STUDY - Technical - New Dacian's Medicine
Aphasia
and other Focal Disorders (3)
Translation Draft
I will continue with transcortical aphasias addressing its fluent "shape" (transcortical sensory aphasia).
I will continue with transcortical aphasias addressing its fluent "shape" (transcortical sensory aphasia).
Clinical characters are
similar to those in Wernicke aphasia, but repeated speech is
intact. The lesion disconnects the center of the language
network from other areas of temporoparietal association.
Hemianopsia may be one of the associated neurological symptoms.
Fluent transcortical aphasia may be associated with
cerebrovascular lesions (e.g. infarction in the posterior of the
vascular crossing area) or neoplasms comprising the
temporoparietal cortex, posterior to the Wernicke area.
In the case of isolation aphasia (a rare syndrome) a combination of the two transcortical aphasia (previously shown) is found. The comprehension is severely altered, and the speech is meaningless.
This condition reflects the pathological functioning of the language network when it is isolated from other regions of the brain. Injuries are not evenly distributed and may be caused by anoxia, carbon monoxide poisoning or complete infarction of the vascular crossing area. The Broca and Wernicke areas are spared, but there are lesions in the temporal, parietal and frontal cortex around them.
Anomic aphasia can be considered as a syndrome of "minimal dysfunction" of the language network. Articulation, comprehension and repeated speech are intact, but appropriation, word-finding, and spelling are altered. The speech is rich in functional words, but poor in nouns and verbs that denote specific actions.
Speech is fluent, but paraphrased, functional and informationless. The location of the lesion can be anywhere in the language network of the left hemisphere, including the middle and lower temporal gyrus. Anomic aphasia is the most common language disorder that occurs after head trauma and metabolic encephalopathy.
It is also the most common aphasia found in Alzheimer's disease. Language disorder in Alzheimer's disease almost always evolves towards fluent aphasia (e.g. anomic aphasia, Wernicke, driving or fluent transcortical). Insidious onset and implacable progression of nonfluent language disorder (Broca or nonfluent transcortical aphasia) may be found in patients with progressive primary aphasia syndrome, a degenerative disease most commonly associated with specific neuronal loss or Pick's disease.
Pure verbal deafness is not a true aphasic syndrome (but it makes introduction into focal brain disorders) because language deficiency is modally specific (but I will present a few things about it because many medical works include it "among" aphasia).
In this case, most commonly, the lesions are bilateral, either localized on the left side of the upper temporal gyrus. The net effect of the underlying lesions is the interruption of the flow of information from the unimodal association cortex of hearing to Wernicke's area. Patients with this syndrome have no difficulty in understanding written texts and can express themselves very well both orally and in writing.
These patients are not really deaf and have no difficulty reacting and interpreting noises in the environment, because the primary cortex of hearing and subcortical hearing centers are intact. However, due to the fact that the information heard cannot be transmitted in the language network, it cannot be decoded into neural representations of words and the patient reacts as if he hears a foreign language that cannot be deciphered. Patients with this syndrome cannot repeat what they hear, but they have no difficulty in naming objects.
Over time, patients with pure verbal deafness learn to read after their lips and their condition may seem improved on a superficial examination. Additional neurological symptoms may be absent, but paranoid agitation reactions are common. Cerebrovascular lesions are the most common causes of this syndrome.
Pure Alexia without graphiness is a visual equivalent syndrome of pure verbal deafness. Injuries (usually a combination of lesions of the left occipital cortex and the posterior part of the body calos - splenium) interrupt the transmission of visual stimuli to the language network. A straight hemianopsia usually occurs, but the center of the language network remains intact.
The patient understands the spoken language and can speak in turn, calls the objects in the left visual hemifield, repeats and writes. However, the patient behaves as if he is illiterate when asked to read even the simplest phrases, because the visual information of the words read (presented in the intact visual hemifield) cannot reach the language network.
Objects in the left visual hemifield can be correctly named because they activate nonvisual associations in the right hemisphere, which can, instead, access the language network through the previous translocal pathways to splenium. Patients with this syndrome may also lose the ability to name colors although they may match them. This manifestation is called color anomis.
The most common cause of pure alexia is a cerebrovascular lesion in the posterior cerebral artery distribution area or an infiltrating neoplasm in the left occipital cortex, comprising both the optical radiation and the cross fibers of the splenium. Because the posterior cerebral artery irrigates and the medial temporal components of the limbic system, patients with pure alexia may also experience amnesia, but this is usually transient.
Afemia is the acute onset of severe alteration of fluency (frequently mutism) that evolves, over time, towards a whispered, hoarse speech. Reading, writing and comprehension are intact, so this is not a true aphasic syndrome. Partial damage to the Broca area or subcortical lesions that interrupt its connections to other areas of the brain may occur. Occasionally, the lesion may involve the additional motor cortex of the left hemisphere.
Apraxia is the generic term that designates a complex motor deficit that cannot be attributed to a pyramidal, extrapyramidal, cerebellar or sensory dysfunction and is not determined by the subject's inability to understand the meaning of the command. The most common form is ideomotor apraxia. The commands to perform a specific motor act ("coughing", "blow and extinguish the flame of a match") or to mimic the use of a common object (comb, hammer, straw or toothbrush) in its absence, cannot be followed.
The patient's ability to understand command is demonstrated by the presentation of several movements, from which the patient can recognize the correct one. Some patients with this type of apraxia may emit the correct movement (after it is presented by the examiner) and have no difficulty when the actual object is handed to them, indicating that the sensory and motor mechanisms required for movement are intact.
Ideomotor apraxia is the disconnection of the language network from the pyramidal motor systems (commands to perform complex movements are understood, but cannot be transmitted to the corresponding motor areas, even if the motor mechanism involved is intact). Bucolic apraxia involves apraxic deficits of the face and mouth. Apraxia of the limbs includes apraxic deficits in the movement of hands and feet. Ideomotor apraxia is commonly associated with aphasic syndromes, especially Broca aphasia and driving syndromes.
The presence of ideomotor aphasia cannot be demonstrated in patients with language comprehension difficulties. As we have previously presented, the ability to perform commands involving axial musculature ("close your eyes", "get up") is replaced in various ways and may be intact in patients with severe apraxia and aphasia. Patients with anterior calos body lesions may have a special type of ideomotor apraxia, limited to the left half of the body. Since the use of real objects is not disturbed, ideomotor apraxia, by itself, does not produce any limitation in daily activity.
Other types of apraxia are the ideative apraxia and the kinetic apraxia. The ideastative apraxia designates a deficiency in the execution of a succession of movements having a finality in patients who do not have difficulty in the separate realization of the components of the succession.
For example, when asked to take a pen and write, the string of movements to remove the pen cover, to put the cap at the other end and, pointing the tip towards the sheet, to start writing, can be interrupted and the patient tries to write with the other end of the pen or without removing the cap.
Such difficulties in tracking the sequence of movements usually occur in confused states and dementia, rather than after associated focal injuries or aphasia. Kinetic apraxia of the limbs implies a lack of skill in the use of objects, which cannot be attributed to sensory, cerebellar, pyramidal or extrapyramidal dysfunctions. This condition may occur after focal lesions in the premotor cortex or in corticobasal ganglion degeneration.
Another landmark of this post is Gertsmann syndrome. The association of acalculation (alteration of simple arithmetic), dysgraphy (alteration of writing), anomy of the fingers (inability to name fingers separately, such as index finger or thumb) and left-right confusion (inability to tell whether a hand, foot or arm of the patient or examiner is on the right or left side of the body), is known as Gertsmann syndrome.
In developing this diagnosis it is important to determine whether the difficulties of appointing the fingers of the hand or the right-left confusion are not part of a generalized syndrome of anomie and whether the patient is not aphasic in other respects. When this syndrome occurs in isolation, it is usually associated with damage to the lower parietal lobe (especially the angular gyrus) in the left hemisphere.
Now, things about aprosody. The variation in melodic accents and intonation influences the meaning and impact of spoken language. For example, the sentences "X is smart." and "X is smart?" contain the same words and have the same syntax, but they convey different messages because of differences in intonation and the accent with which they are spoken. This aspect of the language is called prosody.
Damage to the perisylvian areas in the right hemisphere may interfere with speech prosody and lead to symptoms of aprosody. It was pointed out that the damage to the regions of the right hemisphere corresponding to Thernicke's area causes greater alteration in the decoding of speech prosody, while damage to the right hemisphere regions corresponding to the Broca area causes a greater disorder in the inability to use prosody according to the meaning in spoken language.
The last deficiency is the most common type of aprosodia identified in clinical practice (the patient uses grammatically correct language, the words are also used correctly, but the phrases are pronounced monotonous, which interferes with the ability to convey a particular message or emotional state. Patients with this type of aprosody or the mistaken impression that they are depressed or indifferent).
To complete this post I must point out a few things about subcortical aphasia. Major aphasic syndromes presented are classified according to the location of cortical lesions. However, damage to the subcortical components of the language network (e.g. the head of the caudate nucleus and the thalamus of the left hemisphere) can also lead to aphasia.
The syndromes that occur are associations of deficits in various aspects of language, but rarely correspond to the specific patterns described. Anomic aphasia accompanied by dysartria or fluent aphasia with hemiparesis is a deviation from the major syndromes listed and must raise the suspicion of a subcortical lesion.
In the case of isolation aphasia (a rare syndrome) a combination of the two transcortical aphasia (previously shown) is found. The comprehension is severely altered, and the speech is meaningless.
This condition reflects the pathological functioning of the language network when it is isolated from other regions of the brain. Injuries are not evenly distributed and may be caused by anoxia, carbon monoxide poisoning or complete infarction of the vascular crossing area. The Broca and Wernicke areas are spared, but there are lesions in the temporal, parietal and frontal cortex around them.
Anomic aphasia can be considered as a syndrome of "minimal dysfunction" of the language network. Articulation, comprehension and repeated speech are intact, but appropriation, word-finding, and spelling are altered. The speech is rich in functional words, but poor in nouns and verbs that denote specific actions.
Speech is fluent, but paraphrased, functional and informationless. The location of the lesion can be anywhere in the language network of the left hemisphere, including the middle and lower temporal gyrus. Anomic aphasia is the most common language disorder that occurs after head trauma and metabolic encephalopathy.
It is also the most common aphasia found in Alzheimer's disease. Language disorder in Alzheimer's disease almost always evolves towards fluent aphasia (e.g. anomic aphasia, Wernicke, driving or fluent transcortical). Insidious onset and implacable progression of nonfluent language disorder (Broca or nonfluent transcortical aphasia) may be found in patients with progressive primary aphasia syndrome, a degenerative disease most commonly associated with specific neuronal loss or Pick's disease.
Pure verbal deafness is not a true aphasic syndrome (but it makes introduction into focal brain disorders) because language deficiency is modally specific (but I will present a few things about it because many medical works include it "among" aphasia).
In this case, most commonly, the lesions are bilateral, either localized on the left side of the upper temporal gyrus. The net effect of the underlying lesions is the interruption of the flow of information from the unimodal association cortex of hearing to Wernicke's area. Patients with this syndrome have no difficulty in understanding written texts and can express themselves very well both orally and in writing.
These patients are not really deaf and have no difficulty reacting and interpreting noises in the environment, because the primary cortex of hearing and subcortical hearing centers are intact. However, due to the fact that the information heard cannot be transmitted in the language network, it cannot be decoded into neural representations of words and the patient reacts as if he hears a foreign language that cannot be deciphered. Patients with this syndrome cannot repeat what they hear, but they have no difficulty in naming objects.
Over time, patients with pure verbal deafness learn to read after their lips and their condition may seem improved on a superficial examination. Additional neurological symptoms may be absent, but paranoid agitation reactions are common. Cerebrovascular lesions are the most common causes of this syndrome.
Pure Alexia without graphiness is a visual equivalent syndrome of pure verbal deafness. Injuries (usually a combination of lesions of the left occipital cortex and the posterior part of the body calos - splenium) interrupt the transmission of visual stimuli to the language network. A straight hemianopsia usually occurs, but the center of the language network remains intact.
The patient understands the spoken language and can speak in turn, calls the objects in the left visual hemifield, repeats and writes. However, the patient behaves as if he is illiterate when asked to read even the simplest phrases, because the visual information of the words read (presented in the intact visual hemifield) cannot reach the language network.
Objects in the left visual hemifield can be correctly named because they activate nonvisual associations in the right hemisphere, which can, instead, access the language network through the previous translocal pathways to splenium. Patients with this syndrome may also lose the ability to name colors although they may match them. This manifestation is called color anomis.
The most common cause of pure alexia is a cerebrovascular lesion in the posterior cerebral artery distribution area or an infiltrating neoplasm in the left occipital cortex, comprising both the optical radiation and the cross fibers of the splenium. Because the posterior cerebral artery irrigates and the medial temporal components of the limbic system, patients with pure alexia may also experience amnesia, but this is usually transient.
Afemia is the acute onset of severe alteration of fluency (frequently mutism) that evolves, over time, towards a whispered, hoarse speech. Reading, writing and comprehension are intact, so this is not a true aphasic syndrome. Partial damage to the Broca area or subcortical lesions that interrupt its connections to other areas of the brain may occur. Occasionally, the lesion may involve the additional motor cortex of the left hemisphere.
Apraxia is the generic term that designates a complex motor deficit that cannot be attributed to a pyramidal, extrapyramidal, cerebellar or sensory dysfunction and is not determined by the subject's inability to understand the meaning of the command. The most common form is ideomotor apraxia. The commands to perform a specific motor act ("coughing", "blow and extinguish the flame of a match") or to mimic the use of a common object (comb, hammer, straw or toothbrush) in its absence, cannot be followed.
The patient's ability to understand command is demonstrated by the presentation of several movements, from which the patient can recognize the correct one. Some patients with this type of apraxia may emit the correct movement (after it is presented by the examiner) and have no difficulty when the actual object is handed to them, indicating that the sensory and motor mechanisms required for movement are intact.
Ideomotor apraxia is the disconnection of the language network from the pyramidal motor systems (commands to perform complex movements are understood, but cannot be transmitted to the corresponding motor areas, even if the motor mechanism involved is intact). Bucolic apraxia involves apraxic deficits of the face and mouth. Apraxia of the limbs includes apraxic deficits in the movement of hands and feet. Ideomotor apraxia is commonly associated with aphasic syndromes, especially Broca aphasia and driving syndromes.
The presence of ideomotor aphasia cannot be demonstrated in patients with language comprehension difficulties. As we have previously presented, the ability to perform commands involving axial musculature ("close your eyes", "get up") is replaced in various ways and may be intact in patients with severe apraxia and aphasia. Patients with anterior calos body lesions may have a special type of ideomotor apraxia, limited to the left half of the body. Since the use of real objects is not disturbed, ideomotor apraxia, by itself, does not produce any limitation in daily activity.
Other types of apraxia are the ideative apraxia and the kinetic apraxia. The ideastative apraxia designates a deficiency in the execution of a succession of movements having a finality in patients who do not have difficulty in the separate realization of the components of the succession.
For example, when asked to take a pen and write, the string of movements to remove the pen cover, to put the cap at the other end and, pointing the tip towards the sheet, to start writing, can be interrupted and the patient tries to write with the other end of the pen or without removing the cap.
Such difficulties in tracking the sequence of movements usually occur in confused states and dementia, rather than after associated focal injuries or aphasia. Kinetic apraxia of the limbs implies a lack of skill in the use of objects, which cannot be attributed to sensory, cerebellar, pyramidal or extrapyramidal dysfunctions. This condition may occur after focal lesions in the premotor cortex or in corticobasal ganglion degeneration.
Another landmark of this post is Gertsmann syndrome. The association of acalculation (alteration of simple arithmetic), dysgraphy (alteration of writing), anomy of the fingers (inability to name fingers separately, such as index finger or thumb) and left-right confusion (inability to tell whether a hand, foot or arm of the patient or examiner is on the right or left side of the body), is known as Gertsmann syndrome.
In developing this diagnosis it is important to determine whether the difficulties of appointing the fingers of the hand or the right-left confusion are not part of a generalized syndrome of anomie and whether the patient is not aphasic in other respects. When this syndrome occurs in isolation, it is usually associated with damage to the lower parietal lobe (especially the angular gyrus) in the left hemisphere.
Now, things about aprosody. The variation in melodic accents and intonation influences the meaning and impact of spoken language. For example, the sentences "X is smart." and "X is smart?" contain the same words and have the same syntax, but they convey different messages because of differences in intonation and the accent with which they are spoken. This aspect of the language is called prosody.
Damage to the perisylvian areas in the right hemisphere may interfere with speech prosody and lead to symptoms of aprosody. It was pointed out that the damage to the regions of the right hemisphere corresponding to Thernicke's area causes greater alteration in the decoding of speech prosody, while damage to the right hemisphere regions corresponding to the Broca area causes a greater disorder in the inability to use prosody according to the meaning in spoken language.
The last deficiency is the most common type of aprosodia identified in clinical practice (the patient uses grammatically correct language, the words are also used correctly, but the phrases are pronounced monotonous, which interferes with the ability to convey a particular message or emotional state. Patients with this type of aprosody or the mistaken impression that they are depressed or indifferent).
To complete this post I must point out a few things about subcortical aphasia. Major aphasic syndromes presented are classified according to the location of cortical lesions. However, damage to the subcortical components of the language network (e.g. the head of the caudate nucleus and the thalamus of the left hemisphere) can also lead to aphasia.
The syndromes that occur are associations of deficits in various aspects of language, but rarely correspond to the specific patterns described. Anomic aphasia accompanied by dysartria or fluent aphasia with hemiparesis is a deviation from the major syndromes listed and must raise the suspicion of a subcortical lesion.
A good, pleasant and
restful weekend!
Dorin, Merticaru