of neurophysiology, neuroendocrinology, psychoneuroimmunology, genetics, or psychopharmacology show a big overlap between both groups of disorders. This overlap of symptoms and markers of both disorders intensified the discussion and the proposals for new criteria for the classification of psychiatric disorders. By means of findings from the field of psychoneuroimmunology and inflammation it will be shown that different pathological mechanisms in depression and schizophrenia may lead to the same final common pathway of inflammation. These mechanisms include the immunolog…

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From inflammation to sickness and depression: when the immune system subjugates the brain.

In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.

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Chronic stress-induced hippocampal vulnerability: the glucocorticoid vulnerability hypothesis.

The hippocampus, a limbic structure important in learning and memory, is particularly sensitive to chronic stress and to glucocorticoids. While glucocorticoids are essential for an effective stress response, their oversecretion was originally hypothesized to contribute to age-related hippocampal degeneration. However, conflicting findings were reported on whether prolonged exposure to elevated glucocorticoids endangered the hippocampus and whether the primate hippocampus even responded to glucocorticoids as the rodent hippocampus did. This review discusses the seemingly inconsistent findings about the effects of elevated and prolonged glucocorticoids on hippocampal health and proposes that a chronic stress history, which includes repeated elevation of glucocorticoids, may make the hippocampus vulnerable to potential injury. Studies are described to show that chronic stress or prolonged e…

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Risk factors for anxiety and depression in the elderly: a review.

Background: Although a number of studies have examined risk factors for anxiety and depression at a later age, there have been no systematic comparisons of risk profiles across studies. Knowledge on such risk profiles may further our understanding of both the etiology and early recognition of these highly prevalent disorders. This paper gives a comprehensive overview and compares risk factors associated with anxiety and depression in the elderly. Methods: The databases MEDLINE, PsycINFO and Sociological Abstracts were systematically searched, and relevant English-language articles from January 1995 to December 2005 were reviewed. Cross-sectional and longitudinal studies on risk factors in elderly from a community or primary care setting were included. The associations between risk factors and pure anxiety or depressive symptoms or disorders were summarized and compared. Results: The abst…

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Vagus nerve stimulation for epilepsy and depression.

Many patients with epilepsy suffer from persistent seizures despite maximal antiepileptic drug (AED) therapy. Chronic, intermittent vagus nerve stimulation (VNS) has proven to be a safe, effective option for patients suffering from refractory seizures who are not candidates for surgical resection. Although only a small minority of patients will be entirely seizure-free, VNS as an adjunct to medical therapy does appear to provide a significant amount of improvement in quality of life. Reports of antidepressant effects independent of seizure control, along with the use of multiple AEDs in the treatment of depression, has led to the investigation of VNS as a potential adjunctive treatment for major depressive disorder. Both the number of severely depressed patients refractory to available pharmacologic options and the need for repeated treatments and significant side effects associated with…

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Inflammation, depression and dementia: are they connected?

Chronic inflammation is now considered to be central to the pathogenesis not only of such medical disorders as cardiovascular disease, multiple sclerosis, diabetes and cancer but also of major depression. If chronic inflammatory changes are a common feature of depression, this could predispose depressed patients to neurodegenerative changes in later life. Indeed there is now clinical evidence that depression is a common antecedent of Alzheimer's disease and may be an early manifestation of dementia before the cognitive declines becomes apparent. This review summarises the evidence that links chronic low grade inflammation with changes in brain structure that could precipitate neurodegenerative changes associated with Alzheimer's disease and other dementias. For example, neuronal loss is a common feature of major depression and dementia. It is hypothesised that the progress from depressio…

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Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression.

Glucocorticoids play an essential role in the response to environmental stressors, serving initially to mobilize bodily responses to challenge and ultimately serving to restrain neuroendocrine and immune reactions. A number of diseases including autoimmune, infectious and inflammatory disorders as well as certain neuropsychiatric disorders such as major depression have been associated with decreased responsiveness to glucocorticoids (glucocorticoid resistance), which is believed to be related in part to impaired functioning of the glucocorticoid receptor (GR). Glucocorticoid resistance, in turn, may contribute to excessive inflammation as well as hyperactivity of corticotropin releasing hormone and sympathetic nervous system pathways, which are known to contribute to a variety of diseases as well as behavioral alterations. Recent data indicate that glucocorticoid resistance may be a resu…

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Genetic and hormonal regulation of tryptophan kynurenine metabolism: implications for vascular cognitive impairment, major depressive disorder, and aging.

Impairment of cognition that is caused by (or associated with) vascular factors has been termed vascular cognitive impairment (VCI). The hallmark of VCI is an impairment of brain executive, or planning, functions caused by inflammatory changes of brain microvessels. VCI is characterized by impairment of the executive function and is distinct from Alzheimer's-type and multi-infarct dementias, although VCI might overlap with Alzheimer's disease. This review focuses on the possible contribution of the kynurenine pathway of tryptophan (Try) catabolism to the inflammatory changes in brain microvessels. One mechanism of brain microvessel inflammation is activation of the inducible nitric oxide synthase (iNOS) by the proinflammatory cytokine interferon gamma (IFN-gamma). The effect of IFN-gamma on iNOS might be mediated by kynurenine derivatives of tryptophan because (1) IFN-gamma stimulates th…

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