In principle, personality is usually lifelong, while moods come and go. But dysthymia has to last longer than any other psychiatric disorder in the manual. That can make it difficult to distinguish from a personality disorder — especially the group that includes avoidant, dependent, and obsessive-compulsive personality, with their symptoms of timidity, excessive worry, helplessness, and social withdrawal.
Some would prefer to speak of a depressive personality disorder instead. That diagnosis was removed from the official manual in but has been re-introduced as a possible topic of investigation.
The proposed symptoms include a strong tendency to be critical of oneself and others, pessimism, guilt, brooding, and gloominess. Anhedonia and physical symptoms are not part of the definition, but this personality disorder otherwise has a great deal in common with dysthymia. Mood and personality are the emotional weather and emotional climate of individuals, so the symptoms of mood and personality disorders naturally overlap.
The thought schemas that cognitive therapists find at the roots of major depression and dysthymia — certain beliefs about the self, the world, and the future — are also the basis of depressive personality. Disturbances in mood can have effects on a person's emotional state and social life that resemble a personality disorder.
And people are more easily demoralized and recover more slowly from any stress or misfortune if they are pessimistic and self-critical by nature — or emotionally unstable, impulsive, and hypersensitive to loss. Like major depression, dysthymia has roots in genetic susceptibility, neurochemical imbalances, childhood and adult stress and trauma, and social circumstances, especially isolation and the unavailability of help.
Depression that begins as a mood fluctuation may deepen and persist when equilibrium cannot be restored because of poor internal regulation or external stress.
Dysthymia runs in families and probably has a hereditary component. There are few twin or adoption studies, so it's uncertain how much of this family connection is genetic. Nearly half of people with dysthymia have a symptom that also occurs in major depression, shortened REM latency — that is, they start rapid eye movement vivid dreaming sleep unusually early in the night.
The stress that provokes dysthymia, at least the early-onset form, is usually chronic rather than acute. Studies show that it usually has a gradual onset and does not follow distinct upsetting events. In old age, dysthymia is more likely to be the result of physical disability, medical illness, cognitive decline, or bereavement. 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.
In the ensuing weeks, the patient may notice they are getting better quality sleep. They may begin to feel more energized. Many patients notice they are more focused and can concentrate better. By the end of the treatment period, overall mood is improved as well. TMS is well tolerated, with few side effects reported. Some patients have reported mild headaches or scalp tenderness, but these effects tend to resolve on their own as treatments continue.
There are certain situations, such as patients with a pacemaker or other electrical implants, patients with stents in the neck or brain, shrapnel or bullet fragments in or near the head, and other conditions may not allow someone to be a candidate for TMS. Because dysthymia is a long-term disorder, CBT can be very helpful in changing entrenched negative thought patterns and focusing patients toward constructive behaviors or responses. Another benefit of TMS therapy for treating major depression or dysthymia is its effectiveness in also treating co-occurring anxiety disorder.
Since these two disorders frequently present together, patients who had sought TMS treatment for depression soon discovered that their anxiety symptoms were also better as a result. Anew Era TMS can provide a comprehensive treatment plan for dysthymia, including psychiatric, psychotherapy, and TMS therapy interventions.
To learn if you are a candidate for this promising alternative treatment for dysthymia, please contact Anew Era TMS today at We may request cookies to be set on your device. We use cookies to let us know when you visit our websites, how you interact with us, to enrich your user experience, and to customize your relationship with our website.
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. Apathy syndrome is associated with many diseases, but whether medications are applicable across this spectrum of background diseases remains unknown.
For example, would cholinesterase inhibitors that are used in patients with Alzheimer's disease be effective for apathy associated with major depression? These issues should be examined in future studies. National Center for Biotechnology Information , U. Journal List Depress Res Treat v. Experts say mushrooms contain a number of nutrients, including potassium and B vitamins, that can boost physical as well as mental health. Health Conditions Discover Plan Connect. Mental Health. Persistent Depressive Disorder Dysthymia.
Medically reviewed by Marc S. Symptoms of persistent depressive disorder. Causes of persistent depressive disorder. Risk factors for persistent depressive disorder. Diagnosing persistent depressive disorder. Treating persistent depressive disorder. Long-term outlook for people with persistent depressive disorder. Read this next. Somatic Symptom Disorder. Medically reviewed by Timothy J. Legg, Ph. Affective Disorders. Could It Be Bipolar Disorder? How to Help Someone with Depression Watching a friend live with depression can be painful, but there are ways to help.
What Is Anhedonia? Medically reviewed by Karin Gepp, PsyD.
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