Poststroke depression and lesion location revisited

Seventy patients with one brain infarct on magnetic resonance imaging (MRI) were studied 3 months after ischemic stroke by a standardized protocol to detail side, site, type, and extent of the brain infarct, as well as severity of white matter lesions and brain atrophy. Depression was diagnosed by DSM-III-R and DSM-IV criteria. The brain infarcts that affected structures of the frontal-subcortical circuits, (i.e., the pallidum and caudate, especially on the left side) predisposed stroke patients to depression. The size of the infarcts at these sites in the depressed patients was larger. Using a logistic regression analysis, the authors found that a brain infarct that affected pallidum was a strong independent MRI correlate for poststroke depression (odds ratio = 7.2).     

Post-stroke emotional incontinence after small lenticulocapsular stroke: correlation with lesion location

Although post-stroke emotional incontinence (EI) often occurs after lenticulocapsular strokes, what factors determine the development of EI in these patients has not been identified. I prospectively studied the development of EI in 25 patients (13 men and 12 women, mean age 58.5 years) with single, unilateral, first-ever stroke (24 infarcts and one hemorrhage) of ≤ 2 cm in diameter at 2–6 months after the stroke. The patients with major depression were excluded. The lesion location was analysed by CT and/or MRI. The results showed that 13 patients (52 %) had post-stroke EI. The presence of EI was not related to age, gender, the presence of motor or sensory dysfunction, Barthel index score or the size and the laterality of the lesion. Among the lesions involving mainly the globus pallidus, dorsally located lesions were more often associated with EI than ventrally located ones. I conclude that EI is frequent in the patients with small lenticulocapsular stroke, more often associated with the lesions affecting the dorsal than the ventral part of the globus pallidus. The findings appear to be consistent with alleged chemical neuroanatomy that serotonergic fibers are particularly abundant in the internal globus pallidus. Received: 18 April 2001, Received in revised form: 24 October 2001, Accepted: 23 November 2001     

Factors associated with post-stroke depression and emotional incontinence: lesion location and coping styles

Post-stroke depression (PSD) and post-stroke emotional incontinence (PSEI) have attracted worldwide interest in recent years. These emotional disturbances have a negative impact on the rehabilitation process and the associated worse outcome. Consequently, defining the risk factors for development of PSD and PSEI is important. In this study, we evaluated 368 consecutive patients with acute ischemic stroke at admission and at three months later. PSD was evaluated by using the Beck Depression Inventory, and PSEI was evaluated using Kim's criteria. The Social Support Rating Scale and Medical Coping Modes Questionnaire were also used as measurement tools. Multivariate analyses showed that anterior cortex infarction was associated with PSEI three months after stroke occurrence. The appearance of PSD was not related to lesion location. Both motor and sensory dysfunctions was independently associated with PSD at admission, whereas low degree of social utilization was the independent factor associated with PSD 3 months after stroke. Acceptance-resignation is related to PSD and PSEI both at admission and 3 months after stroke. Avoidance was the independent factor related to PSD at 3 months after stroke onset.     

Poststroke emotional incontinence and decreased sexual activity.

BACKGROUND: Although poststroke depression has been shown to be related to decreased sexual activity (SA), the relationship between poststroke emotional incontinence (EI) and SA has not been properly investigated. METHODS: We examined 70 nondepressed, sexually active patients with first-ever stroke approximately 3 months after stroke and conducted a follow-up interview approximately 2 years after stroke in 55 of them. EI (excessive/inappropriate laughing/crying) and SA (libido, coital frequency, erectile function) were assessed with the use of a standardized questionnaire. RESULTS: Of these 70 patients, 24 (34%) had EI 3 months after stroke, which had resolved 2 years after stroke. Libido, coital frequency and erectile function were reported to have declined in 49, 65 and 26% of the patients, respectively, 3 months after stroke, and in 44, 49 and 20% of the patients 2 years after stroke. Multivariate analyses showed that low coital frequency before stroke (CFBS) was significantly (p < 0.05) related to decreased poststroke coital frequency, while the presence of EI (p < 0.05) and low CFBS (p < 0.05) was significantly associated with decreased erectile function 3 months after stroke. Two years after stroke, the presence of EI 3 months after stroke was significantly related to decreased libido, coital frequency and erectile function (p < 0.05 each). Age, gender, laterality of stroke, Barthel Index score, motor dysfunction and the presence of hypertension and diabetes mellitus were not independently related to SA 3 months and 2 years after stroke. CONCLUSION: The presence of EI is a factor related to decreased poststroke SA, more so in chronic than in subacute stages.     

Poststroke restless legs syndrome and lesion location: anatomical considerations

Several case studies have reported on restless legs syndrome (RLS) associated with stroke. In this study, we investigated the prevalence and the lesion topography of poststroke RLS. There were 137 patients with ischemic stroke included in this study. The diagnosis of RLS was made 1 month after the index stroke using the criteria established by the International RLS Study Group. All patients enrolled underwent magnetic resonance imaging within 7 days of the onset of the stroke. The prevalence of stroke-related RLS was calculated, and the topography of the associated ischemic lesions was analyzed. Among 137 patients, 17 patients (12.4%) were diagnosed with RLS after a stroke. Stroke-related RLS was found in 10 out of 33 patients with a basal ganglia/corona radiata infarct (30.3%), 1 out of 8 patients with an internal capsular infarct (12.5%), and 1 out of 7 patients with a thalamic infarct (14.3%). In addition, one out of 54 with a cortical lesion with/without subcortical involvement (1.9%), and 4 out of 18 patients with a pontine lesion (22.2%) had RLS. The analysis of the lesions in the cortical and subcortical group showed only 1 patient in the cortical group had stroke-related RLS, whereas 16 in the subcortical group had stroke-related RLS. The results of this study suggest that lesions of the subcortical brain areas such as the pyramidal tract and the basal ganglia-brainstem axis, which are involved in motor functions and sleep-wake cycles, may lead to RLS symptoms in patients after an ischemic stroke.     

Post‐stroke depression and apathy: Interactions between functional recovery,lesion location,and emotional response

Depression and apathy are often observed after stroke and are often confused with one another. In the present review, we argue that the current concept of ‘post‐stroke depression’ (PSD) in fact consists of two core symptoms or syndromes: (i) affective (depressive) PSD; and (ii) apathetic PSD. We argue that these two core symptoms are each associated with a different underlying neuroanatomical mechanism, a pattern that influences functional recovery. Post‐stroke disabilities can provoke several distinct emotional responses, some of which are associated with severe depression. We examined one of these emotional responses previously, namely ‘insistence on recovery’, which was believed to be a negative indicator of functional improvement in disabled stroke patients. However, an appropriate level of insistence on recovery may, in fact, be associated with reduced depression and apathy, resulting in enhanced recovery from stroke‐related disabilities. Improvements in physical disabilities (trunk stability or activities of daily living, such as walking) also reduce depression and apathy. Therefore, the experience of PSD/apathy may be intertwined with various initial emotional responses and improvements in physical functioning. Effective treatment of PSD/apathy requires a multidisciplinary approach, such that neuroanatomical/neurobiological, emotional, and physical (rehabilitation) domains are all addressed.     

Poststroke depression: psychopharmacological considerations

PSD is a common psychiatric complication of stroke. It is often underrecognized and untreated. Numerous studies show that untreated PSD impedes the rehabilitation and recovery process, jeopardizes quality of life, and increases mortality. Successful management of the PSD requires early recognition and initiation of appropriate treatment to facilitate an optimal level of functioning. As active members of the interdisciplinary treatment team, psychiatric consultative-liaison nurses play a pivotal role in facilitating positive treatment outcomes during both the acute and rehabilitation phases in the management of PSD.     

Poststroke depression and psychosis

Stroke is capable of producing a varied spectrum of neurobehavioral syndromes that may come to the attention of the mental health professional evaluating psychiatric symptoms in elderly individuals. The neurobehavioral effects may include affective or psychotic symptoms and may occur immediately after the stroke or months to years later. The presence of underlying (or pre-existing) brain disease may have an adverse effect on the resolution of the neuropsychiatric symptoms. Although there are no treatment response studies in the area of psychosis following stroke, the response of poststroke depression to antidepressants makes attempted pharmacologic treatment of symptoms justified.     

Poststroke depression: A biopsychosocial approach

Poststroke depression (PSD) is a form of geriatric depression that is associated with various negative outcomes. This article reviews existing research concerning the etiology, treatment, and prevention of PSD with particular emphasis on the development of a biopsychosocial conceptualization of PSD etiology and treatment. Existing intervention trials are reviewed. A behavioral model of PSD treatment is presented based on a biopsychosocial understanding of PSD that highlights the potential utility of the lesion location hypothesis in the early poststroke period and the behavioral and social changes that may be linked to depression in the postacute period after stroke.     

卒中后抑郁与卒中部位的相关研究

目的 探讨卒中后抑郁（post-stroke depression PSI））与卒中病灶部位的关系。方法通过CT或MRI进行卒中病灶定位,采用Hamilton抑郁量表对200例卒中患者在发病2周和3月进行调查评分。结果急性期和恢复期大脑半球左侧、右侧、双侧卒中PSD发生率无统计学差异。2周时大脑半球前部与后部卒中病灶两PSD发生率无统计学差异（x^2=1．9546,P〉0．1）。3月时大脑半球前部与后部卒中痛灶两PSD发生率有统计学差异（x^2=6．04,P〈0．05）。结论PSD的发生无半球偏利性。急性期大脑半球前部卒中病灶与PSD无明显相关性。恢复期走脑半球前部卒中病灶与PSD存在相关性。     

Poststroke depression in patients with small subcortical infarcts

Objectives

Small subcortical infarcts (SSIs) can result from small vessel disease (SVD) and intracranial and extracranial large artery disease (LAD). No study has explored poststroke depression (PSD) in different etiological types of SSIs.

Methods

Patients with SSIs resulting from LAD and SVD were included in the study. Poststroke depression was evaluated with the 15-item version of the geriatric depression scale (GDS) 3 months after stroke.

Results

Of the 127 patients with SSIs, 44 had LAD and 83 had SVD. The LAD group had a significantly higher mean GDS score and higher frequency of PSD (p < 0.05). The etiological type LAD was a significant independent risk factor for PSD.

Conclusion

PSD is more common in patients with SSIs resulting from LAD. This suggests that cerebral blood perfusion may play an important role in the development of PSD.     

Comparison of patients with and without poststroke major depression matched for size and location of lesion

Patients who developed major depression within two years following stroke (n = 13) were compared with patients who did not become depressed in the same period (n = 13) but who did have a similar size and location of lesion as in the depressed group. Although the depressed patients were not significantly different from the nondepressed patients in background characteristics, history of depressive disorder, neurological impairment, or social functioning, the depressed group had greater cognitive impairment as measured by Mini-Mental State score. In addition, the depressed group had significantly larger lateral and third ventricular to brain ratios than nondepressed patients on computed tomographic scan analysis. The results suggest that poststroke depression itself may produce an intellectual impairment; subcortical atrophy, which likely preceded the stroke lesion, may produce a vulnerability for depression following stroke.     

Post-stroke affective or apathetic depression and lesion location: left frontal lobe and bilateral basal ganglia

This study was designed to examine the correlation between damage to the basal ganglia or frontal lobe and depression status (both affective and apathetic dimensions) in 243 stroke patients. We assessed the affective dimension in post-stroke depression (PSD) using the Zung Self-rating Depression Scale (SDS) and the apathetic dimension in PSD using the apathy scale (AS). We classified basal ganglia or frontal lobe damage into four groups: no damage, damage to the left side only, damage to the right side only, and damage to both sides. Affective and/or apathetic PSD was found in 126 patients (51.9%). The severity of affective depression (SDS score) was associated with left frontal lobe (but not basal ganglia) damage, and that of apathetic depression (AS score) was related to damage to the bilateral basal ganglia (but not to the frontal lobe). The anatomical correlates of PSD differ depending on the PSD dimension (affective or apathetic) and may explain interstudy differences regarding the association between lesion location and type of PSD.