There are many different, and often conflicting, hypotheses that attempt to explain the deficits associated with<unk> . These theories have resulted in several models designed to conceptualize the symptom-complex found in<unk> s. These models are not ordered chronologically, but rather follow a general increasing trend of presence in the field of knowledge regarding<unk> s. Some models may be stronger than others, but that is not necessarily reflected here. Models and hypothesis toward the end of the list are more heavily debated and thus typically have a greater wealth of knowledge surrounding their topic. Continuum model The "Glosser and Friedman (continuum) model" is based upon the concept that<unk>  and phonological<unk>  are opposite endpoints on a "continuum" of reading disability.<unk>  appears to be a more severe form of phonological<unk> ; however, symptoms in patients can change over time so that an initial diagnosis of<unk>  is later better described as strictly a phonological<unk> . These observations suggest recovery is possible along the semantic pathway. Friedman justifies the continuum hypothesis with two sets of evidence. The first involves five patients who started with<unk> , but whose disorders shifted to phonological<unk>  during recovery. Semantic paralexias were the first symptom to diminish, either partially or totally, in each case and then other symptoms were resolved to varying degrees after that. However, nonword reading was always the last symptom to go and complete recovery was never reached by any patient. Her second set of evidence in support of the continuum was found in her review of eleven patients with<unk>  or phonological<unk>  in whom she found a predictable succession of symptoms. She placed great emphasis on the order in which reading symptoms emerged (poor nonword reading first, then visual errors, then noun > functor, then noun > verb, concrete > abstract, and finally, semantic errors) and suggested that the continuum hypothesis was supported by this pattern of symptoms. Connectionist model<unk> s have sufficient activation of a written word's features; but, this activation decays quickly, leading to errors in speech output. The "connectionist model" suggests that the phonological and semantic features of a word are activated, but this activation decays at a rate too quick for cognitive processing- thus, errors in speech output are produced as a result of this fading activation. This hypothesis explains the broad symptom-complex of<unk> s without resorting to a multiple loci damage approach as seen in other models. It eliminates the need to attribute a specific locus of damage to each symptom of<unk>  dylsexia, and instead states that all symptoms are due to decay of a large activation area. Distributed attractor networks Plaut and Shallice have hypothesized that units in the brain interact in such a way that semantic features form stable attractors in the space of all possible representations of words. These unit interactions correspond to particular attractor patterns, and if the particular attractor pattern is activated, the network remains in that pattern. However, they hypothesize that when the pattern is distorted, there is a pull on the pattern, and it gravitates toward the correct pattern, almost as if this semantic space is filled with basins, where if one point on the pattern falls to the edge of the basin, it will still gravitate toward the middle. If you lesion this area, the neurons die and the basins change their shape. When this happens, you may now have the same distorted starting pattern that will end up in a neighboring basin, which is a semantically related area, but not the correct one, and this would account for<unk>  patients to incorrectly identify "river" as "ocean". Lesions that occur early in the network change the basins that send different semantic words to different areas of the network, whereas if they occur later, the words will be much closer semantically. This may account for severity of the deficit in individual patients. Failure of inhibition hypothesis The "failure of inhibition hypothesis" states that the presentation of a target word activates semantic memory of that word, along with memory for other words that are semantically related. For example, the target word "dog" may activate "bark", "cat", "squirrel", "ball", "fetch".<unk>  patients are unable to inhibit the other related words, so they are likely to substitute one of these words for the target word in speech production (explicit output). This hypothesis contradicts the belief of other researchers that the deficits seen in<unk> s are due to processing problems. Researchers believe that "failure of inhibition" has no effect on implicit processing, but instead is the cause of impairments in the explicit task of speech production. They believe that explicit characteristics of reading involve only the conscious production of speech (reading). Information about written words is internalized without awareness (implicitly); the ability to access this information and process it into words that can be read or spoken is an explicit process. Implicit knowledge involves phonological awareness, understanding of the morphology, and a semantic understanding of written words. This implicit aspect of reading may be completely intact, and yet reading errors can still occur through defects in explicit output, or production. Researchers have studied the dissociation of implicit and explicit processes to thus unravel the underlying deficiencies in<unk> . Studies in support of "failure of inhibition" show intact implicit processing of<unk> s. For instance, studies have shown<unk> s that are equally fast in a lexical decision task with a rhyming pair of words (book-took) in comparison to a non-rhyming pair of words (bough-tough), indicating that the patients are able to use implicit phonological knowledge and phonics to process the words. Additionally, they are faster in a lexical decision task with words that sound like they are spelled (couch, pouch) than they are with words that do not sound like they are spelled (touch), again showing that patients are using phonology. These data show that implicit processing is in fact occurring in<unk>  patients. Thus, some researchers believe that the impairments present in<unk> s are only in explicit phonological output (i.e., reading aloud). They believe that the problems of<unk> s are due to production errors, and that<unk> s have normal phonological processing at the implicit level. This is supported by the fact that<unk>  is often present in patients suffering from production errors resulting from Expressive aphasia. Riley and Thompson expanded on this theory in 2010. Previous studies had shown that typical in patients with<unk> , typical members of a semantic category (like "robin" in the category of "birds") are processed faster than atypical members of the same category (like "ostrich"), known as the semantic typicality effect. According to their research, this typicality effect may indicate an inability to efficiently select a correct lexical-semantic representation. They suggest that selection inhibition becomes impaired beginning at the level of semantics rather than the later levels of production like the original failure of inhibition hypothesis suggests. Dual route model<unk>  can affect both pathways in the dual-route hypothesis of reading. The "Morton and Patterson (dual route) model" is based upon the dual route hypothesis of reading. It proposes that the occurrence of semantic errors alongside an inability to read non-words aloud must be due to multiple loci of damage within this dual-route model. Because a<unk>  cannot read aloud non-words, a disruption in the phonological process is assumed, forcing reading to proceed through the semantic route. However,<unk> s also produce semantic errors while reading, alluding to damage in this pathway as well. Other researchers refer to the phonological and semantic route as "modules". They believe that patients have a partially functioning lexical module and a completely deficient nonlexical module. The lexical module is analogous to the semantic route in the dual route model and relies on lexical memory, or the memory for words, to name words. In using the lexical module, an individual accesses a "mental dictionary" of words. The nonlexical module is comparable to the phonological route and uses knowledge of spelling and graphemes to create phonemes to name words and nonwords. The absent nonlexical module in<unk> s explains why patients cannot name nonwords. Right and left hemisphere hypotheses Activation areas in the left hemisphere when hearing or reading a word. The "left-hemisphere hypothesis", supports the idea of a damaged left hemisphere-based reading system. Normal reading is typically a function of a left hemisphere-based system. The right hemisphere plays a minimal role in reading. One hypothesis, the "left hemisphere hypothesis", supports the idea of a damaged left hemisphere-based reading system associated with<unk> .<unk> s may be attempting to use this damaged left hemisphere, resulting in severe reading deficits. On the other hand, the "right hemisphere hypothesis" states that<unk> s attempt to read using a completely different reading system. According to this hypothesis, they are using the right hemisphere for orthographic and semantic processing, but given that this system does not usually play a role in reading,<unk> s
Deep dyslexia
Surface dyslexia
Phonological dyslexia
Specific language impairment
Global developmental delay
Nonverbal learning disorder
Intellectual disability
Nonverbal autism