Mild Cognitive Impairment in Primary Care

Mild Cognitive Impairment in Primary Care Dewanto Andoko, M.D.1,2 1 Faculty of Medicine, Maranatha Christian University 2 Department of Psychiatry, Cipto Mangunkusumo Hospital Abstract Currently, more and more attention is paid to mild and moderate cognitive impairment that does not cause occupational, social problems, or family relationship disturbance are especially common in primary care practice. Cognitive disorders that do not reach the degree of dementia often co-occur with disorders of the anxiety-depressive spectrum. Diagnosis and management of mild cognitive impairment in primary care, must be carried out at the initial stages of the pathological process, long before the onset of dementia, and proves to be an extremely important task for primary care physicians. Keywords: mild cognitive impairment, mood disorders, sleep disturbances, primary care. Overview Studies of recent decades, shows that in 12 - 17% of people aged 55-65 years suffers from mild cognitive impairment and cognitive functions below standard levels, but did not reach the severity of dementia [3]. There is a high prevalence of cognitive impairment in everyday outpatient neurological practice. Up to 70% of elderly patients who visits a neurologist had some degree of cognitive deficiency. Among the risk factors for cognitive impairment, a low level of education and occupation associated with physical labor were identified. It is assumed that active intellectual activity in young and middle years of life helps to slow down the physiological process of apoptosis of functionally inactive neurons [31]. Also, the cause of these disorders may be a violation of systemic metabolism; for example, various diseases of internal organs, altering systemic metabolism, can lead to cognitive impairment. Psychogenic cognitive impairments are often associated with disorders of the anxiety-depressive spectrum. An increased risk of dementia is observed in older patients with a hereditary history of dementia, speech impairment, hippocampal atrophy on brain MRI, as well as carriers of the pathological gene APOE 4 [7]. Mild cognitive impairment is detected only with a thorough neuropsychological workup and does not affect everyday life, although it can cause subjective anxiety of the patient. According to a research by Sechenov, it is concluded that at the stage of mild cognitive impairment, the predominantly neurodynamic component of higher brain functions is impaired: the reaction rate, the ability to maintain intense intellectual activity for a long period of time, and the ability to work with several sources of information simultaneously. The paucity of clinical symptoms at the stage of mild cognitive impairment makes epidemiological studies of their prevalence among the elderly highly problematic [27]. Moderate cognitive impairment goes beyond the age norm, without, however, leading to limitations in everyday activities and affecting only its most complex forms; such patients generally maintain independence and autonomy. However, these violations in 10-15% of cases within one year tend to progress. According to long-term observations, the risk of developing dementia within 5 years after the diagnosis of “Mild cognitive impairment” is 55-70%. Thus, early detection of individuals with mild cognitive impairment is due to the fact that timely diagnosis of these disorders expands the potential for secondary prevention and therapeutic intervention designed to delay or prevent the onset of professional and social maladaptation due to the development of dementia [28]. However, in most cases, moderate cognitive impairment remains stable for a long time or undergoes reverse development. The reversible cognitive disorder syndrome is usually based on dysmetabolic, dysthymic or functional disorders [26, 46]. As clinical experience shows, against the background of cognitive deficit caused by either affective impairment proper or the presence of a concomitant organic damage to the central nervous system, anxiety-depressive disorders often occur. It is noted that both affective disorders and cognitive deficit can be an early manifestation of organic dementing disease of both vascular and degenerative nature. The issue of differentiating these states has acquired particular relevance in recent years [18; 41; 9; fourteen]. Moreover, as shown by the results of a study conducted by E.J. Bierman et al., Cognitive impairment, are associated more with depressive rather than disturbing symptoms [33]. Many researchers have noted a link between depression in young and middle age and the development of cognitive impairment in the elderly. It is possible that in some cases, emotional disorders are the first symptom of a brain disease, which subsequently leads to dementia. The increased interest in impaired cognitive functions in depression is due to significant changes in the general system of ideas about the etiology and pathogenesis of this disease due to the expansion of the methodological capabilities of the structural and functional study of the brain. It is known that depression is accompanied by activation of the hypothalamic-pituitary-adrenal system, against which the degenerative process develops more rapidly [4, 29, 40]. Neurocognitive dysfunction is as much an integral part of a depressive disorder as mood disorder. This fact served as an impetus for conducting numerous studies aimed at the study of individual cognitive functions. It was shown that the general neuropsychological deficit in depression leads to complete social and family maladaptation of patients [43, 44, 45,]. D.M. Tsarenko in his dissertation research proved that the occurrence of affective-cognitive distortions is associated with a shortage of executive functions that provide planning, regulation and control over targeted activities. Violations of these functions in disorders of the anxietydepressive spectrum were manifested by impaired regulation of attention, working memory and flexibility of thinking. Clinically, this was expressed in a slowdown in thinking, a decrease in speech activity, motor retardation, and impaired performance [25]. Cognitive Impairment due to Anxiety-Depressive Disorder Anxiety-depressive disorders are associated with clinical manifestations and the dynamics of cognitive disorders. These disorders have a complex structure and are characterized by a combination of a deficit of neurocognitive functions (decreased attention, memory, psychomotor speed, impaired speech processes, optical-spatial functions, the ability to set goals and process information), affective-cognitive distortions (associated with the affect of pathological selectivity, inconsistency, and limitation perception, thinking and memory), as well as unbalanced metacognitive processes (self-awareness, self-esteem and self-regulation of cognitive functions). Since depressive symptoms often come to the fore, such patients are regarded for a long time as suffering from anxiety-depressive disorders and do not receive specific care [29, 42, 48]. Cognitive impairment is especially important for protracted depression, which occurs in patients of older age groups. In this regard, the correct clinical qualification of cognitive impairment is an important condition for a comprehensive diagnostic assessment of various options for anxiety-depressive disorders and affects the management tactics of such patients, both in relation to psychotherapy and pharmacotherapy [10, 11, 24]. Elderly people with depressive disorders are less likely than young people to complain about low mood even when their depression is noticeable from the outside. In addition, in the elderly, more often than in the young, hypochondriacal fixation is detected - excessive preoccupation with the state of health and fear of somatic disease. These features are the reason that older people with depressive disorders see their general practitioner with complaints of general health rather than symptoms specific to depressive disorder [12]. It was revealed that depression in old age is characterized by atypical symptomatology, a tendency to chronic subsyndromic course, the prevalence of masked and somatized forms, and a high risk of completed suicides. The social isolation of the elderly, the high incidence of somatic and neurological diseases, and dementia manifestations themselves complicate the diagnosis of depression in these cases, as well as lead to untimely initiation of therapy [2, 22, 26]. Numerous studies emphasize that patients with depression perform worse neuropsychological tests for attention, memory, psychomotor and visual-spatial functions, and speech activity than people who do not suffer from depression [21]. They also have a deficit of attention, memory, psychomotor retardation, impaired executive functions, speed characteristics, basic visual functions [16, 30, 35, 37, 38]. The presence of cognitive impairment, as it were, “increases” the severity of depression when it already exists. A similar combination of vascular depression with severe executive dysfunction leads to a loss of independence, motivational disturbances, an increase in behavioral motor disorders, and worsening of social and family relationships in elderly patients [39, 47]. Disorders of memory and intelligence make it difficult to have productive contact with the patient, which prevents the identification of actually depressive symptoms and an assessment of its role in the structure of the syndrome. Only after the spontaneous end of the depressive phase or the use of antidepressants is it found that dementia is reversible [1]. It was found that with a late debut of depression, especially if depression is accompanied by cognitive impairment, the risk of dementia is increased by 1.5–3 times [49]. According to epidemiological studies, from 50 to 90% of patients with depression complain of poor sleep quality [19]. Sleep anomalies associated with depression include insomnia, which manifests itself in difficulty falling asleep, an increase in the number of night awakenings, early morning awakenings, a decrease in sleep duration, depth and uncomfortable dreams. Results from prospective epidemiological studies indicate that people with insomnia have an increased risk of developing a depressive disorder. D.E. Ford and D.B. Kamerow [36] was the first to demonstrate that individuals complaining of insomnia have a higher risk of developing a new episode of depression. W.W. Eaton et al. [34] found that sleep disturbances accompany 47% of new cases of severe depression that occur next year and serve as a more reliable predictor of severe depression than suicidal thoughts, feelings of worthlessness and guilt, psychomotor lethargy, weight loss, and a feeling of constant fatigue. In a study by N. Breslau et al. [32], it was found that in people with insomnia, the risk of developing a new depressive disorder over the next 3.5 years increased almost four times. Epidemiological studies suggest that the risk of new cases of anxiety disorder and alcohol abuse is also higher in this category of individuals [36]. Some authors, [15, 17, 20], showed that sleep disorders can be detected before the appearance of affective disorders proper, and in the case of masked conditions they are the only symptoms of depression [5, 8, 23]. It is also noted that sleep disorders persist after a certain time after the disappearance of the clinical signs of depression [13]. Conclusion Thus, the results of the studies indicate that the relationship between cognitive and mood disorders may be multidirectional: cognitive impairment may be the result of depression, or depression may be a reaction to a progressive deterioration in cognitive function. 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