Dyslexic children require special instruction for word analysis and spelling from an early age. While there are fonts that may help people with dyslexia better understand writing, this might simply be due to the added spacing between words. The prognosis, generally speaking, is positive for individuals who are identified in childhood and receive support from friends and family.

Through the use of compensation strategies, therapy and educational support, dyslexic individuals can learn to read and write. There are techniques and technical aids which help to manage or conceal symptoms of the disorder. Removing stress and anxiety alone can sometimes improve written comprehension. For dyslexia intervention with alphabet-writing systems, the fundamental aim is to increase a child's awareness of correspondences between graphemes (letters) and phonemes (sounds), and to relate these to reading and spelling by teaching how sounds blend into words. It has been found that reinforced collateral training focused on reading and spelling yields longer-lasting gains than oral phonological training alone. Early intervention that is done for children at a young age can be successful in reducing reading failure.

There is some evidence that the use of specially-tailored fonts may help with dyslexia. These fonts, which include Dyslexie, OpenDyslexic, and Lexia Readable, were created based on the idea that many of the letters of the Latin alphabet are visually similar and may, therefore, confuse people with dyslexia. Dyslexie and OpenDyslexic both put emphasis on making each letter more distinctive in order to be more easily identified. The benefits, however, might simply be due to the added spacing between words.

There have been many studies conducted regarding intervention in dyslexia. Among these studies one meta-analysis found that there was functional activation as a result.

There is no evidence demonstrating that the use of music education is effective in improving dyslexic adolescents' reading skills.

A reading disability is a condition in which a sufferer displays difficulty reading resulting primarily from neurological factors. Developmental Dyslexia, Alexia (acquired dyslexia), and Hyperlexia (word-reading ability well above normal for age and IQ).

National Institute of Neurological Disorders and Stroke defines reading disability or dyslexia as follows: "Dyslexia is a brain-based type of learning disability that specifically impairs a person's ability to read. These individuals typically read at levels significantly lower than expected despite having normal intelligence. Although the disorder varies from person to person, common characteristics among people with dyslexia are difficulty with spelling, phonological processing (the manipulation of sounds), and/or rapid visual-verbal responding. In adults, dyslexia usually occurs after a brain injury or in the context of dementia. It can also be inherited in some families, and recent studies have identified a number of genes that may predispose an individual to developing dyslexia."

The NINDS definition is not in keeping with the bulk of scientific studies that conclude that there is no evidence to suggest that dyslexia and intelligence are related. The Rose Review 2009 Definition is more in keeping with modern research and debunked discrepancy model of dyslexia diagnosis:

- Dyslexia is a learning difficulty that primarily affects the skills involved in accurate and fluent word reading and spelling.

- Characteristic features of dyslexia are difficulties in phonological awareness, verbal memory and verbal processing speed.

- Dyslexia occurs across the range of intellectual abilities.

- It is best thought of as a continuum, not a distinct category, and there are no clear cut-off points.

- Co-occurring difficulties may be seen in aspects of language, motor co-ordination, mental calculation, concentration and personal organisation, but these are not, by themselves, markers of dyslexia.

- A good indication of the severity and persistence of dyslexic difficulties can be gained by examining how the individual responds or has responded to well founded intervention.

The most common cause of cortical blindness is ischemia (oxygen deprivation) to the occipital lobes caused by blockage to one or both of the posterior cerebral arteries. However, other conditions have also been known to cause acquired and transient cortical blindness, including:

- Bilateral lesions of the primary visual cortex

- Side effect of some anti-epilepsy drugs (AEDs)

- Creutzfeldt–Jakob disease, in association with a rapid onset of dementia

- Infection

- Head trauma to the occipital lobe of the brain

- Congenital abnormalities of the occipital lobe

- Eclampsia and, rarely, pre-eclampsia

- Hyperammonemia

The most common causes of congenital cortical blindness are:

- Traumatic brain injury (TBI) to the occipital lobe of the brain

- Congenital abnormalities of the occipital lobe

- Perinatal ischemia

- Encephalitis

- Meningitis

Pure alexia results from cerebral lesions in circumscribed brain regions and therefore belongs to the group of acquired reading disorders, alexia, as opposed to developmental dyslexia found in children who have difficulties in learning to read.

Semantic dyslexia is, as the name suggests, a subtype of the group of cognitive disorders known as alexia (acquired dyslexia). Those who suffer from semantic dyslexia are unable to properly attach words to their meanings in reading and/or speech. When confronted with the word "diamond", they may understand it as "sapphire", "shiny" or "diamonds"; when asking for a bus ticket, they may ask for some paper or simply "a thing".

Semantic dementia (SD) is a degenerative disease characterized by atrophy of anterior temporal regions (the primary auditory cortex; process auditory information) and progressive loss of semantic memory. SD patients often present with surface dyslexia, a relatively selective impairment in reading low-frequency words with exceptional or atypical spelling-to-sound correspondences.

Phonological dyslexia is a reading disability that is a form of alexia (acquired dyslexia), resulting from brain injury, stroke, or progressive illness and that affects previously acquired reading abilities. The major distinguishing symptom of acquired phonological dyslexia is that a selective impairment of the ability to read pronounceable non-words occurs although the ability to read familiar words is not affected. It has also been found that the ability to read non-words can be improved if the non-words belong to a family of pseudohomophones.

The prognosis of a patient with acquired cortical blindness depends largely on the original cause of the blindness. For instance, patients with bilateral occipital lesions have a much lower chance of recovering vision than patients who suffered a transient ischemic attack or women who experienced complications associated with eclampsia. In patients with acquired cortical blindness, a permanent complete loss of vision is rare. The development of cortical blindness into the milder cortical visual impairment is a more likely outcome. Furthermore, some patients regain vision completely, as is the case with transient cortical blindness associated with eclampsia and the side effects of certain anti-epilepsy drugs.

Recent research by Krystel R. Huxlin and others on the relearning of complex visual motion following V1 damage has offered potentially promising treatments for individuals with acquired cortical blindness. These treatments focus on retraining and retuning certain intact pathways of the visual cortex which are more or less preserved in individuals who sustained damage to V1. Huxlin and others found that specific training focused on utilizing the "blind field" of individuals who had sustained V1 damage improved the patients' ability to perceive simple and complex visual motion. This sort of 'relearning' therapy may provide a good workaround for patients with acquired cortical blindness in order to better make sense of the visual environment.

Pure alexia, also known as agnosic alexia or alexia without agraphia or pure word blindness, is one form of alexia which makes up "the peripheral dyslexia" group. Individuals who have pure alexia suffer from severe reading problems while other language-related skills such as naming, oral repetition, auditory comprehension or writing are typically intact.

Pure alexia is also known as: "alexia without agraphia", "letter-by-letter dyslexia", "spelling dyslexia", or "word-form dyslexia". Another name for it is "Dejerine syndrome", after Joseph Jules Dejerine, who described it in 1892; however, when using this name, it should not be confused with medial medullary syndrome which shares the same eponym.

Stroke-associated AOS is the most common form of acquired AOS, making up about 60% of all reported acquired AOS cases. This is one of the several possible disorders that can result from a stroke, but only about 11% of stroke cases involve this disorder. Brain damage to the neural connections, and especially the neural synapses, during the stroke can lead to acquired AOS. Most cases of stroke-associated AOS are minor, but in the most severe cases, all linguistic motor function can be lost and must be relearned. Since most with this form of AOS are at least fifty years old, few fully recover to their previous level of ability to produce speech.

Other disorders and injuries of the brain that can lead to AOS include (traumatic) dementia, progressive neurological disorders, and traumatic brain injury.

Agraphia is an acquired neurological disorder causing a loss in the ability to communicate through writing, either due to some form of motor dysfunction or an inability to spell. The loss of writing ability may present with other language or neurological disorders; disorders appearing commonly with agraphia are alexia, aphasia, dysarthria, agnosia, and apraxia. The study of individuals with agraphia may provide more information about the pathways involved in writing, both language related and motoric. Agraphia cannot be directly treated, but individuals can learn techniques to help regain and rehabilitate some of their previous writing abilities. These techniques differ depending on the type of agraphia.

Agraphia can be broadly divided into central and peripheral categories. Central agraphias typically involve language areas of the brain, causing difficulty spelling or with spontaneous communication, and are often accompanied by other language disorders. Peripheral agraphias usually target motor and visuospatial skills in addition to language and tend to involve motoric areas of the brain, causing difficulty in the movements associated with writing. Central agraphia may also be called aphasic agraphia as it involves areas of the brain whose major functions are connected to language and writing; peripheral agraphia may also be called nonaphasic agraphia as it involves areas of the brain whose functions are not directly connected to language and writing (typically motor areas).

The history of agraphia dates to the mid-fourteenth century, but it was not until the second half of the nineteenth century that it sparked significant clinical interest. Research in the twentieth century focused primary on aphasiology in patients with lesions from strokes.

Neuroscientists have learned a lot about the role of the brain in numerous cognitive mechanisms by understanding corresponding disorders. Similarly, neuroscientists have come to learn a lot about music cognition by studying music-specific disorders. Even though music is most often viewed from a "historical perspective rather than a biological one" music has significantly gained the attention of neuroscientists all around the world. For many centuries music has been strongly associated with art and culture. The reason for this increased interest in music is because it "provides a tool to study numerous aspects of neuroscience, from motor skill learning to emotion".

Recent research has established the existence of primary progressive apraxia of speech caused by neuroanatomic motor atrophy. For a long time, this disorder was not distinguished from other motor speech disorders such as dysarthria and in particular primary progressive aphasia. Many studies have been done trying to identify areas in the brain in which this particular disorder occurs or at least to show that it occurs in different areas of the brain than other disorders. One study observed 37 patients with neurodegenerative speech disorders to determine whether or not it is distinguishable from other disorders, and if so where in the brain it can be found. Using speech and language, neurological, neuropsychological and neuroimaging testing, the researchers came to the conclusion that PAS does exist and that it correlates to superior lateral premotor and supplementary motor atrophy. However, because PAS is such a rare and recently discovered disorder, many studies do not have enough subjects to observe to make data entirely conclusive.

Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills (needed for both written and oral language) as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.

The prognosis for children with LKS varies. Some affected children may have a permanent severe language disorder, while others may regain much of their language abilities (although it may take months or years). In some cases, remission and relapse may occur. The prognosis is improved when the onset of the disorder is after age 6 and when speech therapy is started early. Seizures generally disappear by adulthood. Short-term remissions are not uncommon in LKS but they create difficulties in evaluating a patient's response to various therapeutic modalities.

The following table demonstrate the Long-Term Follow-up of Acquired Epileptic Aphasia across many different instrumental studies:.

Lower rates of good outcomes have been reported, ranging between 14% to 50%. Duran "et al." used 7 patients in his study (all males, aged 8–27 years of age) with LKS. On long-term followup, most of his patients did not demonstrate total epilepsy remission and language problems continued. Out of the seven patients, one reported a normal quality of life while the other six reported aphasia to be a substantial struggle. The Duran "et al." study is one of few that features long-term follow up reports of LKS and utilizes EEG testing, MRIs, the Vineland Adaptive Behavior Scales, the Connor's Rating Scales-revised, and a Short-Form Health Survey to analyze its patients.

Globally, more than 200 cases of acquired epileptic aphasia have been described in the literature. Between 1957 and 1980, 81 cases of acquired epileptic aphasia were reported, with 100 cases generally being diagnosed every 10 years.

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

Visuospatial dysgnosia is a loss of the sense of "whereness" in the relation of oneself to one's environment and in the relation of objects to each other. Visuospatial dysgnosia is often linked with topographical disorientation.

There are a variety of medical conditions affecting cognitive ability. This is a broad concept encompassing various intellectual or cognitive deficits, including intellectual disability, deficits too mild to properly qualify as intellectual disability, various specific conditions (such as specific learning disability), and problems acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. These disabilities may appear at any age.

Associative visual agnosia is a form of visual agnosia. It is an impairment in recognition or assigning meaning to a stimulus that is accurately perceived and not associated with a generalized deficit in intelligence, memory, language or attention. The disorder appears to be very uncommon in a "pure" or uncomplicated form and is usually accompanied by other complex neuropsychological problems due to the nature of the etiology. Afflicted individuals can accurately distinguish the object, as demonstrated by the ability to draw a picture of it or categorize accurately, yet they are unable to identify the object, its features or its functions.

Several studies have found that different levels of brain damage can lead to the occurrence of varying forms of non-word reading disorders. It has been found that during certain tasks, dyslexics had activated one of two regions of the brain: the Broca's area, which is responsible for speech, or the Wernicke's area, which is responsible for forming and understanding. Both areas were seldom active together. This study has led to the conclusion that there exist neural connection breakdowns between the language centers that may be causing dyslexia.

Global aphasia typically results from an occlusion to the trunk of the middle cerebral artery (MCA), which affects a large portion of the perisylvian region of the left cortex. Global aphasia is usually a result of a thrombotic stroke, which occurs when a blood clot forms in the brain's blood vessels. In addition to stroke, global aphasia can also be caused by traumatic brain injury (TBI), tumors, and progressive neurological disorders. The large areas in the anterior (Broca's) and posterior (Wernicke's) area of the brain are either destroyed or impaired because they are separate branches of the MCA that are supplied by its arterial trunk. Lesions usually result in extensive damage to the language areas of the left hemisphere, however global aphasia can result from damage to smaller, subcortical regions. It is well known that a lesion to the cortex can cause aphasia. However, a study by Kumar et al. (1996) suggests that lesions to the subcortical regions of the cortex such as the thalamus, basal ganglia, internal capsule, and paraventricular white matter can also cause speech and language deficits. This is due to the fact that the subcortical regions are closely associated with the language centers in the brain. Kumar et al. state that while lesions to the subcortical regions could cause certain types of aphasia, a lesion to these regions would rarely cause global aphasia. In a study performed by Ferro (1992), it was found that five different brain lesion locations were linked to aphasia. These locations include: "fronto-temporo-parietal lesions", "anterior, suprasylvian, frontal lesions", "large subcortical infarcts", "posterior, suprasylvian, parietal infarcts", and "a double lesion composed of a frontal and a temporal infarct".

Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or low intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. There are two types of visual agnosia: apperceptive agnosia and associative agnosia.

Recognition of visual objects occurs at two primary levels. At an apperceptive level, the features of the visual information from the retina are put together to form a perceptual representation of an object. At an associative level, the meaning of an object is attached to the perceptual representation and the object is identified. If a person is unable to recognize objects because they cannot perceive correct forms of the objects, although their knowledge of the objects is intact (i.e. they do not have anomia), they have apperceptive agnosia. If a person correctly perceives the forms and has knowledge of the objects, but cannot identify the objects, they have associative agnosia.

The affected individual may not realize that they have a visual problem and may complain of becoming "clumsy" or "muddled" when performing familiar tasks such as setting the table or simple DIY.

Anosognosia, a lack of awareness of the deficit, is common and can cause therapeutic resistance. In some agnosias, such as prosopagnosia, awareness of the deficit is often present; however shame and embarrassment regarding the symptoms can be a barrier in admission of a deficiency. Because agnosias result from brain lesions, no direct treatment for them currently exists, and intervention is aimed at utilization of coping strategies by patients and those around them. Sensory compensation can also develop after one modality is impaired in agnostics

General principles of treatment:

- restitution

- repetitive training of impaired ability

- development of compensatory strategies utilizing retained cognitive functions

Partial remediation is more likely in cases with traumatic/vascular lesions, where more focal damage occurs, than in cases where the deficit arises out of anoxic brain damage, which typically results in more diffuse damage and multiple cognitive impairments. However, even with forms of compensation, some afflicted individuals may no longer be able to fulfill the requirements of their occupation or perform common tasks, such as, eating or navigating. Agnostics are likely to become more dependent on others and to experience significant changes to their lifestyle, which can lead to depression or adjustment disorders.

For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.