Aphasia can occur as a result of damage to the areas of the brain that control speech. a disease characterized by partial or complete loss of speech. As a rule, the disease is sudden and occurs as a result of a stroke. However, in some cases, the disease can develop gradually, for example due to infection, brain tumor, dementia.
With aphasia, a person almost completely loses the ability to speak and understand speech. In addition, the sick person is unable to read and write. This disease mainly affects older people, but aphasia can also develop in children.
Classification of aphasias
Sensory aphasia. a disorder resulting from damage to the temporal lobe of the brain, usually the left. This disease is also called Wernicke's aphasia. Patients with this disease can speak in long sentences that do not make sense, construct new words on their own and add them to sentences. Because of this, their speech is almost impossible to understand. Also, with Wernicke's aphasia, it is difficult for a person to understand someone else's speech. Since the areas of the brain that control movement are not damaged, the patient's behavior and movements are quite adequate.
Motor aphasia. speech impairment, which occurs due to damage to the frontal lobe of the brain. Another name is Broca's aphasia. Since speech is difficult for those suffering from aphasia, they are able to pronounce only simple, short sentences, omitting prepositions and some words. The frontal lobe of the brain partially regulates motor skills, so Broca's aphasia can often be accompanied by weakness of the right arm and leg or paralysis.
Symptoms of aphasia
A person with sensory aphasia speaks normal words fluently, including nonsense phonemes in sentences without being aware of their meaning. Patients with this condition realize that their speech cannot be understood by others.
People with motor aphasia are able to understand the speech of others relatively well. But there are difficulties with pronouncing words. Writing and speech production are usually impaired, which creates difficulties in communication. Anomia (inability to name objects correctly) may also be present.
Aphasia: treatment of the disease
Aphasia therapy is aimed primarily at restoring normal communication. The services of a professional speech therapist in the early stages of the disease give good results: the sooner therapy is started, the greater the chance of recovery.
One of the most important conditions for successful treatment is the direct participation of family members. Relatives of a patient with aphasia should adhere to the following recommendations:
speak in simple, short sentences;
repeat, if necessary, important phrases;
communicate in a natural manner, without focusing on the disease;
try not to correct the patient’s speech;
talk with the patient as often as possible;
do not rush, giving time to pronounce the proposal.
From this article you learned about a disease such as aphasia: what it is, what are the causes, symptoms and methods of treatment.
Owners of patent RU 2380111:
The invention relates to medicine, to the section of neurology and can find application in neurological and neurorehabilitation clinics in the treatment of patients with aphasia. To do this, against the background of speech therapy classes, akatinol memantine is administered according to a certain scheme. During the first week of therapy at a dose of 5 mg/day in the morning with meals. During the second week at a dose of 10 mg/day, 5 mg morning and evening. During the third week, increase the dose to 15 mg/day, administering 10 mg in the morning and 5 mg in the evening. In the fourth week, the dose is increased to 20 mg/day. The maintenance dose is 20 mg/day. The method provides effective treatment of severe severe aphasia due to cerebrovascular accident. 2 tables
The invention relates to medicine, to the section of neurology and can find application in neurological and neurorehabilitation clinics in the treatment of patients in need of speech restoration - aphasia that occurs after strokes or traumatic brain injuries.
Neurorehabilitation is a branch of medicine associated with the restoration and compensation of impaired higher mental functions (HMF), including speech, in patients with focal brain lesions of various origins. Neurorehabilitation is a multi-level, comprehensive system of rehabilitation measures, which also includes drug therapy, physiotherapy, psycho- and occupational therapy, methods of social and psychological adaptation to the environment.
Aphasias are speech disorders that arise from local lesions of the brain, predominantly of the left hemisphere in right-handed people, and represent systemic disorders of various forms of speech activity - independent, dialogical and narrative speech, nominative and reflected speech, grammatical structure of speech and its understanding, written speech . The location and size of the lesion, as well as the mechanisms underlying this or that speech pathology, determine the variability of systemic speech disorders, i.e. forms of aphasia, on the basis of which various classifications of aphasia have been created. In this work, the classification of A.R. Luria was used (Luria A.R. Traumatic aphasia. M., ed. AMNSSSR, 1947).
Patients in need of speech neurorehabilitation receive primary care from speech therapists and neuropsychologists-rehabilitation specialists. Depending on the form and severity of aphasia, various methods and techniques of logotherapy and remedial training are used. To increase the effectiveness of logotherapeutic effects on patients with speech disorders and other congenital disorders, pharmacological agents of targeted action are used.
The first experiments of such medicinal effects have been known since the Second World War and the post-war period. In order to restore normal synaptic conduction and activate temporarily inhibited functions, anticholinesterase drugs began to be used: proserin, eserin, dibazol. The use of prozerin in the observations of Perelman (1947), given in the monograph by A.R. Luria, had a positive effect on tactile and pain sensitivity, as well as on motor function in paretic limbs, but did not improve gnostic, practical and speech functions. The positive effect of anticholinesterase substances (proserine, galantamine, amipyridine) on the efferent part of speech activity in motor aphasia was noted by other authors (for example, Gogitidze N.K. Dynamics of neuropsychological syndromes under the influence of various neurotropic drugs in patients with traumatic brain injury. Abstract of thesis. Candidate of medical sciences. M., 1990, pp. 14-16).
Muscle relaxant drugs (mydocalm, elatin, melliktin) in the drug therapy of patients with aphasia had a positive effect on the latent periods of the patients’ responses in dialogue (Krylova N.A., Alyakrinsky V.V. The influence of curare-like drugs on the state of the speech motor analyzer in aphasia. "Journal. Neuropathology and Psychiatry named after S.S. Korsakov." 1996, v. 66, asp. 12; Markov G. On the treatment of aphasia and dysarthria with psychophorin (Tofranil) and mydocalm. "Journal of Neuropathology and Psychiatry named after S.S. Korsakov". 1973, vol. 73, vosp. 4, pp. 512-513).
There is a known method of treating aphasia with drugs with nootropic and stimulating effects (instenon, complamin, encephabol, piracetam, picamilon, gammalon). The use of the drug instenon in patients with motor aphasia had a positive effect on the dynamics of speech and the emotional-volitional sphere of patients (Popova L.T., Pylaeva N.M., Tsvetkova L.S., Shovskaya N.Yu. On the issue of targeted pharmacological effects in the process of rehabilitation training for patients with aphasia in the post-stroke period. Problems of aphasia and rehabilitation training, Moscow State University, 1975, pp. 206-214).
Experiments using gammalon for the treatment of 48 post-stroke patients with aphasia showed that their general and speech activity increased, reflected and nominative speech, reading and writing improved.
The use of all of the listed medications for the treatment of patients with motor aphasia in most cases was carried out without taking into account the form, severity, duration of the disease, and without assessing the dynamics of individual symptoms. In addition, pharmacotherapy in the treatment of aphasia was not always selective and often caused side effects in the form of disorders of the cardiovascular and respiratory systems (anticholinesterase, nootropic drugs, muscle relaxants).
The closest in technical essence and achieved result to the proposed method is a method for treating aphasia by administering a pharmacological drug to a patient (RU, patent No. 2123858, class A61K 38/11, 1994).
The neuropeptide vasopressin analogue of arginine vasopressin (DDAVP) was used as a pharmacological drug. 45 patients (44 post-stroke and 1 after traumatic brain injury) with various forms of aphasia received treatment. Each patient underwent a thorough examination with each speech symptom assessed. The use of this method reduced the severity of speech disorders, improved the expressive and impressive speech of patients with various forms of aphasia (except for afferent motor aphasia), optimized the attention and performance of patients, and improved the quality of logotherapy.
The disadvantage of the known method of treating aphasia is its low effectiveness.
Interest in targeted medication support for patients with aphasia has contributed to the search for new, more effective drugs that help improve speech in the process of traditional rehabilitation.
The technical result to which the present invention is aimed is to increase the effectiveness of treatment. This technical result is achieved by the fact that in the method of treating aphasia by administering a pharmacological drug to a patient, according to the invention, akatinol memantine is used as a drug according to the following scheme: during the first week of therapy - a dose of 5 mg/day (in the morning with meals); during the second week - a dose of 10 mg/day (5 mg in the morning and evening); during the third week, increase the dose to 15 mg/day (10 mg in the morning and 5 mg in the evening); in the fourth week, the dose is increased to 20 mg/day, with a maintenance dose of 20 mg/day.
In addition, treatment with akatinol memantine can be carried out against the background of speech therapy sessions.
The treatment of various forms of dementia with akatinol memantine, currently carried out at the V.M. Bekhterev Institute, including at the stage when, in addition to intellectual-mnestic disorders, agnostic-apractical and aphasic disorders appear, has made it possible to stabilize the state of cognitive functions for some time in these patients.
This made it necessary to test the effect of akatinol on post-stroke patients suffering from various forms of aphasia in combination, in some cases, with the pathology of other HMFs.
akatinol, the active component of which is memantine, is a non-competitive antagonist of NMDA-N-methyl-D-aspartate receptors, has a modulating effect on the glutamatergic system. Glutamate is the most important excitatory neurotransmitter in the central nervous system, controlling 70% of excitatory neurons. Glutamatergic transmission is responsible for the physiological processes of memory formation, long-term potentiation and synaptic plasticity. Disturbances in the glutamatergic neurotransmission system associated with pathologically prolonged calcium influx into postsynoptic cortical and subcortical neurons contribute to a chronic increase in glutamate concentrations and lead to loss of function and neuronal death. Clinically, this may manifest as signs of progressive dementia. Akatinol memantine, having fast receptive kinetics, prevents pathological activation of NMDA receptors caused by chronically high concentrations of glutamate, improves the process of nerve impulse transmission, compensates for cognitive and functional deficits, improves memory processes, learning ability, and increases daily activity.
When cerebral circulation is impaired, the concentration of glutamate increases. Akatinol, by blocking excess calcium ion channel, remains bound to the receptor even in the presence of increased concentrations of glutamate. It improves the functioning of neurons located on the periphery of the lesion, normalizes the membrane potential of surviving neurons, improves and accelerates the process of nerve impulse transmission, strengthening and expanding synaptic connections. This mechanism of action of akatinol is, according to the authors, the basis for the positive effect of its use - restoration of speech in aphasia. In clinical studies, the safety and tolerability of akatinol memantine was assessed as good to very good. The total incidence of side effects was no different from that in the placebo group. Memantine does not interact with other substances that are necessary for post-stroke patients.
The use of akatinol memantine in the study group of patients was carried out according to the following scheme: during the 1st week of therapy, a dose of 5 mg per day (in the morning with meals), during the 2nd week - at a dose of 10 mg per day (5 mg in the morning and in the evening), during the 3rd week - the dose was increased to 15 mg (10 mg - 1 tablet - in the morning and 5 mg - half a tablet in the evening). At week 4, the dose was increased to 20 mg per day (10 mg in the morning and 10 mg in the evening). The maintenance dose remained 20 mg per day.
In terms of chemical composition and pharmacological action, akatinol memantine has no analogue. To compare the results of treatment with akatinol compared with other drugs for targeted drug treatment of aphasia, we chose DDAVP (1-deamino-8-D-argnine vasopressin). The argument in favor of this decision was that the process of conducting the study and processing the results obtained, previously carried out by the authors on vasopressin, was identical to the study on akatinol. The study was conducted at the V.M. Bekhterev Scientific Research Institute of Scientific Research in the Department of Rehabilitation of Neurological Patients. A detailed neuropsychological examination of patients with aphasia was carried out according to the program adopted at the institute; the severity of symptoms was assessed according to a four-point system we developed: from 0 - normal or minimal impairment, to 3 points - deep decay of the assessed function (Wasserman L.I. (ed.) Standardized set of diagnostic tests neuropsychological methods. L., 1987; and Wasserman L.I., Dorofeeva S.A., Meerson Ya.A. Methods of neuropsychological diagnostics. St. Petersburg, 1997, ed. The state of oral and written speech was scored. 9 speech functions were assessed using 84 indicators: expressive speech - 9, reflected speech (repetition) - 15, pronunciation features of speech - 4, paraphasia (distortion of words) - 3, nominative speech (naming) - 4, speech understanding - 14 each, writing - 5 each, phonemic analysis of words - 6 each, reading - 13 each, auditory speech retention - 1 indicator each. In addition, during a neuropsychological examination in aphasia syndrome, the state of non-speech HMF was also determined: visual and auditory gnosis, various types of praxis: motor, ideamotor, ideational, dynamic, constructive, oral. Orientation in space, in a geographical map, in right-left, in the “body diagram” was studied; the safety of accounting transactions was determined.
The state of non-speech higher mental functions was assessed by their presence or absence. 0 - no violations, 1 - there are violations. The results of the examination were recorded in the form of a protocol, and the assessment of each symptom was entered in the patient’s individual questionnaire twice: before treatment with akatinol and at discharge. Upon repeated admissions, the patient’s speech capabilities were assessed over time.
Treatment with akatinol was carried out against the background of speech therapy sessions.
The drug was used on 30 patients with different forms and varying degrees of severity of aphasia.
The result of using the drug is illustrated by an example.
Patient Ezd-va A., 69 years old, worked as a chief accountant before her retirement. She became acutely ill on 09/20/06, when her speech suddenly became impaired and right-sided hemiparesis developed. She was hospitalized in a city hospital with a diagnosis of acute ischemic cerebrovascular accident in the left middle cerebral artery with mild right-sided hemiparesis and aphasia. During treatment, 2 days later (09.22.06) she suffered a recurrent disorder with worsening right-sided hemiparesis and worsening symptoms of aphasia. CT data: ischemic stroke in the territory of the left middle cerebral artery, cyst in the territory of the left posterior cerebral artery. After a course of treatment with slight improvement, on 11/16/06 she was admitted to the department of rehabilitation of neurological patients at the V.M. Bekhterev Research Institute for Rehabilitation for a course of rehabilitation treatment.
Upon admission: complaints of speech disorders, limitation of movements in the right limbs.
Neurologically, deep right-sided hemiparesis, more pronounced in the arm, hypoesthesia in the right half of the body, areflexia in the right extremities were determined. There were no pathological reflexes. The patient is right-handed.
Clinical diagnosis: stage III hypertension, atherosclerosis of cerebral vessels, consequences of repeated cerebrovascular accidents in the left middle cerebral artery with right-sided hemiparesis and aphasia.
For the first time, the department conducted a neuropsychological examination of the state of higher speech and non-speech functions. The survey data are shown in the table. Severe amnestic (parietal) aphasia was diagnosed in combination with apraxic agraphia and severe parietal symptoms (Gerstmann syndrome) with the lesion localized in the left parietal-temporal, occipital region.
On examination: spontaneous and dialogic speech is phrasal, without distinct agrammatism, lexically impoverished, replete with multiple verbal substitutions (paraphasias), making the patient’s speech often incomprehensible. Constantly repeats the words of a given question or task. There are no pronunciation speech disorders. Oral and symbolic oral praxis are normal. Automated speech is incomplete. Narrative speech is not available. When composing sentences for a single-plot picture, he gives a lengthy description consisting of verbal substitutions that have nothing to do with the plot. Reflected speech was virtually unaffected. Difficulties arose when reproducing complex words, complex and polysyllabic sentences. Gross violations were revealed during the study of the nominative function of speech. Difficulties in naming manifested themselves in two ways: replacing the nomination with verbal paraphasia, which had nothing to do with the semantics of the word, or attempts to give a description of the purpose of the object, which also did not reflect its meaning. Understanding everyday and situational speech was possible. She did not understand the meaning of individual words well. Pronounced violations were revealed when studying the understanding of complex logical and grammatical structures. Gross violations in the study of written speech: reading, writing, sound-letter analysis of words. There was no reading aloud or silently. I added captions - words to subject pictures incorrectly. Writing and copying (with the left hand) was not possible. When trying to write down individual letters or her last name, she drew several short lines with circles intersecting each other, which did not resemble graphemes. The letter system - generalized ideas about the letter (classification) was not affected.
When examining parietal (non-speech) symptoms, gross constructive apraxia, acalculia and finger agnosia (Gerstmann syndrome) were revealed.
In addition to antihypertensive therapy, the patient was prescribed akatinol memantine according to the manufacturer’s recommended regimen: 1 week - 5 mg - in the morning, 2 week 5 mg - 2 times a day, 3 week 10 mg - morning, 5 mg - evening, 4 week and further 10 mg - 2 times a day.
From the first days, rehabilitation speech therapy classes were conducted. During treatment, the general condition improved, the patient became more active, and her interest in logotherapy increased. Positive dynamics were noted in expressive (spontaneous and dialogic) speech. Adequate words appeared and the understanding of individual words improved. Global (ideogram) reading began to recover.
The patient was discharged after three weeks, and a month later she was admitted for re-treatment. As an outpatient, the patient continued to take antihypertensive therapy, akatinol memantine at a dose of 10 mg, 2 times a day. I did not work with a speech therapist during this period.
A repeated neuropsychological examination revealed significant positive dynamics in speech and other higher mental functions (table, column 3). Spontaneous and especially dialogic speech improved. It became clearer, the number of verbal substitutions decreased, perseveration occurred much less frequently - the patient practically stopped repeating the words of the question in her answers. Narrative and monologue speech became possible. Thus, the patient was able to coherently tell her biography, compose a sentence or story based on the plot picture. The understanding of the meanings of words was restored, the ability to perform simple tasks was restored, and the volume of verbal and auditory memory increased. The understanding of complex logical and grammatical structures has significantly improved. The nominative function of speech began to recover. Verbal paraphasias during nomination became closer to the conceptual semantics of the word. The description of the item became more adequate in cases where there was no nomination.
The dynamics of written speech and parietal symptoms turned out to be especially effective. It became possible to read aloud and silently. The nature of reading has changed. If at first the process of putting words-names under the corresponding object pictures was guessing, i.e. was carried out according to the type of ideogram “grasping”, now the patient, although often syllable by syllable with slight paralexia, read the word and only then found the corresponding pictures. Restoring analytical reading contributed to improved reading comprehension, both when reading aloud and when reading silently. It became possible to understand written instructions by silent reading. The restoration of constructive praxis - copying, copying and, partly, independent drawing - contributed to the restoration of apractical agraphia, the mechanism of which was closely related to the collapse of constructive praxis. Not only the process of copying was restored, but it became possible to write letters, syllables, words and phrases under dictation. When writing, there were rare literal paragraphs (like replacing one grapheme with another (Pskov-Tskov, courage-bougestvo), and the mirror spelling of some letters (Я-R, И-N)). The syllabic and letter composition of words was preserved. Other parietal symptoms were restored: finger gnosis, counting within the first ten and, partially, with the transition through ten, orientation in the right-left and in the geographical map.
Table 1 shows changes in individual speech functions during treatment of a patient with amnestic (parietal) aphasia with akatinol memantine.
Table 2 shows changes in individual non-speech higher mental functions during treatment of a patient with amnestic (parietal) aphasia with akatinol memantine.
No side effects were observed when taking akatinol memontine.
The proposed method for the treatment of aphasia compared to the treatment of DDAVP has the following advantages.
1. More effective in the treatment of all forms of aphasia (motor, sensory, “parietal”), including gross afferent motor aphasia with the collapse of articulatory patterns, the treatment method of which DDAVP does not produce results or provides a slight improvement in speech not in the articulatory part.
2. More effective in the treatment of all types of disorders of expressive, impressive written speech.
3. Particularly effective with complex effects - a combination of pharmacotherapy with akatinol memantine and logotherapy.
4. Influences the process of logotherapy, shortening the time for positive dynamics to appear and improving results.
5. Improves speech function in a shorter period of time.
6. Positive dynamics do not depend on the duration of the disease.
7. Constant use of the drug promotes progressive improvement of speech function without logotherapy.
8. Restores or improves the condition of non-speech HMF.
9. Has a more significant therapeutic effect on such mental states of patients as performance, speech activity, emotional-volitional sphere.
10. Restores the dynamics of the speech process itself: readiness and ability to independently engage in speech, strengthening the ability for verbal communication, along with the restoration of the speech process itself.
| Table 1 Changes in individual speech functions during treatment with akatinol memantine in a patient with amnestic (parietal) aphasia |
|||
| No. | Separate speech functions and indicators characterizing them | Example 1 | |
| to | after | ||
| treatment | |||
| 1.0 | Expressive speech: | 3 | 2+ |
| 1.1 | overall rating | ||
| 1.2 | Spontaneous speech | 3 | 2+ |
| 1.3 | Dialogical | 2 | 1+ |
| 1.4 | Narrative | 3 | 2+ |
| 1.5 | Compilation | 3 | 2+ |
| suggestions for the picture | |||
| 1.6 | Writing a story based on | 3 | 2+ |
| 2.0 | picture | ||
| 2.1 | Automated: | ||
| 2.2 | a) counting from 1 to 10 | 1 | 0+ |
| 2.3 | b) days of the week | 2 | 0+ |
| 2.4 | c) naming the months | 3 | 0+ |
| 2.5 | Reflected speech: general | 0 | 0 |
| 2.6 | grade | ||
| 2.7 | Repetition of consonants | 0 | 0 |
| 2.8 | Vowel repetition | 0 | 0 |
| Repeating simple words | 0 | 0 | |
| 2.9 | |||
| 2.10 | |||
| Repetition of syllables | 0 | 0 | |
| 2.11 | Repetition of complex | 2 | 1+ |
| 2.12 | words | ||
| 2.13 | Repetition of foreign | 2 | 1+ |
| 2.14 | words | ||
| 3.0 | Repetition of pseudowords | 2 | 1+ |
| Repeating a series of vowels | 0 | 0 | |
| 3.1 | Repeating a series of syllables | 1 | 0+ |
| 3.2 | Repetition | 0 | 0 |
| 3.3 | sentences of 2-3 words | ||
| 4.0 | Repetition | 2 | 1+ |
| 4.1 | sentences of 4-7 words | ||
| 4.2 5.0 |
Repeating a series of words | 1 | 0+ |
| 5.1 | Repetition | 0 | 0 |
| 5.2 | opposition syllables | ||
| 5.3 | Repetition | 0 | 0 |
| 6.0 | opposition words | ||
| 6.1 | Pronunciation | 0 | 0 |
| 6.2 6.3 |
peculiarities | ||
| 6.4 | overall rating: | ||
| Efforts, tensions, | 0 | 0 | |
| memorization | |||
| Delivering speeches | 0 | 0 | |
| sounds | |||
| Prosody | 0 | 0 | |
| Paraphasia: general | 2 | 2 | |
| grade | |||
| Paraphasia literal | 0 | 0 | |
| Verbal paraphasias | 2 | 1+ | |
| Name: general | 3 | 2+ | |
| item assessment | 3 | 2+ | |
| actions | 3 | 2+ | |
| several at the same time | 3 | 3 | |
| items | |||
| 7.0 | understanding: general assessment | 0 | 0 |
| 7.1 | |||
| 7.2 | |||
| situational speech | 0 | 0 | |
| 7.3 | individual words | 2 | 0+ |
| 7.4 | simple tasks | 0 | 0 |
| 8.0 | difficult grammatical | 3 | 1+ |
| 8.1 | designs: | ||
| a) relationships, | 1 | 0+ | |
| 8.2 | expressed by one | ||
| 8.3 | pretext | ||
| 8.4 | b) -"- two prepositions | 2 | 1+ |
| 8.5 | c) inflectional | 2 | 1+ |
| 9.0 | relationship | ||
| 9.1 | |||
| 9.2 | d) -"- inverted | ||
| designs | 2 | 1+ | |
| 9.3 | |||
| d) passive voice | |||
| 9.4 9.5 |
e) Head's tests | 2 | 1+ |
| 9.6 | g) temporary | 2 | 1+ |
| 9.7 9.8 |
designs | 1 | 0+ |
| 9.9 | h) designs | ||
| 9.10 | genitive case | 2 | 1+ |
| 9.11 | i) sensitized | ||
| 9.12 | samples | 2 | 2 |
| j) retention of speech | |||
| rows by ear | 3 | 2+ | |
| Writing: overall score | |||
| Cheating | 3 | 1+ | |
| writing words under | 3 | 0+ | |
| dictation | 3 | 1+ | |
| writing phrases under | |||
| dictation | 3 | 1+ | |
| independent writing | |||
| phonemic analysis: | 3 | 2+ | |
| overall rating | 3 | 1+ | |
| determination of quantity | |||
| letters in a word | 3 | 2+ | |
| determining the number of letters in | 3 | 2+ | |
| recalled word | |||
| - "- determination of the number of syllables in a word | 0 | 0 | |
| - "- the first letter in the word | 2 | 1+ | |
| -"-last-"- | 3 | 1+ | |
| Reading: Overall Score | 3 | 1+ | |
| Putting captions under pictures | 3 | 1+ | |
| Adding captions to story pictures | 3 | 1+ | |
| Reading | 3 | 1+ | |
| automated ideograms | |||
| Reading individual letters | 3 | 1+ | |
| Reading individual syllables | 3 | 1+ | |
| Reading simple words | 3 | 1+ | |
| Reading difficult words | 3 | 1+ | |
| Reading sentences | 3 | 1+ | |
| Reading text aloud | 3 | 1+ | |
| Reading written instructions to yourself | 3 | 1+ | |
| Silent reading and text comprehension | 3 | 2+ | |
| Reading pseudowords | 3 | 2+ | |
| Legend: | |||
| +improved performance |
| Table 2 Changes in individual non-speech higher mental functions during treatment with akatinol memantine in a patient with amnestic (parietal) aphasia |
||
| Before treatment | After treatment | |
| 10.0 | ||
| 10.0 exploration of movements and actions | ||
| 10.1 spatial praxis - one-handed hand tests | 0 | 0 |
| 10.2 two-handed - hand - hand | 0 | 0 |
| 10.3 Head tests: one-sided | 0 | 0 |
| 10.4 Head tests: cross | 1 | 1 |
| 11.0 dynamic praxis: | ||
| 11.1 right hand | 0 | 0 |
| 11.2 left hand | 1 | 0 |
| 12.reciprocal coordination | 0 | 0 |
| 13. constructive praxis | ||
| 13.1 copying | 1 | 0 |
| 13.2 inversion | 1 | 0 |
| 13.3 drawing independently | 1 | 0 |
| 13.4 sketching | 1 | 0 |
| 13.5 tracing | 1 | 0 |
| 14.0 praxis | ||
| 14.1. articulatory praxis | 0 | 0 |
| 14.2 oral praxis | 0 | 0 |
| 14.3 symbolic oral praxis | 0 | 0 |
| 14.4 motor praxis | 0 | 0 |
| 14.5 ideational praxis | 0 | 0 |
| 14.6 ideamotor praxis | 0 | 0 |
| 15.0 study of the counting system | ||
| 15.1 Reading Prime Numbers | 1 | 0 |
| 15.2 reading complex numbers | 1 | 1 |
| 16.3 writing complex numbers | 1 | 1 |
| 17.0 performing simple counting operations | ||
| 17.1 addition within the first ten | 1 | 0 |
| 17.2 subtraction within the first ten | 1 | 1 |
| 17.3 addition with passing through ten | 1 | 1 |
| 17.4 subtraction with passing tens | 1 | 1 |
| 17.5 repetition of the multiplication table | 1 | 1 |
| 17.6 Performing a serial count | 1 | 1 |
| 18.0 study of somatosensory gnosis | ||
| 18.1 finger gnosis | 0 | 0 |
| 18.2 finger pose | 1 | 0 |
| 18.3 stereognosis | 0 | 0 |
A method of treating severe, severe aphasia due to cerebrovascular accident, characterized by the fact that, against the background of speech therapy sessions, akatinol memantine is administered according to the following scheme: during the first week of therapy at a dose of 5 mg/day in the morning with meals; during the second week at a dose of 10 mg/day, 5 mg in the morning and evening; during the third week, increase the dose to 15 mg/day, administering 10 mg in the morning and 5 mg in the evening; in the fourth week, the dose is increased to 20 mg/day, with a maintenance dose of 20 mg/day.
Main symptoms:
- Replacing some sounds with others
- Impaired concentration
- Writing disorders
- Reading disorders
- Unnatural speech
- Misunderstanding the meaning of spoken words
- Speech decay
- Abrupt switching from one word to another
- Difficulty in naming objects
- Difficulties in speech recognition
- Difficulty constructing sentences
Aphasia is a pathological process in which there is a complete or partial loss of the ability to speak. At the same time, the patient cannot independently express his thoughts in words and understand speech addressed to him. Aphasia occurs when the cerebral cortex is damaged. In the most complex forms of development of this pathological process, the clinical picture is complemented by psychiatric disorders and deterioration in the functioning of the musculoskeletal system. The treatment is complex. Consultation with a neurologist, psychotherapist and speech therapist is required.
Etiology
Etiological factors that can trigger the development of this disease include:
- acute and chronic;
- education ;
- serious cardiovascular diseases – , ;
- infectious diseases that affect the central nervous system;
- degenerative pathologies;
- poisoning with toxic substances.
In addition, risk factors for developing this disease should be highlighted separately:
- or character;
Elderly people are also at risk.
Classification
Depending on the etiological factor and pathogenesis of this disease, the following types of aphasia are distinguished:
- sensory aphasia or Wernicke's aphasia;
- amnestic aphasia;
- sensorimotor aphasia;
- semantic;
- dynamic;
- afferent-motor aphasia.
Depending on the severity of the disease, the following forms of aphasia are distinguished:
- total aphasia – complete impairment of the patient’s speech;
- partial – the ability to express one’s thoughts and speak is observed partially.
It should be noted that in addition to the general clinical picture, this disease will be supplemented by specific symptoms, the nature of which will depend on the form of the disease.
Symptoms
The first and most reliable sign of the development of amnestic and other forms of aphasia is a violation of speech function. The further clinical picture will depend on the location of the pathology.
Sensory aphasia is characterized by the following symptoms:
- the patient hears the speech of another person as an incomprehensible stream of sounds;
- the person does not understand the meaning of the spoken words;
- the patient has difficulty concentrating;
- the patient himself may not perceive his defect.
With amnestic aphasia, the following clinical signs may be observed:
- difficulties in naming objects - the patient knows their name, but cannot express it in words;
- is able to adequately conduct dialogue;
- periodically has difficulty constructing sentences.
With dynamic aphasia, the patient experiences a complete breakdown of speech, although clarity of consciousness and adequate perception of others are maintained.
Broca's aphasia is characterized by the following symptoms:
- the patient speaks in an unnatural way;
- replaces some sounds with others;
- during a conversation can abruptly switch from one word to another;
- Gross impairments in reading and writing are clearly evident.
With the semantic form of aphasia, the patient practically does not perceive logical-grammatical constructions and cannot construct them independently. In some cases, a person may simply not perceive words.
If you have the above symptoms, you should immediately seek medical help and not self-medicate.
Diagnostics
To make an accurate diagnosis and determine the correct course of treatment, consultation may be required, and. The diagnostic program may include the following:
- objective examination, collection of anamnesis and clarification of complaints, time of onset of the clinical picture;
- neurological examination of the patient;
- electroencephalography;
- CT scan of the brain;
- magnetic resonance imaging.
In addition, psychodiagnostics and examination by a speech therapist can be carried out to assess speech function.
Based on the examination results, a final diagnosis is made and the correct course of treatment is prescribed.
Treatment
The treatment of amnestic aphasia and other forms of this disease is based on the elimination of the underlying illness against which aphasia developed. It should be noted that conservative methods of therapy are not always effective, so surgery may be required.
In general, treatment for this disease may include the following:
- surgical removal of tumor formation in the brain;
- taking anticonvulsants if the cause of the disease is epilepsy;
- stabilization of blood pressure, etc.
As for psychotropic drugs, they are prescribed only when absolutely necessary. The regimen and duration of taking such drugs is prescribed strictly by the attending physician.
Speech restoration in aphasia is carried out during classes with a speech therapist. The exercise program is prescribed individually, and will largely depend on the form and degree of development of the disease. However, you need to understand that the effectiveness of this type of therapy will largely depend on the restoration of brain function.
In addition to the course of treatment prescribed by the doctor, there are also general recommendations:
- stimulation of written and oral speech, independent reading;
- the patient must be protected from stress, nervous tension, negative psycho-emotional environment;
- It is better to carry out treatment at home, in a person’s familiar environment;
- since often the patient cannot independently express his thoughts and needs, the support of loved ones is important;
- daily walks in the fresh air;
- social adaptation of the patient.
It should be understood that such patients may require constant supervision, especially if they are elderly.
Forecast
The prognosis of this disease will depend on the etiology and form of the disease. It should also be understood that speech restoration may take several months or several years.
Prevention
There are no targeted recommendations, since most etiological factors cannot be prevented. You can reduce the risk of developing such a disease if you lead a healthy lifestyle and monitor your physiological and psychological health. At the first alarming symptoms, you should consult a doctor.
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Diseases with similar symptoms:
Delayed psycho-speech development is a disease that is characterized by a disruption in the rate of mental development of a child. In most cases, this disease is caused by abnormalities in the development of the nervous system, in particular the brain. The latter may be due to a number of etiological factors, and the incorrect lifestyle of parents is no exception. According to the International Classification of Diseases, Tenth Revision (ICD-10), this pathology is assigned code F80. Whether it is possible to completely cure this disease, only a doctor can say after examining the patient. The earlier this disorder is diagnosed, the greater the child’s chances of recovery.
inability to understand language
inability to speak not due to paralysis or muscle weakness
inability to speak spontaneously
inability to form words
inability to name objects (anomia)
bad diction
excessive creation and use of personal neologisms
inability to repeat a phrase
persistent repetition of one syllable, word, or phrase (stereotypy)
paraphasia (substitution of letters, syllables or words)
agrammatism (inability to speak in a grammatically correct way)
dysprosody (changes in inflection, stress and rhythm of speech)
inability to write
limited verbal output
difficulty naming objects
speech disorder
crazy speech
inability to understand simple requests
Associated Behaviors
Based on the signs and symptoms listed earlier, the following behaviors are common in people with aphasia as a result of attempting to compensate for speech and language deficits: Self-correction: Further impairment of speech fluency as a result of inappropriate attempts to correct incorrect speech production. Loss of verbal fluency: Includes the previously mentioned difficulties, including repetition and prolongation at the phoneme, syllabic and word levels, at abnormal levels of frequency. Struggle with loss of fluency in aphasia: Serious efforts to reproduce speech, provided that the patient was previously able to speak and communicate easily, can cause depression. Stored and automatic language: Behavior in which speech or language sequences that were frequently used before the onset of aphasia can still be produced with greater ease than other speech structures.
Types
Acute aphasia
Subcortical aphasia The characteristics and symptoms of subcortical aphasia depend on the location and size of the subcortical lesion. Possible sites of injury include the thalamus, internal capsule, and basal ganglia.
Reasons
Aphasia is most often caused by a stroke, however, any disease or damage to the parts of the brain that control language can lead to aphasia. Some of these diseases may include brain tumors, traumatic brain injury, and progressive neurological disorders. In rare cases, aphasia may also result from herpetic encephalitis. Herpes simplex virus affects the frontal and temporal lobes, subcortical structures and hippocampal tissue, which can cause aphasia. In acute disorders such as head injury or stroke, aphasia usually develops quickly. If aphasia is caused by a brain tumor, infection, or dementia, it develops more slowly. There are two types of strokes: ischemic stroke and hemorrhagic stroke. An ischemic stroke occurs when a person's arteries, which supply blood to different areas of the brain, become clogged with a blood clot. This type of stroke occurs in 80% of cases. A blood clot can form in a blood vessel, or it can travel somewhere in the blood system, called an embolus. A hemorrhagic stroke occurs when a blood vessel in the brain ruptures. In general, bleeding occurs in or around the brain tissue. This type of stroke occurs in 20% of cases and is very serious. The most common cause of hemorrhagic stroke is aneurysm. Although all of the above diseases are potential causes of aphasia, aphasia usually develops only when there is significant damage to the left hemisphere (responsible for language functions) of the brain, either in the cerebral cortex (outer layer) and/or in the white matter. Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, internal and external capsules, and the caudate nucleus of the basal ganglia. The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. A very small number of people may experience aphasia after damage to only the right hemisphere. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps a greater overall reliance on the right hemisphere for language skills than in the general population. Primary Progressive Aphasia (PPA), despite its name, is actually a form of dementia, some of whose symptoms are closely related to several forms of aphasia. It is characterized by a gradual loss of language functioning while other cognitive domains, including memory and character, are largely preserved. PPA usually begins when a person begins to experience sudden difficulty finding the right word, and progresses to decreased ability to formulate grammatically correct sentences (syntax) and impaired comprehension. The etiology of PPA is not related to stroke, traumatic brain injury (TBI), or infectious disease; It is still unclear what exactly triggers the onset of PPA. Finally, some chronic neurological disorders, such as epilepsy or migraine, may also include transient aphasia as a prodromal or episodic symptom. Aphasia is also a rare side effect of fentanyl patches, an opioid used to treat chronic pain.
Classification
Aphasia is best viewed as a collection of different disorders rather than a single problem. Each person with aphasia exhibits a unique combination of language strengths and weaknesses. A major challenge, therefore, is simply documenting the various difficulties that different people may experience, let alone deciding how they can best be treated. Most classifications of aphasia tend to divide various symptoms into broad classes. The general approach is to distinguish between fluent aphasia (where speech remains fluent, but the content may be lacking and the person may have difficulty understanding others), and non-fluent aphasia (where speech is very restrained and effortful, and may consist of only one or two words for a certain time). However, none of these broad groupings have proven to be adequate. There is enormous variation among patients within the same broad grouping, and aphasias can be highly selective. For example, patients with naming deficits (anomic aphasia) may be unable to name only buildings, people, or flowers. It is important to note that there are common difficulties associated with speech and language that are also observed during the normal aging process. As people age, speech production can become more difficult, leading to slower verbal comprehension, poorer reading abilities, and a greater likelihood of word-finding difficulties. With each, however, unlike some types of aphasia, functionality in everyday life remains unchanged.
Classical-localizationist approaches
Locationist approaches aim to classify aphasias according to their main characteristics and the brain regions that are most likely to be their source. Inspired by the early work of nineteenth-century neurologists Paul Broca and Carl Wernicke, these approaches distinguish two main subtypes of aphasia and several smaller subtypes: Expressive aphasia (also known as "motor aphasia" or "Broca's aphasia"), characterized by choppy, fragmented speech that requires effort , but with a relatively well-preserved understanding. The damage is typically seen in the anterior part of the left hemisphere, primarily in Broca's area. Individuals with Broca's aphasia often have right-sided arm and leg paralysis because the left frontal lobe is also important for body movement, especially on the right side. Wernicke's aphasia (also known as "sensory aphasia") is characterized by fluent speech but marked difficulty understanding words and sentences. Speech, although free, may not include key basic words (nouns, verbs, adjectives), and may contain irregular words or even nonsense words. This subtype has been associated with damage to the left posterior temporal cortex, namely Wernicke's area. These people typically do not have physical illness because their brain injury is not near the parts of the brain that control movement. Conduction aphasia, where speech remains fluent and comprehension is maintained, but the person may have disproportionate difficulty repeating words or sentences. As a rule, the arcuate bundle of nerves and the left parietal region are damaged. Dynamic aphasia and transcortical sensory aphasia are similar to Broca's and Wernicke's aphasia, respectively, but the ability to repeat words and phrases is disproportionately preserved. Recent classification schemes using this approach, such as the Boston Neoclassical Model, also group these classical aphasia subtypes into two broad classes: nonfluent aphasia (which includes Broca's aphasia and dynamic aphasia) and fluent aphasia (which includes Wernicke's conduction aphasia). aphasia and transcortical sensory aphasia). These frameworks also identify several additional subtypes of aphasia, including anomic aphasia, which is characterized by selective difficulty finding names for things; and global aphasia, in which speech expression and comprehension are severely affected. Many localizationist approaches also recognize the existence of additional, more “pure” forms of language disorder that may affect only one language skill. For example, in pure alexia, a person may be able to write but may not be able to read, and in pure word deafness, a person may be able to produce speech and read, but cannot understand speech when spoken to.
Cognitive neuropsychological approaches
Although localizationist approaches provide a useful way to classify different patterns of linguistic complexity into large groups, one problem is that a significant number of individuals do not fit into one category or another. Another problem is that the categories, in particular the main categories such as Broca's and Wernicke's aphasias, are still quite broad. Consequently, even among people who meet the criteria for classification into a subtype, there may be enormous variability in the types of difficulties they experience. Rather than categorizing each individual into a specific subtype, cognitive neuropsychological approaches aim to identify key language skills or "modules" that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with several modules. This approach requires a framework or theory regarding what skills/modules are needed to perform different types of language tasks. For example, the Max Coltheart model identifies a module that recognizes phonemes as they are spoken, which is essential for any task, including word recognition. Additionally, there is a module that stores the phonemes that a person plans to produce in speech, and this module is critical for any task that involves producing long words or long lines of speech. Once the theoretical framework was established, the performance of each module could be assessed using a specific test or set of tests. In clinical settings, use of this model typically involves conducting a battery of assessments, each testing one or more of these modules. Once the area of greatest impact has been identified, therapy can be prescribed to improve these skills. In practice, a cognitive neuropsychological approach can be difficult to implement due to the wide range of skills that potentially need to be tested. Additionally, it is perhaps best suited for milder cases of aphasia: If a person has little expressive or receptive language ability, performance on a test can sometimes be difficult to interpret. In practice, clinicians often use a combination of assessment approaches that include broad subtypes based on a localization framework, and some more refined studies of specific language skills are based on cognitive neuropsychological frameworks.
Progressive aphasia
Primary progressive aphasia (PPA) is a focal dementia that may be associated with progressive diseases or dementias, such as frontotemporal dementia/complex motor neuron disease of Pick, progressive supranuclear palsy and Alzheimer's disease, a gradual process associated with the gradual loss of the ability to think . Gradual loss of language function occurs in the context of relatively well-preserved memory, visual processing, and character, up to an advanced stage. Symptoms typically begin with problems with word retrieval (naming) and a progressive decline in the functions of grammar (syntax) and comprehension (sentence processing and semantics). People suffering from PPA may have difficulty understanding what others say. They may also have difficulty finding the right words and forming sentences. There are three classifications of primary progressive aphasia: nonfluent progressive aphasia (PNFA), semantic dementia (SD), and logopenic progressive aphasia (LPA). Progressive jargon aphasia is a free or receptive aphasia in which the patient's speech is difficult to understand but appears meaningful to the patient. Speech is fluent and effortless with correct syntax and grammar, but the patient has trouble choosing names for things. Patients will either replace the target word with another that sounds or looks like the original word, or they will replace it with sounds. Thus, patients with slang aphasia often use neologisms when trying to replace words that they cannot remember or can be expressed with sounds. Substitution usually involves another word that begins with the same sound, the choice of another word that is semantically related to the first one, or the choice of a word that is phonetically similar to the desired one.
Voiceless aphasia
There are many cases showing that there is a form of aphasia among deaf individuals. Sign language, after all, is a form of communication that has been shown to use the same areas of the brain as verbal forms of communication. Mirror neurons are activated when an animal acts in a certain way or observes another animal performing that action. These mirror neurons play an important role in a person's ability to imitate hand movements. Broca's speech production area has been shown to contain some of these mirror neurons, resulting in significant similarities in brain activity between sign language and vocal speech communication. Facial communication is a significant part of how animals interact with each other. People use facial movements to create what other people perceive as emotions. When these facial movements are combined with speech, a more complete form of language is created that allows the species to interact with a much more complex form of communication. Sign language also uses these facial movements and emotions, along with the primary hand movements. These forms of communication associated with facial movements occur in the same areas of the brain. When we deal with damage in certain areas of the brain, vocal forms of communication are at risk of severe forms of aphasia. Since these same areas of the brain are used in sign language, the same, or at least very similar, forms of aphasia may be observed in the deaf community. People can demonstrate a form of Wernicke's aphasia with sign language, and they show deficits in the ability to produce any form of facial expression. Broca's aphasia also occurs in some patients.
Prevention
Below are some precautions you should take to avoid aphasia by reducing the risk of stroke, which is the main cause of aphasia:
Regular exercise
Healthy eating
Low alcohol consumption and tobacco cessation
Blood pressure control
Control
In the most severe cases of aphasia, some or most speech-language skills are restored by working with a speech therapist. This rehabilitation can take two or more years and is most effective if started quickly. Once aphasia occurs, there is a period of spontaneous recovery of approximately six months. During this time, the brain tries to repair damaged neurons. Aphasia therapy during this period promotes even greater levels of recovery. Improvement varies widely, depending on the cause, type, and severity of the aphasia. Recovery also depends on the patient's age, health, motivation and education level. There is no one treatment that is effective for all types of aphasia. The reason for this is the nature of the disorder and the different ways in which it is presented, as described in the previous sections. Aphasia rarely presents in the same way, which means treatment must be specific to each case. Research has shown that although there is no consensus in the literature regarding the methodology for treating aphasia, there is ample evidence that treatment generally has positive results. Treatment for aphasia ranges from improving functional communication to improving speech accuracy, depending on the severity of the illness, the needs of the individual, and the support of family and friends. Group therapy allows people to work on their pragmatic and communication skills with other people with aphasia (skills that often do not respond to individual therapy). Group therapy can also help improve self-confidence and social skills in a comfortable environment. A multidisciplinary team including physicians (often a physician is involved, but it is more likely that the treatment team will be led by a clinical neuropsychologist), a physical therapist, an occupational therapist, a speech therapist, and a social worker working as a team to treat aphasia. For the most part, treatment relies heavily on repetition and focuses on improving language performance and working on task-specific skills. The main goal is to help the person and their loved ones adjust to language changes and limitations. Treatment methods mainly include two approaches:
The replacement model is an approach that uses additional factors to improve spoken language, such as the writing board.
Direct treatment model – an approach that targets deficits through specific exercises
Several treatments include the following:
Melodic intonation therapy is used to treat non-fluent aphasia. The method has proven effective in some cases. However, there is still no evidence from randomized controlled trials to support the effectiveness of MIT for chronic aphasia. MIT is used to help people with aphasia use vocal skills through spoken songs, and this skill then transfers to spoken words. Good candidates for this therapy include patients who have had a stroke in the left hemisphere, patients with nonfluent aphasia such as Broca's aphasia, good auditory comprehension, poor repetition and articulation abilities, and good emotional stability and memory. It has been suggested that MIT is an effective method because prosody and singing are influenced by areas of the right hemisphere of the brain; these may be areas of the right hemisphere that are used for natural speech production after intensive training. An alternative explanation is that the effectiveness of MIT depends on neural circuits involved in the processing of rhythmicity and patterned expressions (examples: “I'm fine,” “how are you?”, “thank you”); while rhythmic features associated with melodic intonation may occupy primarily subcortical regions of the left hemisphere of the brain, and the use of patterned expressions is supported by cortical and subcortical bilateral neural networks of the right hemisphere. More recently, computer technology has been incorporated into treatment options. The key indicator for a good prognosis is the intensity of treatment. To obtain positive results, a minimum of two to three hours of treatment per week is required. The main advantage of using computers is that it can significantly increase the intensity of therapy. These programs include a wide variety of exercises and can be done at home in addition to face-to-face therapy with a therapist. However, because aphasia presents differently among individuals, these programs must be dynamic and flexible to adapt to variability in impairment. Another obstacle is the ability of computer programs to imitate normal speech and keep up with the speed of normal conversations. Thus, computer technology appears to be limited in communication settings, however, it is effective in training communication skills.
Treatment intensity
The intensity of aphasia therapy is determined by the length of each session, the total number of hours of therapy per week, and the total duration of therapy. There is no consensus on what “intensive” aphasia therapy entails, or how intensive the therapy should be to get the best results. In general, treatment is considered more intensive when the total number of hours of therapy per week is increased, and on average, studies show that more intensive therapy leads to better results. For example, one study found that patients who received treatment for 8.8 hours per week for 11.2 weeks experienced greater progress than patients who received treatment for 2 hours per week for 22.9 weeks. The results of another study confirm these findings. The researchers found that patients who received 100 hours of intensive therapy over 62 weeks scored higher on language measures than a control group of individuals who received less intensive therapy. Although there is general agreement that intensive treatment produces greater benefits, there is no explicit definition of “intensive” treatment. The intensity of treatment should be individualized based on the duration of the stroke, the goal of therapy, and other characteristics of the individual patient, such as age, lesion size, general health, and motivation. Each person responds differently to the intensity of treatment and is able to tolerate treatment at different points in time after a stroke. Some patients cannot tolerate therapy immediately after a stroke because of confusion or exhaustion, but may tolerate therapy better later. The intensity of treatment after a stroke should depend on the patient's motivation, endurance and tolerance to therapy. The level of intensity of therapy also depends on the goals of therapy; for certain purposes, non-intensive therapy is more beneficial. For example, non-intensive therapy is more effective than intensive therapy in influencing naming accuracy in patients with anomia. This is because more time between sessions allows long-term learning to be rehearsed and reinforced. The intensity of therapy also depends on the duration of the stroke. Patients respond differently to intensive treatment in the acute phase (0-3 months after stroke), subacute phase (3-6 months after stroke), or chronic phase (6+ months after stroke). Intensive therapy has been found to be effective for patients with nonfluent and fluent chronic aphasia, but less effective for patients with acute aphasia. Patients with subacute aphasia also respond well to intensive 100-hour therapy over 62 weeks. This suggests that patients in the subacute phase may experience significant improvements in language and functional communication scores with intensive care compared with usual care. Research has shown that intensive treatment is most beneficial in the subacute or chronic phase, rather than immediately after a stroke. More research is needed to determine the optimal time to provide intensive care for all patients with aphasia. Intensive therapy may alternatively be characterized by the amount of demands placed on the client during the session. According to this definition, intensive therapy includes several specific methods, such as restrictive induced aphasia therapy (CIAT) and intensive speech rehabilitation (SP-I-R-IT). CIAT places high demands on the patient, limiting the use of the patient's strongest areas of the brain and requiring the use of the weakest areas. Typical CIAT therapy sessions are intensive and last approximately 3 hours. One study found that when intensive CIAT therapy is used, the patient's quality of verbal communication in daily life improves significantly. Each study participant also demonstrated improvement in at least one of the subtests within the Aachen Aphasia Test; which assesses language efficiency and comprehension in patients with aphasia. These results suggest that intensive CIAT therapy is effective for patients with moderate, fluent aphasia in the chronic recovery stage. SP-I-R-IT focuses heavily on speech production and intervention strategies. SPIRIT therapy has been found to be effective; Patients participating in intensive SPIRIT therapy demonstrated a 15% increase in performance on standardized measures after 50 weeks of therapy. Overall, treatment intensity for aphasia is an area that requires more research. Current research shows that intensive treatment is effective, although the definition of "intensity" is variable. Most importantly, the intensity of treatment should be determined on an individual basis and should depend on the duration of the stroke and the patient's endurance, tolerance to therapy, motivation, general health, and treatment goals.
Forecast
There are several effects that contribute to the overall outcomes of a patient diagnosed with aphasia, including: neuroplasticity, age, general health, and patient motivation. Neuroplasticity is the brain's ability to change in response to its environment. Neuroplasticity underlies normal processes such as typical development, learning and maintenance during aging, and the brain's response to severe injury. Positive outcomes are most noticeable when the aphasic patient's neuroplasticity is greatest, and is predicted by the patient's response to other specified outcomes. The age of the patient directly affects the neuroplasticity of the brain - the younger the patient, the greater the plasticity. In general, health status also significantly influences outcomes in patients with aphasia. If a patient has no underlying health problems and is young, they will perform better than older patients with serious health problems (such as obesity, heart disease, cancer, high blood pressure, etc.). ) in combination with aphasia. However, the most important factor influencing the clinical outcome of a patient with aphasia is the patient's motivation. The success of treatment, regardless of the contributing results, is ensured by the patient's high motivation. If a patient is not motivated, greater success in treatment is much less likely than for patients with good motivation. All of these outcomes contribute to success in Wernicke's aphasia, Broca's aphasia, global aphasia, and conduction aphasia and are described in detail below.
Wernicke's aphasia
Wernicke's aphasia is considered a more severe form of aphasia, and is more common in older populations. Wernicke's aphasia has high recovery rates and often evolves into other forms of aphasia. Although some cases of Wernicke's aphasia show more improvement than milder forms of aphasia, people with Wernicke's aphasia may not achieve the same level of language ability as people with mild forms of aphasia.
Broca's aphasia
The term "anomic aphasia" generally refers to patients whose only common symptom is difficulty finding the right word in spoken and written language. Typically, the spontaneous speech of a person with anomic aphasia is fluent and grammatically correct, but contains many errors when searching for words. These failures lead to unusual pauses in communication, talking “around the bush” without directly indicating the desired word, or replacing the desired word with another word. Anomic aphasia is a mild form of aphasia, indicating a likely opportunity for better recovery. Patients with Broca's aphasia may also have difficulty finding the right word, or anomia. In addition, patients with Broca's aphasia understand spoken and written language better than they can speak or write themselves. These patients are aware of their communication disorders. Antecedent factors correlate with good prognosis for patients with Broca's aphasia. Many patients with acute-onset Broca's aphasia eventually progress to milder forms of aphasia, such as conduction or anomic aphasia. Therapy for Broca's aphasia (non-fluent aphasia) is beneficial, even for patients with severe non-fluent aphasia. Marangolo and associates (2013) conducted a study using talk therapy for patients with severe nonfluent aphasia. The study results showed a significant increase in the patient's expressive language. The authors suggested that intensive conversation therapy should be considered for patients with moderately severe nonfluent aphasia in order to improve the patient's quality of life and improve language expressiveness. Additionally, although anomic aphasia is considered less severe than other types of aphasia, therapy is still needed to help reduce word-finding deficits. In a study conducted by Harnisch et al (2014), intensive treatment was given to patients with anomic aphasia. According to the study results, there was a significant improvement in the expressive language of the participants. These results suggest that an intensive intervention program for patients with anomic aphasia produces remarkably rapid improvements in expressive language. Specifically, these patients relearned how to correctly pronounce problem words after 1 to 3 hours of speech-language therapy.
Global aphasia
Global aphasia is considered a severe impairment in many aspects of language as it affects expressive and receptive language, reading and writing. Despite these many deficits, there is evidence demonstrating the benefits of speech language therapy. Although each case is different, it has been noted that individuals with global aphasia showed greater improvements during the second six months after stroke compared to the first six months. Intensive and frequent speech therapy was more effective with additional sessions at home daily. Improvement was also shown when the person demonstrated attentiveness, motivation, and when information was presented in a variety of ways. In one study, 23 people who had previously received speech therapy but stopped treatment because further recovery was not expected participated in a course of intensive speech therapy. Results showed significant improvements in oral and written sentence and noun production, action naming, and everyday communication. Even if people with global aphasia do not become competent speakers, listeners, writers, or readers, treatment can help improve the quality of life for these patients. Collins (1991) suggests that therapy that focuses on achievable goals will have the greatest impact on a person's daily life. Individuals with global aphasia generally respond well to treatment that includes personally relevant information that is also important to consider in therapy.