Post-stroke depression (PSD) is considered the most frequent and important consequence of neuropsychiatry of stroke. About one-third of stroke sufferers are severely depressed. In addition, this condition can have adverse effects on cognitive function, functional recovery, and survival.
Diagnostic and Statistical Statistics Manual (DSM) IV categorizes post-stroke depression as "mood disorder due to common medical conditions" (ie stroke) with determinants of depressive features, depressive episodes-such as large, bead features, or mixed features. Utilizing patient data from acute hospital admissions, previous community surveys or patient clinics, previous studies have identified two types of depressive disorders associated with cerebral ischemia: severe depression, occurring in 25% of patients; and mild depression, which has been defined for research purposes by DSM-IV criteria as depressed mood or loss of interest and at least two but fewer than four symptoms of major depression. Mild depression occurs in up to 30% of patients after a stroke.
Prevalence clearly varies over time with clear peaks 3-6 months after stroke and subsequent declines in prevalence in one year account for about 50% of baseline. Robinson and colleagues marked a natural course of severe depression after a stroke with spontaneous remission usually 1 to 2 years after a stroke. However, it is also noted that in some cases the depression becomes chronic and can last more than 3 years after a stroke. On the other hand, mild depression appears to be more variable, both with short-term and long-term depression occurring in these patients.
Post-stroke depression is very common among post-stroke men and women; however, it seems that post-stroke depression is more common in women when prevalence is compared between sexes.
Women are two times more likely to experience post-stroke depression than men. This was hypothesized, based on CT scans, that of the two sexes who experienced post-stroke depression, women who experienced post-stroke depression had higher rates of left hemisphere lesions than men. However, the risk of post-stroke depression can not be determined effectively based on the location of lesions in the brain and more research in this area is required.
It has also been postulated that the risk of developing post-stroke depression in male patients is partly related to having high levels of disability and disability in function, especially in conducting daily life activities (ADL's), as a result of their stroke; the larger the limit, the greater the severity. The risk of developing post-stroke depression in women is partly related to a history of psychological disorders as well as limitations that involve cognition as a result of their stroke.
The scientific community is divided into two "camps" that support opposing views: some propose a primary biological mechanism with strokes affecting the neural circuitry involved in mood regulation which in turn leads to post-stroke depression, while other researchers claim that post-stroke depression is caused by social and psychological pressure arising from a stroke.
While integrated bio-psycho-social models including the biological and psychosocial aspects of post-stroke depression seem to be needed, a number of studies clearly show that biological mechanisms play a major role in the development of post-stroke depression.
- stroke patients showed higher rates of depression compared with orthopedic patients with comparable severity.
- Several studies suggest linkages with specific lesions (lesions and lesions of the left anterior and left basal ganglia close to the frontal pole) and the occurrence of post-stroke depression.
- Several studies have reported an association between post-stroke mania and right orbital frontal lesions, basotemporal, basal ganglia.
- It has been shown that patients with anosognosia who are unaware of their disability still experience post-stroke depression.
Despite this evidence, the post-stroke depression relationship with certain brain lesions is still blurred and requires replication from various independent groups. Furthermore, the cause of post-stroke depression at the functional level is unclear.
The only biological model proposed by Robinson and co-workers: They hypothesize that the depletion of monoaminergic amines that occur after stroke play a role in post-stroke-depression. They show that the norepinephrinergic and serotonergic nuclei send the projection into the frontal cortex and curve posteriorly, traveling through the deep cortical layer, where they centralize and send the projection of the terminal to a shallow cortical layer. This norepinephrinergic and serotoninergic pathway is impaired in basal ganglia and frontal lobe lesions - sites that have been shown to be associated with post-stroke depression.
However, this model is far from universally accepted and there are serious objections both to their models and findings which show the relationship between post-stroke depression and site lesions.
Behavior such as depression is shown in the cortical intracerebral hemorrhage rat model.
Video Post-stroke depression
References
- Gainotti G.Mcmarra C: Determinants and consequences of post-stroke depression. Curr Opin Neurol 2002; 15: 85-89
- American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders - DSM-IV. Washington DC: Am Psychiat. Press 1994
- Robinson RG, Starr LB, Kubos KL, Price TR: A two-year longitudinal study of post-stroke mood disorders: findings during the initial evaluation. Stroke 1983; 14: 736-44
- Gainotti G, Azzoni A, Marra C: Frequency, phenomenology and anatomical-clinical correlates with major post-stroke depression. Br J Psychiatry 1999; 175: 163-167 Robinson RG, Starksein SE: Recent research in affective disorder after stroke. A Neuropsyhiatrical Clin Neurosci 1990; 2: 1-14
- Robinson RG, Starksein SE: Recent research on affective disorders after a stroke. A Neuropsyhiatrical Clin Neurosci 1990; 2: 1-14
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