Behavioural Neurology

Behavioural Neurology / 2017 / Article
Special Issue

Behavioural and Cognitive Changes in Neurodegenerative Diseases and Brain Injury

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Research Article | Open Access

Volume 2017 |Article ID 5181024 |

Frank G. van Rooij, Nicole O. Plaizier, Sarah E. Vermeer, Bozena M. Góraj, Peter J. Koudstaal, Edo Richard, Frank-Erik de Leeuw, Roy P. C. Kessels, Ewoud J. van Dijk, "Subjective Cognitive Impairment, Depressive Symptoms, and Fatigue after a TIA or Transient Neurological Attack: A Prospective Study", Behavioural Neurology, vol. 2017, Article ID 5181024, 7 pages, 2017.

Subjective Cognitive Impairment, Depressive Symptoms, and Fatigue after a TIA or Transient Neurological Attack: A Prospective Study

Academic Editor: Gabriella Santangelo
Received09 Jul 2017
Revised30 Sep 2017
Accepted08 Oct 2017
Published19 Nov 2017


Introduction. Subjective cognitive impairment (SCI), depressive symptoms, and fatigue are common after stroke and are associated with reduced quality of life. We prospectively investigated their prevalence and course after a transient ischemic attack (TIA) or nonfocal transient neurological attack (TNA) and the association with diffusion-weighted imaging (DWI) lesions. Methods. The Cognitive Failures Questionnaire, Hospital Anxiety and Depression Scale, and Subjective Fatigue subscale from the Checklist Individual Strength were used to assess subjective complaints shortly after TIA or TNA and six months later. With repeated measure analysis, the associations between DWI lesion presence or clinical diagnosis (TIA or TNA) and subjective complaints over time were determined. Results. We included 103 patients (28 DWI positive). At baseline, SCI and fatigue were less severe in DWI positive than in DWI negative patients, whereas at follow-up, there were no differences. SCI () and fatigue () increased in severity only in DWI positive patients. There were no differences between TIA and TNA. Conclusions. Subjective complaints are highly prevalent in TIA and TNA patients. The short-term prognosis is not different between DWI-positive and DWI negative patients, but SCI and fatigue increase in severity within six months after the event when an initial DWI lesion is present.

1. Introduction

Subjective cognitive impairment (SCI), depressive symptoms, and fatigue are highly prevalent after stroke and are related to stroke severity [14]. Although by definition the symptoms of a transient ischemic attack (TIA) subside completely within 24 hours [5], subjective cognitive complaints, depressive symptoms, and fatigue often persist in these patients as well [68].

Diagnosing TIA is notoriously difficult [9]. Patients often report attacks of atypical or nonfocal neurological symptoms. In the absence of an alternative diagnosis, these episodes are referred to as transient neurological attack (TNA) [10]. In one-third of TIA patients, diffusion-weighted imaging (DWI) shows signs of acute ischemia beyond the point of symptom resolution, ascertaining a cerebrovascular etiology of the attack [11]. Acute DWI lesions are however also present in more than 20% of clinically diagnosed TNA patients [12].

Previous studies on subjective complaints after short-lasting attacks of neurological symptoms have focused solely on TIA, did not take DWI findings into account, and were cross-sectional in nature [68]. Since subjective complaints are associated with a reduced quality of life and are possible harbingers of forthcoming cognitive decline, it is important to understand their prevalence and determinants [13, 14].

We prospectively investigated the prevalence, severity, and course of SCI, depressive symptoms, anxiety, and fatigue in a cohort of TIA and TNA patients and determined the relation with event type and DWI results. We hypothesized that patients with acute DWI lesions would report an increase in severity of complaints in the months after the initial event. Since TIA and TNA have a comparable prevalence of DWI positivity, we expected to find no differences between these patient categories [12].

2. Methods

2.1. Study Design and Patients

This study was part of the prospective Cohort study ON Neuroimaging, Etiology, and Cognitive consequences of Transient neurological attacks (CONNECT), the details of which have been previously reported [15]. Consecutive stroke-free patients aged ≥ 45 years referred to a specialized outpatient TIA clinic within 7 days after an event of acute onset neurological symptoms lasting < 24 hours were included. Baseline measurements took place within seven days after the qualifying event, and follow-up was performed six months later. All baseline assessments were performed before the final diagnosis was discussed with the patient. The Medical Review Ethics Committee region Arnhem-Nijmegen approved the study, and written informed consent was obtained from all participants.

2.2. Classification of Qualifying Event

Based on a detailed description of the signs and symptoms of the event including a structured assessment of the presence or absence of eighteen specific predefined symptoms (Table 1), three specialized stroke neurologists adjudicated each event as TIA, TNA, or a specified other diagnosis, using previously determined definitions of TIA and TNA [5, 10]. Events with both focal and nonfocal symptoms were classified as TIA. Qualifying neurologists were blinded to results from MRI, and in case of disagreement, a consensus meeting was held.


HemiparesisDecreased consciousness or unconsciousness
HemianopiaNonrotatory dizziness
Transient monocular blindnessPositive visual phenomena
DiplopiaBilateral weakness of arms or legs
VertigoUnwell feelings

Symptoms should have sudden onset, rapid clearance, and duration of <24 hours. Referable to the nervous system if the referring physician considered TIA but patients were unable to specify further.
2.3. Brain Imaging

Brain MRI was performed within seven days after the qualifying event on a 1.5 Tesla Magnetom Scanner (Siemens, Erlangen, Germany) and included DWI, FLAIR, T1-, T2-, and T2-weighted sequences. Two experienced raters individually evaluated the severity of white matter hyperintensities, the presence of (silent) territorial infarcts, lacunes, and microbleeds [16, 17]. DWI was visually assessed for signs of acute infarction. Raters were unaware of clinical information, and a consensus meeting was held in case of disagreement.

2.4. Subjective Cognitive Impairment

At baseline and follow-up, the presence and severity of SCI in the previous month was assessed with a 15-item semistructured interview based on the Cognitive Failures Questionnaire (CFQ) [18]. Items concerning remembering, word finding, planning, concentration, and slowness of thought were given a wider score range (0–3) than other items (0-1). SCI was considered present if ≥1 moderate problem (score ≥ 2) on an item with a score range of 0 to 3 or a score of 1 on a dichotomous item was reported [19]. Trained examiners, unaware of clinical diagnosis and DWI status, administered all semistructured interviews.

2.5. Other Measurements

At both baseline and follow-up, the Hospital Anxiety and Depression Scale (HADS) was administered to measure the severity of symptoms of depression and anxiety [20]. Relevant symptoms of depression or anxiety were defined as a value of >7 on the subscales [21]. Fatigue was assessed with the subscale Subjective Fatigue of the Checklist Individual Strength (CIS20R-fatigue) with a score > 35 considered indicative for severe fatigue [22]. Level of education was classified using seven categories (1 = less than primary school; 7 = academic degree) [23]. Vascular risk factors were assessed at baseline. Incident vascular events (stroke, TIA, and myocardial infarction) between baseline and follow-up were assessed with a standardized, structured questionnaire. All questionnaires were handed out at the baseline or follow-up visit. In case of limited time, these were filled in at home and returned within one week.

2.6. Statistical Analysis

Only patients who completed follow-up were included. Baseline characteristics were compared between patients with complete and incomplete follow-up, between TIA and TNA between patients, and patients with and without DWI lesion, using Student’s t-test, χ2 test, or Mann–Whitney U test as appropriate.

Differences in prevalence of SCI, symptoms of depression or anxiety, and severe fatigue between groups (clinical diagnosis and DWI status) and time points were analyzed with McNemar’s test. Subsequently, the effect of DWI lesion and clinical diagnosis on change in subjective outcomes over time was determined with repeated measures analyses of variance. Associations between SCI, fatigue, and depressive and anxiety symptoms were assessed with multivariate regression analysis.

Age, sex, and level of education were regarded as potential confounders and adjusted for in all repeated measures analyses. Alpha was set at 0.05 and statistical analyses were performed with IBM SPSS Statistics version 24.0 (IBM Corp., Armonk, NY).

3. Results

CONNECT included 150 patients, 87 of whom were diagnosed as TIA, 56 as TNA, and 7 with a specific diagnosis. Patients in the last category were excluded from further analyses, as were those with incomplete baseline or follow-up assessments, leading to 103 included patients (Figure 1). Reasons for incomplete assessment were failure to return questionnaires (>95%) and refusal (<5%). Patients with incomplete HADS or CIS20R-fatigue were slightly younger (mean 61.8 [SD 10.7] years versus 65.8 [SD 9.1] years, ) than those with complete evaluations. There were no differences concerning clinical diagnosis, DWI lesion presence, level of education, or presence of vascular risk factors between patients with complete and incomplete assessments. Baseline characteristics of participants with complete assessments are presented by DWI results in Table 2. DWI lesions were more often present in clinically defined TIA patients, although 13% of included TNA patients also had a DWI lesion. Most DWI lesions were small cortical or subcortical lesions. There were no incident strokes or myocardial infarctions between baseline and follow-up, and five patients had an incident TIA. Excluding patients with incident TIA from the analyses did not change the results.

(n = 28)
(n = 75)

Women8 (29)29 (39)0.34
Age, mean (SD)66.7 (8.5)65.6 (9.3)0.60
Level of education, median (IQR)5 (3)5 (2)0.10
TIA23 (82)42 (56)0.01
Hypertension25 (89)60 (80)0.27
Dyslipidemia18 (64)53 (71)0.53
Diabetes mellitus2 (7)7 (9)0.73
Atrial fibrillation3 (11)10 (13)0.72
Smoking13 (46)17 (23)0.02
Diffusion-weighted imaging lesions, total n45N/AN/A
 Lesion type
  Small cortical26 (58)
  Small subcortical14 (31)
  Territorial5 (11)
Fazekas score, median (IQR)1 (1)1 (1)0.30
Lacunes5 (18)12 (16)0.82
Territorial infarcts2 (7)8 (11)0.59
Microbleeds (available for 72 patients)1 (6)6 (11)0.49

Values are n (%) unless stated otherwise. For difference using Student’s t-test, χ2 test, or Mann–Whitney U test as appropriate. DWI: diffusion-weighted imaging; IQR: interquartile range; TIA: transient ischemic attack; N/A: not applicable.
3.1. Subjective Cognitive Impairment ()

The overall prevalence of SCI in TIA and TNA patients was 82% at baseline and 77% at follow-up and was not significantly different between time points, DWI status, or clinical diagnosis. At baseline, the mean number of subjective cognitive failures was lower in patients with a DWI lesion than in those without (mean (SD) 1.83 (1.75) versus 3.77 (3.27), ), while at follow-up, this increased to 3.00 (2.70) in the first group and decreased slightly to 3.14 (3.17) in the latter () (Figure 2(a)). Repeated measures analysis (adjusted for age, sex, and level of education) showed that change over time in the number of subjective cognitive failures was significantly different between DWI positive and DWI negative patients (). There was no difference in SCI between TIA and TNA patients.

3.2. Depressive Symptoms and Anxiety ()

Relevant depressive symptoms (HADS-depression subscore > 7) were present in 8% of all patients at baseline and 9% at follow-up. The prevalence of relevant anxiety symptoms (HADS-anxiety subscore > 7) was 15% at baseline and 11% at follow-up. Depressive and anxiety symptoms did not differ between DWI negative and DWI positive patients or between TIA and TNA patient groups (Figures 2(b) and 2(c)).

3.3. Fatigue ()

Severe fatigue (CIS20R-fatigue score > 35) was present in 23% of patients at baseline and in 19% six months later. Prevalence of severe fatigue did not differ between DWI positive and DWI negative patients or between TIA and TNA patients.

Mean (SD) CIS20R-fatigue score was 25.0 (12.7) at baseline and 24.8 (11.5) at follow-up. Baseline scores were lower in DWI positive patients (21.0 (12.7) compared to 26.6 (12.4) for those without; ) but equal at follow-up (24.9 (11.6) in the DWI positive group versus 24.7 (11.6) in the DWI negative group; ). Patients with and without DWI lesions differed with respect to change in CIS20R-fatigue scores () (Figure 2(d)). The clinical diagnosis was unrelated to severity or change over time of fatigue.

At both baseline and follow-up, SCI was associated with higher CIS20R-fatigue scores (), but not with symptoms of depression or anxiety.

4. Discussion

Subjective complaints, especially SCI and fatigue, are highly prevalent in TIA and TNA patients both directly before the event and after six months. The initial qualifying diagnosis was unrelated to the presence, severity, and course of subjective complaints. Patients with signs of acute ischemia on DWI reported less severe SCI and fatigue in the month before the TIA or TNA than those without such a lesion. In this group of patients, severity subsequently increased in the six months after the event to a level equal to that of DWI negative patients.

Some methodological issues need to be considered when interpreting these results. First, given the loss to follow-up, selection bias might have occurred. Patients with missing follow-up HADS and CIS20R-fatigue assessments were on average slightly younger than participants. Since especially fatigue is more often reported in older patients, this might have resulted in an overestimation of its prevalence [24]. Alternatively, patients with incomplete assessments might have dropped out because of complaints, resulting in an underestimation. Other demographic variables however did not differ between patients with and without complete assessments, and we adjusted for age in our analyses. Therefore, we feel that selection bias has not largely influenced our results. The relatively small patient numbers in our study however limit statistical power, and our results need to be replicated in a larger cohort. Secondly, we used questionnaires to obtain information on the presence of SCI, depression, anxiety, and fatigue. These screening instruments, although validated, indicate whether patients experience dysfunction when actively asked about it. This differs from spontaneously reported complaints and may explain the high frequency of SCI observed in our cohort. The CFQ handles a strict cutoff for SCI, making it a sensitive but perhaps not very specific screening instrument. Thirdly, our study did not include a control group, limiting the interpretation of an added effect of TIA or TNA on subjective complaints.

The prevalence of SCI in our study is comparable to that in both stroke patients and those with evidence of small vessel disease on neuroimaging, using the same screening instrument [2, 19, 25]. Patients in those studies were on average older, had more often suffered stroke instead of TIA, and were tested several years after the initial event. Also, vascular lesions on neuroimaging were relatively sparse in our cohort, as compared to these studies [19, 25]. The high prevalence of SCI in TIA and TNA patients is therefore remarkable. Severe fatigue was less prevalent in our patients than in other stroke cohorts, as were depressive symptoms [4, 26, 27].

Interestingly, DWI positive patients reported less subjective cognitive failures and fatigue in the month before the event than those without a lesion. The DWI positive group by definition consisted of patients with a recent cerebrovascular event, independent of the clinical diagnosis. The DWI negative group possibly included some patients whose transient complaints have noncerebrovascular causes such as somatization, depression, or anxiety. Although this may explain the higher prevalence of premorbid SCI and fatigue, the lack of observed higher frequencies of depressive or anxiety symptoms does not support this hypothesis. Furthermore, we found no changes in subjective complaints in the DWI negative group, although one could expect these to increase after a disturbing event such as a TIA or TNA.

Within six months after TIA or TNA, severity of SCI and fatigue increased significantly in DWI positive patients. This can be explained in several ways. First, DWI hyperintensities are associated with permanent brain damage, which in turn is associated with cognitive decline, SCI, mood disorders, and fatigue in stroke patients [1, 3, 4, 28, 29]. Although the exact etiology remains to be established, a relationship between minor cognitive decline and recent lacunar infarct has been suggested [30]. Since the DWI lesions in our cohort were predominantly small cortical and subcortical lesions, a similar relationship may exist between these lesions and increasing subjective complaints over time. Second, the knowledge of having a DWI lesion could have influenced the perception of cognitive performance and have led to more subjective cognitive complaints. Third, secondary preventive medications including statins will more often have been started in the DWI positive patient group. Statins have been associated with cognitive complaints and fatigue. However, there are no consistent negative effects of statins on these outcome measures [31]. Finally, the increase in severity of SCI and fatigue observed in the DWI positive patient group could be merely a correction of an unexplained baseline difference, that is, regression towards the mean. However, no changes in prevalence or severity of these complaints were found in the DWI negative group, countering this explanation.

Fatigue was associated with subjective cognitive dysfunction. Possibly, both fatigue and SCI, as measured in our study, are expressions of the same underlying sense of unwell-being. We found no association between depressive symptoms and subjective cognitive dysfunction, suggesting that the increased severity of SCI observed in DWI positive patients was not influenced by mood changes.

5. Conclusions

Subjective complaints are highly prevalent in TIA and TNA patients. Larger sampled studies with longer follow-up need to determine whether subjective complaints last beyond six months after TIA or TNA and assess the course over time with respect to DWI lesion presence and the association with cognitive performance. Furthermore, the etiology of subjective cognitive impairment and fatigue after short-lasting cerebral ischemia and the association with radiological markers of cerebrovascular damage such as lacunes and cerebral atrophy should be subject to further research. Our results nevertheless add to the growing notion that TIA and TNA are more than just transient attacks but are associated with ongoing deficits and problems. This can be used to inform patients on the potential long-term prognosis of their TIA or TNA.

Conflicts of Interest

The authors declare that there is no conflict of interest regarding the publication of this article.


This study was supported by a fellowship from the Netherlands Brain Foundation received by Dr. Ewoud J. van Dijk (Grant F2009(1)-16).


  1. F. Lamb, J. Anderson, M. Saling, and H. Dewey, “Predictors of subjective cognitive complaint in postacute older adult stroke patients,” Archives of Physical Medicine and Rehabilitation, vol. 94, no. 9, pp. 1747–1752, 2013. View at: Publisher Site | Google Scholar
  2. N. A. Maaijwee, P. Schaapsmeerders, L. C. Rutten-Jacobs et al., “Subjective cognitive failures after stroke in young adults: prevalent but not related to cognitive impairment,” Journal of Neurology, vol. 261, no. 7, pp. 1300–1308, 2014. View at: Publisher Site | Google Scholar
  3. N. El Husseini, L. B. Goldstein, E. D. Peterson et al., “Depression and antidepressant use after stroke and transient ischemic attack,” Stroke, vol. 43, no. 6, pp. 1609–1616, 2012. View at: Publisher Site | Google Scholar
  4. A. Lerdal, L. N. Bakken, S. E. Kouwenhoven et al., “Poststroke fatigue—a review,” Journal of Pain and Symptom Management, vol. 38, no. 6, pp. 928–949, 2009. View at: Publisher Site | Google Scholar
  5. National Institute of Neurological Disorders and Stroke Committee, “Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III,” Stroke, vol. 21, no. 4, pp. 637–676, 1990. View at: Publisher Site | Google Scholar
  6. M. Fens, C. M. van Heugten, G. H. Beusmans et al., “Not as transient: patients with transient ischaemic attack or minor stroke experience cognitive and communication problems; an exploratory study,” The European Journal of General Practice, vol. 19, no. 1, pp. 11–16, 2013. View at: Publisher Site | Google Scholar
  7. H. J. Luijendijk, B. H. Stricker, R. G. Wieberdink et al., “Transient ischemic attack and incident depression,” Stroke, vol. 42, no. 7, pp. 1857–1861, 2011. View at: Publisher Site | Google Scholar
  8. C. Winward, C. Sackley, Z. Metha, and P. M. Rothwell, “A population-based study of the prevalence of fatigue after transient ischemic attack and minor stroke,” Stroke, vol. 40, no. 3, pp. 757–761, 2009. View at: Publisher Site | Google Scholar
  9. J. Castle, M. Mlynash, K. Lee et al., “Agreement regarding diagnosis of transient ischemic attack fairly low among stroke-trained neurologists,” Stroke, vol. 41, no. 7, pp. 1367–1370, 2010. View at: Publisher Site | Google Scholar
  10. M. J. Bos, M. J. van Rijn, J. C. Witteman, A. Hofman, P. J. Koudstaal, and M. M. Breteler, “Incidence and prognosis of transient neurological attacks,” JAMA, vol. 298, no. 24, pp. 2877–2885, 2007. View at: Publisher Site | Google Scholar
  11. M. Brazzelli, F. M. Chappell, H. Miranda et al., “Diffusion-weighted imaging and diagnosis of transient ischemic attack,” Annals of Neurology, vol. 75, no. 1, pp. 67–76, 2014. View at: Publisher Site | Google Scholar
  12. F. G. van Rooij, S. E. Vermeer, B. M. Goraj et al., “Diffusion-weighted imaging in transient neurological attacks,” Annals of Neurology, vol. 78, no. 6, pp. 1005–1010, 2015. View at: Publisher Site | Google Scholar
  13. P. Montejo, M. Montenegro, M. A. Fernandez, and F. Maestu, “Memory complaints in the elderly: quality of life and daily living activities. A population based study,” Archives of Gerontology and Geriatrics, vol. 54, no. 2, pp. 298–304, 2012. View at: Publisher Site | Google Scholar
  14. R. J. Kryscio, E. L. Abner, G. E. Cooper et al., “Self-reported memory complaints: implications from a longitudinal cohort with autopsies,” Neurology, vol. 83, no. 15, pp. 1359–1365, 2014. View at: Publisher Site | Google Scholar
  15. F. G. van Rooij, A. M. Tuladhar, R. P. Kessels et al., “Cohort study ON Neuroimaging, Etiology and Cognitive consequences of Transient neurological attacks (CONNECT): study rationale and protocol,” BMC Neurology, vol. 15, no. 1, p. 36, 2015. View at: Publisher Site | Google Scholar
  16. F. Fazekas, J. B. Chawluk, A. Alavi, H. I. Hurtig, and R. A. Zimmerman, “MR signal abnormalities at 1.5 T in Alzheimer’s dementia and normal aging,” American Journal of Roentgenology, vol. 149, no. 2, pp. 351–356, 1987. View at: Publisher Site | Google Scholar
  17. J. M. Wardlaw, E. E. Smith, G. J. Biessels et al., “Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration,” Lancet Neurology, vol. 12, no. 8, pp. 822–838, 2013. View at: Publisher Site | Google Scholar
  18. D. E. Broadbent, P. F. Cooper, P. FitzGerald, and K. R. Parkes, “The Cognitive Failures Questionnaire (CFQ) and its correlates,” The British Journal of Clinical Psychology, vol. 21, no. 1, pp. 1–16, 1982. View at: Publisher Site | Google Scholar
  19. J. C. de Groot, F. E. de Leeuw, M. Oudkerk, A. Hofman, J. Jolles, and M. M. Breteler, “Cerebral white matter lesions and subjective cognitive dysfunction: the Rotterdam Scan Study,” Neurology, vol. 56, no. 11, pp. 1539–1545, 2001. View at: Publisher Site | Google Scholar
  20. A. S. Zigmond and R. P. Snaith, “The Hospital Anxiety and Depression Scale,” Acta Psychiatrica Scandinavica, vol. 67, no. 6, pp. 361–370, 1983. View at: Publisher Site | Google Scholar
  21. I. Bjelland, A. A. Dahl, T. T. Haug, and D. Neckelmann, “The validity of the Hospital Anxiety and Depression Scale. An updated literature review,” Journal of Psychosomatic Research, vol. 52, no. 2, pp. 69–77, 2002. View at: Publisher Site | Google Scholar
  22. J. H. Vercoulen, C. M. Swanink, J. F. Fennis, J. M. Galama, J. W. van der Meer, and G. Bleijenberg, “Dimensional assessment of chronic fatigue syndrome,” Journal of Psychosomatic Research, vol. 38, no. 5, pp. 383–392, 1994. View at: Publisher Site | Google Scholar
  23. J. Hochstenbach, T. Mulder, J. van Limbeek, R. Donders, and H. Schoonderwaldt, “Cognitive decline following stroke: a comprehensive study of cognitive decline following stroke,” Journal of Clinical and Experimental Neuropsychology, vol. 20, no. 4, pp. 503–517, 1998. View at: Publisher Site | Google Scholar
  24. J. H. Loge, O. Ekeberg, and S. Kaasa, “Fatigue in the general Norwegian population: normative data and associations,” Journal of Psychosomatic Research, vol. 45, no. 1, pp. 53–65, 1998. View at: Publisher Site | Google Scholar
  25. A. G. van Norden, W. F. Fick, K. F. de Laat et al., “Subjective cognitive failures and hippocampal volume in elderly with white matter lesions,” Neurology, vol. 71, no. 15, pp. 1152–1159, 2008. View at: Publisher Site | Google Scholar
  26. N. A. Maaijwee, R. M. Arntz, L. C. Rutten-Jacobs et al., “Post-stroke fatigue and its association with poor functional outcome after stroke in young adults,” Journal of Neurology, Neurosurgery & Psychiatry, vol. 86, no. 10, pp. 1120–1126, 2015. View at: Publisher Site | Google Scholar
  27. L. Snaphaan, S. van der Werf, K. Kanselaar, and F. E. de Leeuw, “Post-stroke depressive symptoms are associated with post-stroke characteristics,” Cerebrovascular Diseases, vol. 28, no. 6, pp. 551–557, 2009. View at: Publisher Site | Google Scholar
  28. C. Oppenheim, C. Lamy, E. Touze et al., “Do transient ischemic attacks with diffusion-weighted imaging abnormalities correspond to brain infarctions?” American Journal of Neuroradiology, vol. 27, no. 8, pp. 1782–1787, 2006. View at: Google Scholar
  29. S. T. Pendlebury and P. M. Rothwell, “Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis,” Lancet Neurology, vol. 8, no. 11, pp. 1006–1018, 2009. View at: Publisher Site | Google Scholar
  30. L. Blanco-Rojas, A. Arboix, D. Canovas, M. Grau-Olivares, J. C. Oliva Morera, and O. Parra, “Cognitive profile in patients with a first-ever lacunar infarct with and without silent lacunes: a comparative study,” BMC Neurology, vol. 13, p. 203, 2013. View at: Publisher Site | Google Scholar
  31. C. S. Desai, S. S. Martin, and R. S. Blumenthal, “Non-cardiovascular effects associated with statins,” BMJ, vol. 349, article g3743, 2014. View at: Publisher Site | Google Scholar

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