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Diagnostic features of neurocognitive disorders


Dementia and Cognitive Impairment: Epidemiology, Diagnosis, and Treatment

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Classifying neurocognitive disorders: the DSM-5 approach

Review

. 2014 Nov;10(11):634-42.

doi: 10.1038/nrneurol.2014.181. Epub 2014 Sep 30.

Perminder S Sachdev  1 , Deborah Blacker  2 , Dan G Blazer  3 , Mary Ganguli  4 , Dilip V Jeste  5 , Jane S Paulsen  6 , Ronald C Petersen  7

Affiliations

Affiliations

  • 1 Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Prince of Wales Hospital, Barker Street, Randwick, NSW 2031, Australia.
  • 2 Department of Psychiatry, Massachusetts General Hospital/Harvard Medical School, 401 Park Drive, Boston, MA 02215, USA.
  • 3 Duke Institute for Brain Sciences, Duke University, 3521 Hospital South, Durham, NC 27710, USA.
  • 4 Department of Psychiatry, University of Pittsburgh, 3811 O'Hara Street, Pittsburgh, PA 15213, USA.
  • 5 Department of Psychiatry, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
  • 6 Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
  • 7 Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
  • PMID: 25266297
  • DOI: 10.1038/nrneurol.2014.181

Free article

Review

Perminder S Sachdev et al. Nat Rev Neurol. 2014 Nov.

Free article

. 2014 Nov;10(11):634-42.

doi: 10.1038/nrneurol.2014.181. Epub 2014 Sep 30.

Authors

Perminder S Sachdev  1 , Deborah Blacker  2 , Dan G Blazer  3 , Mary Ganguli  4 , Dilip V Jeste  5 , Jane S Paulsen  6 , Ronald C Petersen  7

Affiliations

  • 1 Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Prince of Wales Hospital, Barker Street, Randwick, NSW 2031, Australia.
  • 2 Department of Psychiatry, Massachusetts General Hospital/Harvard Medical School, 401 Park Drive, Boston, MA 02215, USA.
  • 3 Duke Institute for Brain Sciences, Duke University, 3521 Hospital South, Durham, NC 27710, USA.
  • 4 Department of Psychiatry, University of Pittsburgh, 3811 O'Hara Street, Pittsburgh, PA 15213, USA.
  • 5 Department of Psychiatry, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
  • 6 Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
  • 7 Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
  • PMID: 25266297
  • DOI: 10.1038/nrneurol.2014.181

Abstract

Neurocognitive disorders--including delirium, mild cognitive impairment and dementia--are characterized by decline from a previously attained level of cognitive functioning. These disorders have diverse clinical characteristics and aetiologies, with Alzheimer disease, cerebrovascular disease, Lewy body disease, frontotemporal degeneration, traumatic brain injury, infections, and alcohol abuse representing common causes. This diversity is reflected by the variety of approaches to classifying these disorders, with separate groups determining criteria for each disorder on the basis of aetiology. As a result, there is now an array of terms to describe cognitive syndromes, various definitions for the same syndrome, and often multiple criteria to determine a specific aetiology. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) provides a common framework for the diagnosis of neurocognitive disorders, first by describing the main cognitive syndromes, and then defining criteria to delineate specific aetiological subtypes of mild and major neurocognitive disorders. The DSM-5 approach builds on the expectation that clinicians and research groups will welcome a common language to deal with the neurocognitive disorders. As the use of these criteria becomes more widespread, a common international classification for these disorders could emerge for the first time, thus promoting efficient communication among clinicians and researchers.

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Publication types

MeSH terms

Grant support

  • P50 AG005134/AG/NIA NIH HHS/United States
  • R01 MH099987/MH/NIMH NIH HHS/United States
  • K07 AG044395/AG/NIA NIH HHS/United States

classification, main causes and treatment uMEDp

The article provides a definition, classification, diagnostic criteria, principles of pathogenetic and symptomatic therapy of non-dementia cognitive impairment. The possibilities of using the dopaminergic and noradrenergic drug piribedil (Pronoran) for the treatment of mild and moderate cognitive impairments that do not reach the severity of dementia are considered in detail.

Table 1. Cognitive Functions (according to DSM-V)

Table 2. DSM-V

Diagnostic Criteria for Moderate and Severe Neurocognitive Impairment

Table 3. Classification of cognitive impairment by severity [5]

Table 4. Diagnostic criteria for depression according to the International Classification of Diseases, 10th Revision

Fig. 1. The increase in the sum of points on the Montreal scale for assessing cognitive functions during therapy with Pronoran (group A), piracetam (group B), ginkgo biloba (group C) and vinpocetine (group D)

Fig. 2. Dynamics of subjective neurological symptoms during therapy with Pronoran (p < 0.05)

About 90% of the area of ​​the human cerebral cortex is involved in cognitive activity. Therefore, most neurological diseases with an interest in the brain are accompanied by certain cognitive disorders. Usually they are combined with changes in the emotional-behavioral sphere, being united by a common pathomorphological and pathophysiological substrate. A practicing neurologist needs to assess the presence and characteristics of cognitive and other neuropsychiatric disorders and take this information into account when diagnosing syndromic, topical and nosological diseases of the nervous system.

Cognitive impairment is of equal importance to clinicians in other medical specialties. The target organ of many somatic diseases, in particular, diseases of the cardiovascular system that are widespread in old age, is the brain. In this case, the assessment of the state of the brain is extremely important for assessing the effectiveness of controlling the underlying disease and choosing a therapeutic tactic.

The presence of cognitive impairments has an extremely negative impact on the quality of life of the patient and his immediate family, makes it difficult to treat concomitant diseases and carry out rehabilitation measures. Therefore, timely diagnosis and the earliest possible start of therapy for existing cognitive disorders are very important.

Definition and classification of cognitive impairments

According to the latest revision of the international recommendations for the diagnosis of mental disorders (Diagnostic and statistical manual of mental diseases - DSM-V), cognitive disorders include a decrease in comparison with the premorbid level of one or more higher brain functions that provide the processes of perception, storage, transformation and transmission of information (Table 1) [1].

It is important not only to establish cognitive decline and conduct its qualitative analysis, but also to quantify the severity of existing disorders. It is known that some drugs that are effective in severe cognitive impairment (dementia) have a much lesser effect on cognitive impairment that does not reach the degree of dementia. This is probably due to various neurochemical changes that are noted at the early and later stages of the pathological process [2-4].

Dementia (or, according to DSM-V, severe neurocognitive impairment) is characterized by significant impairment of higher brain functions that interfere with the normal functioning of the patient. With dementia, due to severe cognitive impairment, the patient is at least partially deprived of independence and needs outside help in the most common life situations (for example, when orienting in the area, shopping in a store) (Table 2) [1].

In the treatment of patients with severe cognitive disorders, priority should be given to drugs with a symptomatic effect, which can reduce the severity of disorders and thereby improve the quality of life of patients and their relatives.

The diagnosis of non-dementia cognitive impairment is established in cases where, despite the existing intellectual defect, the patient retains independence in everyday life. At the same time, the patient may feel some difficulties in mental work, which is reflected in complaints. However, the patient overcomes these difficulties without resorting to outside help (Table 2) [1]. In the treatment of patients with non-dementia cognitive disorders, one should not only use symptomatic therapy, but also take measures to prevent dementia.

According to the classification of Academician N.N. Yakhno, non-dementia cognitive disorders are divided into mild and moderate (Table 3) [5]. At the same time, patients with moderate impairments may experience difficulties in the most complex and unusual activities for the patient. At the same time, patients with mild disorders are completely independent and independent in all types of activity, including the most difficult one.

In recent years, the attention of neurologists, psychiatrists and representatives of other neurosciences has increased to an even earlier stage of cognitive deficiency - the so-called subjective cognitive impairment. The wording "subjective cognitive impairment" (subjective memory impairment, cognitive complaints) is currently widely used both in the scientific literature and in everyday clinical practice as an independent diagnosis. This diagnosis is made if there are cognitive complaints, while the results of objective cognitive tests remain within the age norm.

Patients may complain of increased forgetfulness, decreased concentration of attention, increased fatigue during mental work, and sometimes difficulty in finding the right word in a conversation. These complaints are a very urgent problem for the patient, which can serve as an independent or main reason for contacting a doctor. At the same time, the use of standard cognitive tests does not reveal any significant deviations from the accepted standards. Patients with subjective cognitive disorders fully maintain independence in everyday life. Cognitive difficulties are also invisible from the outside: relatives, colleagues and other persons always assess the patient's cognitive abilities as quite intact.

Currently, the following international diagnostic criteria (2014) for the syndrome of subjective cognitive impairment are known [6]:

  • patient complaints about a persistent deterioration in mental performance compared to the past, which arose for no apparent reason;

  • the absence of any deviations from the age norm according to the cognitive tests used to diagnose Alzheimer's disease and other dementing diseases;

  • cognitive complaints are not associated with any established diagnosis of a neurological, psychiatric disease or intoxication.

The dissociation between patient complaints, test results, and patients' day-to-day functioning raises legitimate questions about the true nature of the complaints. These issues are still far from being resolved and are being actively studied. At the present stage of scientific knowledge, it seems that patients with subjective cognitive impairments represent a very heterogeneous group, which includes both patients with the earliest stages of the dementing process, and patients with disorders of the anxiety-depressive and hypochondria spectrum.

In some cases, the predominantly subjective nature of disorders is explained by methodological difficulties in objectifying cognitive status. Currently, there are no generally accepted recommendations on the use of specific methods for the diagnosis of dementia or non-dementia cognitive impairment. Therefore, in practice, tests of varying degrees of sensitivity, specificity and reproducibility are used. The use of tests with low sensitivity will lead to underdiagnosis of mild and moderate cognitive impairments and to overdiagnosis of so-called subjective impairments.

The diagnosis of "subjective cognitive impairment" is often received by patients with a high premorbid intellectual level. The cognitive functions reduced as a result of a cerebral disease in comparison with the individual norm will formally be within the average statistical standard for a long time. Consequently, cognitive decline can remain formally unconfirmed for a long time, in other words, “subjective”.

Complaints of a cognitive nature may be due to anxiety-depressive disorders in the absence of an organic cerebral disease. Thus, patients with a high level of anxiety will be overly concerned about minor situational forgetfulness. In this case, the reason for going to the doctor is such widespread complaints, including among healthy people, such as “I don’t remember why I came to the room”, “I don’t remember what I put where”, “I didn’t recognize a familiar person or didn’t remember him surname", etc.

However, the greatest research interest in a heterogeneous group of patients with subjective cognitive impairments is caused by patients with reduced tolerance to mental stress, since this pathological phenomenon may indeed be the earliest clinical manifestation of the dementing process. As is known, at the very initial stages of a neurodegenerative or cerebrovascular disease, clinical symptoms may be absent, despite the presence of organic brain damage, sometimes significant. This is due to the so-called cerebral reserve, that is, the compensatory capabilities of the brain. The presence of such opportunities will lead to a false negative test result. At the same time, in everyday life, the patient may experience difficulties in special conditions when the cerebral reserve is depleted and cannot overcome the difficulties that arise, for example, in a state of fatigue or emotional stress. At present, the development of the "intellectual treadmill" methodology is being carried out very actively in the world. It will allow assessing the degree of tolerance to increased mental stress, which may decrease to the development of clinically defined cognitive disorders.

International studies show that the risk of developing dementia among patients with subjective cognitive impairment is significantly higher than the average in the population [6]. Therefore, even isolated complaints that are not confirmed by cognitive tests should not be ignored by the attending physicians. They cannot serve as a basis for any specific clinical diagnosis, but their presence is an indication for active prevention, primarily non-pharmacological (mental and physical activity, optimization of nutrition and lifestyle).

Diagnosis of moderate cognitive impairment

As follows from the above criteria (Table 2), the diagnosis of the syndrome of moderate neurocognitive impairment is based, firstly, on the complaints of patients and / or their relatives, and secondly, on objective test results. At the same time, it should be borne in mind that complaints of a cognitive nature are far from always straightforward. Usually, patients with the so-called amnestic type of the syndrome of moderate neurocognitive impairment complain of a decrease in memory or increased forgetfulness, in which progressive memory disorders predominate in their cognitive status. In such patients, Alzheimer's disease is most often established in the future. However, according to the analysis of specialized outpatient admission of patients with cognitive impairment, the most common cause of the syndrome of moderate cognitive impairment is cerebrovascular pathology. Thus, the experience of the first Russian clinic of memory disorders shows that dyscirculatory encephalopathy or the consequences of acute cerebrovascular accidents cause 68% of moderate cognitive impairments [7].

Vascular cognitive impairments in most cases are of the so-called subcortical-frontal type. At the same time, the memory for current events and life events practically does not suffer, and the cognitive status is dominated by a decrease in the concentration of attention and the pace of cognitive activity (bradyphrenia), a violation of frontal control functions (planning and control). A characteristic feature is also the frequent combination of cognitive and emotional-behavioral disorders: depression, apathy or affective lability. It should be emphasized that emotional and behavioral disorders in chronic cerebrovascular insufficiency are of an organic nature and are caused by the same brain damage (dysfunction of fronto-striatal connections) as cognitive impairment. The comorbidity of vascular depression and vascular cognitive impairment is at least 80% [8–11].

Patients with vascular cognitive disorders rarely complain of forgetfulness, since their memory is relatively intact. The structure of complaints is dominated by the so-called subjective neurological symptoms: headache, non-systemic dizziness, noise and heaviness in the head, increased fatigue, sleep disturbances. These symptoms are quite typical for the initial stages of dyscirculatory encephalopathy and in the recent past were considered as an important sign of chronic ischemic brain damage. It is now obvious that headache, dizziness and other unpleasant sensations in the head cannot be a direct result of cerebral ischemia. The pathogenesis of subjective neurological symptoms is more complex and is associated primarily with existing cognitive, emotional and motor disorders. So, headache most often has the character of a tension headache, which, as you know, is almost always caused by anxiety and / or depression. Sleep disturbances also have an emotional cause. Increased fatigue can either be a sign of depression (Table 4) or reflect a decrease in mental performance. In the latter case, this complaint is the subjective equivalent of cognitive disorders. Dizziness in chronic cerebrovascular insufficiency is usually non-systemic and is described as a feeling of unsteadiness when walking. Behind this sensation, as a rule, there are real imbalances due to damage to the fronto-striatal and fronto-cerebellar connections.

Subjective neurological symptoms are almost always present in the initial stages of chronic cerebrovascular insufficiency. They cannot be the basis for a diagnosis, but should lead the doctor to suspect a chronic cerebrovascular disease. To confirm the diagnosis, a thorough assessment of the cognitive and emotional status using objective methods is required. At the stage of moderate (non-dementic) cognitive disorders, the most sensitive methods should be used, for example, the Montreal Cognitive Assessment Scale [12].

Pathogenetic and symptomatic therapy of non-dementia cognitive impairments

To date, a unified generally accepted protocol for the management of patients with cognitive impairments that do not reach the severity of dementia has not been finally developed. Many international studies have failed to demonstrate that pharmacotherapy with drugs such as acetylcholinesterase inhibitors, piracetam, non-steroidal anti-inflammatory drugs prevents or reduces the risk of dementia [2-4]. At the same time, the same studies showed the ability of some of the above drugs to reduce the severity of symptoms in patients with mild cognitive impairment syndrome.

Currently, vasotropic and neurometabolic drugs, the dopaminergic and noradrenergic drug piribedil (Pronoran), and NMDA receptor blockers are widely used empirically in everyday clinical practice.

The results of a number of large studies and practical experience indicate the clinical effectiveness of the drug piribedil (Pronoran). Pronoran has a complex mechanism of action: it stimulates postsynaptic D 2 / D 3 - dopamine receptors and blocks presynaptic alpha-adrenergic receptors. At the same time, the blockade of presynaptic adrenergic receptors leads to an increase in cerebral noradrenergic activity. Thus, against the background of the use of this drug, the activity of two cerebral neurotransmitter systems increases: dopaminergic and noradrenergic. Both of these systems are directly involved in cognitive activity. At the same time, it is believed that dopaminergic stimulation of the prefrontal cortex, indirectly through the mesocortical dopaminergic pathway, plays an important role in attention processes and provides intellectual flexibility, that is, the ability to change the behavioral paradigm. Noradrenergic activation is important for the processes of memorization and reproduction of information, since it provides the optimal level of concentration and motivation for mnestic activity. With age, the synthesis and activity of both dopamine and norepinephrine decrease. Therefore, the correction of these neurotransmitter disorders against the background of the use of Pronoran helps to reduce the severity of age-associated disorders of attention and memory. In addition, due to the adrenoblocking and dopaminergic action, Pronoran also has a favorable vasotropic effect, which creates additional benefits in case of cognitive impairment of vascular etiology [13-16].

In clinical practice, Pronoran is used to treat mild and moderate cognitive impairment that does not reach the severity of dementia in patients over 50 years of age. The drug can be prescribed both for vascular cognitive impairment and at the initial stages of the neurodegenerative process. A large number of clinical studies have been performed for this indication, including those using a double-blind method. For example, in France in the 1980s. 14 clinical studies were conducted, in which more than 7 thousand patients with non-dementia cognitive impairments took part. It has been shown that Pronoran contributes to a significant improvement in memory, concentration and intellectual flexibility, that is, the ability to change the paradigm of behavior depending on external conditions [17, 18]. In 2001, the clinical efficacy of Pronoran was again demonstrated by D. Nagaradja and S. Jayashree. The authors used Pronoran in the syndrome of moderate cognitive impairment in accordance with modern diagnostic criteria. It was shown that against the background of the study drug, there was a more than two-fold increase in the frequency of cognitive improvement on the short mental status assessment scale compared with placebo, which was statistically and clinically significant [19].

Currently, Russian specialists also have significant experience in using Pronoran in patients with cognitive impairments that do not reach the severity of dementia. Thus, as part of the PROMETHEUS study, 574 patients from 33 cities in 30 regions of Russia, including 336 women and 207 men, aged 60 to 89 years (mean age 69. 5 ± 5.5 years) received Pronoran with mild or moderate cognitive impairment. . Patients with cognitive complaints who scored 25–27 points on the Mini Mental Status Scale or who performed the clock drawing test with errors but did not meet the diagnostic criteria for dementia were selected for treatment. During therapy, a statistically significant improvement in cognitive functions was recorded, which was noted as early as the sixth week of treatment and further increased until the end of the 12-week follow-up. At the same time, one part of the patients received Pronoran monotherapy, and the other part received Pronoran in combination with vasotropic and / or neurometabolic drugs. No significant difference was shown between these groups of patients, that is, the combination of Pronoran with vasotropic and neurometabolic therapy had no advantages over monotherapy with the study drug [20, 21].

In the largest Russian non-comparative study, Pronoran was treated by more than 2,000 patients aged 50 to 94 years (mean age 64. 9 ± 8.3 years) with a diagnosis of stage 1 or 2 dyscirculatory encephalopathy and with mild or moderate cognitive impairment. violations. All patients took Pronoran for three months. According to the attending physicians, in 2/3 of cases there was a significant or moderate improvement in cognitive and other neurological functions [22].

According to some data, the magnitude of the therapeutic effect of dopamine and noradrenergic therapy in relation to non-dementia cognitive disorders may be greater than that of other vasotropic and neurometabolic drugs actively used in clinical practice. In the FUETE study, 189 patients were observed, including 139 women and 57 men, aged 42 to 82 years (mean age 63.6 ± 8.5 years) with cognitive disorders that did not reach the severity of dementia, against the background of arterial hypertension and cerebral atherosclerosis . The patients were treated with various drugs, while the representatives of the therapeutic groups did not differ in age, level of education and clinical features of the underlying disease. Against the background of the therapy, there was a regression of both subjective and objective cognitive disorders in all compared therapeutic groups. At the same time, the severity of subjective improvement and objective dynamics of cognitive tests against the background of the use of Pronoran after two months of therapy were significantly greater compared with vasotropic and neurometabolic therapy (Fig. 1) [23].

Regression of cognitive disorders, according to special tests, is the main criterion for the effectiveness of the therapy. However, as noted above, many patients with moderate cognitive impairment, primarily of a vascular nature, also complain of headache, non-systemic dizziness, noise, heaviness or other unpleasant sensations in the head, increased fatigue and sleep disturbances. These complaints are of the same nature and are associated with both cognitive impairment and changes in the emotional status of patients at the initial stage of chronic cerebrovascular insufficiency. They significantly reduce the quality of life of patients and are often the main reason for visiting a neurologist. Therefore, the dynamics of subjective neurological symptoms in patients with a syndrome of moderate neurocognitive disorders of vascular etiology during therapy is extremely important for assessing the significance of the clinical effect and the degree of influence of therapy on the daily life of patients. Regression of subjective neurological symptoms contributes most to adherence to therapy.

In the study by N.N. Yakhno et al. (2006) 29 patients with a diagnosis of "moderate cognitive impairment" against the background of dyscirculatory encephalopathy of the first or second stage received Pronoran for three months [24]. At the same time, no other vasotropic or neurometabolic drugs were used. During treatment with Pronoran, the frequency and severity of headache, dizziness, fatigue and subjective feeling of forgetfulness significantly decreased (Fig. 2). Other authors also reported on the weakening of subjective neurological symptoms during the use of Pronoran [17, 18]. Thus, dopamine and noradrenergic therapy contributes to a significant improvement in the well-being of patients, and, consequently, improves the quality of life and adherence to ongoing therapeutic measures.

It can be summarized that to date, Pronoran has established itself as an effective drug that improves cognitive abilities and well-being in patients with the initial stages of organic cerebral diseases without dementia. In contrast to Parkinson's disease, in which significantly higher doses are used, for non-demented cognitive impairment, Pronoran is prescribed at a dose of 50 mg / day once a day. The recommended duration of therapy is at least three months.

Diagnosis of mental disorders in the elderly: modern classifications | Savina

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