**5. Poststroke depression in elderly**

Although there is a growing prevalence of stroke in patients aged 65 and younger, the majority of strokes affect patients that are elderly. With the prolonged life expectancy, there is an increased risk for stroke in the aging population, with 70% risk being after the age of 65 [29]. In patients older than 80 years old that suffer from strokes, there is a greater risk of fatality, prolonged hospitalization, complications, and increased postacute care needs [30]. In elderly patients that suffer from stroke, depression may be difficult to diagnose. This is largely due to the symptoms being a vegetative phenotype. It is also confounded because depression is the most common psychiatric disorder among the elderly—with 1% of the elderly population having a formal diagnosis of major depression, and 15% with depressive symptoms according to the National Institutes of Health Consensus development conference [31]. This poses a challenge that practitioners face in distinguishing between premorbid depression, inherent stroke symptoms and poststroke depression, given that many of the features overlap. Some such features include cognitive impairment, psychomotor retardation, and social withdrawal [29]. One measure used to assess poststroke depression in the elderly is the geriatric depression scale (GDS) [32]. This is a self-reported scale where patients answer yes and no questions to determine if a patient is experiencing some form of depression. A score greater than 6 indicates that the patient is likely experiencing some form of depression.

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*Post Stroke Depression*

*DOI: http://dx.doi.org/10.5772/intechopen.86935*

those with cognitive impairments caused by a stroke.

**5.1 Vascular dementia and poststroke depression**

had lesions in the basal ganglia and thalamus [31, 33].

rehabilitation in elderly stroke patients.

stroke and vascular depression [31].

This scale is highly sensitive and predictive of poststroke depression in the geriatric population [32]. However, the GDS cannot be used by aphasic stroke patients or

Alexopoulos and colleagues found that elderly stroke patients that suffered ischemic strokes demonstrated increased encephalomalacia and MRI hyperintensities that would predispose these patients to develop depression [33]. Their study suggested that these changes were not seen in elderly patients that had depression without vascular risk factors. Elderly patients that have been observed to have signs of depression, but do not have any vascular risk factors were found to have less white matter hyperintensities on MRI, which were similar to the nondepressed controls [31]. It has also been demonstrated that patients that suffered from depression without vascular insult had phenotypically different depression with features of more agitation, aggression, feelings of guilt and dysphoria. This is the theory of vascular depression in the elderly [33]. The hypothesis behind vascular depression states that chronic small vessel changes or non-symptomatic cerebrovascular events accumulate over time, resulting in the disruption of cortico-striato-pallido-thalamo-cortical (CSPTC) pathways [31]. Vascular dementia is described as a subcortical phenomenon. This type of depression differs from poststroke depression, in that they are silent, and the patient is not aware that they have suffered a stroke [31]. In a Japanese sample, greater than 80% of the patients that had major depression had MRI evidence of multiple silent infarcts [32]. Up to 75% of these depressed patients

Three pathways associated with CSPTC were proposed in the way that vascular depression can present phenotypically. Within the CSPTC are the orbitofrontal pathway, the cingulate pathway, and the dorsolateral pathway. Injury over time to the orbitofrontal pathway can result in irritability and disinhibition [31]. The cingulate pathway can cause apathy, and lack of initiative if injured, and lastly, injury to the dorsolateral pathway can result in poor speech productions, and inability to learn. These symptoms can all be seen in elderly depression. Prefrontal dysfunction has shown to have a poor or delayed response to antidepressants in elderly patients [31, 33]. However, early administration of antidepressants, particularly selective serotonin reuptake inhibitors have been shown to improve neuropsychological

Lacunar infarcts have been seen to result in more depression among Alzheimer patients especially basal ganglia strokes and cortical strokes were found to have more cognitive impairment [31]. Severe cognitive impairment was also seen to be one of the leading causes of depression in the elderly. There are some questions of whether cognitive impairment or dementia can increase the risk of stroke, and thus poststroke depression among the elderly, or do strokes result in cognitive decline and vascular depression [31]. Dementia and depression can be difficult to differentiate. In the elderly, pseudodementia can be secondary to depression however, the opposite is also true. This is a "what came first" type of scenario with dementia,

Although vascular depression and poststroke depression are different in the way they affect a patient, they likely lay on a continuum. Both are secondary to a vascular event, and both result in depression. Vascular depression has a higher incidence in elderly patients as they have an accumulation of more subcortical white matter changes that are seen as hyperintensities on MRI FLAIR. Poststroke depression is less subtle since the patient is usually aware that they have had a stroke [31, 33]. There may be a growing incidence of vascular depression among young patients,

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

**4.4 Psychosocial association with poststroke depression**

services like physical therapy or occupational therapy [11, 12].

Although there is a growing prevalence of stroke in patients aged 65 and younger, the majority of strokes affect patients that are elderly. With the prolonged life expectancy, there is an increased risk for stroke in the aging population, with 70% risk being after the age of 65 [29]. In patients older than 80 years old that suffer from strokes, there is a greater risk of fatality, prolonged hospitalization, complications, and increased postacute care needs [30]. In elderly patients that suffer from stroke, depression may be difficult to diagnose. This is largely due to the symptoms being a vegetative phenotype. It is also confounded because depression is the most common psychiatric disorder among the elderly—with 1% of the elderly population having a formal diagnosis of major depression, and 15% with depressive symptoms according to the National Institutes of Health Consensus development conference [31]. This poses a challenge that practitioners face in distinguishing between premorbid depression, inherent stroke symptoms and poststroke depression, given that many of the features overlap. Some such features include cognitive impairment, psychomotor retardation, and social withdrawal [29]. One measure used to assess poststroke depression in the elderly is the geriatric depression scale (GDS) [32]. This is a self-reported scale where patients answer yes and no questions to determine if a patient is experiencing some form of depression. A score greater than 6 indicates that the patient is likely experiencing some form of depression.

**5. Poststroke depression in elderly**

chromosome 17q11.1-17q12, which encodes the serotonin transporter [25–27]. In a meta-analysis of 7 studies, there was a significant relationship between 5-HTTLPR

Lastly, psychosocial factors must be considered when assessing who is at risk for poststroke depression. After suffering a life-altering event such as a stroke, even if there are no severe deficits, patients can undergo an adjustment period. They may feel depressed about the new diagnosis of a stroke. There is also the concern of getting back to their normal life routine such as working, caring for dependents, and caring for their own activities of daily living (ADLS) [11, 12]. Patients that do not have good social support tend to experience more depression after a stroke due to feeling helpless, and alone. Patients may also experience anxiety, related to the fear that another stroke may occur. Financial costs of health care also play a role in postacute stroke depression. If a patient is unable to work there may be a concern about medication compliance, affording medication, affording postacute special

polymorphism and the development of poststroke depression symptoms. 5-HTTLPR is an exon of the 5-HT transporter gene polymorphism [25, 26]. The hypothesis is that this gene polymorphism responds to the increased activity of the amygdala when responding to negative stimuli. An increase in 5-HTTLPR serum level has been positively associated with threefold increased risk of developing poststroke depression [25–28]. Another 5-HT polymorphism that has been analyzed is the STin2 VNTR, which is located within intron 2. It has variable number tandem repeats 9, 10, or 12. Repeats of the 9-allele have been well documented to be associated with multiple psychiatric disorders such as bipolar disorder, and major depression [25–28]. Repeats of the twelfth allele have been linked to the development of schizophrenia and bipolar affective disorder. It has been demonstrated that patients with variable tandem repeats of 9/12 and 12/12 were likely to have more depression

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after a stroke [25–28].

This scale is highly sensitive and predictive of poststroke depression in the geriatric population [32]. However, the GDS cannot be used by aphasic stroke patients or those with cognitive impairments caused by a stroke.
