Symptoms of depression vs anxiety, pregnant having trouble sleeping at night - Try Out

If you think you may be experiencing symptoms of clinical depression or anxiety, talk with your primary care provider about your concerns. Until some years ago, there was a common understanding that when people talked about depression or anxiety, they were talking about exclusively Western problems. Images from the web about depression and anxiety an international perspective, hope you like them.
Most heart patients will suffer from depression, anxiety, or both at some point along the etiological continuum, and effective treatment of these problems has been shown to improve cardiac outcomes, yet evidence-based treatment for depression and anxiety remains elusive for the vast majority of cardiac patients. The author, having recently published a patient self-help manual on this topic, calls for emphasis on developing innovative new methods for the treatment of depression, anxiety, and subsyndrome distress for cardiac patients that are effective, rapid, and reasonable in cost. Prevalence rates for depression among women are higher than rates for men both in the general population (15), and among cardiac patients (16).
In sum, the correlation between depression and cardiovascular problems appears to be comparable to the correlation between smoking and CVD (18). These longitudinal studies indicate that depression most frequently occurs before the onset of clinically significant CAD.
A range of studies have found high rates of clinically meaningful depressive symptoms among cardiac patients. When we look prognostically at the risks associated with higher morbidity and mortality for patients with a diagnosis of CVD and depression, we see the mortality rate among clinically depressed patients is quite high and increases with the severity of symptoms and passage of time.
A recent study designed to assess the impact of changes in symptoms of depression for heart failure patients found that worsening symptoms of depression were associated with higher rates of cardiac death and cardiovascular hospitalization, even after controlling for baseline depression and established risk factors like HF cause, age, ejection fraction, plasma N-terminal pro-B-type natriuretic peptide level, and prior hospitalizations (44).
Studies show that there are several depression-driven biological factors that promote increased morbidity and mortality for people with heart disease (46). Depression also causes increased platelet aggregation (55) and higher platelet monoamine oxidase (MAO) activity, especially in women (56). Research has substantiated the role that chronic stress and depression play in pro-inflammatory processes. Anxiety’s association with CVD has been less well studied than the effect of depression for this population, though the research base is substantial and growing, to such a degree that many researchers in the US have called on the American Heart Association to list anxiety as a major independent risk factor for heart disease.
Anxiety is a negative affective state resulting from an individual’s perception of threat, characterized by a perceived inability to predict, control, or gain preferred results in given situations (61). A number of studies have shown that anxiety predicts a higher incidence of cardiac events, higher morbidity and mortality, and poorer quality of life for CHD patients in both the short and long term, independent of conventional risk factors and disease severity (69–71). Anxiety has been shown to predict future coronary events and long-term survival after MI, even after controlling for disease severity and conventional risk factors (79–81). A very large prospective, comparative, cross-cultural investigation by Moser and De Jong was designed to evaluate the impact of anxiety on patient health soon after MI in five countries: Australia, England, Japan, South Korea, and the US (86). Data from the Moser and DeJong cross-cultural study was separately evaluated for gender differences in the presentation of anxiety across culture. There are several studies which find that anxiety predicts an increased risk of subsequent negative cardiac events for people who already have a diagnosis of CHD.
The biophysical mechanisms whereby anxiety may contribute to the onset of CHD and negative CHD outcomes appear to be several and, as with depression, chiefly focus on the role of the SNS. It has been found that patients with GAD have lower vagal tone than those with low levels of anxiety, which allows SNS activity to predominate (101,102).
Cardiovascular reactivity (CVR) is exaggerated in people with anxiety so that stressful stimuli can produce frequent, pronounced, and sustained changes in blood pressure, heart rate, stroke volume, and total peripheral resistance, which may then contribute to the etiology of heart disease and poor prognosis (104).
Several studies have examined the incidence rates for diagnosable depression and anxiety among patients waiting for heart transplant.
Research shows that depression is a known cause or correlate of many of these established psychosocial and behavioral risk factors, namely less exercise, poor diet, obesity and smoking, especially in women (148), failure to use social support resources (149,150), and triple the risk of noncompliance with physician-ordered medical regimens (151).
Chronic stress, depression, and anxiety, to varying degrees, are factors in the onset and severity of diagnoses that frequently co-occur with or presage CVD: hypertension, metabolic syndrome (MetS), and diabetes. There is a substantial research base, nearly a century in the making, linking hypertension to negative affect, anxiety, depression, stress in general, and negative personality traits.
Depression and distress are associated with MetS in the research literature, though more research needs to be done on this association. In another study by Skilton et al., 1,598 subjects at risk of CVD were assessed for metabolic syndrome, depression, and anxiety to investigate whether metabolic syndrome is associated with anxiety or depression, whether these relationships vary by gender, and whether they are independent of age, obesity, smoking status, socioeconomic factors, and lifestyle (172).
Chronic stress is now believed to be the leading cause of depression (173) and acute stress, especially if it is encountered in childhood, the most significant factor in the development of anxiety disorders and depressive disorders later in life (174). More than a dozen potential biomarkers that interact with stress to promote the etiology of clinical depression and anxiety have been identified, including monoamine regulators, proinflammatory cytokines, and other inflammatory mediators, mediators of glutaminergic activity, and GABAergic activity, as well as regulators of neurogenesis (186).
Table 1 provides list of the most common symptoms of stress and Table 2 the list of clinical criteria for depression and anxiety. People who have four or fewer symptoms from the checklists in Table 2 are considered subsyndromal, regardless of symptom severity. Anxiety and depression have symptoms in common but overall their symptoms exhibit distinct central tendencies: anxiety is usually accompanied by excessive, exaggerated worry about everyday events and hyperactivity, while depression tends to be dominated by feelings of sadness, guilt, lack of self-worth, in-activity, and withdrawal.
Research evidence suggests genetic and neurobiologic similarities between depressive and anxiety disorders, many of which have been reviewed in this article. It should be noted that a substantial number of patients satisfy full diagnostic criteria for both depression and anxiety, evidencing true comorbidity. Frasure-Smith and Lesperance assessed the prognostic importance of MDD and GAD together with self-reports of anxiety and depression and their co-occurrence during 2-year follow up of 804 men and women with stable CAD, measuring incidence of major adverse cardiac events or MACEs (cardiac death, MI, cardiac arrest, or nonelective revascularization) in the 2 years following baseline (197). It is remarkable that depression, in and of itself without any specific comorbidity, is associated with a decrement in health status almost as bad as the decrement associated with congestive heart failure after each group is adjusted for the presence of comorbidities (200).
While there are no reliable nationwide data on rates of anxiety in India, limited data from the WHO place the current point-prevalence rate of GAD at 8.5% (206).
Increasing rates of chronic stress, distress, depression, and anxiety in India should be of great concern from both the clinical and public health perspectives. Depression, anxiety, and distress in the cardiac patient can be treated effectively, even cured, resulting in vastly improved cardiovascular health and reduced risk of future adverse cardiac events and lower utilization of costly health and allied health services (212).
CVD is a multifactor problem that requires a multifactor solution, and the same is true for depression, anxiety, and subsyndrome distress.
In 2008 The American Heart Association published physician guidelines for the diagnosis and treatment of depression in heart patients (221).
Given the popularity of the two-stage PHQ series for assessing and monitoring depression, similar 2- and 7-step anxiety screeners were developed by Spitzer et al. The underdiagnosis of depression in cardiac care is highly significant, greater even than in primary care settings, where doctors fail to diagnose depression more than half the time. Studies have shown that the symptomology of depression in cardiac patients often differs from that observed in general psychiatric patients. In the majority of cardiology practices in the US, a cardiac patient with positive screening results for depression, anxiety, or distress is referred for evaluation to a mental health professional who is qualified in the diagnosis and treatment of these disorders. Ideally, treatment of depression and anxiety in cardiac patients should be based on a differential diagnosis of patient need within the larger framework of mind-body medicine, using a multifactor approach, and treatment should be formulated using evidence-based modalities. Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs), Serotonin Antagonist and Reuptake Inhibitors (SARIs), and benzodiazepines are considered the prescriptive choice for people with depression and anxiety in the general population. In the majority of cardiac settings, treatment for depression and anxiety is still mostly limited to the dispensing of SSRI medications, despite their limitations and recent challenges to their efficacy.
There is some evidence that SSRIs may improve depressive symptoms and reduce the frequency of reinfarction and death due to MI for extremely depressed patients with CAD, but they do not render these benefits with consistency. In the hands of a properly trained doctoral-level clinician, psychotherapy can reverse the neurobiologic and psychological consequences of chronic stress, depression and anxiety, is preferred over medication therapy by many patients, and can be combined with medication to increase medication efficacy in patients with more severe psychiatric diagnoses (260).
IPT is an empirically validated treatment proven effective for clinical depression, social phobias, majoranxiety disorder, bipolar disorder, and post-traumatic stress disorder (276,277). Keywords: depression and anxiety, depression and anger, depression and pregnancy, depression and bipolar support alliance, depression and sleep, depression and anxiety test, depression and relationships, depression and weight gain, depression and alcohol, depression and sex, depression and anxiety an international perspective .


Depression and depressive symptoms are also associated with 2–3 times higher mortality rates for patients with stable CAD and for those who suffer myocardial infarction (MI), unstable angina, and coronary artery bypass.
Clearly, a diagnosis of CVD, the physical degradations and disabilities associated with it, and the stress of medical procedures and surgery, are significant enough to cause or exacerbate depression in people with heart disease. One authoritative study by Denollet and Brutsaert placed the incidence rate of clinical depression among cardiac patients as high as 50.5% (19). The relative risk ratio for death within 6 months among post-MI patients with MDD, versus post-MI patients without depressive disorder, was reported as 3.1 by both Schleifer at al. It is well-established that depression is associated with higher rates of healthcare utilization and costs for all heart patients (45).
Depression is associated with alterations in immunological functioning relevant to pro-inflammatory processes. There are several different subtypes of anxiety, including panic disorder, social anxiety disorder, generalized anxiety disorder (GAD), simple phobia, obsessive-compulsive disorder, and post-traumatic stress disorder. The Normative Aging Study, a large prospective study conducted in Boston, found that higher levels of worry (a key symptom of anxiety) were found to predict increased risks of both MI and fatal CHD in male subjects at 20-year follow up (66). Persistent anxiety predicts worse disability, more physical symptoms, and poorer functional status in CHD patients (72,73).
Anxiety post MI is also associated with increased in-hospital complications such as lethal dysrhythmias, continued ischemia, and reinfarction (82), longer stays in the cardiac care unit and hospital (83)[, more frequent and severe symptoms, regardless of the severity of a patient’s physical condition (84), higher consumption of healthcare resources, and lower quality of life post-discharge (85). Overall, women reported mean anxiety levels 25% higher than those reported by men – a pattern of higher anxiety in women that was seen in each country studied, which (according to the study authors) may account for poorer prognosis seen in women post-MI (88).
This study found that patients with high anxiety had twice the occurrence of complications as patients with low anxiety, independent of age, diabetes, previous AMI, type of AMI, and Killip class. Anxiety, both episodic and chronic, contributes to excessive activation of the SNS, and release of epinephrine, norepinephrine, and cortisol. Research has also shown that anxiety can lead to increased blood cortisol levels that promote elevated resting blood pressure and heart rate (103). Magni and Bogherini (126) found that 35% of patients waiting for heart transplant suffered from anxiety disorders and more than 20% suffered from marked depressive symptoms. The relative risk of cardiac death in patients with type D personality versus patients asymptomatic for depression and anxiety in this study was 4.3 (133). MSI, covered previously in this article, is driven by fairly low levels of anxiety and nervousness typical for the general population, yet has disastrous consequences for the heart patient. It is well-documented that the incidence of chronic stress, depression, and anxiety is higher among people of lower socioeconomic status (146).
Anxiety, both clinical and subclinical, is also associated in the research literature with behaviors that are contraindicated for a healthy heart. This study concluded that metabolic syndrome is associated with depression and depressive symptoms, but not statistically significantly associated with anxiety, irrespective of gender, and obesity in subjects at risk for CVD.
On observation, the symptoms for depression and anxiety are nearly identical to the symptoms of stress.
Subsyndromal depression and anxiety is very frequently seen in patients with heart disease and, as previously cited, these distressed patients are more than twice as likely to develop CVD and up to three times more likely to have a poorer prognosis than patients with normal mood (190). It is quite common for patients with clinical depression to have symptoms from the anxiety checklist and vice versa.
They found that anxiety and depression both predict greater MACE risk in patients with stable CAD.
Unfortunately, high rates of chronic and acute stress, a cultural disdain for seeking help with mental problems, and a lack of early intervention and treatment alternatives have combined to fuel an epidemic of depression and anxiety in India. Senior fellows at the National Institute of Mental Health and Neurosciences estimate the point prevalence for anxiety disorders to be 20–25%, or one out of every four or five Indians (207). Jon Kabat-Zinn in the US developed the MBSR, a mindfulness-based stress reduction program involving mild forms of Hatha Yoga in combination with meditation, exercise, and a healthy diet, which demonstrated statistically significant levels of stress-reduction, positive changes in brain activity, improved emotional processing, better immune functioning, better circulation, and other symptom reduction in people who suffer from heart disease and breast cancer (217,218). To answer this challenge, a great deal of research has been devoted to depression and anxiety screening instruments that are valid, specific, and brief. Despite its brevity, the PHQ-9 provides the sensitivity and specificity needed for assigning a provisional diagnosis of depression. Complaints of tiredness or lack of energy are more frequent for people who suffer from heart disease and depression, whereas melancholy or depressed mood states are more common for psychiatric patients in general (230–232). Recent research, reviewed in prior sections of this article, shows that serotonin depletion is but one of multiple neurobiologic effects of chronic distress, depression, and anxiety. Citalopram showed antidepressant efficacy (reduction of depressive symptoms) in some patients and no evidence of harm, but also failed to show any statistically significant improvements in cardiovascular health for study participants (251). In all these trials, patients suffering from CHD and psychological disorders experienced treatment efficacy (remission of psychological symptoms) but little statistically meaningful reduction in coronary morbidity and mortality. The American Psychiatric Association practice guidelines state that CBT and interpersonal psychotherapy (IPT) have the best-documented efficacy for treatment of MDD and anxiety disorders (271,272). On this basis the American Heart Association listed depression as a major independent risk factor for heart disease in February of 2014 and strengthened its guidelines for the screening and treatment of depression in people with heart disease. The wide range of risk across studies is associated with different scales used to measure depression and subsyndrome depressive symptoms, great variation in study length, and substantial difference in study cohort characteristics (age, gender, socioeconomic status, diagnosis).
The incidence and severity of depression were evaluated according to the Zung Self-Rating Depression Scale (SDS).
This study found that, after multivariate adjustment for traditional CAD risk factors, depressive symptoms predicted CAD severity and increased risk of death in women 55 and younger, but not in men 55 or younger, nor in women over the age of 55. They found that CHF patients who met DSM-IV criteria for major depression had a mortality rate more than twice that of those who were not depressed, and three times as many hospitalizations.
Specifically, depression has been associated with an elevation of interleukin-6 (IL-6), a primary pro-inflammatory cytokine (59,60). Anxiety disorders can evolve as a normal reaction to chronic stress and cumulative adversity, and acutely stressful situations (like having an MI) can trigger anxiety. Rates of anxiety in the general population are higher for women than for men, and women tend to suffer higher anxiety than men post-MI, a finding that is consistent across a variety of Western and Asian cultural groups (89).
In a review article, von Kanel concluded that patients with atherosclerosis who experience anxiety and mental stress may tend toward hypercoagulation due to endothelial dysfunction and reduced fibrinolysis (125). Those with anxiety are more likely to eat an unhealthy diet, smoke, use drugs or alcohol or both, fail to adhere to physician instructions, experience sleep disturbance, and be physically inactive (152–154). Study participants were regularly interviewed for stress symptomology and received CT examinations in 1968, 1974, 1980, 1992, and 2000. This study found that teenage boys who had some depressive symptoms at the start of the study, together with high levels of circulating morning cortisol (as measured in their saliva) were 14 times more likely to develop major depression within the following 3 years than boys without any signs of depression and low levels of cortisol, and 2–4 times more likely to develop clinical depression than boys with either depressive symptoms or high levels of morning cortisol. In this study, researchers found the SKA2 mutation was associated with higher levels of cortisol and glucocorticoids and significantly interacted with chronic stress and anxiety to explain about 80% of suicidal behavior and progression from suicidal ideation to suicide attempt (188). The difference between stress symptomology and the clinical criteria for a psychiatric diagnosis lies primarily in symptom volume and chronicity. Approximately 85% of patients with depression also have significant symptoms of anxiety, an association that holds true for men in the particular, and significant depressive symptoms occur in up to 90% of patients with anxiety disorders (192,193). This study found that younger age at onset of HF and depressive symptoms were independent predictors of anxiety (199). The excessive morbidity associated with depression is well-documented in the scientific literature, but its implications have been largely ignored by mainstream medicine until recently, owing to unprecedented increase in rates of depression, anxiety, and distress worldwide. A score of 3 or more has been shown to have a sensitivity of 83% and a specificity of 92% for major depression (222)[2; 3 is considered the optimal cut-point for further screening and a score of 0 virtually excludes depression.
It also provides a severity measure for treatment planning purposes, serves as a diagnostic instrument for the depression criteria listed in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (the DSM IV), and it has been proven accurate for patients with CAD (224,225). This series is called the GAD-2 and GAD-7, respectively, with GAD meaning generalized anxiety disorder . A score of 3 or higher warrants assessment with the GAD-7, which provides severity measures across all 7 diagnostic criteria for anxiety in the DSM IV.

An SSRI, while a helpful adjunct to the treatment of depression, major depression especially, does not target the most frequent underlying cause of depression: mental distress and stress-related neuroendocrine pathology.
Patients with depression were randomized into a protocol that included low-intensity cognitive behavioral therapy (CBT) (6 individual and group sessions over 11 weeks).
Although benzodiazepines have long been prescribed for short-term use by the post-MI patient to reduce anxiety, there are no controlled trials documenting the benefits of this protocol (258) and recent research suggests that sustained use of benzodiazepines may contribute to heart failure and cardiac death (259).
Problem-solving therapy and relaxation therapies are also proven adjuncts to treatment for depression and anxiety, and in heart patients, emotionally focused therapy (EFT) for couples and families has been shown to improve cardiac outcomes (273). Depressive symptoms were scaled from 0 to 4, with a grade of 2 or higher equivalent to clinical depression. The authors conclude that younger women may be especially vulnerable to the adverse cardiovascular effects of depression (35). They also found the relationship between depression and higher rates of mortality and re-hospitalization was independent of advanced age and severity of ischemic etiology of CHF. Although smoking and ventricular arrhythmias are more common in depressed patients, depression adversely affects the course of heart disease independent of these factors (58).
In a similar study of 2,280 community dwelling men with a 32-year follow up, the rate of sudden death due to heart disease was 4.46 times higher for anxious individuals than for those without anxiety. For patients with low perceived control, 20% experiencing low anxiety versus 80% experiencing high anxiety experienced complications. Patients with CHD and elevated anxiety or prolonged stress and a history of AMI have higher plasma norepinephrine levels (98). High anxiety is also associated with prolonged QTc intervals, and has been shown to increase risk for lethal cardiac dysrhythmias (106).
In this survey, men with a history of depression were not significantly more likely to develop MetS. Girls with some depressive symptoms and high levels of cortisol were 4 times more likely to develop major depression within 3 years than same-age girls who had no symptomology and low cortisol levels at the start of the study (187). At least five of the symptoms on the Table 2 checklists must be present nearly every day, most of the time, in order to make a diagnosis of clinical depression or anxiety. Although depression and anxiety symptoms co-occur with great frequency and they share a substantial component of general affective distress, they can be differentiated based on factors specific to each syndrome (194). The World Health Organization (WHO) estimates that, owing to the rise of chronic stress globally, depression has become a pandemic. In this study, the incidence of depressive episodes was higher for women than for men by a ratio of 2:1, which also holds true in the US (203).
The AHA recommends, based on research evidence, that patients with heart disease who are being treated for depression (and anxiety) should undergo careful monitoring for adherence to their medical treatment regimen, and for the efficacy and safety of drug therapy for their medical and mental health conditions (235).
For all these reasons, the standard of practice for major depression requires both psychotherapy and anti-depressive medication to be administered.
Patients who showed less than a 50% reduction in Beck Depression Inventory scores after 5 weeks of CBT were referred to a psychiatrist for pharmacotherapy, usually sertraline. Indeed, subsequent analysis of data from SADHART showed that treatment with sertraline compared with placebo did not support improved cardiovascular status among patients with depression at statistically significant levels (250). The Recurrent Coronary Prevention Project, in which 1,013 MI patients with depressive symptoms were randomly assigned to receive psychotherapy and social support, showed a reduction in depressive symptoms and a 44% reduction in cardiac death and nonfatal MI for the treatment group (268). Meditation has been proven effective in the treatment of coronary artery disease (CAD) and for mild to moderate depression and anxiety but most cardiac patients quit its practice before it can deliver clinical benefit, and it is not effective as a stand-alone intervention for moderate to major depression and anxiety. The definition of CAD included MI, angina pectoris, chronic heart disease, and other types of symptomatic disease that required coronary artery bypass surgery or percutaneous transluminal coronary angioplasty. In this study, patients with major depression had a 4.5-times higher risk of experiencing a heart attack (MI) during a 13-year follow up than those without major depressive disorder (MDD).
In this study, the higher the depression grade, the greater the incidence of morbidity and mortality due to heart-related pathology. Patients who were moderately to severely depressed had a 69% higher risk of cardiac death and 78% higher risk of all-cause mortality when compared to patients without depression. Research strongly suggests that anxiety at every step along the continuum has comparable cognitive, neurobiological, and behavioral effects, and that clinical and subclinical anxiety are not fundamentally different phenomena – both have dilatory effects on patient health (62).
MetS was associated with a current diagnosis of major depression and overeating, but not with age or sex (169). The study authors found that higher SLE and higher social strain were associated with a higher incidence of CVD and hemorrhagic stroke, independent of sociodemographic factors and depressive symptoms (180). Patients who meet these criteria are then assessed for symptom severity to determine whether their clinical presentation is mild, moderate, or severe. This study found that anxiety symptoms were the strongest predictor of future negative cardiac events, rehospitalization, and increased healthcare consumption for men (198). Doctors from The National Institute of Mental Health and Neurosciences and leading psychiatrists in private practice report that the incidence of depression is rising precipitously, especially in urban areas, where the current point prevalence of depression among Indians is estimated to be 10% (204).
Scores of 5, 10, and 15 represent cut-points for mild, moderate, and severe anxiety respectively.
The cumulative incidence of clinical depression in this cohort of 1,190 participants at 40 years of follow up was 12% (lower than the incidence of depression in the general population). Patients with depressive symptoms that fell below the clinical criteria for major depression were twice as likely to die of MI as patients with no depressive symptoms whatsoever.
A high depression grade correlated with an almost threefold increase in risk for angina pectoris. In all these studies, anxiety was found to predict subsequent cardiac events independent of conventional risk factors and disease severity.
Major depressive episodes were the most frequent psychiatric disorder, followed by anxiety disorders. Chronic stress and acute stress induce the neurobiologic changes that lead to distress, depression, and anxiety. When screening for anxiety disorders, the recommended cut-point for further evaluation is a score of 10 or greater, which has a sensitivity of 89% and specificity of 82% for GAD.
In this study, clinical depression was associated with a more than twofold higher risk of later CAD.
Subclinical, fairly common depressive features like feelings of guilt and low self-assertiveness were also associated with an increased risk of MI. Patients with MDD (a score of 10 or more on the Beck Depression Inventory [BDI]) had a rate of death due to MI at 1-year follow up that was almost five times higher than patients without depression – a risk ratio that remained after controlling for baseline electrocardiographic evidence of ischemia, left ventricular ejection fraction, and number of diseased coronary arteries. In all these studies, the relationship between anxiety and poor cardiac outcomes was independent of traditional cardiovascular risk factors and there was evidence of a dose–response effect whereby higher levels of anxiety correlated with poorer cardiac health outcomes.
Similar high rates of postoperative depression and anxiety have been observed in the year following transplantation, with post-traumatic stress disorder being the primary diagnosis (130). Although originally developed to diagnose GAD, the GAD-7 is also proven to have good sensitivity and specificity as a screener for panic, social anxiety, and post-traumatic stress disorder (227).
In the study by Vaccarino, depressive symptoms of 391 patients 50 years old or older who were hospitalized with CHF were measured, and all patients were followed for 6 months with a focus on mortality and functional capacity (activities of daily living [ADL]). In this study, mortality at 6 months was two to three times higher in patients with greater depressive symptoms compared to patients with lesser symptoms or patients considered to have normal mood.
Patients with moderate depressive symptoms also experienced significant functional declines during follow up.

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