How do you diagnose dysthymia

Due to the stigma still associated with depression, many people with this disorder may be unrecognized and untreated. Although dysthymia has long been considered to be less severe than major depression, the consequences of this condition are increasingly recognized as potentially grave, including severe functional impairment, increased morbidity from physical disease, and even an increased risk of suicide.

The pathophysiology of dysthymia is not fully understood. Most people, especially those with early onset dysthymia, have a family history of mood disorders, including bipolar disorder. One or both parents may have suffered from major depression. A family history of this illness makes it more likely for dysthymia to appear in the teenage years or early 20s. Compared with major depression, patients with dysthymia tend to have more subjective symptoms and less dramatic psychomotor disturbance or neurovegetative symptoms including abnormalities of sleep, appetite, and energy levels.

Persons with dysthymia who have major depressive episodes tend to suffer from depression for long periods and spend less time fully recovered [ 9 ]. In a year follow-up study of persons with dysthymia, The validity of making a distinction between depressive personality disorder and dysthymia has been a matter of debate since depressive personality disorder and dysthymia are both classified among the lesser severity spectrum of depressive disorders.

Depressive personality disorder is characterized by a gloomy or negative outlook on life, introversion, a tendency toward self-criticism, and pessimistic cognitive processes, with fewer than mood and neurovegetative symptoms, seen in dysthymia. Dysthymia or depression may coexist with depressive personality disorder, and persons who have depressive personality disorder are at greater risk of developing dysthymia than healthy persons after followup for 3 years [ 11 ]. The best treatment for dysthymia appears to be a combination of psychotherapy and medication.

The positive clinical response to medications like selective serotonin reuptake inhibitors SSRIs [ 12 — 19 ], serotonin norepinephrine reuptake inhibitors SNRIs [ 20 , 21 ], and tricyclic antidepressants TCAs [ 14 , 15 ] suggests that serotoninergic and noradrenergic systems involve the mechanism of dysthymia. A systematic review [ 22 , 23 ] of antidepressant treatment for dysthymia suggests that SSRIs, TCAs, and monoamine oxidase inhibitors are all equally effective, but SSRIs may be slightly better tolerated.

Success has also been reported with more noradrenergic agents, such as mirtazapine, nefazodone, venlafaxine, duloxetine, and bupropion. Second-generation antipsychotics showed beneficial effects compared to placebo for major depressive disorder or dysthymia, but most second-generation antipsychotics have shown worse tolerability, mainly due to sedation, weight gain, or laboratory data abnormalities such as prolactin increase.

Some evidence indicated beneficial effects of low-dose amisulpride for dysthymic people [ 24 ]. Psychotherapy and medication are both effective treatment modalities for dysthymia and their use in combination is common. There are many different types of psychotherapy, including cognitive behavioral therapy, psychodynamic, and insight-oriented or interpersonal psychotherapy, which are available to help persons with dysthymia. CBASP is a form of psychotherapy that was specifically developed for patients with chronic depression.

It encourages patients to focus on the consequences of their behavior and to use a social problem-solving algorithm to address interpersonal difficulties. CBASP is more structured and directive than interpersonal psychotherapy and differs from cognitive therapy by focusing primarily on interpersonal interactions, including interactions with therapists.

Through this psychotherapy, patients come to recognize how their cognitive and behavioral patterns produce and perpetuate interpersonal problems and learn how to remedy maladaptive patterns of interpersonal behavior.

The combination of medication and psychotherapy may be much more effective than either one alone [ 26 ]. Dysthymia is essentially defined by the existence of depressive symptoms at some level. However, some patients who are treated for dysthymia only present with loss of interest and do not have a depressed mood.

This condition should be regarded as apathy. Marin [ 27 ] defined the apathy syndrome as a syndrome of primary lack of motivation, that is, loss of motivation that is not attributable to emotional distress, intellectual impairment, or diminished consciousness.

Starkstein [ 28 ] described the features of apathy as lack of motivation characterized by diminished goal-oriented behavior and cognition, and a diminished emotional connection to goal-directed behavior.

Levy and Dubois [ 29 ] proposed that apathy could be defined as the quantitative reduction of self-generated voluntary and purposeful behavior. At present, apathy is treated symptomatically. There is no decision tree for apathy in DSM-IV-TR, but there is a possibility that apathy will come to be managed independently from mood disorders if the mechanisms involved or treatment strategy is more fully established in the future. Marin [ 27 ] and Starkstein [ 30 ] have suggested diagnostic criteria for this condition.

As the basis of specific diagnostic criteria for apathy, abnormalities in aspects of emotion, cognition, motor function, and motivation have been suggested. Marin has also developed an apathy rating scale [ 31 ], while diagnostic criteria for apathy have been proposed by Starkstein et al. Table 1. Adapted from Starkstein [ 30 ].

Apathy has received increasing attention because of its effects on emotion, behavior, and cognitive function. It seems likely that apathy in persons with depression results from alterations of the emotional and affective processing, but it may typically occur in the absence of a depressed mood Figure 1.

Apathy occurs in persons with a variety of psychiatric and neurological disorders including schizophrenia [ 32 , 33 ], stroke [ 34 , 35 ], traumatic brain injury [ 36 ], Parkinson's disease [ 28 , 37 , 38 ], progressive supranuclear palsy [ 38 ], Huntington's disease [ 39 , 40 ], and dementias such as Alzheimer's disease [ 30 , 41 , 42 ], vascular dementia [ 43 ], frontotemporal dementia [ 41 , 42 ], and dementia due to HIV [ 44 ]. Marin et al. Mean apathy scores were significantly higher than healthy elderly scores in right hemispheric stroke, Alzheimer's disease, and major depression.

Elevated apathy scores were associated with low depression in Alzheimer's disease, high depression in major depression, and intermediate scores for depression in right hemispheric stroke. They found that the level of apathy and depression varied among diagnostic groups although apathy and depression were significantly correlated within each group.

Thus, apathy is most often seen clinically within the setting of depression, dementia, or stroke, and problems related to apathy tend to be important because of its frequency, increasing prevalence, impact on daily life, poorer rehabilitation outcomes after stroke, and burden on caregivers. Levy et al. Furthermore, they reported that apathy was not correlated with depression in a combined patient sample, including those with Alzheimer's disease, frontotemporal dementia, progressive supranuclear palsy, Parkinson's disease, and Huntington's disease.

Apathy, but not depression, was correlated with lower cognitive function as measured by the mini mental state examination [ 48 ]. These results imply that apathy might be a specific neuropsychiatric syndrome that is distinct from depression but is associated with both depression and dementia. Symptomatologically, it is important to understand that apathy can occur concomitantly with depression, but is usually different from it.

Starkstein et al. The apathetic patients were older, had a higher frequency of major but not minor depression, had more severe physical and cognitive impairment, and had lesions involving the posterior limb of the internal capsule.

In their study, there was a significantly higher frequency of apathy among the patients with major depression but not those with minor depression or no depression. These findings indicate that although major depression and apathy occur independently, apathy remains significantly associated with major depression but not with minor depression.

This is consistent with the results of previous studies that have differentiated between major and minor depression, including differences of cognitive function and cortisol suppression after dexamethasone administration [ 49 , 50 ], which were seen in patients with major depression but not minor depression.

Apathy is often seen in patients with lesions of the prefrontal cortex [ 51 , 52 ] and is also frequent after focal lesions of specific structures in the basal ganglia such as the caudate nucleus, the internal pallidum, and the medial dorsal thalamic nuclei [ 53 — 56 ]. Apathy is, therefore, one of the clinical sequelae of disruption of the prefrontal cortex-basal ganglia axis, which is one of the functional systems involved in the origin and control of self-generated purposeful behavior.

Anatomical localization of regional dysfunction associated with apathy and depression appears to overlap considerably. Depression has been reported to be more frequent when focal lesions are anterior and left-sided [ 57 ].

Taking into consideration the facts that apathy is related to cognitive function and disruption of the prefrontal cortex-basal ganglia axis, apathy can be considered to resemble subcortical dementia and to be treatable using dopaminergic agents in central nervous system. A growing number of reports have documented the treatment of apathy with a variety of psychoactive agents. Various small studies have indicated that psychostimulants, dopaminergics, and cholinesterase inhibitors might be of benefit for this syndrome.

However, there is no current consensus about treatment for apathy, and information on pharmacotherapy for this condition mainly depends upon underlying etiology and background disease. For example, dopamine agonists appear to be promising for ameliorating apathy in patients with Parkinson's disease while atypical antipsychotics used in schizophrenia and cholinesterase inhibitors have been reported to be useful for treating apathy in Alzheimer's disease and other dementias.

Therefore, the treatment of apathy should be selected according to its etiology. Depressed patients with apathy should be given antidepressants, which may also alleviate other symptoms.

However, caution has been raised about using SSRIs for depressed elderly persons because it may worsen apathy [ 58 ]. Since frontal lobe dysfunction is considered to be one of the causes of apathy, patients with primary apathy may respond to psychostimulants such as methylphenidate or dextroamphetamine. There have also been reports about improvement of apathy and cognitive function after stroke by treatment with cilostazol [ 59 ].

As nonpharmacological methods, cranial electrotherapy stimulation for apathy after traumatic brain injury [ 60 ], and cognitive stimulation therapy for neuropsychiatric symptoms in Alzheimer's disease [ 61 ] might have some value, but evidence awaits future studies.

In some older men, low testosterone may also be a factor. Physical brain trauma — concussions and the like — can also have surprising long-term effects on mood that often take the form of dysthymia. At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, drug addiction, or alcoholism.

In these cases, it is difficult to distinguish the original cause, especially when there is a vicious cycle in which, say, depression exacerbates alcoholism or heart disease exacerbates depression. The same vicious cycle exists in many other situations. For a person who is vulnerable to depression, every problem seems more difficult to solve and every misfortune causes more suffering.

Depressed people give discouraging interpretations to every event in their lives, and these interpretations make them still more depressed. Depression often alienates others, and the resulting isolation and low social support make the symptoms worse. The experience of chronic depression may sensitize the brain to stress, heightening its vulnerability to further depression.

Most people with dysthymia are undertreated. They usually see only their family doctors, who often fail to diagnose the problem. They may only complain about physical symptoms, or fail to complain at all because the disorder has become so much a part of them that they believe that is simply how life is. In older people, dysthymia may be disguised as dementia, apathy, or irritability.

A physician might ask an open question like, "How are things at home? There are also several brief screening questionnaires, including the Hamilton Rating Scale for Depression and the Patient Health Questionnaire.

If the answers suggest dysthymia, a standard clinical interview can be used to confirm the diagnosis. Like major depression, dysthymia is treated with psychotherapy and medications — usually the same medications and the same kinds of psychotherapy.

The most common drug treatments are selective serotonin reuptake inhibitors like fluoxetine Prozac and sertraline Zoloft , or one of the dual action antidepressants such as venlafaxine Effexor. Some patients may do better with a tricyclic antidepressant like imipramine Tofranil. Supportive therapy provides advice, reassurance, sympathy, and education about the disorder.

Cognitive therapy identifies and corrects thought patterns that promote self-defeating attitudes. Behavioral treatment improves social skills and teaches ways to manage stress and unlearn learned helplessness.

Psychodynamic therapy helps patients resolve emotional conflicts, especially those derived from childhood experience. Interpersonal therapy helps patients cope with personal disputes, loss and separation, and transitions between social roles.

Depression and Bipolar Support Alliance toll free www. A review of controlled research found that medication is slightly superior to psychotherapy in the treatment of dysthymia. But a statistical difference among a large number of patients in many different situations is not necessarily a guide for any individual case. Some patients — especially older people — will not or cannot take drugs, sometimes because of side effects or drug interactions. For many others, a combination of long-term psychotherapy and medication may be most effective.

A solid relationship with a psychotherapist or other professional can be important in maintaining a willingness to continue medications. Recovery from dysthymia often takes a long time, and the symptoms often return. Another study found an average time to recurrence of nearly six years. After recovery, many patients find it helpful to continue doing whatever made them well — whether it was a drug or psychotherapy. While the search continues for better drugs and better forms of psychotherapy, the problem remains that, despite much improvement, most people with dysthymia are not receiving even the imperfect available treatments.

Even when they do see professionals, they may not fill their prescriptions or take their drugs consistently, and they may abandon psychotherapy too soon. And a survey commissioned by the National Depressive and Manic Depressive Association now the Depression and Bipolar Support Alliance found that doctors and patients often communicate poorly about the symptoms and treatment. Patients may stop taking drugs because they do not receive enough information about side effects or routine follow-up visits.

For both the public and professionals, what is most important may be recognizing that dysthymia is a treatable disorder, identifying it, and following through. Treatment for PDD typically consists of medication and psychotherapy. You may need to try different medications and dosages to find an effective solution for your specific situation. This requires patience, as many medications take several weeks to take full effect.

Talk with your doctor if you continue to have concerns about your medication. Your doctor may suggest changing dosage or medication. Never stop taking your medication as directed without speaking with your doctor first. Stopping treatment suddenly or missing several doses may cause withdrawal-like symptoms and make depressive symptoms worse.

A combination of medication and psychotherapy is the most effective method for treating PDD. Medical professionals will commonly suggest taking part in psychotherapy or cognitive-behavioral therapy CBT. Psychotherapy, which may be referred to as talk therapy, typically involves sessions with a mental health professional. These can happen either in person or remotely via phone or video calls. You may also participate in group sessions.

CBT focuses on your actions and behaviors in addition to your thoughts and emotions. In CBT, you will work to identify and deal with what is causing your depression. This will include talking with mental health professionals to help you accept your symptoms and establish safe coping habits for PDD.

This form of therapy can not only help you in the short term but may also reduce your risk of future relapses. Making certain lifestyle adjustments can complement medical treatments and help ease symptoms. However, identifying symptoms and seeking help is a crucial first step to improving the long-term outlook for people with PDD.

Research shows that a combination of psychotherapy and medication programs can be effective in treating PDD symptoms and preventing future relapses. Alongside these treatments, lifestyle changes, such as eating a healthful diet and exercising regularly, may also help you manage PDD and improve your long-term outlook.

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