Table of Contents
2. CLASSIFICATION OF ACQUIRED ALEXIAS
2.1 Traditional Approach
2.1.1 Posterior Alexia
2.1.2 Central Alexia
2.1.3 Anterior Alexia
2.2 A Psycholinguistic Approach
2.2.1 Surface Alexia
2.2.2 Phonological Alexia
2.2.3 Deep Alexia
There have always been people with reading difficulties, but they haven’t been noticed for a long time, because it was not customary to be able to read. Since literacy is now widespread and the majority of the society is able to read, a wide range of reading disabilities have been brought to light and have aroused the interest of scientists and neurologists, who have been trying to analyze and classify them. First of all, in the case of reading disorders, it is to distinct between acquired and developmental reading disabilities. The term alexia only refers to a reading deficit caused by brain damage. Thus, it is an acquired disorder, which can only occur in a patient, who had been able to read before and has lost that ability. A developmental reading disability on the other hand is usually called dyslexia. It refers to a reading deficit from childhood on, due to which the individual is unable to learn to read. Although most scientists accept and use these terms in that manner, it is to mention, that this distinction of terms is not universally accepted. (Benson 1928: 107)
The focus of this term paper is on the varieties of acquired reading disorders, thus, the alexias. It is intended to provide a broad and understandable overview of the different forms of alexia with their underlying defects. They will be presented with respect to two main approaches, namely the traditional approach from a neurological point of view and the psycholinguistic approach from a neurolinguistic point of view.
The traditional approach divides alexias into major clinical syndromes with regard to the reading deficit. There exists a wide range of terms for the syndrome, referring either to accompanying deficits like apraxia, agraphia or acalculia or to the anatomical locus of the lesion. Referring to accompanying deficits, Déjerine distinguished between alexia with agraphia and alexia without agraphia. Frankl and Alajouarine on the other hand distinguished between aphasic alexia and agnostic alexia. Referring to proposed site of the lesion, Wernicke and Kleist used the terms cortical alexia and subcortical alexia, whereas Benson used the terms central alexia and posterior alexia to refer to alexia with and alexia without agraphia. He then added a third variety, namely anterior alexia, which is associated with pathology in the frontal language area and therefore completes his classification system based on the locus of the lesion. The terms introduced by Benson will be representative for the traditional approach in this term paper, since his classification covers all brain areas, that could be damaged in alexic patients. (Boller/Grafman 1988: 377)
“With the development of cognitive neuropsychology in recent decades, theorists have developed a new classification system for reading disturbances that follow brain damage.” (Obler/Gjerlow 1999: 114) They were interested in developing a model of how the psycholinguistic process of reading operates based on the sorts of reading patterns they see in alexic patients. Therefore, their psycholinguistic approach divides alexias with respect to the reading mechanisms of brain-damaged people. The three linguistic subtypes, which result from that division, are surface alexia, phonological alexia and deep alexia.
2. Classification of acquired alexias
2.1 Traditional Approach
„The classical alexic syndromes have been defined on the basis of patterns of observations made by clinical neurologists. Their descriptions tend to center around the presence of a reading disturbance and the accompanying neurological symptoms”. (Heilman/Valenstein 1985: 49)
“One standard practice has been to divide the alexias into major clinical syndromes with respect to the reading deficit” (Heilman/Valenstein 1985: 50): literal alexia, verbal alexia and global alexia. The term literal alexia refers to ‘letter-without- word-blindness’ and is also called pure letter blindness. A patient with literal alexia is relatively able to read words, but unable to read letters. The term verbal alexia refers to the exact opposite syndrome, namely ‘word-without-letter-blindness’, and is also called pure word blindness. A patient with verbal alexia is relatively able to read letters, but unable to read words. The term global alexia refers to the co- occurrence of both syndromes, thus, the inability to read letters or words. Many authors consider verbal and literal alexia to be points on a continuum rather than discrete entities, due to the fact that most patients, who are considered to be wordblind, can recognize certain highly familiar words without relying upon a letter-by- letter analysis and at the same time have at least some difficulty identifying individual letters as well as words. (Heilman/Valenstein 1985: 50)
2.1.1 Posterior Alexia
Posterior alexia, occipital alexia, alexia without agraphia , pure alexia, pure word blindness or agnostic alexia – all of these terms refer to a spectacular but rare clinical syndrome: the “serious inability to read contrasted with an almost uncanny preservation of writing ability”. (Benson 1928: 111) In other words, a patient with posterior alexia has no language deficit except for the reading disability. There are no signs of agraphia, paralysis, aphasia, sensory deficit or any other basic neurologic defect. The only symptom, that is seen and is present in most cases is the right homonymous hemianopsia, which is a significant unilateral field defect. Most cases without the right homonymous hemianopsia are caused by a tumor, “either a meningioma compressing the medial occipital region or a glioma infiltrating this region.” (Benson 1928: 112)
Due to the total impairment of the comprehension of written language, a patient who suffers from pure alexia is not even capable of reading what he has just finished writing himself. His ability to written acalculia and to copy is also impaired, whereas he has lesser difficulty in producing words to dictation. His oral language and spelling are even close to normal. (Heilman/Valenstein 1985: 51) The patient performs excellently, both when he is asked to spell a word out loud and when he is tested to recognize written words that are spelled out loud for him during the reading process. Thus, he suffers a verbal alexia, but not a literal alexia. This phenomenon is contrary to the syndrome of central alexia, which is why the recognition of spelled words becomes an important test for differentiating these two varieties of alexia.
The ability to write is also on an almost normal level; there are no signs of agraphia. But, due to the long absence of visual monitoring, some patients do gain some difficulties over the years. Often, they gain a tendency to slant their writing upwards and their writing tends to get worse over the years. (Benson 1928: 111)
Besides these minor writing difficulties, the most frequent neighborhood findings are a right homonymous hemianopsia, as mentioned earlier, and a color anomia regarding the visual-verbal association process of naming a color or pointing to a named color. Despite that “color-naming disturbance”, patients are able to use color names correctly in conversation or in auditory comprehension and they also perform excellently when they are asked to sort colors. Thus, it’s only a two-way-defect and “can be considered a true agnosia for colors.” (Benson 1928: 112)
Other neighborhood findings with less consistency are a mild degree of anomia, difficulty in number-reading, acalculia, visual agnosia for objects or colors, lost musical notation-reading or a mild degree of hemiplegia, which is the paralysis of one vertical half of the body. (Heilman/Valenstein 1985: 51)
The majority of reported cases of pure alexia result from cerebrovascular lesions, with cerebral destruction in “the territory of the posterior cerebral artery, rather than of the middle cerebral artery, which had been found to be the territory responsible for oral language disorders.” (Heilman/Valenstein 1985: 52) The distruction is “usually affecting the fusiform and lingual gyri […]. In addition, pathological involvement of the splenium of the corpus callosum is present in most cases.” (Benson 1928: 114) Some reported cases have also been secondary to tumors or arterio-venous malformation.
The mechanisms underlying the syndrome of posterior alexia are still disputed. (Heilman/Valenstein 1985: 51) According to Quensel’s disconnection theory, which derived from the theory of a disconnection syndrome and has been stressed by most authors since then, there are two brain lesions required for pure alexia: one to the left occipital lobe so that written information into the left hemisphere can’t be passed on left-hemisphere language areas, and one back to the back portion of the corpus callosum, so that the written information that get into the right hemisphere also can’t be passed to left-hemisphere language areas. In other words, information from the right visual field can’t get to the language area because of damage to the left occipital lobe; nor can information from the left visual field get to the language area. It gets to the right occipital lobe but cannot cross to the left hemisphere because of damage to the corpus. (Obler/Gerlow 1999: 114-115)
The fact that a patient with posterior alexia is able to “recognize individual letters when they are drawn in the palm or palpated from embossed blocks and can decipher words presented in this manner […] [also shows that he] has not lost the power to read; rather, it appears that visual stimuli have only limited access to the language area.” (Benson 1928: 111)
As for the chance of recovery, most patients are able to regain some of their reading skills. Eventually, they recover their ability to read many or even all individual letters and to read them aloud. By reading them aloud, patients might be able to put them together to form words and decipher them in that way. The recovery process does take a lot of time, but with continued improvement, the reading pace becomes faster and more fluent, to the point that patients no longer need to spell the words out loud to comprehend them. It is to mention though, that the reading is still accomplished by “identifying individual letters and putting them together to form words.” (Benson 1928: 111)
2.1.2 Central Alexia
The second major syndrome is the syndrome of central alexia, also referred to as alexia with agraphia, aphasic alexia or parietal-temporal alexia, indicating a dominant parietal lobe lesion (Benson 1928: 108). Its major feature is the disturbance of both, reading and writing, thus, the alexia and agraphia. The loss hereby often occurs in degrees of incompleteness.
“Clinically, the reading disorder appears as letter blindness plus word blindness.” (Heilman/ Valenstein 1985: 54) Thus, patients with central alexia are unable to read letters or words. Both, the ability to read out loud and the ability to comprehend written language are disturbed. Cues like tracing the letter with the finger or getting the word spelled aloud are of little help; they are still not able to decipher the word. In this variety of alexia, the reading disturbance also applies to the comprehension of numbers and musical notation. Patients suffer an acquired illiteracy; they can be considered illiterate for written and printed language symbols. (Benson 1928: 109)
“Disorders of writing are severe, and appear in all aspects of writing.” (Heilman/ Valenstein 1985: 54) In sharp contrast to a patient with posterior alexia, a patient with central alexia is not able to produce words to dictation. In fact, he is not able to produce any letter combinations correctly. His ability to copy written and printed words on the other hand is far better.
- Quote paper
- Stella Fritz (Author), 2018, Two approaches to the classification of acquired alexias, Munich, GRIN Verlag, https://www.grin.com/document/465276