Problems with using or understanding language (aphasia) appear, according to statistics from studies conducted by NABI (National Stroke Association), in 25 patients out of 100. Every fourth patient experiences difficulties associated with verbal communication - the ability to speak, write or understand spoken language. and written language. This indicates that acute cerebrovascular accident affected one or more language control centers.
Aphasia is a symptom of brain damage, not a disease. As individual as the picture of damage is, the manifestation of aphasia in each patient is as individual. This condition determines the individual nature of the selection of speech restoration techniques after a stroke for each patient.
There are four main types of post-stroke speech disorders
Damage to the language center in the dominant hemisphere - Broca's area - leads to the fact that patients lose the ability to convey their thoughts using coherent and grammatically correct language structures. Conversely, pathological changes in Wernicke's area (sensory center) lead to problems in receptivity to language. Such patients have difficulty understanding spoken or written language. They often use correct grammatical structures, but their statements may not make sense. The most severe form of aphasia (global or total) occurs in patients with extensive damage to several areas of the brain responsible for understanding and language. The mildest form of aphasia—amnestic—leads to difficulty working with vocabulary.
How do these types of aphasia manifest themselves in practice?
Damage to the language center in the dominant hemisphere - Broca's area - leads to the fact that patients lose the ability to convey their thoughts using coherent and grammatically correct language structures. Conversely, pathological changes in Wernicke's area (sensory center) lead to problems in receptivity to language. These patients have difficulty understanding spoken or written language. They often use correct grammatical structures, but their statements may not make sense. The most severe form of aphasia (global or total) occurs in patients with extensive damage to several areas of the brain responsible for understanding and language. The mildest form of aphasia—amnestic—leads to difficulty working with vocabulary.
How do these types of aphasia manifest themselves in practice?
- Motor aphasia. You know what you want to say, but you can’t find (remember, use and pronounce) the right words.
- Sensory aphasia. You hear someone speak or see printed text, but cannot understand the meaning of the words.
- Amnestic aphasia. You find it difficult to select and use the correct words to refer to certain people, objects, places or events.
- Global aphasia. You cannot speak, write, read and do not understand what is being said to you.
SENSORY APHASIA
Stage of severe disorders
1. Accumulation of everyday passive vocabulary:
— display of pictures depicting objects and actions by their names, functional, classification and other characteristics
— display of pictures depicting objects belonging to certain categories (“clothing”, “dishes”, “furniture”, etc.);
- showing body parts in the picture and in yourself;
- choosing the correct name of the object and action among the correct and conflicting designations based on the picture.
2. Stimulation of understanding of situational phrasal speech:
- answering questions with words “yes”, “no”, affirmative or negative gesture;>
- following simple oral instructions;
— capturing semantic distortions in simple phrases deformed in meaning.
3. Preparation for restoration of written speech:
— laying out captions for subject and simple plot pictures;
— answers to questions in a simple dialogue based on visual perception of the text of the question and answer;
- writing words, syllables and letters from memory;
- “voiced reading” of individual letters, syllables and words (the patient reads “to himself”, and the teacher reads out loud);
- development of the “phoneme-grapheme” connection by selecting a given letter and syllable by name, writing letters and syllables under dictation.
Moderate stage of disorders
1. Restoration of phonemic hearing:
- differentiation of words that differ in length and rhythmic structure;
- highlighting the same 1st sound in words of different lengths and rhythmic structures, for example: “house”, “sofa”, etc.;
- highlighting different 1st sounds in words with the same rhythmic structure, for example, “work”, “care”, “gate”, etc.;
- differentiation of words that are similar in length and rhythmic structure with disjunctive and oppositional phonemes by identifying differentiated phonemes, filling in gaps in words and phrases; capturing semantic distortions in a phrase; answers to questions containing words with oppositional phonemes; reading texts with these words.
2. Restoring understanding of the meaning of a word:
— development of generalized concepts by classifying words into categories; selection of a generalizing word for groups of words belonging to one or another category;
— filling in gaps in phrases;
- selection of definitions for words.
3. Overcoming oral speech disorders:
— “imposing a framework” on a statement by composing sentences from a given number of words (instructions: “Make a sentence of 3 words!”, etc.);
— clarification of the lexical and phonetic composition of the phrase using the analysis of verbal and literal paraphasias admitted by the patient;
— elimination of elements of agrammatism using exercises to “revitalize” the sense of language, as well as analysis of grammatical distortions.
4. Restoration of written speech:
- strengthening the “phoneme-grapheme” connection by reading and writing letters under dictation;
— various types of sound-letter analysis of the composition of a word with a gradual “collapse” of external supports;
- writing from dictation of words and simple phrases;
- reading words and phrases, as well as simple texts, followed by answers to questions;
- independent writing of words and phrases from pictures or written dialogue.
Stage of mild disorders
1. Restoring understanding of extended speech:
— answers to questions in an expanded, non-situational dialogue;
- listening to texts and answering questions about them;
— capturing distortions in deformed compound and complex sentences;
— understanding of logical and grammatical figures of speech;
— implementation of oral instructions in the form of logical and grammatical figures of speech.
2. Further work to restore the semantic structure of the word:
- selection of synonyms as homogeneous members of a sentence and out of context;
- work on homonyms, antonyms, phraseological units.
3. Correction of oral speech:
— restoration of the self-control function by fixing the patient’s attention on his mistakes;
- compiling stories based on a series of plot pictures;
- retelling texts according to plan and without plan;
— drawing up plans for texts;
- composing speech improvisations on a given topic;
— speech sketches with elements of “role-playing games”.
4. Further restoration of reading and writing:
— reading expanded texts, various fonts;
- dictations;
- written statements;
- written essays;
- mastering samples of congratulatory letters, business notes, etc.
Stroke: restoration of speech. Exercises
Patients diagnosed with aphasia and speech disorders are concerned with the following questions: is it possible to fully recover from a stroke and how long will it take?
First of all, it is necessary to take into account the irreversibility of the process of destruction of brain cells. To restore the patient’s ability to speak, specialists will need to select means of recovery after a stroke that will help switch speech functions to the closest areas of the brain not affected by the disease. And the timing depends, among other things, on the high inertia of brain cells - after all, it is necessary to switch them to functions unusual for them
Many methods have been developed for restoring speech after a stroke that can speed up this process - speech, melodic, visual, artistic, etc. These speech therapy methods are used along with drug therapy - the patient is prescribed drugs that can stimulate the formation of new neural connections.
The method of intonation (melodic) therapy is based on “singing”. The patient is asked to sing words that cannot be pronounced clearly. Visual therapy uses the ability to form associations between words denoting an object and their visual image.
The most common method of treating aphasia is speech therapy. Classes on the method are conducted with a speech therapist-aphasiologist and are included in the course of intensive rehabilitation of patients after a stroke to the extent necessary for a particular patient.
Exercises to restore speech after a stroke begin with a complex that is designed to gradually restore the patient’s articulatory skills. This could be pronouncing individual sounds, syllables or words, or pronouncing tongue twisters. The exercises are performed with a speech therapist, and the results are consolidated independently in your free time. The more intense the exercise, the greater the likelihood of recovery.
Prognostic role of IS-related factors
A retrospective analysis of data from the acute period of stroke from the study cohort ( n
= 40) revealed a direct positive relationship between the initial severity of IS (NIHSS scores on the 1st day of IS) and the initial degree of aphasia on days 1-3 of IS (β = 0.08;
p
≤0.02), while the severity of IS (NIHSS scores on day 1) is an independent prognostic factor for the risk of severe aphasia on days 1–3 of IS (OR 4.07; 95% CI [1.25– 13.24]).
Similar results were obtained in a number of clinical studies of the acute period of stroke [35, 36]. The independent prognostic value of this indicator also remains for assessing the degree of aphasia by the 3rd month of AI (OR 3.27; 95% CI [1.02–9.77]). The degree of functional recovery of patients by the 21st day (mRs scores) is significantly positively associated with the recovery of speech functions by the 3rd month of AI (β=1.24; p
≤0.002), although this indicator is not an independent prognostic factor.
The initial severity of aphasia on the 1st day of IS is considered as an independent risk factor for the severity of aphasia by the 3rd month of IS and the 1st year of the disease [37, 38]. The results obtained do not confirm the independent prognostic significance of the initial severity of aphasia for the subsequent restoration of speech function by the 3rd month of the disease. At the same time, linear regression data revealed a direct relationship between the severity of aphasia on the 1st day and the degree of speech impairment by the 3rd month of the disease (β=1.2; p
≤0,000).
In the acute period of IS, 9 (22.5%) patients had a combination of aphasia and dysarthria syndromes. By the 3rd month of the disease, 6 (15%) of them had a regression of dysarthria while maintaining aphasia, and 3 (7.5%) had a regression of aphasia while maintaining dysarthria. In patients with a combination of aphasia and dysarthria in the acute period of IS, the likelihood of persistence of aphasic syndromes after 3 months is associated with a high degree of disability according to mRs ( p
<0, OR=0.31; 95% CI [0.27–0.35] [39].
Analysis of the statistical significance of the influence of focal motor and sensory neurological deficits in the early recovery period of the disease (total NIHSS score) on the severity of aphasia (average score on speech subtests of the 10-point scoring method) by the 3rd month of the disease before the course of therapy revealed a significant dependence of these signs ( p
=0.005, OR 4.6; 95% CI [1.39–15.11]). The distribution of the severity of speech disorders depending on the initial NIHSS value is presented in Fig. 3.
Rice. 3. Linear positive relationship between the degree of speech impairment and the severity of focal neurological deficit on the NIHSS scale (y-axis) upon admission of patients to the hospital. The x-axis shows scores on the speech subtests of the 10-point HPF assessment method; the y-axis shows NIHSS scores. A similar relationship was observed between the functional recovery of patients (total Barthel index score) and the degree of speech impairment ( p
= 0.004, OR 3.92; 95% CI [1.01–15.21]).
After a course of rehabilitation treatment, an independent effect on regression of aphasia was associated only with the severity of focal neurological deficit according to the total NIHSS score ( p
= 0.001, OR 6.4; 95% CI [1.75–23.35]).
Thus, the severity of motor and sensory deficits is an independent factor influencing the degree of recovery of speech functions by the 3rd month of the disease. The above data suggest that it is one of the pathogenetic factors that worsens the processes of post-stroke plasticity of neuronal networks.
According to neuropsychological examination, all patients showed a decrease in the severity of speech disorders. A significant improvement in speech function was observed in 6 (15%) patients with gross sensory function (by an average of 1.05 points - from 5.09 to 6.14 points according to the 10-point assessment method for HMF) and gross sensorimotor function (by an average of 1.05 points). 03 points - from 2.91 to 3.94 points) aphasia (Fig. 4).
Rice. 4. Dynamics of speech restoration after a course of complex rehabilitation therapy in patients with different forms of aphasia [22]. The abscissa axis shows forms of aphasia; the ordinate axis shows the dynamics of speech restoration, scores. Preserved speech function corresponds to a scale value of 10 points. The observed significant (by more than 1 point) regression of aphasia in patients with mixed and sensory types in all cases led to a change in the degree of its severity to a lighter one at discharge. This result is consistent with observations of maximum regression of sensory aphasia during directed speech therapy in the early recovery period of IS. In the late recovery period of IS, the highest effectiveness of speech therapy was revealed [40] for mixed sensorimotor aphasia.
Thus, the results of our study do not support the hypothesis that certain clinical forms of aphasia have an unfavorable prognostic significance on the effect of rehabilitation treatment. There was no unfavorable prognosis for sensory aphasia for regression of symptoms after a course of rehabilitation treatment. These results do not agree with the data of a number of authors [41–43] about the low therapeutic effectiveness and negative prognostic value of sensory aphasia. This issue probably requires further research. No statistically significant relationship was found between the degree of restoration of speech function and a specific form of aphasia.
A high rate of regression of non-speech disorders was observed in 32 (80%) patients with mixed and sensory (40% of cases each) and 8 (20%) with complex motor aphasia. In 70% of cases, significant regression according to the 10-point assessment method was combined with the presence of severe aphasia, in 40% - moderate. Insignificant dynamics of recovery of non-speech functions was observed in initially mild aphasia: 28 (71%) patients had mild to moderate speech impairment. Thus, in patients with severe speech disorders, cognitive rehabilitation is highly effective in restoring non-speech disorders.
A high significant positive correlation was found between the degree of non-speech impairment and the severity of aphasia ( r
=0.73;
p
<0.05) in patients under 65 years of age.
When calculating this indicator for the entire sample, a high significant positive correlation was also obtained, although the value of the correlation coefficient was lower ( r
= 0.64;
p
< 0.05).
It has been shown that as patients age, the severity of speech disorders becomes more related to the degree of neurodynamic impairment. Thus, in patients over 65 years of age, a significant high correlation was obtained between the degree of non-speech and neurodynamic disorders ( r
= 0.74;
p
< 0.05).
Depressive disorder, qualified as a single depressive episode of varying duration, was identified in 23 (57%) patients according to the psychiatrist’s conclusion and the results of testing according to IASOD-10 (total score ≥6). Upon admission to TsPRiN, the average score on IASOD-10 was M 15.5; 95% CI [6.6–24.4]. According to the regression analysis, a direct positive relationship was revealed between the severity of aphasia (according to the 10-point assessment method) and the development of post-stroke depression (total score ≥6 on the ASHOD-10; β=0.17; p
≤0.03). Determining the severity, clinical features of the course and typological distinctions of depressive disorders in patients who are not capable of verbally describing complaints and emotional state presents significant difficulties [44]. In these cases, it is impossible to use classical diagnostic methods associated with questionnaires using special scales or detailed interviews with patients. Therefore, for the initial identification of depression in the presence of speech dysfunction, it is necessary to use standardized observational scales that record the external manifestations of psychopathological symptoms and syndromes [45, 46]. Using screening using the Russian version of the hospital version of IASHOD-10 and examination by a psychiatrist, depressive disorder was identified in 57% of cases [19, 45]. The results of studies [47, 48], which used other observational scales, also indicate 44–70% of cases of anxiety and depressive disorders in post-stroke aphasia. The identified direct relationship between the severity of aphasia and psychopathological symptoms probably reflects the predominantly exogenous nature of depression. A direct relationship between the severity of focal neurological deficit and depression, showing the reactive nature of the latter, was also observed in the recovery period of IS in other clinical studies [49, 50].
According to a number of studies, the size and localization of post-infarction changes in the speech areas of the left hemisphere, as well as the basal ganglia, are unfavorable predictors of aphasia regression [5, 35, 51], while the localization of the lesion in the left superior temporal gyrus is associated with an unfavorable prognosis for the restoration of speech functions [52]. In contrast to the above data, in the present study, no reliable negative prognostic value was obtained for MRI signs associated with the size of the lesion, damage to various structures of the left perisylvian region and basal ganglia, however, an intact (according to structural MRI) area of the left superior temporal gyrus associated with good recovery of speech function.
The results obtained indicate that there is no direct dependence of the regression of aphasia on the localization of the focus in the early recovery period of I.I. This is likely due to significant variability in the recovery or compensation of speech function associated with the reorganization of intra- and interhemispheric speech neuronal networks. This is consistent with previously obtained data [53] that traditional MRI predictors of regression of post-stroke aphasia in the acute period of IS are insignificant for the later (90 days of IS) period of the disease.
In contrast to the regression of aphasia syndrome, a number of MRI signs showed a significant relationship with the dynamics of non-speech cognitive impairment. A positive linear relationship was revealed between lesions of the left angular gyrus (β=0.92; p
≤0.01) and the absence of regression of non-speech cognitive impairment.
A negative linear relationship was obtained between the localization of post-stroke changes in the left frontotemporal region (β= –0.6; p
≤0.05) and regression of non-speech cognitive, while the volume of the lesion turned out to be significant (β=0.002;
p
≤0.000).
It is known that the leading cause of the formation of chronic cerebrovascular accident is damage to small-caliber arteries caused by hypertension, atherosclerosis, diabetes and their combination [54]. In the study cohort, 80% of patients had MRI signs of varying severity of microangiopathy, probably caused by this underlying vascular pathology. However, according to logistic regression, the severity of MRI signs of microangiopathy is not associated with regression of aphasia (β= –0.19; p
≤0.39) and non-dementia cognitive impairment (β= –0.06;
p
≤0.95).
Modifiable vascular risk factors for IS and aphasia prognosis
According to logistic regression, there was no significant influence of vascular risk factors for IS on the regression of aphasia. Probably, the absence of a direct pathogenetic connection in this case is due to the complex individual functional reorganization of the speech structures of the brain caused by neuroplasticity [55].
According to the results of prospective clinical studies [56, 57], a number of cardiovascular risk factors for IS, including hypertension, type 2 diabetes, hyperlipidemia, are also risk factors for the progression of non-dementia cognitive impairment and the formation of vascular dementia. Our patients revealed a significant linear relationship between the presence of type 2 diabetes (β=0.06; p
≤0.02), hyperlipidemia (β=0.11;
p
≤0.000) and the degree of non-speech (non-dementia) cognitive impairment using a 10-point assessment method. This cause-and-effect relationship confirms the significance of vascular risk factors associated with the pathology of intracerebral arteries and microvasculature for impaired autoregulation of cerebral blood flow, one of the pathogenetic mechanisms of cognitive disorders [58].
Thus, to optimize the process of rehabilitation therapy and develop new approaches to neurorehabilitation of patients with post-stroke aphasia, it is necessary to take into account prognostic factors that influence the regression of speech and non-speech cognitive impairment. A number of risk factors associated with I.I. have been identified. For regression of aphasia both in the acute and recovery periods of the disease, the initial severity of neurological symptoms (total NIHSS score on days 1–3 of stroke) has an independent prognostic value. At the 3rd month of the disease, the independent effect on regression of aphasia is associated with the severity of focal neurological deficit (NIHSS score) and the degree of functional recovery (Barthel index). A number of MRI signs (localization of post-stroke changes in the left angular gyrus, frontotemporal region and lesion volume) had a significant effect on the dynamics of non-speech cognitive impairment. At the same time, traditional MRI predictors of regression of post-stroke aphasia in the acute period of IS turned out to be insignificant for the recovery period of the disease. Therefore, the search for other significant prognostic factors must continue. Biological and social factors (age, gender, education) do not have independent prognostic significance, although a direct relationship between age and certain clinical forms of aphasia has been shown, as well as a significant influence of higher education on the regression of aphasia. Neuropsychological data indicate the influence of its severity on the degree of improvement in speech function. A significant improvement in speech function was revealed in patients with initially severe forms of aphasia, in particular sensory and sensorimotor. In these cases, the effect of speech therapy led to a change in the severity of the disorders. The study results indicate a high level of depression in patients with aphasia. A direct relationship has been revealed between depression and the severity of speech disorders. Considering the negative impact of depression on the rehabilitation process, continued research is necessary for the early diagnosis of affective disorders in this category of patients.
This work was supported by the Russian Science Foundation grant No. 16−15−10419.
The authors declare no conflict of interest.
Causes
Amnestic aphasia is usually observed when the white matter is damaged at the junction of the parietal, occipital and temporal parts of the left or right hemisphere of the brain. It is important to note that the disease does not appear on the affected side, but on the opposite side. In left-handers, the right hemisphere is damaged, and in right-handers, the left. The main etiological reasons are the following factors:
- Traumatic damage to the above-described areas of the brain. Most often this occurs during road traffic accidents and blunt blows to the temporal region of the head with a heavy object. In this case, a rupture of axonal connections of the white matter of the brain of a traumatic nature may form.
- Surgical interventions on brain structures. Damage to neighboring brain structures cannot be ruled out, since anatomically all zones and regions of the brain are closely connected.
- Infectious and inflammatory diseases such as meningitis, encephalitis and brain abscess. Infectious diseases can be of viral or bacterial etiology and often lead to generalized brain damage.
- Neoplasms of a benign or malignant nature.
- Acute and chronic cerebrovascular accidents causing stroke, thrombosis of cerebral vessels or discirculatory encephalopathy.
- Acute intoxication of the body, especially with neurotoxic poisons, or as a result of an overdose of certain medications.
- Separately, lesions of nervous tissue are distinguished in acute renal or liver failure. In this form, metabolic and breakdown products are not removed from the body in a timely manner and lead first to dysfunctional disorders and then to organic damage to brain tissue.
- Mental illnesses.
- Alzheimer's disease and Pick's disease. In Alzheimer's disease, a combination of sensory aphasia with amnestic aphasia is often characteristic, and in Pick's disease, a combination with motor aphasia is more often observed.
There are several risk groups for amnestic aphasia:
- Genetic predisposition. If there are relatives in the family with similar diseases, then the hereditary history is burdened and significantly increases the risk of aphasia for the reasons described above.
- Elderly and senile age. Common extragenital diseases: coronary heart disease, hypertension, epileptic seizures or cluster headache.
Forget like a bad dream
At the Neurospectr Center for Children's Speech Neurology and Rehabilitation, a complex method is used for sensorimotor aphasia in children. The patient receives treatment from a neurologist, and receives speech correction from a speech therapist.
The specialists at our center are well acquainted with the disorders that accompany aphasia. We treat movement disorders and behavioral problems. All this can be done in parallel, and this tactic is considered optimal. The faster recovery begins after damage to the nervous system, the calmer the child, the faster and better the result.
The task of a speech therapist is to help the child restore neural connections or, if brain damage is irreversible, develop new connections to replace the lost ones. For this, exercises are used, some of which are taught by specialists to parents: it is impossible to ensure the necessary intensity of classes in the center, because the child needs to exercise several times a day.
Often, specialists encounter high levels of anxiety in children suffering from sensorimotor aphasia. This is due both to the child’s loss of the usual way of contact with the world, and to the consequences of the damaging factor that led to aphasia. A child’s anxiety and hyperactivity significantly complicates sessions with a speech therapist. But this problem can be solved within the framework of an integrated approach to therapy: a neurologist can prescribe sedatives, which are acceptable for the child’s current condition, or physical therapy. Perhaps the doctor will recommend additional sessions with a psychologist that will help the baby adapt to his temporary condition and believe that everything can be fixed. When the child becomes calmer, progress in his studies with a speech therapist will become even more noticeable.
In children, recovery from sensorimotor aphasia is rapid: mild impairments are compensated for in 4-5 weeks, moderate impairments are usually compensated for in six months. With severe lesions, the exact time required for rehabilitation cannot be predicted in advance. The timing can be clarified as the patient’s condition improves.
