Post-stroke depression: an update | Neurología (English Edition)

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However, studies have recently demonstrated that there are other aspects such as cognition, behaviour, and emotion that greatly affect the impact that stroke will have on a patient's life.Within the emotional-cognitive sphere, depression will be a determining factor for these patients. We currently know that depression is the most frequent neuropsychological complication of stroke.<a class="elsevierStyleCrossRefs" href="#bib0005">1,2</a> Nevertheless, in addition to post-stroke depression (PSD), many other neuropsychological symptoms may be present after stroke: anxiety, irritability, agitation, and emotional incontinence; changes in emotional experience; sleep disturbances; behavioural disorders such as disinhibition; apathy and fatigue; and psychotic symptoms such as delusions and hallucinations.<a class="elsevierStyleCrossRefs" href="#bib0005">1–3</a>We also know that PSD is the main predictor of poor functional outcome after stroke. Presence of PSD is associated with poorer functional and cognitive recovery, increased limitations on daily life activities, and social and interpersonal activities, poorer quality of life, and higher mortality rates (up to 10 times higher than in patients without PSD).<a class="elsevierStyleCrossRefs" href="#bib0015">3,4</a>Furthermore, we know that there are many risk factors for developing PSD, including more severe motor deficit, a higher degree of disability, and a poorer social support network. Identifying these factors permits early application of prevention and treatment strategies.<a class="elsevierStyleCrossRef" href="#bib0005">1</a>However, although prevalence of PSD is high, it is generally underdiagnosed and usually undertreated, as we will discuss in a later section.PSD is a frequent complication with severe negative repercussions for both patients and their carers, and yet it is clearly predictable and treatable. Therefore, it is essential to understand the risk factors for PSD and identify it in patients as soon as possible.Prevalence of PSDEstimating the real prevalence of PSD is not an easy task due to the methodological differences between the studies that have been conducted.<a class="elsevierStyleCrossRefs" href="#bib0005">1,2</a> First, the diagnostic criteria for depression are not the same in all studies, although it must be said that most of them conducted structured interviews and followed the criteria from the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV).Second, the scales applied to assess the results also vary from one study to the other. Some use PSD-specific scales whereas some other studies use general scales, such as the Hamilton Rating Scale for Depression (Ham-D); furthermore, some studies use self-evaluation scales and others do not.Third, inclusion criteria vary considerably. In fact, some studies excluded patients that other studies included (for example, patients with aphasia or dementia), and inclusion criteria also differed with regard to the target populations, age groups, or phases of the disease (acute- vs chronic-phase stroke).Lastly, it has been demonstrated that prevalence rates of PSD depend on the setting where patients are examined.<a class="elsevierStyleCrossRef" href="#bib0025">5</a>In general, prevalence rates of PSD range from 25% to 79% depending on the patient selection criteria used by each of the different studies.<a class="elsevierStyleCrossRefs" href="#bib0025">5,6</a>Community-dwelling patients have the lowest prevalence rates; in this setting, 14% of patients present major depression, and 9%, minor depression. In hospital settings, including acute-care patients and those in rehabilitation, prevalence rates of major and minor depression were 21.6% and 20.0%, respectively. Among patients discharged from hospital, prevalence rates of major and minor depression were 24.0% and 23.9% at times ranging from 3 months to 3 years after stroke. Other studies show similar rates, although the percentage of patients reporting major depression is lower than that diagnosed with minor depression.<a class="elsevierStyleCrossRef" href="#bib0035">7</a>White et al.<a class="elsevierStyleCrossRef" href="#bib0040">8</a> recently published data from patients with lacunar stroke only, extracted from a larger study, Secondary Prevention of Small Subcortical Strokes (SPS3). They examined the prevalence of depression, its correlation to other factors, and the course of depression over time in a cohort of 2477 patients with a history of lacunar stroke. Prevalence of depression at 4 months after stroke was 19%. Older age, male sex, and absence of cognitive impairment were the factors associated with a lower risk of depression. On the contrary, functional disability, living with a spouse or family, and presenting risk factors for stroke were associated with a high risk of depression. The study stated that likelihood of depression decreased with age at a rate of 1.12 times lower per year (95% CI: 1.06-1.17).<a class="elsevierStyleCrossRef" href="#bib0040">8</a>However, the impact of certain factors on PSD prevalence is a controversial topic. Some studies have found a higher prevalence of PSD in patients with cognitive impairment, while others have not.<a class="elsevierStyleCrossRef" href="#bib0005">1</a> Similarly, and contrary to the results from the SPS3 study, many authors claim that older age constitutes a risk factor for PSD, resulting in increased prevalence in elderly patients.<a class="elsevierStyleCrossRefs" href="#bib0025">5,6</a>Diagnosis of PSDDiagnosis of PSD is complex due to the frequent presence of other symptoms, especially those associated with cognitive impairment, such as aphasia, agnosia, apraxia, and changes in memory.<a class="elsevierStyleCrossRef" href="#bib0005">1</a> Additionally, some symptoms of stroke or of depression may overlap and be indistinguishable from each other. Symptoms common to both entities include sleep disorders, difficulty concentrating, and loss of appetite. These similarities may lead to overestimating depression in stroke patients.<a class="elsevierStyleCrossRef" href="#bib0045">9</a> On other occasions, many symptoms are not identified as the result of depression. In these cases, they are mistaken for consequences of stroke or old age (in elderly patients), which may lead to an underestimation of the diagnosis.<a class="elsevierStyleCrossRefs" href="#bib0010">2,10</a>Due to these diagnostic difficulties, between 50% and 80% of all PSD cases are not identified by doctors who are not psychiatrists.<a class="elsevierStyleCrossRefs" href="#bib0030">6,9</a>Some studies have compared several diagnostic tools in order to determine the most appropriate one. Some authors state that the Geriatric Depression Scale (GDS) is a better diagnostic tool than other scales, such as the Hospital Anxiety and Depression Scale (HADS).<a class="elsevierStyleCrossRef" href="#bib0055">11</a> GDS is especially indicated for patients with a high level of functional ability and mild cognitive impairment.<a class="elsevierStyleCrossRef" href="#bib0060">12</a>Quaranta et al.<a class="elsevierStyleCrossRef" href="#bib0065">13</a> evaluated the diagnostic accuracy of the Poststroke Depression Rating Scale (PSDRS), a tool specifically designed for diagnosing PSD. They then compared the results with those of Ham-D. Both scales were reliable diagnostic tools, and they both showed good sensitivity and specificity. Cognitive impairment had a considerable effect on Ham-D, whereas PSDRS was influenced by the patient's age. Healey et al.<a class="elsevierStyleCrossRef" href="#bib0070">14</a> compared 3 depression scales: the Beck Depression Inventory-Fast Screen (BDI-FS), Brief Assessment Schedule Depression Cards (BASDEC), and HADS. BASDEC demonstrated the greatest validity and precision. Similarly, Berg et al.<a class="elsevierStyleCrossRef" href="#bib0075">15</a> compared different screening tools and concluded that the Ham-D, BDI-FS, and Clinical Global Impression (CGI) assessments carried out by professionals were useful for evaluating depression alongside DSM diagnostic criteria (DSM-III-R or other versions). They found no significant differences between these scales. In addition, these authors do not recommend using the Visual Analogue Mood Scale (VAMS) in patients with aphasia or other cognitive dysfunctions.Other authors<a class="elsevierStyleCrossRef" href="#bib0080">16</a> have demonstrated that PSD can be successfully diagnosed by using structured or semi-structured neuropsychiatric interviews following current DSM criteria. They concluded that no specific diagnostic instruments were necessary. PSD is generally diagnosed according to DSM guidelines, sometimes differentiating major from minor depression.However, a study<a class="elsevierStyleCrossRef" href="#bib0085">17</a> published in Stroke in 2012 investigated the diagnostic value of the 9-item and 2-item Patient Health Questionnaire (PHQ-9 and PHQ-2) and compared it with other scales (HADS, BDI-II, Distress Thermometer, and Kessler-10) in acute stroke patients with preserved ability to communicate. PHQ-9 includes all 9 symptoms of depression established by the DSM, whereas PHQ-2 only includes 2: anhedonia and depressed mood. The study showed a good diagnostic value for PHQ-9 scores ≥10 and for PHQ-2 scores ≥2. This group also recommends using PHQ-2 in all patients, and PHQ-9 only in those with a positive result on the PHQ-2 because this approach demonstrates the greatest sensitivity. The authors suggest these 2 screening tools for stroke patients since they are brief and easy to use, their only limitation being that they cannot be used in patients with significant cognitive and verbal impairment (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>).<elsevierMultimedia ident="tbl0005"></elsevierMultimedia>DSM IV-TR<a class="elsevierStyleCrossRef" href="#bib0090">18</a> categorises PSD as a mood disorder resulting from a general medical condition (stroke in this case). It can be classified into subtypes according to the following specifiers: depressive features, major depressive-like episode, and mixed features (manic features, depression). According to this classification, depression must be a direct physiological consequence of stroke.Therefore, we normally use the term PSD to refer to major depressive-like episodes that follow stroke. Diagnosis of PSD requires evidence from the patient's medical history, and findings from the clinical examination and complementary tests, confirming that depression is a direct physiological consequence of stroke.According to DSM-IV-TR diagnostic criteria, 5 or more symptoms must be present during at least 2 weeks for major depression to be diagnosed.Pathophysiological mechanisms of PSDThe pathophysiological mechanisms of PSD are not yet fully understood. Biological, behavioural, and social factors are thought to be involved, and PSD is therefore a multifactorial process.Biological factors can be divided into several different types: stroke location, stroke type, neurobiological pathways involved, mechanisms of inflammation and apoptosis, and genetic factors.Stroke location and PSDThe first studies on the origin of PSD focused on the connection between cerebrovascular lesion location and development of PSD. Robinson et al.,<a class="elsevierStyleCrossRef" href="#bib0095">19</a> for example, were the first to suggest a connection between PSD and a lesion in the left hemisphere. According to these authors, the lesions supposedly responsible for PSD were located in the left frontal and dorsolateral cortical regions and in the left basal ganglia. Many other studies have later corroborated this association.<a class="elsevierStyleCrossRefs" href="#bib0030">6,20</a> Other researchers<a class="elsevierStyleCrossRef" href="#bib0105">21</a> found that lesions located in the left lateral frontal lobe, caudate nucleus, and putamen were significantly more likely to cause depression after acute stroke than similar lesions located in the right hemisphere. However, several other studies did not confirm this connection. A meta-analysis performed by Carson et al.<a class="elsevierStyleCrossRef" href="#bib0110">22</a> could not support the connection between the stroke location or laterality, and risk of developing PSD. Another study<a class="elsevierStyleCrossRef" href="#bib0115">23</a> showed that frontal or basal ganglia lesion location was a risk factor for PSD, but it found no correlation between laterality and depression. Likewise, a subsequent review of the methodological limitations of the studies addressing lesion location and PSD observed that the link between risk of developing PSD and frontal/basal ganglia lesions depended on the study population; studies in hospital inpatients showed a stronger association than those in community-dwelling patients.<a class="elsevierStyleCrossRef" href="#bib0120">24</a> In another study, Nishiyama et al.<a class="elsevierStyleCrossRef" href="#bib0125">25</a> found that presence of lesions in the left lenticulocapsular area, as well as hypertension and education level, was an independent predictor of symptoms of depression after stroke.Therefore, and given that results from different studies are contradictory, mainly because of methodological biases, we can conclude that the evidence is insufficient to support a correlation between lesion laterality and risk of developing PSD.Another structure that has been investigated extensively in connection with PSD is the amygdala. It is well-known today that the amygdala is involved in the regulation of mood and emotions. In the Sydney Stroke Study, Sachdev et al.<a class="elsevierStyleCrossRef" href="#bib0130">26</a> showed that amygdala was smaller in patients who had suffered a stroke or a transient ischaemic attack (TIA), and especially in patients with cognitive impairment.Stroke type and PSDThe vascular depression hypothesis proposes that ischaemic vascular lesions (acute, chronic, silent infarctions, leukoaraiosis, etc.) can damage mood and emotion regulation and provoke late-onset depression. Based on that hypothesis, some authors suggest that PSD may lead to cognitive dysfunction of vascular origin which may in turn cause new depressive symptoms, therefore establishing a reciprocal connection between depression and cerebrovascular disease.<a class="elsevierStyleCrossRef" href="#bib0135">27</a>In the present study we aim to explain the impact of different types of stroke on the development of PSD. Firstly, white matter lesions caused by leukoaraiosis or small lacunar strokes seem to play a role in PSD pathogenesis. White matter hyperintensities have been associated with depression and executive dysfunction.<a class="elsevierStyleCrossRef" href="#bib0140">28</a> Silent infarctions and white matter hyperintensities are frequently found in elderly patients with depression. Studies have proved that vascular risk factors and cerebrovascular lesions affect the course of depression, especially in older patients. This suggests that lesions affect not only medium- and large-calibre blood vessels, but also small-calibre vessels.<a class="elsevierStyleCrossRef" href="#bib0145">29</a> In fact, Chen et al.<a class="elsevierStyleCrossRef" href="#bib0150">30</a> studied PSD in patients with small subcortical strokes by comparing the 2 possible aetiologies: small vessel disease, and intracranial and extracranial large artery disease. The authors found that PSD was more frequent among patients with small subcortical strokes derived from lesions in large-calibre vessels. This suggests that cerebral perfusion plays a major role in the development of PSD.Santos et al.<a class="elsevierStyleCrossRef" href="#bib0155">31</a> analysed 41 autopsies of patients who had presented initial onset of depression within the first 2 years after stroke. Researchers found no connection between macroinfarct location and development of PSD for any of the locations included in the study. Lacunar strokes within the thalamus and basal ganglia were associated with a higher risk of PSD. However, microinfarcts and periventricular and diffuse demyelination did not occur more frequently in PSD patients. They concluded that the damage resulting from chronic accumulation of lacunar strokes in the thalamus, basal ganglia, and deep white matter may be a more important predictor of PSD than the localisation of a single infarct.In a more recent study, Tang et al.<a class="elsevierStyleCrossRef" href="#bib0160">32</a> examined the association between PSD (defined as a GDS score ≥7) and presence of cerebral microhaemorrhages (evaluated with MRI) in 235 patients at 3 months after stroke. The researchers observed that patients with PSD were more likely to present lobar microhaemorrhages than patients without PSD. Lobar microhaemorrhage was therefore considered an independent predictor of PSD.Neurobiological pathways and PSDThe connection between PSD and lesions in different cerebral pathways has also been studied. We now know that frontal-subcortical lesions of the monoaminergic pathways reduce biogenic amine release and result in increased likelihood of depression.<a class="elsevierStyleCrossRef" href="#bib0165">33</a>Another plausible mechanism would involve changes in glutamatergic transmission after stroke. In fact, a study<a class="elsevierStyleCrossRef" href="#bib0170">34</a> found changes in frontal lobe glutamate/glutamine levels in PSD patients assessed by magnetic resonance spectroscopy.On the other hand, hypothalamo-pituitary adrenal axis dysregulation has been observed in 40% of all stroke patients, and adrenocortical hyperactivity appears almost immediately after stroke onset. Additionally, the resulting persisting hypercortisolaemia has been associated with the development of depression, poorer prognosis, and increased mortality rate.<a class="elsevierStyleCrossRef" href="#bib0175">35</a>Inflammation and PSDInflammatory processes seem to be involved in PSD pathogenesis. Cerebral ischaemia has been shown to cause increased production of proinflammatory cytokines, such as interleukin-1β (IL-1β), tumour necrosis factor α (TNF-α), or interleukin-18 (IL-18). In turn, these cytokines may cause decreased serotonin production in certain brain areas, thereby favouring depression.<a class="elsevierStyleCrossRef" href="#bib0180">36</a> More specifically, changes in IL-18 serum levels seem to be linked to depression severity.<a class="elsevierStyleCrossRef" href="#bib0185">37</a>A recent review by Pascoe et al.<a class="elsevierStyleCrossRef" href="#bib0190">38</a> on inflammatory processes in stroke patients confirms that depression and ischaemia are related to inflammation. Both conditions are associated with increased circulating levels of proinflammatory cytokines. Since cytokines play a mediating role in ischaemia-related cell death and limbic region apoptosis is associated with depression, the authors concluded that ischaemic inflammation is likely to contribute to development of PSD.<a class="elsevierStyleCrossRef" href="#bib0190">38</a> Another study<a class="elsevierStyleCrossRef" href="#bib0195">39</a> found increased levels of cytokines IL-6, IL-10, TNF-α, and interferon-γ (IFN-γ), and elevated ratios of IL-6/IL-10 and TNF-α/IL-10, in patients with PSD compared to stroke patients without depression.However, some authors did not observe a clear association between the increase in inflammatory markers and the development of PSD.<a class="elsevierStyleCrossRef" href="#bib0200">40</a>In any case, other studies provide interesting information about the anti-inflammatory effects of antidepressants.<a class="elsevierStyleCrossRefs" href="#bib0205">41,42</a> These drugs can reduce depressive symptoms by acting on the inflammatory markers involved in mood regulation. More specifically, animal models have shown that antidepressants reduce the levels of pro-inflammatory interleukins IL-1 and IL-2, while increasing the level of anti-inflammatory interleukin IL-10. Additionally, they inhibit the expression of IL-6, TNF-α, and IFN-γ.Genetic factors and PSDGenetic variability seems to be involved in PSD. For example, patients with the s/s polymorphism of the serotonin transporter-linked gene region 5-HTTLPR are 3.1 times more likely to present PSD than those with the l/l or l/χl variant. Additionally, patients with the 9/12 or 12/12 variants of the serotonin transporter locus STin2 were 4.1 times more likely to develop depression than patients with the STin2 10/10 genotype.<a class="elsevierStyleCrossRef" href="#bib0215">43</a> A more recent study<a class="elsevierStyleCrossRef" href="#bib0220">44</a> found a connection between the s/s variant of the 5-HTT gene-linked promoter region and post-stroke emotional incontinence. Yet another study<a class="elsevierStyleCrossRef" href="#bib0225">45</a> stated that s/s homozygosity for serotonin transporter gene SLC6A4 may be involved in development of PSD.Based on the above, it seems that certain genetic features determine the degree of vulnerability to depression.Symptoms of PSDAlthough PSD can occur shortly after a cerebrovascular event, it usually develops within the first few months following a stroke.<a class="elsevierStyleCrossRefs" href="#bib0005">1,2</a> In a study of 100 stroke patients, 46% of those with depressive symptoms at 2 months after stroke also presented depressive symptoms at 12 months, whereas only 12% presented the first symptoms 12 months after stroke.<a class="elsevierStyleCrossRef" href="#bib0230">46</a> The term ‘early-onset PSD’ has been proposed to refer to PSD occurring within the first 3 months after stroke, while ‘late-onset PSD’ refers to PSD developing after 3 months.<a class="elsevierStyleCrossRef" href="#bib0005">1</a> In early-onset PSD, somatic depressive symptoms tend to be more numerous than psychological symptoms.<a class="elsevierStyleCrossRef" href="#bib0135">27</a>Although depressive symptoms are usually similar, some differences have been found between PSD patients and patients with depression but no associated neurological disease. PSD patients, especially those with right-hemisphere damage, are less likely to present dysphoric depression and more likely to present vegetative signs and symptoms than patients with other types of late-onset PSD.<a class="elsevierStyleCrossRefs" href="#bib0025">5,47</a> Greater social withdrawal and fewer agitation symptoms have been reported in elderly stroke patients with depression compared to depressive patients with other conditions.<a class="elsevierStyleCrossRefs" href="#bib0025">5,48</a> A subsequent study<a class="elsevierStyleCrossRef" href="#bib0245">49</a> found that PSD patients presented ‘inability to feel’ and ‘disturbed sleep’ more frequently than depressed patients with no prior history of stroke.It is therefore important to perform differential diagnosis to rule out other cognitive-behavioural syndromes presenting with mood and emotional changes after stroke, since their symptoms may be similar to those of PSD.<a class="elsevierStyleCrossRef" href="#bib0135">27</a> Those syndromes include emotional lability, athymhormic syndrome, aboulia and apathy, affective aprosody, and frontal dysexecutive syndromes. Other disorders that may appear in the absence of PSD include certain autonomic disorders, changes in sleep patterns after stroke, and vegetative symptoms such as post-stroke anxiety and subjective fatigue. Gusev and Bogolepova<a class="elsevierStyleCrossRef" href="#bib0250">50</a> state that some 2% to 3% of first-time stroke patients may present masked depression, that is, presence of depressive symptoms but absence of depressive mood. The main manifestations of this type of depression are biological rhythm disturbances and somatisation disorders, especially vegetative-vascular dystonia, vertigo, and various algic phenomena. These symptoms, which are common to stroke and depression, may lead to overestimating depression in stroke patients.<a class="elsevierStyleCrossRef" href="#bib0045">9</a> However, underestimation of PSD is even more frequent, since depressive symptoms are rarely identified despite the high incidence and prevalence of PSD.<a class="elsevierStyleCrossRef" href="#bib0255">51</a>Treatment of PSDSeveral anti-depressants have proved to cause an improvement in cognitive skills and functional recovery in PSD patients. Selective serotonin reuptake inhibitors (SSRI) and tricyclic antidepressants (TAD) are the most extensively studied drug treatments.The first study on PSD treatment, performed by Lipsey et al.,<a class="elsevierStyleCrossRef" href="#bib0260">52</a> was a placebo-controlled study that found improvement in Ham-D scores in 11 patients treated with nortriptyline (25-100mg/d) for 6 weeks.The first study using SSRIs<a class="elsevierStyleCrossRef" href="#bib0265">53</a> found that patients receiving citalopram showed more symptomatic improvement (with lower scores on Ham-D at 3 and 6 weeks) than those on fluoxetine. However, 2 double-blind placebo-controlled trials found both citalopram and fluoxetine to be effective for PSD treatment after assessing 66 and 31 patients respectively over 6 weeks.<a class="elsevierStyleCrossRefs" href="#bib0270">54,55</a> Another placebo-controlled trial<a class="elsevierStyleCrossRef" href="#bib0280">56</a> compared nortriptyline to fluoxetine in 104 patients over 12 weeks. Nortriptyline proved to be more effective than fluoxetine and placebo since it caused a more marked decrease in Ham-D scores. The study by Jorge et al.<a class="elsevierStyleCrossRef" href="#bib0285">57</a> found that patients treated with either fluoxetine or nortriptyline presented significantly lower mortality rates than placebo-treated patients.Rampello et al.<a class="elsevierStyleCrossRef" href="#bib0290">58</a> found that patients on reboxetine experienced a more pronounced decrease in Ham-D scores than those treated with placebo.More recent studies have focused on the effectiveness of SSRIs. Ried et al.<a class="elsevierStyleCrossRef" href="#bib0295">59</a> conducted a retrospective study on mortality and found that SSRI treatment, administered either before or after stroke, was associated with a significantly lower risk of mortality during the first year after stroke (HR=0.31; 95% CI: 0.11-0.86). However, mortality rates increased after 7 years. The authors concluded that SSRI treatment was associated with better survival rates, and they therefore recommend starting or resuming SSRI treatment after stroke, especially in patients with prior history of depression or those treated with SSRIs before stroke. Another study<a class="elsevierStyleCrossRef" href="#bib0300">60</a> found that discontinuing escitalopram treatment can increase occurrence of post-stroke depressive symptoms over the first 6 months after treatment withdrawal, compared to placebo and problem-solving therapy (PST). Jorge et al.<a class="elsevierStyleCrossRef" href="#bib0305">61</a> conducted a double-blind placebo-controlled trial in 129 patients evaluated using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). The authors found that patients receiving escitalopram after stroke showed improvement in the higher cognitive functions, specifically in verbal and visual memory functions, compared to patients receiving placebo or PST. The beneficial effect of escitalopram was independent of its effect on depressive symptoms. Similarly, it has been proven that fluoxetine improves quality of life in patients with emotional disorders, including PSD, after stroke.<a class="elsevierStyleCrossRef" href="#bib0310">62</a> In a recent controlled trial, Cramer<a class="elsevierStyleCrossRef" href="#bib0315">63</a> assessed the effect of fluoxetine in patients at 5 to 10 days after stroke using the Fugl-Meyer Assessment of Motor Recovery after Stroke (FMA) and found improved motor function at 90 days after stroke. These patients also showed a lower level of disability according to modified Rankin Scale scores.The efficacy of drugs other than antidepressants has also been investigated. For example, certain stimulants, such as amphetamines and methylphenidate, have been studied in patients with severe depression and rapid cognitive decline, with contradictory results.<a class="elsevierStyleCrossRef" href="#bib0320">64</a> In another study, PSD patients treated with the calcium agonist nimodipine showed improvement of depressive symptoms and a lower risk of recurrence.<a class="elsevierStyleCrossRef" href="#bib0325">65</a>Finally, although pharmacological treatment with SSRIs is recommended for PSD, there are no studies providing conclusive data on the superiority of a specific drug.<a class="elsevierStyleCrossRef" href="#bib0135">27</a> Nevertheless, SSRIs are safer, provoke fewer adverse effects, are relatively quick-acting with a latency period ranging from 7 to 10 days, and they also exert an anxiolytic effect. For this reason, they are considered first-line antidepressants, especially in stroke patients, who are usually elderly with underlying cardiovascular problems, and on polytherapy, which can lead to drug interactions (<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>).<elsevierMultimedia ident="tbl0010"></elsevierMultimedia>In any case, many questions about PSD treatment remain unanswered, such as the best moment for initiating treatment, the effect of antidepressants in areas other than emotion (for example, cognition and motor function), and the importance of antidepressants for reducing mortality in stroke patients.ConclusionStroke has traditionally been considered a disease affecting motor function. Therefore, approaches to hospital care, rehabilitation, and follow-up have focused on this aspect almost exclusively. However, we currently know that PSD is a common problem in daily clinical practice since it is present in 1 out of every 3 stroke patients. Additionally, PSD is the main factor limiting patient recovery and rehabilitation, and increasing morbidity and mortality rates. Strangely enough, more than half of the cases are neither diagnosed nor treated. In this scenario, neurologists play a major role in caring for and managing recovery in stroke patients, and they must therefore be familiar with early detection and treatment of PSD. This way, neurologists will be able to facilitate patients’ functional recovery and social integration, and improve quality of life in patients and their families.Conflicts of interestThe authors have no conflicts of interest to declare." "textoCompletoSecciones" => array:1 [ "secciones" => array:18 [ 0 => array:3 [ "identificador" => "xres848373" "titulo" => "Abstract" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0005" "titulo" => "Introduction" ] 1 => array:2 [ "identificador" => "abst0010" "titulo" => "Development" ] 2 => array:2 [ "identificador" => "abst0015" "titulo" => "Conclusions" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec843480" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres848374" "titulo" => "Resumen" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0020" "titulo" => "Introducción" ] 1 => array:2 [ "identificador" => "abst0025" "titulo" => "Desarrollo" ] 2 => array:2 [ "identificador" => "abst0030" "titulo" => "Conclusiones" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec843479" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Prevalence of PSD" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Diagnosis of PSD" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Pathophysiological mechanisms of PSD" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Stroke location and PSD" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Stroke type and PSD" ] 10 => array:2 [ "identificador" => "sec0035" "titulo" => "Neurobiological pathways and PSD" ] 11 => array:2 [ "identificador" => "sec0040" "titulo" => "Inflammation and PSD" ] 12 => array:2 [ "identificador" => "sec0045" "titulo" => "Genetic factors and PSD" ] 13 => array:2 [ "identificador" => "sec0050" "titulo" => "Symptoms of PSD" ] 14 => array:2 [ "identificador" => "sec0055" "titulo" => "Treatment of PSD" ] 15 => array:2 [ "identificador" => "sec0060" "titulo" => "Conclusion" ] 16 => array:2 [ "identificador" => "sec0065" "titulo" => "Conflicts of interest" ] 17 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2012-04-14" "fechaAceptado" => "2012-06-27" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec843480" "palabras" => array:5 [ 0 => "Antidepressants" 1 => "Post-stroke depression" 2 => "Cerebrovascular disease" 3 => "Stroke" 4 => "Selective serotonin reuptake inhibitors" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec843479" "palabras" => array:5 [ 0 => "Antidepresivos" 1 => "Depresión post ictus" 2 => "Enfermedad cerebrovascular" 3 => "Ictus" 4 => "Inhibidores selectivos de la recaptación de serotonina" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:3 [ "titulo" => "Abstract" "resumen" => "IntroductionPost-stroke depression (PSD) is the most common mood disorder following a stroke, and also the main factor limiting recovery and rehabilitation in stroke patients. In addition, it may increase mortality by up to ten times. DevelopmentPSD occurs in 1 in 3 stroke patients and more than half of all cases are neither diagnosed nor treated. Several mechanisms, including biological, behavioural, and social factors, are involved in its pathogenesis. Symptoms usually occur within the first three months after stroke (early onset PSD), and less frequently at a later time (late onset PSD). Symptoms resemble those of other types of depression, although there are some differences; PSD patients experience more sleep disturbances, vegetative symptoms, and social withdrawal. For PSD diagnosis, we recommended vigilance and use of specific diagnostic tools such as the Patient Health Questionnaire-2 (PHQ-2). The treatments of choice are selective serotonin reuptake inhibitors (SSRI). However, there are still many unanswered questions in the treatment of PSD, such as the best time to start treatment or the effects of antidepressants on cognition and motor function, among others. ConclusionsNeurologists play a pivotal role in the care and management of patients recovering from stroke. They must be familiar with methods for early detection and treatment of PSD, as this can facilitate a patient's functional recovery and social reintegration, and improve quality of life for patients and their families." "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0005" "titulo" => "Introduction" ] 1 => array:2 [ "identificador" => "abst0010" "titulo" => "Development" ] 2 => array:2 [ "identificador" => "abst0015" "titulo" => "Conclusions" ] ] ] "es" => array:3 [ "titulo" => "Resumen" "resumen" => "IntroducciónLa depresión post ictus (DPI) es el trastorno afectivo más frecuente tras un ictus y el principal factor que limita la recuperación y rehabilitación de los pacientes, además de poder incrementar su mortalidad hasta 10 veces. DesarrolloLa DPI se presenta en uno de cada 3 pacientes con ictus y en más de la mitad de los casos no se diagnostica ni se trata. En su etiopatogenia son varios los mecanismos implicados: biológicos, conductuales y sociales. Los síntomas suelen aparecer en los primeros 3 meses tras el ictus (DPI «precoz») y menos frecuentemente más tarde (DPI «tardía»). Los síntomas son similares a los de otras depresiones, aunque con algunas diferencias, como presentar más trastornos del sue¿no, síntomas vegetativos e introversión para las relaciones sociales. Para su diagnóstico se recomienda mantener una actitud vigilante y emplear herramientas diagnósticas específicas, como el Patient Health Questionaire-2 (PHQ-2). Finalmente, el tratamiento de elección son los inhibidores selectivos de la recaptación de serotonina (ISRS). No obstante, aún son muchas las cuestiones por resolver en el tratamiento de la DPI, como cuándo es el mejor momento para iniciar el tratamiento o el efecto de los antidepresivos sobre la cognición y la función motora, entre otros. ConclusionesLos neurólogos desempe¿nan un papel fundamental en la recuperación de los enfermos con ictus. Es necesario que estén familiarizados con la detección temprana y el trata-miento de la DPI, para así facilitar la recuperación funcional del paciente, su reinserción social y la mejora en la calidad de vida del enfermo y su familia." "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0020" "titulo" => "Introducción" ] 1 => array:2 [ "identificador" => "abst0025" "titulo" => "Desarrollo" ] 2 => array:2 [ "identificador" => "abst0030" "titulo" => "Conclusiones" ] ] ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "Please cite this article as: Espárrago Llorca G, Castilla-Guerra L, Fernández Moreno MC, Ruiz Doblado S, Jiménez Hernández MD. Depresión post ictus: una actualización. Neurología. 2015;30:23–31." ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:2 [ "leyenda" => "Positive score >2." "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head " align="left" valign="top" scope="col">Name \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " colspan="4" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Date of visit</th></tr><tr title="table-row"><th class="td" title="table-head " align="" valign="top" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Not at all \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Several days \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">More than half the days \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Nearly every day \t\t\t\t\t\t\n \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry " colspan="5" align="left" valign="top">Over the past 2 weeks, how often have you been bothered by any of the following problems?</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">1. Little interest or pleasure in doing things \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">3 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">2. Feeling down, depressed or hopeless \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">0 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">2 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="char" valign="top">3 \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1431789.png" ] ] ] ] "descripcion" => array:1 [ "en" => "Patient Health Questionnaire (PHQ-2)" ] ] 1 => array:7 [ "identificador" => "tbl0010" "etiqueta" => "Table 2" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:3 [ "leyenda" => "NSAID: non-steroidal anti-inflammatory drugs; SSRI: selective serotonin reuptake inhibitors; TAD: tricyclic antidepressants." "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">TADs \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Antiarrhythmic agents: increased risk of ventricular arrhythmias when TADs are administered in combination with amiodarone, flecainide, procainamide, quinidine, propafenone, or beta-blockers \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Antibiotic agents: increased risk of ventricular arrhythmias when TADs are administered in combination with moxifloxacin \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Anticoagulant agents: TADs may increase or reduce anticoagulant effects \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Antiepileptic agents: TADs antagonise the anticonvulsant effect of antiepileptic agents (reduced seizure threshold) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Antihistaminic agents: antimuscarinic and sedative effects increase when TADs are administered with antihistamines \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Diuretic agents: increased risk of postural hypotension when TADs are administered in combination with diuretics \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">SSRIs<a class="elsevierStyleCrossRef" href="#tblfn0005">a</a> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Analgesic agents: increased risk of haemorrhage when SSRIs are administered in combination with NSAIDs or acetylsalicylic acid \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Antiarrhythmic agents: fluoxetine increases flecainide level in plasma; paroxetine may inhibit propafenone metabolism (increasing the risk of toxicity) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Anticoagulant agents: SSRIs may increase anticoagulant effect \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Antiepileptic agents: SSRIs antagonise the anticonvulsant effect of antiepileptic agents (reduced seizure threshold) \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Anti-ulcer agents: cimetidine increases plasma levels of citalopram, escitalopram, and sertraline; omeprazole increases plasma levels of escitalopram \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Beta-blockers: paroxetine may increase metoprolol plasma levels; citalopram and escitalopram increase plasma levels of metoprolol; fluvoxamine increases propranolol plasma levels \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Theophylline: fluvoxamine increases theophylline plasma levels \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1431790.png" ] ] ] "notaPie" => array:1 [ 0 => array:3 [ "identificador" => "tblfn0005" "etiqueta" => "a" "nota" => "SSRI interactions fundamentally depend on inhibitory effect of SSRIs on cytochrome P450. 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Post-stroke depression: an update

Depresión post ictus: una actualización

G. Espárrago Llorcaa, L. Castilla-Guerrab, M.C. Fernández Morenoc,

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castillafernandez@hotmail.com

Corresponding author.

, S. Ruiz Dobladoa, M.D. Jiménez Hernándezd

a Servicio de Psiquiatría, Hospital de la Merced, Osuna, Sevilla, Spain

b Servicio de Medicina Interna, Hospital de la Merced, Osuna, Sevilla, Spain

c Servicio de Neurología, Hospital de Valme, Sevilla, Spain

d Servicio de Neurología y Neurofisiología, Hospital Virgen del Rocío, Sevilla, Spain

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in addition to post-stroke depression &#40;PSD&#41;&#44; many other neuropsychological symptoms may be present after stroke&#58; anxiety&#44; irritability&#44; agitation&#44; and emotional incontinence&#59; changes in emotional experience&#59; sleep disturbances&#59; behavioural disorders such as disinhibition&#59; apathy and fatigue&#59; and psychotic symptoms such as delusions and hallucinations&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#8211;3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We also know that PSD is the main predictor of poor functional outcome after stroke&#46; Presence of PSD is associated with poorer functional and cognitive recovery&#44; increased limitations on daily life activities&#44; and social and interpersonal activities&#44; poorer quality of life&#44; and higher mortality rates &#40;up to 10 times higher than in patients without PSD&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Furthermore&#44; we know that there are many risk factors for developing PSD&#44; including more severe motor deficit&#44; a higher degree of disability&#44; and a poorer social support network&#46; Identifying these factors permits early application of prevention and treatment strategies&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">However&#44; although prevalence of PSD is high&#44; it is generally underdiagnosed and usually undertreated&#44; as we will discuss in a later section&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">PSD is a frequent complication with severe negative repercussions for both patients and their carers&#44; and yet it is clearly predictable and treatable&#46; Therefore&#44; it is essential to understand the risk factors for PSD and identify it in patients as soon as possible&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Prevalence of PSD</span><p id="par0035" class="elsevierStylePara elsevierViewall">Estimating the real prevalence of PSD is not an easy task due to the methodological differences between the studies that have been conducted&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> First&#44; the diagnostic criteria for depression are not the same in all studies&#44; although it must be said that most of them conducted structured interviews and followed the criteria from the Diagnostic and Statistical Manual of Mental Disorders&#44; 4th edition &#40;DSM-IV&#41;&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Second&#44; the scales applied to assess the results also vary from one study to the other&#46; Some use PSD-specific scales whereas some other studies use general scales&#44; such as the Hamilton Rating Scale for Depression &#40;Ham-D&#41;&#59; furthermore&#44; some studies use self-evaluation scales and others do not&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Third&#44; inclusion criteria vary considerably&#46; In fact&#44; some studies excluded patients that other studies included &#40;for example&#44; patients with aphasia or dementia&#41;&#44; and inclusion criteria also differed with regard to the target populations&#44; age groups&#44; or phases of the disease &#40;acute- vs chronic-phase stroke&#41;&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Lastly&#44; it has been demonstrated that prevalence rates of PSD depend on the setting where patients are examined&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">In general&#44; prevalence rates of PSD range from 25&#37; to 79&#37; depending on the patient selection criteria used by each of the different studies&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;6</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Community-dwelling patients have the lowest prevalence rates&#59; in this setting&#44; 14&#37; of patients present major depression&#44; and 9&#37;&#44; minor depression&#46; In hospital settings&#44; including acute-care patients and those in rehabilitation&#44; prevalence rates of major and minor depression were 21&#46;6&#37; and 20&#46;0&#37;&#44; respectively&#46; Among patients discharged from hospital&#44; prevalence rates of major and minor depression were 24&#46;0&#37; and 23&#46;9&#37; at times ranging from 3 months to 3 years after stroke&#46; Other studies show similar rates&#44; although the percentage of patients reporting major depression is lower than that diagnosed with minor depression&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">White et al&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> recently published data from patients with lacunar stroke only&#44; extracted from a larger study&#44; Secondary Prevention of Small Subcortical Strokes &#40;SPS3&#41;&#46; They examined the prevalence of depression&#44; its correlation to other factors&#44; and the course of depression over time in a cohort of 2477 patients with a history of lacunar stroke&#46; Prevalence of depression at 4 months after stroke was 19&#37;&#46; Older age&#44; male sex&#44; and absence of cognitive impairment were the factors associated with a lower risk of depression&#46; On the contrary&#44; functional disability&#44; living with a spouse or family&#44; and presenting risk factors for stroke were associated with a high risk of depression&#46; The study stated that likelihood of depression decreased with age at a rate of 1&#46;12 times lower per year &#40;95&#37; CI&#58; 1&#46;06-1&#46;17&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">However&#44; the impact of certain factors on PSD prevalence is a controversial topic&#46; Some studies have found a higher prevalence of PSD in patients with cognitive impairment&#44; while others have not&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Similarly&#44; and contrary to the results from the SPS3 study&#44; many authors claim that older age constitutes a risk factor for PSD&#44; resulting in increased prevalence in elderly patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;6</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Diagnosis of PSD</span><p id="par0075" class="elsevierStylePara elsevierViewall">Diagnosis of PSD is complex due to the frequent presence of other symptoms&#44; especially those associated with cognitive impairment&#44; such as aphasia&#44; agnosia&#44; apraxia&#44; and changes in memory&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Additionally&#44; some symptoms of stroke or of depression may overlap and be indistinguishable from each other&#46; Symptoms common to both entities include sleep disorders&#44; difficulty concentrating&#44; and loss of appetite&#46; These similarities may lead to overestimating depression in stroke patients&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> On other occasions&#44; many symptoms are not identified as the result of depression&#46; In these cases&#44; they are mistaken for consequences of stroke or old age &#40;in elderly patients&#41;&#44; which may lead to an underestimation of the diagnosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;10</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Due to these diagnostic difficulties&#44; between 50&#37; and 80&#37; of all PSD cases are not identified by doctors who are not psychiatrists&#46;<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;9</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Some studies have compared several diagnostic tools in order to determine the most appropriate one&#46; Some authors state that the Geriatric Depression Scale &#40;GDS&#41; is a better diagnostic tool than other scales&#44; such as the Hospital Anxiety and Depression Scale &#40;HADS&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> GDS is especially indicated for patients with a high level of functional ability and mild cognitive impairment&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Quaranta et al&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> evaluated the diagnostic accuracy of the Poststroke Depression Rating Scale &#40;PSDRS&#41;&#44; a tool specifically designed for diagnosing PSD&#46; They then compared the results with those of Ham-D&#46; Both scales were reliable diagnostic tools&#44; and they both showed good sensitivity and specificity&#46; Cognitive impairment had a considerable effect on Ham-D&#44; whereas PSDRS was influenced by the patient&#39;s age&#46; Healey et al&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> compared 3 depression scales&#58; the Beck Depression Inventory-Fast Screen &#40;BDI-FS&#41;&#44; Brief Assessment Schedule Depression Cards &#40;BASDEC&#41;&#44; and HADS&#46; BASDEC demonstrated the greatest validity and precision&#46; Similarly&#44; Berg et al&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> compared different screening tools and concluded that the Ham-D&#44; BDI-FS&#44; and Clinical Global Impression &#40;CGI&#41; assessments carried out by professionals were useful for evaluating depression alongside DSM diagnostic criteria &#40;DSM-III-R or other versions&#41;&#46; They found no significant differences between these scales&#46; In addition&#44; these authors do not recommend using the Visual Analogue Mood Scale &#40;VAMS&#41; in patients with aphasia or other cognitive dysfunctions&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">Other authors<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> have demonstrated that PSD can be successfully diagnosed by using structured or semi-structured neuropsychiatric interviews following current DSM criteria&#46; They concluded that no specific diagnostic instruments were necessary&#46; PSD is generally diagnosed according to DSM guidelines&#44; sometimes differentiating major from minor depression&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">However&#44; a study<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> published in <span class="elsevierStyleItalic">Stroke</span> in 2012 investigated the diagnostic value of the 9-item and 2-item Patient Health Questionnaire &#40;PHQ-9 and PHQ-2&#41; and compared it with other scales &#40;HADS&#44; BDI-II&#44; Distress Thermometer&#44; and Kessler-10&#41; in acute stroke patients with preserved ability to communicate&#46; PHQ-9 includes all 9 symptoms of depression established by the DSM&#44; whereas PHQ-2 only includes 2&#58; anhedonia and depressed mood&#46; The study showed a good diagnostic value for PHQ-9 scores &#8805;10 and for PHQ-2 scores &#8805;2&#46; This group also recommends using PHQ-2 in all patients&#44; and PHQ-9 only in those with a positive result on the PHQ-2 because this approach demonstrates the greatest sensitivity&#46; The authors suggest these 2 screening tools for stroke patients since they are brief and easy to use&#44; their only limitation being that they cannot be used in patients with significant cognitive and verbal impairment &#40;<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0105" class="elsevierStylePara elsevierViewall">DSM IV-TR<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> categorises PSD as a mood disorder resulting from a general medical condition &#40;stroke in this case&#41;&#46; It can be classified into subtypes according to the following specifiers&#58; depressive features&#44; major depressive-like episode&#44; and mixed features &#40;manic features&#44; depression&#41;&#46; According to this classification&#44; depression must be a direct physiological consequence of stroke&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">Therefore&#44; we normally use the term PSD to refer to major depressive-like episodes that follow stroke&#46; Diagnosis of PSD requires evidence from the patient&#39;s medical history&#44; and findings from the clinical examination and complementary tests&#44; confirming that depression is a direct physiological consequence of stroke&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">According to DSM-IV-TR diagnostic criteria&#44; 5 or more symptoms must be present during at least 2 weeks for major depression to be diagnosed&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Pathophysiological mechanisms of PSD</span><p id="par0120" class="elsevierStylePara elsevierViewall">The pathophysiological mechanisms of PSD are not yet fully understood&#46; Biological&#44; behavioural&#44; and social factors are thought to be involved&#44; and PSD is therefore a multifactorial process&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Biological factors can be divided into several different types&#58; stroke location&#44; stroke type&#44; neurobiological pathways involved&#44; mechanisms of inflammation and apoptosis&#44; and genetic factors&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Stroke location and PSD</span><p id="par0130" class="elsevierStylePara elsevierViewall">The first studies on the origin of PSD focused on the connection between cerebrovascular lesion location and development of PSD&#46; Robinson et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> for example&#44; were the first to suggest a connection between PSD and a lesion in the left hemisphere&#46; According to these authors&#44; the lesions supposedly responsible for PSD were located in the left frontal and dorsolateral cortical regions and in the left basal ganglia&#46; Many other studies have later corroborated this association&#46;<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;20</span></a> Other researchers<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a> found that lesions located in the left lateral frontal lobe&#44; caudate nucleus&#44; and putamen were significantly more likely to cause depression after acute stroke than similar lesions located in the right hemisphere&#46; However&#44; several other studies did not confirm this connection&#46; A meta-analysis performed by Carson et al&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> could not support the connection between the stroke location or laterality&#44; and risk of developing PSD&#46; Another study<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> showed that frontal or basal ganglia lesion location was a risk factor for PSD&#44; but it found no correlation between laterality and depression&#46; Likewise&#44; a subsequent review of the methodological limitations of the studies addressing lesion location and PSD observed that the link between risk of developing PSD and frontal&#47;basal ganglia lesions depended on the study population&#59; studies in hospital inpatients showed a stronger association than those in community-dwelling patients&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> In another study&#44; Nishiyama et al&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a> found that presence of lesions in the left lenticulocapsular area&#44; as well as hypertension and education level&#44; was an independent predictor of symptoms of depression after stroke&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Therefore&#44; and given that results from different studies are contradictory&#44; mainly because of methodological biases&#44; we can conclude that the evidence is insufficient to support a correlation between lesion laterality and risk of developing PSD&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">Another structure that has been investigated extensively in connection with PSD is the amygdala&#46; It is well-known today that the amygdala is involved in the regulation of mood and emotions&#46; In the Sydney Stroke Study&#44; Sachdev et al&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> showed that amygdala was smaller in patients who had suffered a stroke or a transient ischaemic attack &#40;TIA&#41;&#44; and especially in patients with cognitive impairment&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Stroke type and PSD</span><p id="par0145" class="elsevierStylePara elsevierViewall">The vascular depression hypothesis proposes that ischaemic vascular lesions &#40;acute&#44; chronic&#44; silent infarctions&#44; leukoaraiosis&#44; etc&#46;&#41; can damage mood and emotion regulation and provoke late-onset depression&#46; Based on that hypothesis&#44; some authors suggest that PSD may lead to cognitive dysfunction of vascular origin which may in turn cause new depressive symptoms&#44; therefore establishing a reciprocal connection between depression and cerebrovascular disease&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">In the present study we aim to explain the impact of different types of stroke on the development of PSD&#46; Firstly&#44; white matter lesions caused by leukoaraiosis or small lacunar strokes seem to play a role in PSD pathogenesis&#46; White matter hyperintensities have been associated with depression and executive dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> Silent infarctions and white matter hyperintensities are frequently found in elderly patients with depression&#46; Studies have proved that vascular risk factors and cerebrovascular lesions affect the course of depression&#44; especially in older patients&#46; This suggests that lesions affect not only medium- and large-calibre blood vessels&#44; but also small-calibre vessels&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> In fact&#44; Chen et al&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a> studied PSD in patients with small subcortical strokes by comparing the 2 possible aetiologies&#58; small vessel disease&#44; and intracranial and extracranial large artery disease&#46; The authors found that PSD was more frequent among patients with small subcortical strokes derived from lesions in large-calibre vessels&#46; This suggests that cerebral perfusion plays a major role in the development of PSD&#46;</p><p id="par0155" class="elsevierStylePara elsevierViewall">Santos et al&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">31</span></a> analysed 41 autopsies of patients who had presented initial onset of depression within the first 2 years after stroke&#46; Researchers found no connection between macroinfarct location and development of PSD for any of the locations included in the study&#46; Lacunar strokes within the thalamus and basal ganglia were associated with a higher risk of PSD&#46; However&#44; microinfarcts and periventricular and diffuse demyelination did not occur more frequently in PSD patients&#46; They concluded that the damage resulting from chronic accumulation of lacunar strokes in the thalamus&#44; basal ganglia&#44; and deep white matter may be a more important predictor of PSD than the localisation of a single infarct&#46;</p><p id="par0160" class="elsevierStylePara elsevierViewall">In a more recent study&#44; Tang et al&#46;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> examined the association between PSD &#40;defined as a GDS score &#8805;7&#41; and presence of cerebral microhaemorrhages &#40;evaluated with MRI&#41; in 235 patients at 3 months after stroke&#46; The researchers observed that patients with PSD were more likely to present lobar microhaemorrhages than patients without PSD&#46; Lobar microhaemorrhage was therefore considered an independent predictor of PSD&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Neurobiological pathways and PSD</span><p id="par0165" class="elsevierStylePara elsevierViewall">The connection between PSD and lesions in different cerebral pathways has also been studied&#46; We now know that frontal-subcortical lesions of the monoaminergic pathways reduce biogenic amine release and result in increased likelihood of depression&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a></p><p id="par0170" class="elsevierStylePara elsevierViewall">Another plausible mechanism would involve changes in glutamatergic transmission after stroke&#46; In fact&#44; a study<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a> found changes in frontal lobe glutamate&#47;glutamine levels in PSD patients assessed by magnetic resonance spectroscopy&#46;</p><p id="par0175" class="elsevierStylePara elsevierViewall">On the other hand&#44; hypothalamo-pituitary adrenal axis dysregulation has been observed in 40&#37; of all stroke patients&#44; and adrenocortical hyperactivity appears almost immediately after stroke onset&#46; Additionally&#44; the resulting persisting hypercortisolaemia has been associated with the development of depression&#44; poorer prognosis&#44; and increased mortality rate&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a></p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Inflammation and PSD</span><p id="par0180" class="elsevierStylePara elsevierViewall">Inflammatory processes seem to be involved in PSD pathogenesis&#46; Cerebral ischaemia has been shown to cause increased production of proinflammatory cytokines&#44; such as interleukin-1&#946; &#40;IL-1&#946;&#41;&#44; tumour necrosis factor &#945; &#40;TNF-&#945;&#41;&#44; or interleukin-18 &#40;IL-18&#41;&#46; In turn&#44; these cytokines may cause decreased serotonin production in certain brain areas&#44; thereby favouring depression&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a> More specifically&#44; changes in IL-18 serum levels seem to be linked to depression severity&#46;<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a></p><p id="par0185" class="elsevierStylePara elsevierViewall">A recent review by Pascoe et al&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a> on inflammatory processes in stroke patients confirms that depression and ischaemia are related to inflammation&#46; Both conditions are associated with increased circulating levels of proinflammatory cytokines&#46; Since cytokines play a mediating role in ischaemia-related cell death and limbic region apoptosis is associated with depression&#44; the authors concluded that ischaemic inflammation is likely to contribute to development of PSD&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a> Another study<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">39</span></a> found increased levels of cytokines IL-6&#44; IL-10&#44; TNF-&#945;&#44; and interferon-&#947; &#40;IFN-&#947;&#41;&#44; and elevated ratios of IL-6&#47;IL-10 and TNF-&#945;&#47;IL-10&#44; in patients with PSD compared to stroke patients without depression&#46;</p><p id="par0190" class="elsevierStylePara elsevierViewall">However&#44; some authors did not observe a clear association between the increase in inflammatory markers and the development of PSD&#46;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a></p><p id="par0195" class="elsevierStylePara elsevierViewall">In any case&#44; other studies provide interesting information about the anti-inflammatory effects of antidepressants&#46;<a class="elsevierStyleCrossRefs" href="#bib0205"><span class="elsevierStyleSup">41&#44;42</span></a> These drugs can reduce depressive symptoms by acting on the inflammatory markers involved in mood regulation&#46; More specifically&#44; animal models have shown that antidepressants reduce the levels of pro-inflammatory interleukins IL-1 and IL-2&#44; while increasing the level of anti-inflammatory interleukin IL-10&#46; Additionally&#44; they inhibit the expression of IL-6&#44; TNF-&#945;&#44; and IFN-&#947;&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Genetic factors and PSD</span><p id="par0200" class="elsevierStylePara elsevierViewall">Genetic variability seems to be involved in PSD&#46; For example&#44; patients with the s&#47;s polymorphism of the serotonin transporter-linked gene region 5-HTTLPR are 3&#46;1 times more likely to present PSD than those with the l&#47;l or l&#47;&#967;l variant&#46; Additionally&#44; patients with the 9&#47;12 or 12&#47;12 variants of the serotonin transporter locus STin2 were 4&#46;1 times more likely to develop depression than patients with the STin2 10&#47;10 genotype&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">43</span></a> A more recent study<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a> found a connection between the s&#47;s variant of the 5-HTT gene-linked promoter region and post-stroke emotional incontinence&#46; Yet another study<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a> stated that s&#47;s homozygosity for serotonin transporter gene SLC6A4 may be involved in development of PSD&#46;</p><p id="par0205" class="elsevierStylePara elsevierViewall">Based on the above&#44; it seems that certain genetic features determine the degree of vulnerability to depression&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Symptoms of PSD</span><p id="par0210" class="elsevierStylePara elsevierViewall">Although PSD can occur shortly after a cerebrovascular event&#44; it usually develops within the first few months following a stroke&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> In a study of 100 stroke patients&#44; 46&#37; of those with depressive symptoms at 2 months after stroke also presented depressive symptoms at 12 months&#44; whereas only 12&#37; presented the first symptoms 12 months after stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a> The term &#8216;early-onset PSD&#8217; has been proposed to refer to PSD occurring within the first 3 months after stroke&#44; while &#8216;late-onset PSD&#8217; refers to PSD developing after 3 months&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> In early-onset PSD&#44; somatic depressive symptoms tend to be more numerous than psychological symptoms&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a></p><p id="par0215" class="elsevierStylePara elsevierViewall">Although depressive symptoms are usually similar&#44; some differences have been found between PSD patients and patients with depression but no associated neurological disease&#46; PSD patients&#44; especially those with right-hemisphere damage&#44; are less likely to present dysphoric depression and more likely to present vegetative signs and symptoms than patients with other types of late-onset PSD&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;47</span></a> Greater social withdrawal and fewer agitation symptoms have been reported in elderly stroke patients with depression compared to depressive patients with other conditions&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;48</span></a> A subsequent study<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a> found that PSD patients presented &#8216;inability to feel&#8217; and &#8216;disturbed sleep&#8217; more frequently than depressed patients with no prior history of stroke&#46;</p><p id="par0220" class="elsevierStylePara elsevierViewall">It is therefore important to perform differential diagnosis to rule out other cognitive-behavioural syndromes presenting with mood and emotional changes after stroke&#44; since their symptoms may be similar to those of PSD&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Those syndromes include emotional lability&#44; athymhormic syndrome&#44; aboulia and apathy&#44; affective aprosody&#44; and frontal dysexecutive syndromes&#46; Other disorders that may appear in the absence of PSD include certain autonomic disorders&#44; changes in sleep patterns after stroke&#44; and vegetative symptoms such as post-stroke anxiety and subjective fatigue&#46; Gusev and Bogolepova<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a> state that some 2&#37; to 3&#37; of first-time stroke patients may present masked depression&#44; that is&#44; presence of depressive symptoms but absence of depressive mood&#46; The main manifestations of this type of depression are biological rhythm disturbances and somatisation disorders&#44; especially vegetative-vascular dystonia&#44; vertigo&#44; and various algic phenomena&#46; These symptoms&#44; which are common to stroke and depression&#44; may lead to overestimating depression in stroke patients&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> However&#44; underestimation of PSD is even more frequent&#44; since depressive symptoms are rarely identified despite the high incidence and prevalence of PSD&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Treatment of PSD</span><p id="par0225" class="elsevierStylePara elsevierViewall">Several anti-depressants have proved to cause an improvement in cognitive skills and functional recovery in PSD patients&#46; Selective serotonin reuptake inhibitors &#40;SSRI&#41; and tricyclic antidepressants &#40;TAD&#41; are the most extensively studied drug treatments&#46;</p><p id="par0230" class="elsevierStylePara elsevierViewall">The first study on PSD treatment&#44; performed by Lipsey et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> was a placebo-controlled study that found improvement in Ham-D scores in 11 patients treated with nortriptyline &#40;25-100<span class="elsevierStyleHsp" style=""></span>mg&#47;d&#41; for 6 weeks&#46;</p><p id="par0235" class="elsevierStylePara elsevierViewall">The first study using SSRIs<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> found that patients receiving citalopram showed more symptomatic improvement &#40;with lower scores on Ham-D at 3 and 6 weeks&#41; than those on fluoxetine&#46; However&#44; 2 double-blind placebo-controlled trials found both citalopram and fluoxetine to be effective for PSD treatment after assessing 66 and 31 patients respectively over 6 weeks&#46;<a class="elsevierStyleCrossRefs" href="#bib0270"><span class="elsevierStyleSup">54&#44;55</span></a> Another placebo-controlled trial<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> compared nortriptyline to fluoxetine in 104 patients over 12 weeks&#46; Nortriptyline proved to be more effective than fluoxetine and placebo since it caused a more marked decrease in Ham-D scores&#46; The study by Jorge et al&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> found that patients treated with either fluoxetine or nortriptyline presented significantly lower mortality rates than placebo-treated patients&#46;</p><p id="par0240" class="elsevierStylePara elsevierViewall">Rampello et al&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a> found that patients on reboxetine experienced a more pronounced decrease in Ham-D scores than those treated with placebo&#46;</p><p id="par0245" class="elsevierStylePara elsevierViewall">More recent studies have focused on the effectiveness of SSRIs&#46; Ried et al&#46;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a> conducted a retrospective study on mortality and found that SSRI treatment&#44; administered either before or after stroke&#44; was associated with a significantly lower risk of mortality during the first year after stroke &#40;HR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;31&#59; 95&#37; CI&#58; 0&#46;11-0&#46;86&#41;&#46; However&#44; mortality rates increased after 7 years&#46; The authors concluded that SSRI treatment was associated with better survival rates&#44; and they therefore recommend starting or resuming SSRI treatment after stroke&#44; especially in patients with prior history of depression or those treated with SSRIs before stroke&#46; Another study<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a> found that discontinuing escitalopram treatment can increase occurrence of post-stroke depressive symptoms over the first 6 months after treatment withdrawal&#44; compared to placebo and problem-solving therapy &#40;PST&#41;&#46; Jorge et al&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">61</span></a> conducted a double-blind placebo-controlled trial in 129 patients evaluated using the Repeatable Battery for the Assessment of Neuropsychological Status &#40;RBANS&#41;&#46; The authors found that patients receiving escitalopram after stroke showed improvement in the higher cognitive functions&#44; specifically in verbal and visual memory functions&#44; compared to patients receiving placebo or PST&#46; The beneficial effect of escitalopram was independent of its effect on depressive symptoms&#46; Similarly&#44; it has been proven that fluoxetine improves quality of life in patients with emotional disorders&#44; including PSD&#44; after stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">62</span></a> In a recent controlled trial&#44; Cramer<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">63</span></a> assessed the effect of fluoxetine in patients at 5 to 10 days after stroke using the Fugl-Meyer Assessment of Motor Recovery after Stroke &#40;FMA&#41; and found improved motor function at 90 days after stroke&#46; These patients also showed a lower level of disability according to modified Rankin Scale scores&#46;</p><p id="par0250" class="elsevierStylePara elsevierViewall">The efficacy of drugs other than antidepressants has also been investigated&#46; For example&#44; certain stimulants&#44; such as amphetamines and methylphenidate&#44; have been studied in patients with severe depression and rapid cognitive decline&#44; with contradictory results&#46;<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">64</span></a> In another study&#44; PSD patients treated with the calcium agonist nimodipine showed improvement of depressive symptoms and a lower risk of recurrence&#46;<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">65</span></a></p><p id="par0255" class="elsevierStylePara elsevierViewall">Finally&#44; although pharmacological treatment with SSRIs is recommended for PSD&#44; there are no studies providing conclusive data on the superiority of a specific drug&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Nevertheless&#44; SSRIs are safer&#44; provoke fewer adverse effects&#44; are relatively quick-acting with a latency period ranging from 7 to 10 days&#44; and they also exert an anxiolytic effect&#46; For this reason&#44; they are considered first-line antidepressants&#44; especially in stroke patients&#44; who are usually elderly with underlying cardiovascular problems&#44; and on polytherapy&#44; which can lead to drug interactions &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">Table 2</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0260" class="elsevierStylePara elsevierViewall">In any case&#44; many questions about PSD treatment remain unanswered&#44; such as the best moment for initiating treatment&#44; the effect of antidepressants in areas other than emotion &#40;for example&#44; cognition and motor function&#41;&#44; and the importance of antidepressants for reducing mortality in stroke patients&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Conclusion</span><p id="par0265" class="elsevierStylePara elsevierViewall">Stroke has traditionally been considered a disease affecting motor function&#46; Therefore&#44; approaches to hospital care&#44; rehabilitation&#44; and follow-up have focused on this aspect almost exclusively&#46; However&#44; we currently know that PSD is a common problem in daily clinical practice since it is present in 1 out of every 3 stroke patients&#46; Additionally&#44; PSD is the main factor limiting patient recovery and rehabilitation&#44; and increasing morbidity and mortality rates&#46; Strangely enough&#44; more than half of the cases are neither diagnosed nor treated&#46; In this scenario&#44; neurologists play a major role in caring for and managing recovery in stroke patients&#44; and they must therefore be familiar with early detection and treatment of PSD&#46; This way&#44; neurologists will be able to facilitate patients&#8217; functional recovery and social integration&#44; and improve quality of life in patients and their families&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Conflicts of interest</span><p id="par0270" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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          "titulo" => "Abstract"
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              "identificador" => "abst0005"
              "titulo" => "Introduction"
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            1 => array:2 [
              "identificador" => "abst0010"
              "titulo" => "Development"
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              "titulo" => "Conclusions"
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          "titulo" => "Keywords"
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          "identificador" => "xres848374"
          "titulo" => "Resumen"
          "secciones" => array:3 [
            0 => array:2 [
              "identificador" => "abst0020"
              "titulo" => "Introducci&#243;n"
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            1 => array:2 [
              "identificador" => "abst0025"
              "titulo" => "Desarrollo"
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            2 => array:2 [
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              "titulo" => "Conclusiones"
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          "titulo" => "Palabras clave"
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          "identificador" => "sec0005"
          "titulo" => "Introduction"
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        5 => array:2 [
          "identificador" => "sec0010"
          "titulo" => "Prevalence of PSD"
        ]
        6 => array:2 [
          "identificador" => "sec0015"
          "titulo" => "Diagnosis of PSD"
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          "identificador" => "sec0020"
          "titulo" => "Pathophysiological mechanisms of PSD"
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        8 => array:2 [
          "identificador" => "sec0025"
          "titulo" => "Stroke location and PSD"
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          "titulo" => "Stroke type and PSD"
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          "titulo" => "Neurobiological pathways and PSD"
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          "identificador" => "sec0040"
          "titulo" => "Inflammation and PSD"
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          "titulo" => "Genetic factors and PSD"
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          "titulo" => "Symptoms of PSD"
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        14 => array:2 [
          "identificador" => "sec0055"
          "titulo" => "Treatment of PSD"
        ]
        15 => array:2 [
          "identificador" => "sec0060"
          "titulo" => "Conclusion"
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          "identificador" => "sec0065"
          "titulo" => "Conflicts of interest"
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          "titulo" => "References"
        ]
      ]
    ]
    "pdfFichero" => "main.pdf"
    "tienePdf" => true
    "fechaRecibido" => "2012-04-14"
    "fechaAceptado" => "2012-06-27"
    "PalabrasClave" => array:2 [
      "en" => array:1 [
        0 => array:4 [
          "clase" => "keyword"
          "titulo" => "Keywords"
          "identificador" => "xpalclavsec843480"
          "palabras" => array:5 [
            0 => "Antidepressants"
            1 => "Post-stroke depression"
            2 => "Cerebrovascular disease"
            3 => "Stroke"
            4 => "Selective serotonin reuptake inhibitors"
          ]
        ]
      ]
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          "titulo" => "Palabras clave"
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          "palabras" => array:5 [
            0 => "Antidepresivos"
            1 => "Depresi&#243;n post ictus"
            2 => "Enfermedad cerebrovascular"
            3 => "Ictus"
            4 => "Inhibidores selectivos de la recaptaci&#243;n de serotonina"
          ]
        ]
      ]
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    "resumen" => array:2 [
      "en" => array:3 [
        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introduction</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Post-stroke depression &#40;PSD&#41; is the most common mood disorder following a stroke&#44; and also the main factor limiting recovery and rehabilitation in stroke patients&#46; In addition&#44; it may increase mortality by up to ten times&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Development</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">PSD occurs in 1 in 3 stroke patients and more than half of all cases are neither diagnosed nor treated&#46; Several mechanisms&#44; including biological&#44; behavioural&#44; and social factors&#44; are involved in its pathogenesis&#46; Symptoms usually occur within the first three months after stroke &#40;early onset PSD&#41;&#44; and less frequently at a later time &#40;late onset PSD&#41;&#46; Symptoms resemble those of other types of depression&#44; although there are some differences&#59; PSD patients experience more sleep disturbances&#44; vegetative symptoms&#44; and social withdrawal&#46; For PSD diagnosis&#44; we recommended vigilance and use of specific diagnostic tools such as the Patient Health Questionnaire-2 &#40;PHQ-2&#41;&#46; The treatments of choice are selective serotonin reuptake inhibitors &#40;SSRI&#41;&#46; However&#44; there are still many unanswered questions in the treatment of PSD&#44; such as the best time to start treatment or the effects of antidepressants on cognition and motor function&#44; among others&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Conclusions</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Neurologists play a pivotal role in the care and management of patients recovering from stroke&#46; They must be familiar with methods for early detection and treatment of PSD&#44; as this can facilitate a patient&#39;s functional recovery and social reintegration&#44; and improve quality of life for patients and their families&#46;</p></span>"
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            "identificador" => "abst0005"
            "titulo" => "Introduction"
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          1 => array:2 [
            "identificador" => "abst0010"
            "titulo" => "Development"
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          2 => array:2 [
            "identificador" => "abst0015"
            "titulo" => "Conclusions"
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      "es" => array:3 [
        "titulo" => "Resumen"
        "resumen" => "<span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Introducci&#243;n</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La depresi&#243;n post ictus &#40;DPI&#41; es el trastorno afectivo m&#225;s frecuente tras un ictus y el principal factor que limita la recuperaci&#243;n y rehabilitaci&#243;n de los pacientes&#44; adem&#225;s de poder incrementar su mortalidad hasta 10 veces&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Desarrollo</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">La DPI se presenta en uno de cada 3 pacientes con ictus y en m&#225;s de la mitad de los casos no se diagnostica ni se trata&#46; En su etiopatogenia son varios los mecanismos implicados&#58; biol&#243;gicos&#44; conductuales y sociales&#46; Los s&#237;ntomas suelen aparecer en los primeros 3 meses tras el ictus &#40;DPI &#171;precoz&#187;&#41; y menos frecuentemente m&#225;s tarde &#40;DPI &#171;tard&#237;a&#187;&#41;&#46; Los s&#237;ntomas son similares a los de otras depresiones&#44; aunque con algunas diferencias&#44; como presentar m&#225;s trastornos del sue¿no&#44; s&#237;ntomas vegetativos e introversi&#243;n para las relaciones sociales&#46; Para su diagn&#243;stico se recomienda mantener una actitud vigilante y emplear herramientas diagn&#243;sticas espec&#237;ficas&#44; como el <span class="elsevierStyleItalic">Patient Health Questionaire-2</span> &#40;PHQ-2&#41;&#46; Finalmente&#44; el tratamiento de elecci&#243;n son los inhibidores selectivos de la recaptaci&#243;n de serotonina &#40;ISRS&#41;&#46; No obstante&#44; a&#250;n son muchas las cuestiones por resolver en el tratamiento de la DPI&#44; como cu&#225;ndo es el mejor momento para iniciar el tratamiento o el efecto de los antidepresivos sobre la cognici&#243;n y la funci&#243;n motora&#44; entre otros&#46;</p></span> <span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusiones</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Los neur&#243;logos desempe¿nan un papel fundamental en la recuperaci&#243;n de los enfermos con ictus&#46; Es necesario que est&#233;n familiarizados con la detecci&#243;n temprana y el trata-miento de la DPI&#44; para as&#237; facilitar la recuperaci&#243;n funcional del paciente&#44; su reinserci&#243;n social y la mejora en la calidad de vida del enfermo y su familia&#46;</p></span>"
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          2 => array:2 [
            "identificador" => "abst0030"
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        "etiqueta" => "&#9734;"
        "nota" => "<p class="elsevierStyleNotepara" id="npar0010">Please cite this article as&#58; Esp&#225;rrago Llorca G&#44; Castilla-Guerra L&#44; Fern&#225;ndez Moreno MC&#44; Ruiz Doblado S&#44; Jim&#233;nez Hern&#225;ndez MD&#46; Depresi&#243;n post ictus&#58; una actualizaci&#243;n&#46; Neurolog&#237;a&#46; 2015&#59;30&#58;23&#8211;31&#46;</p>"
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        "mostrarDisplay" => false
        "tabla" => array:2 [
          "leyenda" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Positive score &#62;2&#46;</p>"
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                  <table border="0" frame="\n
                  \t\t\t\t\tvoid\n
                  \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head  " align="left" valign="top" scope="col">Name&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " colspan="4" align="center" valign="top" scope="col" style="border-bottom: 2px solid black">Date of visit</th></tr><tr title="table-row"><th class="td" title="table-head  " align="" valign="top" scope="col" style="border-bottom: 2px solid black">&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Not at all&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Several days&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">More than half the days&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th><th class="td" title="table-head  " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Nearly every day&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry  " colspan="5" align="left" valign="top"><span class="elsevierStyleItalic">Over the past 2 weeks&#44; how often have you been bothered by any of the following problems&#63;</span></td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>1&#46; Little interest or pleasure in doing things&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">0&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">2&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">3&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span>2&#46; Feeling down&#44; depressed or hopeless&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">0&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">1&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">2&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td><td class="td" title="table-entry  " align="char" valign="top">3&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
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          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Patient Health Questionnaire &#40;PHQ-2&#41;</p>"
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        "tabla" => array:3 [
          "leyenda" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">NSAID&#58; non-steroidal anti-inflammatory drugs&#59; SSRI&#58; selective serotonin reuptake inhibitors&#59; TAD&#58; tricyclic antidepressants&#46;</p>"
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                  <table border="0" frame="\n
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                  \t\t\t\t" class=""><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleItalic">TADs</span>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Antiarrhythmic agents</span>&#58; increased risk of ventricular arrhythmias when TADs are administered in combination with amiodarone&#44; flecainide&#44; procainamide&#44; quinidine&#44; propafenone&#44; or beta-blockers&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Antibiotic agents</span>&#58; increased risk of ventricular arrhythmias when TADs are administered in combination with moxifloxacin&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Anticoagulant agents</span>&#58; TADs may increase or reduce anticoagulant effects&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Antiepileptic agents</span>&#58; TADs antagonise the anticonvulsant effect of antiepileptic agents &#40;reduced seizure threshold&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Antihistaminic agents</span>&#58; antimuscarinic and sedative effects increase when TADs are administered with antihistamines&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Diuretic agents</span>&#58; increased risk of postural hypotension when TADs are administered in combination with diuretics&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleVsp" style="height:0.5px"></span>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleItalic">SSRIs</span><a class="elsevierStyleCrossRef" href="#tblfn0005"><span class="elsevierStyleSup">a</span></a>&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Analgesic agents</span>&#58; increased risk of haemorrhage when SSRIs are administered in combination with NSAIDs or acetylsalicylic acid&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Antiarrhythmic agents</span>&#58; fluoxetine increases flecainide level in plasma&#59; paroxetine may inhibit propafenone metabolism &#40;increasing the risk of toxicity&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Anticoagulant agents</span>&#58; SSRIs may increase anticoagulant effect&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Antiepileptic agents</span>&#58; SSRIs antagonise the anticonvulsant effect of antiepileptic agents &#40;reduced seizure threshold&#41;&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Anti-ulcer agents</span>&#58; cimetidine increases plasma levels of citalopram&#44; escitalopram&#44; and sertraline&#59; omeprazole increases plasma levels of escitalopram&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Beta-blockers</span>&#58; paroxetine may increase metoprolol plasma levels&#59; citalopram and escitalopram increase plasma levels of metoprolol&#59; fluvoxamine increases propranolol plasma levels&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry  " align="left" valign="top"><span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleBold">Theophylline</span>&#58; fluvoxamine increases theophylline plasma levels&nbsp;\t\t\t\t\t\t\n
                  \t\t\t\t</td></tr></tbody></table>
                  """
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              "identificador" => "tblfn0005"
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              "nota" => "<p class="elsevierStyleNotepara" id="npar0005">SSRI interactions fundamentally depend on inhibitory effect of SSRIs on cytochrome P450&#46; Sertraline&#44; citalopram&#44; and escitalopram are the SSRIs with the least pronounced inhibitory effect on cytochrome P450&#46;</p>"
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          ]
        ]
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          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Clinically relevant drug interactions for antidepressants in elderly patients on polytherapy</p>"
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      "titulo" => "References"
      "seccion" => array:1 [
        0 => array:2 [
          "identificador" => "bibs0005"
          "bibliografiaReferencia" => array:65 [
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              "etiqueta" => "1"
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                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Depresi&#243;n postictus &#40;i&#41;&#46; Epidemiolog&#237;a&#44; criterios diagn&#243;sticos y factores de riesgo"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:1 [
                            0 => "F&#46;J&#46; Carod-Artal"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:6 [
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                        "volumen" => "42"
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                            "web" => "Medline"
                          ]
                        ]
                      ]
                    ]
                  ]
                ]
              ]
            ]
            1 => array:3 [
              "identificador" => "bib0010"
              "etiqueta" => "2"
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                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Poststroke depression"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:4 [
                            0 => "R&#46;M&#46; Dafer"
                            1 => "M&#46; Rao"
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                          ]
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                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1310/tsr1501-13"
                      "Revista" => array:6 [
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            2 => array:3 [
              "identificador" => "bib0015"
              "etiqueta" => "3"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
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                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
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                            1 => "S&#46; Paolucci"
                            2 => "U&#46; Bivona"
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                          ]
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                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1111/j.1600-0447.2004.00297.x"
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            ]
            3 => array:3 [
              "identificador" => "bib0020"
              "etiqueta" => "4"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Depression is an independent predictor of poor long-term functional outcome post-stroke"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:5 [
                            0 => "T&#46; Pohjasvaara"
                            1 => "R&#46; Vataja"
                            2 => "A&#46; Leppavuori"
                            3 => "M&#46; Kaste"
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                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:6 [
                        "tituloSerie" => "Eur J Neurol"
                        "fecha" => "2001"
                        "volumen" => "8"
                        "paginaInicial" => "315"
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                        "link" => array:1 [
                          0 => array:2 [
                            "url" => "https://www.ncbi.nlm.nih.gov/pubmed/11422427"
                            "web" => "Medline"
                          ]
                        ]
                      ]
                    ]
                  ]
                ]
              ]
            ]
            4 => array:3 [
              "identificador" => "bib0025"
              "etiqueta" => "5"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Management of depression in elderly stroke patients"
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Article information

ISSN: 21735808
Original language: English

DOI:10.1016/j.nrleng.2012.06.006

The statistics are updated each day

Year/Month	Html	Pdf	Total

2024 November	28	3	31
2024 October	239	13	252
2024 September	275	17	292
2024 August	290	16	306
2024 July	370	28	398
2024 June	284	31	315
2024 May	330	21	351
2024 April	343	23	366
2024 March	461	34	495
2024 February	377	40	417
2024 January	456	45	501
2023 December	365	33	398
2023 November	440	40	480
2023 October	435	47	482
2023 September	332	24	356
2023 August	6176	40	6216
2023 July	9001	50	9051
2023 June	3566	30	3596
2023 May	322	32	354
2023 April	310	46	356
2023 March	488	42	530
2023 February	385	43	428
2023 January	209	23	232
2022 December	218	45	263
2022 November	209	29	238
2022 October	205	34	239
2022 September	196	49	245
2022 August	215	35	250
2022 July	134	26	160
2022 June	176	28	204
2022 May	185	51	236
2022 April	169	45	214
2022 March	259	46	305
2022 February	135	20	155
2022 January	162	25	187
2021 December	160	57	217
2021 November	331	31	362
2021 October	170	44	214
2021 September	133	43	176
2021 August	130	52	182
2021 July	73	31	104
2021 June	203	27	230
2021 May	189	33	222
2021 April	1103	86	1189
2021 March	339	65	404
2021 February	216	57	273
2021 January	232	50	282
2020 December	181	45	226
2020 November	222	56	278
2020 October	95	31	126
2020 September	171	45	216
2020 August	125	37	162
2020 July	106	39	145
2020 June	95	28	123
2020 May	229	68	297
2020 April	207	24	231
2020 March	307	47	354
2020 February	129	28	157
2020 January	193	30	223
2019 December	126	38	164
2019 November	149	36	185
2019 October	96	25	121
2019 September	103	24	127
2019 August	120	25	145
2019 July	107	36	143
2019 June	120	36	156
2019 May	226	78	304
2019 April	125	16	141
2019 March	83	43	126
2019 February	88	16	104
2019 January	74	22	96
2018 December	90	14	104
2018 November	85	11	96
2018 October	79	28	107
2018 September	110	24	134
2018 August	77	23	100
2018 July	56	16	72
2018 June	40	13	53
2018 May	33	21	54
2018 April	50	17	67
2018 March	645	24	669
2018 February	31	9	40
2018 January	63	20	83
2017 December	44	15	59
2017 November	44	12	56
2017 October	50	17	67
2017 September	70	14	84
2017 August	58	15	73
2017 July	48	13	61
2017 June	90	16	106
2017 May	56	15	71
2017 April	55	17	72
2017 March	104	19	123
2017 February	69	9	78
2017 January	67	13	80
2016 December	42	22	64
2016 November	127	18	145
2016 October	97	28	125
2016 September	118	25	143
2016 August	75	27	102
2016 July	65	11	76
2016 June	82	36	118
2016 May	85	47	132
2016 April	92	60	152
2016 March	110	49	159
2016 February	53	22	75
2016 January	51	32	83
2015 December	50	20	70
2015 November	74	29	103
2015 October	61	31	92
2015 September	71	28	99
2015 August	57	22	79
2015 July	53	28	81
2015 June	37	23	60
2015 May	47	34	81
2015 April	59	32	91
2015 March	70	47	117
2015 February	156	46	202

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