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14Wschodnioeuropejskie Czasopismo Naukowe (East European Scientific Journal) #10, 2016
CLINICAL FEATURES OF COGNITIVE IMPAIRMENT AFTER ISCHEMIC STROKE AND FACTORS OF PROGRESSION OF COGNITIVE IMPAIRMENT IN PATIENTS WITH CHRONIC CEREBRAL CIRCULATION ABNORMALITY
Zhukovskyy O.O.
MD, PhD, Associate Professor of the Department of Neurology, Psychiatry and Medical Psychology Bukovinian State Medical
University, Chernivtsi, Ukraine Filipets O.O.
MD, PhD, Associate Professor of the Department of Neurology, Psychiatry and Medical Psychology Bukovinian State Medical
University, Chernivtsi, Ukraine
ne thesis presents the results of defining clinical features of cognitive impairment in patients in the late recovery period after ischemic stroke and determination of factors of progression of cognitive impairment in patients with chronic cerebral flow abnormality. Key words: cognitive impairment, stroke, cerebrovascular disease.
Background. The problem of cognitive impairment is getting more actual social importance that is related to ageing of the population, as well as with the increase of prevalence of diseases and conditions that are associated with cognitive dysfunction (diabetes mellitus, hypothyroidism, circulatory system diseases, somatic pathology, exogenous intoxications, cancer etc.) [3]. Cognitive impairment often develops after stroke and together with neurological deficit leads to social, domestic and professional disadaptation.
Stroke is the second most common cause of dementia which is diagnosed in 20-30% of stroke patients [2]. The risk of early dementia after acute stroke increases five fold and risk of dementia in the first year after brain infarction is nine times higher than in general population.
Cognitive impairment may appear both in acute phase of stroke and in the late recovery period. The type and severity of cognitive decline depends on the type of stroke, localization and volume of lesion, duration of cerebral hypoperfusion, and comorbidities [4]. Cognitive dysfunction in acute phase of stroke can appear as focal deficit such as aphasia, neglect and apraxia, as well as general impairment of memory, attention, executive functions etc.
The most of cognitive functions improve by the end of acute and early recovery period. But some patients experience progressive cognitive decline from mild cognitive impairment to dementia. Many investigators have shown that the decreased cognitive functions may recover during long period of time and the recovery rate differs substantially depending on the preliminary state of patient [5]. The data about dynamics of cognitive functioning after brain infarction that are crucial for finding markers of cognitive decline and improvement of prevention and treatment are lacking
Chronic disturbances of cerebral circulation also manifest clinically with cognitive dysfunction. The main cause of cognitive decline is lesion of small vessels that leads to lacunar infarcts mainly without clinical sighs of stroke. It is presented morphologically as leukoaraiosis or white matter hyperintensities as a result of repeated episodes of transitional local dyscirculation that do not lead to completed infarction [1]. Because of peculiar properties of cerebral blood flow the most frequent localization of lacunar infarctions and leukoaraiosis is basal ganglia and deep structures of white matter. This localization of lesion explains early cognitive impairment.
Untimely diagnosis of the initial stage of cognitive impairment and lack of its effective correction in cerebrovascular disease leads to vascular dementia and patient's disability. Severe decrease of all cognitive functions at the stage of vascular dementia makes
the patient loose independence and self-sufficiency. There are numerous methods for revealing cognitive impairment which can be used even in the outpatient facility. Standard sets of tests with the quantitative assessment of results enable quick evaluation of cognitive functions in a limited time and can be used routinely in neurology practice. Special attention should be paid to the patients who are at high risk of progressive cognitive dysfunction.
The aim of research. In our study we aimed to define clinical features of cognitive impairment in patients in the late recovery period after ischemic stroke and to determine the factors of progression of cognitive impairment in patients with chronic cerebral flow abnormality.
Materials and methods. We have examined 47 patients (26 women and 21 men) with the sequelae of ischemic stroke aged from 48 to 74 years. The mean age of patients was 65.2±1.5 years. The duration of disease was 1-5 years. The study did not include patients with confirmed cognitive impairment before stroke, as well as patients with chronic somatic and endocrine comorbidity that could cause cognitive decline before stroke.
The assessment of dynamics of neurological and cognitive state in patients after stroke was performed with neuroimaging techniques (CT, MRI), neurological scales, neuropsychological scale (MMSE test). Post-stroke cognitive impairment was defined as cognitive deficit that is diagnosed during the first three months after stroke and lasts more than six months and is not associated with the other conditions and diseases (metabolic, endocrine disorders, vasculitis, depression). Post-stroke dementia was diagnosed in case of any type of dementia after stroke independently of its etiology - vascular, degenerative, or combined.
We also examined 48 patients (28 women and 20 men) with cognitive impairment of vascular origin. The mean age of patients was 61.4±4.2 years. All patients underwent neurological and neuropsychological examination, ultrasonography of cerebral arteries and brain CT. Cognitive functions were assessed with MMSE test.
Results and discussion.
According to the results of examination 37 (78.7%) of patients were diagnosed with anterior circulation stroke; among them 19 (51.4%) in the area of left middle cerebral artery, 16 (43.2%) - right middle cerebral artery, 2 (5.4%) - left anterior cerebral artery. Posterior circulation stroke was diagnosed in 10 (21.3%) patients.
Cognitive impairment was found in 80.1% of cases. Clinical presentation of post-stroke cognitive impairment varied from focal neurological deficit to general cognitive dysfunction. We
© Zhukovskyy O. O., Filipets O. O., 2016
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Wschodnioeuropejskie Czasopismo Naukowe (East European Scientific Journal) #10, 2016
have assessed the level of memory, gnosis (attention, perception) and executive functions with MMSE test. The results have shown that more severe cognitive deficit was found in patients with infarctions in the left cerebral hemisphere with anterior circulation stroke. Besides, cognitive impairment was associated with the volume and number of lesions. Large hemispheric infarctions and multiple infarctions were found in patients with moderate cognitive impairment (MMSE score 24-27) and dementia (>23). The peculiarity of cognitive dysfunction was predominance of impairment of praxis and speed of thinking over decrease of memory that is typical for cognitive decline of vascular origin.
In patients with dementia the most prevalent localization of infarctions was left angular gyrus, inferior medial part of temporal lobe, medial area of the frontal lobe, thalamus, genu of the left internal capsule and caudate nucleus. This coincides with the data from the other investigators that the lesion of deep structures of the white matter and basal ganglia plays the leading role in formation of cognitive insufficiency. It leads to weakening of connection between frontal lobes and subcortical ganglia and to secondary dysfunction of frontal lobes. Normal functioning of frontal lobes is very important for cognitive activity, formation of motivation, selection of goals, and creation of a program and control of its realization.
Neurological deficit in patients with chronic cerebral flow abnormality was commonly presented by pyramidal insufficiency, ataxia, cephalgia and cognitive impairment. The comorbid pathology that led to chronic ischemia was cerebral atherosclerosis (72.9%), hypertension (68.8%), hypercholesterolemia (60.4%), heart failure (47.9%), diabetes (18.8%) and myocardial infarction (16.7%).
The results of neuropsychological examination revealed that the average severity of cognitive decline corresponded to pre-dementia. The general level of cognitive productivity according to MMSE was 26.2±1.2. Moderate cognitive impairment was diagnosed in 15 patients (31.2%), mild - 25 (52.1%). In case ofmild cognitive dysfunction we found separate cognitive symptoms that
did not form single clinical syndrome. 8 patients (16.7%) did not show any cognitive dysfunction. The characteristic feature of the patients was that there was impairment of all cognitive spheres but the most affected were attention, intellectual operations, spatial praxis and gnosis.
The study of prevalence of risk factors in patients with different level of cognitive decline has shown that patients with moderate cognitive impairment had hypertension and cerebral atherosclerosis more often than patients with mild dysfunction - 86.7 vs. 66.7% and 88.0 vs. 68.0% respectively. The percentage of patients with cognitive decline in the group with hypertension was significantly higher than in the group without hypertension (58.8 and 38.2%, p<0.05). Patients with cerebral atherosclerosis more frequently had moderate cognitive impairment than patients without clinically significant atherosclerosis (49.9 vs. 34.1%). There was direct correlation between the level of cognitive deficit and atherosclerosis (r=0.32, p<0.05). In the group of patients with leukoaraiosis on brain CT moderate cognitive impairment was diagnosed in 52.1% of cases vs. 37.0% in patients without leukoaraiosis. There was positive correlation between leukoaraiosis and the level of cognitive decline (r=0.41, p<0.05).
Conclusions. We diagnosed cognitive impairment in the majority of patients in the late recovery period of ischemic stroke. Clinical manifestation of post-stroke cognitive impairment is quite heterogeneous and they can have vascular, degenerative or combined etiology. Changes of cognitive functions in patients with the sequelae of cerebral infarction need further study for effective prevention of progressive cognitive decline.
Cognitive disorders also are diagnosed in majority of patients with chronic disturbances of cerebral circulation and they can be the only clinical sign of cerebrovascular disease for a long period of time. Much attention should be paid to the assessment of cognitive sphere in patients with cerebral atherosclerosis and hypertension. Early detection and correction of cognitive disorders is a prerequisite for improved prognosis and effective treatment.
References:
1. Arboix A. Lacunar infarct and cognitive decline. Expert Rev Neurother 2011, 11(9); 1251-4.
2. Danovska M., Stamenov B., Alexandrova M., Peychinska D. Post-stroke cognitive impairment - phenomenology and prognostic factors. Journal of IMAB - Annual Proceeding (Scientific Papers) 2012, 18(3); 290-297.
3. Deary I.J., Corley J., Gow A.J., Harris S.E., Houlihan L.M., Marioni R.E., Penke L., Rafnsson S.B., Starr J.M. Age-associated cognitive decline. Br Med Bull 2009, 92(1); 135-152.
4. Hillis A., Kleinman J., Newhart M., Heidler-Gary J., Gottesman R., Barker P.B., Aldrich E., Llinas R., Wityk R., Chaudry P. Restoring cerebral blood flow reveals neural regions critical for naming. J Neurosci 2006, 26; 8069-73.
5. Hochstenbach J.B., den Otter R., Muilder T.W. Cognitive recovery after stroke: a 2-year follow-up. Arch Phys Med Rehabil 2003, 84(10); 1499-504.
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