What is the difference between dysphoria and dysthymia

Sign in. Thanks for reading Scientific American. Create your free account or Sign in to continue. See Subscription Options. Go Paperless with Digital. James Kocsis, a professor in the department of psychiatry at Cornell University, offers this definition: "Dysthymia has been in the official nomenclature of the American Psychiatric Association since Get smart.

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Health Conditions Discover Plan Connect. Mental Health. Differences Between Dysthymia and Depression. Overview Differences Symptoms Treatment Double depression Takeaway Dysthymia and depression can both result in feelings of deep sadness and hopelessness.

Double depression. The takeaway. Read this next. Types of Depression and How to Recognize Them. Medically reviewed by Karin Gepp, PsyD. 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. 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. Marin et al. 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. 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.

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 ]. Apathy syndrome is associated with many diseases, but whether medications are applicable across this spectrum of background diseases remains unknown. These issues should be examined in future studies.

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Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Academic Editor: Mathias Berger. Received 06 Dec Accepted 24 Apr Published 27 Jun Abstract Dysthymia is a depressive mood disorder characterized by chronic and persistent but mild depression.

Treatment for Dysthymia The best treatment for dysthymia appears to be a combination of psychotherapy and medication. Apathy Dysthymia is essentially defined by the existence of depressive symptoms at some level.

Presence, with lack of motivation, of at least one symptom belonging to each of the following three domains. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

The symptoms are not due to a diminished level of consciousness or the direct physiological effects of a substance e. Adapted from Starkstein [ 30 ]. Figure 1. Table 2. References M. Weissman, P. Leaf, M. Bruce, and L. View at: Google Scholar R. Kessler, K. McGonagle, S. Zhao et al. View at: Google Scholar J. Markowitz, M. Moran, J. Kocsis, and A. Broadhead, D. Blazer, L. George, and C. Brunello, H. Akiskal, P. Boyer et al. Kovacs, H. Akiskal, C.