Pauline Renou

Evolution of depression symptoms following stroke: a prospective study using computerized ambulatory monitoring.

Background: Despite the high prevalence and impact of post-stroke depression (PSD), questions persist concerning the nature and stability of PSD over time. The current study uses state-of-the-art computerized ambulatory monitoring techniques to assess daily life depression symptoms following stroke and examines the evolution of depression levels over a three-month period. Methods: 48 patients admitted to a university hospital neurology unit for ischemic or hemorrhagic stroke participated in ambulatory monitoring of DSM-IV depression symptoms for a one-week period after hospital discharge. Clinician-administered measures of depression were also obtained at discharge and again three months later. Results: The percentage of the sample with elevated depression scores was the same at discharge and three months later, but consistency in depression profiles was low. Ambulatory monitoring revealed that elevated depression levels at hospital discharge were most strongly associated with anhedonia (t ratio = 4.840, p < 0.001) and fatigue (t ratio = 4.00, p < 0.001), whereas individuals with elevated scores at three months were predicted by daily life negative thoughts (t ratio = 4.051, p < 0.001), anxious mood (t ratio = 3.489, p < 0.01), sad mood (t ratio = 2.621, p < 0.05) and emotional reactivity (t ratio = 2.466, p < 0.05). Conclusions: The prevalence of depression may appear stable during the immediate weeks and months following stroke, but it is likely to be composed of very different symptom profiles. The immediate physical and psychological impact of stroke may induce somatic symptoms that explain elevated depression levels and which may not indicate a risk factor for later depression.

Subacute Default Mode Network Dysfunction in the Prediction of Post-Stroke Depression Severity

PURPOSE To identify patterns of rest functional connectivity (FC) in the whole brain with the default mode network (DMN) soon after stroke and to explore the predictive accuracy of the strength of rest FC in specific areas on poststroke severity of depression and anxiety symptoms. MATERIALS AND METHODS The protocol was accepted by the local ethics board, and all patients provided informed consent to participate. Resting-state functional magnetic resonance (MR) images were acquired 10 days after a first stroke in 24 patients without a history of psychiatric illness. Independent component analysis was used to isolate the DMN in each subject. Hamilton Depression Rating Scale (HDRS) 17 and Hamilton Anxiety Rating Scale (HARS) were recorded 10 days and 3 months after the stroke. Associations between severity of anxiety or depression symptoms and DMN functional connectivity were investigated with whole-brain analyses by using statistical parametric mapping software and were adjusted for age, sex, manual laterality, and National Institutes of Health Stroke Severity scores. Correlations were considered significant if P<.001, with a cluster size of more than 50 voxels. RESULTS Ten days after stroke, anxiety severity was correlated with functional connectivity in the middle temporal cortex and the anterior midcingulate cortex, while at 3 months after stroke, a correlation was observed with the middle temporal cortex and the posterior cingulate cortex. Poststroke depressive symptom severity did not correlate with functional connectivity changes at 10-day follow-up, while the HDRS 17 score was correlated with functional connectivity in the left middle temporal cortex and precuneus at 3-month follow-up. CONCLUSION These results suggest that a dysfunction of DMN functional connectivity involved in emotional control is associated with the severity of poststroke depression. Further studies are necessary to determine the mechanisms of this functional impairment.

Final cerebral infarct volume is predictable by MR imaging at 1 week.

BACKGROUND AND PURPOSE: Stroke volume, an increasingly used end point in phase II trials, is considered stationary at least 30 days after the ictus. We investigated whether information conveyed by MR imaging measurements of the “final” infarct volume could be assessed as early as the subacute stage (days 3–6), rather than waiting for the chronic stage (days 30–45). MATERIALS AND METHODS: Ninety-five patients with middle cerebral artery stroke prospectively included in a multicenter study underwent MR imaging during the first 12 hours (MR imaging-1), between days 3 and 6 (MR imaging-2), and between days 30 and 45 (MR imaging-3). We first investigated the relationship between subacute (FLAIR-2) and chronic volumes (FLAIR-3), by using a linear regression model. We then tested the relationship between FLAIR volumes (either FLAIR-2 or FLAIR-3) and functional disability, measured by the mRS at the time of MR imaging-3, by using logistic regression. The performances of the models were assessed by using the AUC in ROC. RESULTS: A linear association between log FLAIR-2 and log FLAIR-3 volumes was observed. The proportion of FLAIR-3 variation, explained by FLAIR-2, was high (R2 = 81%), without a covariate that improved this percentage. Both FLAIR-2 and FLAIR-3 were independent predictors of mRS (OR, 0.79 and 0.73; 95% CI, 0.64–0.97 and 0.56–0.96; P = .026 and .023). The performances of the models for the association between either FLAIR volume and mRS did not differ (AUC = 0.897 for FLAIR-2 and 0.888 for FLAIR-3). CONCLUSIONS: Stroke damage may be assessed by a subacute volume because subacute volume predicts the “true” final volume and provides the same clinical prognosis.

Early Fiber Number Ratio Is a Surrogate of Corticospinal Tract Integrity and Predicts Motor Recovery After Stroke

Background and Purpose— The contribution of imaging metrics to predict poststroke motor recovery needs to be clarified. We tested the added value of early diffusion tensor imaging (DTI) of the corticospinal tract toward predicting long-term motor recovery. Methods— One hundred seventeen patients were prospectively assessed at 24 to 72 hours and 1 year after ischemic stroke with diffusion tensor imaging and motor scores (Fugl-Meyer). The initial fiber number ratio (iFNr) and final fiber number ratio were computed as the number of streamlines along the affected corticospinal tract normalized to the unaffected side and were compared with each other. The prediction of motor recovery (&Dgr;Fugl-Meyer) was first modeled using initial Fugl-Meyer and iFNr. Multivariate ordinal logistic regression models were also used to study the association of iFNr, initial Fugl-Meyer, age, and stroke volume with Fugl-Meyer at 1 year. Results— The iFNr correlated with the final fiber number ratio at 1 year (r=0.70; P<0.0001). The initial Fugl-Meyer strongly predicted motor recovery (≈73% of initial impairment) for all patients except those with initial severe stroke (Fugl-Meyer<50). For these severe patients (n=26), initial Fugl-Meyer was not correlated with motor recovery (R2=0.13; p=ns), whereas iFNr showed strong correlation (R2=0.56; P<0.0001). In multivariate analysis, the iFNr was an independent predictor of motor outcome (&bgr;=2.601; 95% confidence interval=0.304–5.110; P=0.031), improving prediction compared with using only initial Fugl-Meyer, age, and stroke volume (P=0.026). Conclusions— Early measurement of FNr at 24 to 72 hours poststroke is a surrogate marker of corticospinal tract integrity and provides independent prediction of motor outcome at 1 year especially for patients with severe initial impairment.

Stroke Location Is an Independent Predictor of Cognitive Outcome

Background and Purpose— On top of functional outcome, accurate prediction of cognitive outcome for stroke patients is an unmet need with major implications for clinical management. We investigated whether stroke location may contribute independent prognostic value to multifactorial predictive models of functional and cognitive outcomes. Methods— Four hundred twenty-eight consecutive patients with ischemic stroke were prospectively assessed with magnetic resonance imaging at 24 to 72 hours and at 3 months for functional outcome using the modified Rankin Scale and cognitive outcome using the Montreal Cognitive Assessment (MoCA). Statistical maps of functional and cognitive eloquent regions were derived from the first 215 patients (development sample) using voxel-based lesion-symptom mapping. We used multivariate logistic regression models to study the influence of stroke location (number of eloquent voxels from voxel-based lesion-symptom mapping maps), age, initial National Institutes of Health Stroke Scale and stroke volume on modified Rankin Scale and MoCA. The second part of our cohort was used as an independent replication sample. Results— In univariate analyses, stroke location, age, initial National Institutes of Health Stroke Scale, and stroke volume were all predictive of poor modified Rankin Scale and MoCA. In multivariable analyses, stroke location remained the strongest independent predictor of MoCA and significantly improved the prediction compared with using only age, initial National Institutes of Health Stroke Scale, and stroke volume (area under the curve increased from 0.697–0.771; difference=0.073; 95% confidence interval, 0.008–0.155). In contrast, stroke location did not persist as independent predictor of modified Rankin Scale that was mainly driven by initial National Institutes of Health Stroke Scale (area under the curve going from 0.840 to 0.835). Similar results were obtained in the replication sample. Conclusions— Stroke location is an independent predictor of cognitive outcome (MoCA) at 3 months post stroke.

Atraumatic Nonaneurysmal Sulcal Subarachnoid Hemorrhages: A Diagnostic Workup Based on a Case Series

Introduction: Atraumatic and nonaneurysmal sulcal subarachnoid hemorrhage (sSAH) is a rare type of cerebrovascular disease with various etiologies previously reported in small case reports. In this study, we propose to analyze clinical presentations, imaging patterns and etiologies in a large case series of such patients in order to propose a diagnostic workup. Methods: We retrospectively analyzed clinical and radiological data of consecutive patients with a diagnosis of atraumatic and nonaneurysmal sSAH, admitted to our institution between 2008 and 2011. All patients had both computed tomography (CT) and magnetic resonance imaging (MRI) as a part of their initial evaluation. Results: 30 patients (18 women and 12 men, mean age: 60 years) were identified. The main clinical symptoms at presentation were focal and transient neurological deficit (n = 22) and thunderclap headache (n = 10). Four patients had progressive headache and 4 other had partial or generalized epileptic seizures. MRI abnormalities associated with sSAH were prior hemorrhages, microbleeds, severe leukoencephalopathy and hemosiderosis suggesting cerebral amyloid angiopathy (CAA; n = 9), vasogenic edema in parieto-occipital areas compatible with a posterior reversible encephalopathy syndrome (PRES; n = 3), cortical venous thrombosis (n = 2) and concomitant acute cortical stroke (n = 3). Other underlying causes of sSAH, not diagnosed on MRI, were reversible cerebral vasoconstriction syndrome (RCVS) based on clinical criteria and conventional angiography (n = 4), angiitis diagnosed by skin biopsy (n = 1), vascular malformation diagnosed on CT and digital subtraction angiographies (n = 3), and overanticoagulation (n = 1). Four cases remained unresolved. Conclusion: This study confirmed that sSAH is a rare condition related to a wide spectrum of etiologies. Combination of brain MRI and magnetic resonance angiography and eventually digital subtraction angiography allowed the identification of an underlying etiology for 87% of patients. CAA, RCVS and PRES represented more than 50% of the etiological mechanisms. Among older patients, sSAH was mainly related to CAA while in younger patients, RCVS represented the most frequent etiology.

Feasibility and validity of computerized ambulatory monitoring in stroke patients.

Background: Computerized ambulatory monitoring provides real-time assessments of clinical outcomes in natural contexts, and it has been increasingly applied in recent years to investigate symptom expression in a wide range of disorders. The purpose of this study was to examine the feasibility and validity of this data collection strategy with adult stroke patients. Methods: Forty-eight individuals (75% of the contacted sample) agreed to participate in the current study and were instructed to complete electronic interviews using a personal digital assistant 5 times per day over a 1-week period. Results: More than 80% of programmed assessments were completed by the sample, and no evidence was found for fatigue effects. Expected patterns of associations were observed among daily life variables, and data collected through ambulatory monitoring were significantly correlated with standard clinic-based measures of similar constructs. Conclusion: Support was found for the feasibility and validity of computerized ambulatory monitoring with stroke patients. The application of these novel methods with stroke patients should provide complementary information that is inaccessible to standard hospital-based assessments and permit increased understanding of the significance of clinical results and test scores for daily life experience. DSM-IV-R = Diagnostic and Statistical Manual of Mental Disorders, 4th edition, revised; EMA = ecologic momentary assessment; ESM = experience sampling method; HAM-A = Hamilton Anxiety Rating Scale; HAM-D = Hamilton Depression Rating Scale; MMSE = Mini-Mental State Examination; PDA = personal digital assistant; SE = standard error.

Circadian sleep/wake rhythm abnormalities as a risk factor of a poststroke apathy

Background Poststroke apathy affects 19–55% of patients following stroke and has a negative impact on functional recovery, general health, and quality of life, as well as being a source of significant burden for caregivers. Aims A major clinical issue is the delayed diagnosis of post-stroke apathy, and so the aim of our study is to evaluate the relationship between early poststroke alterations of circadian rhythms of sleep/wake cycles and the occurrence of poststroke apathy. Methods Forty-six patients with a recent magnetic resonance imaging confirmed stroke were included. Main exclusion criteria were a mild to severe disability impeding home discharge from the hospital and the presence of apathy or dementia before stroke. Cerebrovascular lesions were evaluated by magnetic resonance imaging. At hospital discharge, an actigraph was used to measure patients global activity as well as parameters of circadian rhythmicity (relative amplitude, interdaily stability, intradaily variability) and sleep (sleep duration, sleep efficiency, fragmentation index) over seven-days. Apathy was assessed at hospital discharge as well as at three-months using the Apathy Inventory and the Lille Apathy Rating Scale. Results Of the 46 patients evaluated, 10 (22%) showed apathy three-months after stroke (median Apathy Inventory = 4·5). Before inclusion, these 10 subjects did not differ significantly from other patients concerning their sleep and, at inclusion, they did not differ concerning apathy, anxiety, depression, or cognitive and functional abilities. However, actigraphy measured at discharged identified significant alterations of sleep (P < 0·005). Future poststroke apathy patients exhibited a decrease in sleep efficiency (actual sleep time expressed as a percentage of time in bed) and an increase in the fragmentation index (degree of fragmentation during the sleep period) at three-months. No association was observed between poststroke apathy and the characteristics of cerebrovascular lesions (stroke location, extent of leucoencephalopathy, number of lacunes and microbleeds). Conclusion These results indicate that early poststroke alterations of sleep/wake circadian rhythms — easily evaluated by actigraphy — are associated with a higher risk of poststroke apathy at three-months. In terms of clinical outcomes, our results provide targets for very early identification of patients at risk to develop apathy after stroke and for assessing when to start specific therapy to optimize rehabilitation efficiency.

Endovascular Embolization of a Nondominant Vertebral Artery Compressed by an Osteophyte to Prevent Recurrence of Vertebrobasilar Infarctions

BACKGROUND Vertebral artery compression by cervical osteophyte is a rare cause of vertebrobasilar ischemic stroke. This mechanism of stroke has been reported as the Bow Hunter syndrome defined by vertebrobasilar insufficiency because of mechanical stenosis of the vertebral artery at the cervical level triggered by head movement. The most common treatment is surgical decompression. However, in most cases, a dominant vertebral artery is involved, and its dynamic extrinsic compression is demonstrated on angiography. CASE REPORT We report a patient with recurrent posterior circulation infarctions because of the compression of a nondominant vertebral artery by a cervical osteophyte. The dynamic angiography did not show any worsening of the vertebral stenosis by head movements but an irregularity of the vertebral artery with regard to the osteophyte compression, suggesting a direct artery wall injury. We concluded to an embolic mechanism through thrombus formation from the artery wall injury at the stenosed site. Because neither surgical decompression nor stenting was deemed to be a relevant treatment option, endovascular coil embolization of the compressed vertebral artery was performed after a clamping test to check the efficiency of the collateral circulation. The procedure was a success. During the 12-month follow-up, the patient did not have any recurrent stroke. CONCLUSIONS In case of recurrent symptomatic extrinsic compression of a nondominant vertebral artery, endovascular embolization after a clamping test may be considered.

Inter- and intraobserver reliability of five MRI sequences in the evaluation of the final volume of cerebral infarct.

To evaluate the reproducibility of fluid attenuated inversion recovery (FLAIR) and four other magnetic resonance imaging (MRI) sequences in the quantitative assessment of final cerebral infarct volume.