There are tests that can indicate with high probability whether a person is a dyslexic. If diagnostic testing indicates that a person may be dyslexic, such tests are often followed up with a full diagnostic assessment to determine the extent and nature of the disorder. Tests can be administered by a teacher or computer. Some test results indicate how to carry out teaching strategies.

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.

In order to assess an individual for agnosia, it must be verified that the individual is not suffering from a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual is suffering from a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual is suffering from a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed.

Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters.

Remediation includes both appropriate remedial instruction and classroom accommodations.

Sensory modality testing allows practitioners to assess for generalized versus specific deficits, distinguishing visual agnosias from optic aphasia, which is a more generalized deficit in semantic knowledge for objects that spans multiple sensory modalities, indicating an impairment in the semantic representations themselves.

Specialists, like ophthalmologists or audiologists, can test for perceptual abilities. Detailed testing is conducted, using specially formulated assessment materials, and referrals to neurological specialists is recommended to support a diagnosis via brain imaging or recording techniques. The separate stages of information processing in the object recognition model are often used to localize the processing level of the deficit.

Testing usually consists of object identification and perception tasks including:

- object-naming tasks

- object categorization or figure matching

- drawing or copying real objects or images or illustrations

- unusual views tests

- overlapping line drawings

- partially degraded or fragmented image identification

- face or feature analysis

- fine line judgment

- figure contour tracking

- visual object description

- object-function miming

- tactile ability tests (naming by touch)

- auditory presentation identification

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).

A patient with cortical blindness has no vision but the response of his/her pupil to light is intact (as the reflex does not involve the cortex). Therefore, one diagnostic test for cortical blindness is to first objectively verify the optic nerves and the non-cortical functions of the eyes are functioning normally. This involves confirming that patient can distinguish light/dark, and that his/her pupils dilate and contract with light exposure. Then, the patient is asked to describe something he/she would be able to recognize with normal vision. For example, the patient would be asked the following:

- "How many fingers am I holding up?"

- "What does that sign (on a custodian's closet, a restroom door, an exit sign) say?"

- "What kind of vending machine (with a vivid picture of a well-known brand name on it) is that?"

Patients with cortical blindness will not be able to identify the item being questioned about at all or will not be able to provide any details other than color or perhaps general shape. This indicates that the lack of vision is neurological rather than ocular. It specifically indicates that the occipital cortex is unable to correctly process and interpret the intact input coming from the retinas.

Fundoscopy should be normal in cases of cortical blindness. Cortical blindness can be associated with visual hallucinations, denial of visual loss (Anton–Babinski syndrome), and the ability to perceive moving but not static objects. (Riddoch syndrome).

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.

The table below demonstrates the extensive and differential diagnosis of acquired epileptic aphasia along with Cognitive and Behavioral Regression:

Note: EEG = electroencephalographic; ESES = electrical status epilepticus of sleep; RL = receptive language; S = sociability

- Continuous spike and wave of slow-wave sleep (>85% of slow-wave sleep).

Though there have been ample attempts to rehabilitate patients with pure alexia, few have proven to be effective on a large scale. Most rehabilitation practices have been specialized to a single patient or small patient group. At the simplest level, patients seeking rehabilitation are asked to practice reading words aloud repeatedly. This is meant to stimulate the damaged system of the brain. This is known as multiple oral re-reading (MOR) treatment. This is a text-based approach that is implemented in order to prevent patients from LBL reading. MOR works by reading aloud the same text repeatedly until certain criteria are reached. The most important criteria for a pure alexic patient is reading at an improved rate. The treatment aims to shift patients away from the LBL reading strategy by strengthening links between visual input and the associated orthographic representations. This repetition supports the idea of using top-down processing initially minimize the effects peripheral processing which were demonstrated in the study above. From here, the goal is to increasing bottom-up processing. This will hopefully aid in word recognition and promote interactive processing of all available information to support reading. 'The supported reading stimulation from MOR has a rehabilitative effect so that reading rate and accuracy are better for untrained text, and word-form recognition improves as evidenced by a reduced word-length effect.' These tactics have seen quite good success.

Another tactic that has been employed is the use of cross modal therapy. In this therapy, patients are asked to trace the words in which they are trying to read aloud. There has been success using cross modal therapy such as kinaesthetic or motor-cross cuing therapy, but tends to be a more feasible approach for those on the slower reading end of the spectrum.

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.

Agraphia cannot be directly treated, but individuals can be rehabilitated to regain some of their previous writing abilities.

For the management of phonological agraphia, individuals are trained to memorize key words, such as a familiar name or object, that can then help them form the grapheme for that phoneme. Management of allographic agraphia can be as simple as having alphabet cards so the individual can write legibly by copying the correct letter shapes. There are few rehabilitation methods for apraxic agraphia; if the individual has considerably better hand control and movement with typing than they do with handwriting, then they can use technological devices. Texting and typing do not require the same technical movements that handwriting does; for these technological methods, only spatial location of the fingers to type is required. If copying skills are preserved in an individual with apraxic agraphia, repeated copying may help shift from the highly intentional and monitored hand movements indicative of apraxic agraphia to a more automated control.

Micrographia is a condition that can occur with the development of other disorders, such as Parkinson's disease, and is when handwriting becomes illegible because of small writing. For some individuals, a simple command to write bigger eliminates the issue.

- Anagram and Copy Treatment (ACT) uses the arrangement of component letters of target words and then repeated copying of the target word. This is similar to the CART; the main difference is that the target words for ACT are specific to the individual. Target words that are important in the life of the individual are emphasized because people with deep or global agraphias do not typically have the same memory for the words as other people with agraphia may. Writing can be even more important to these people as it can cue spoken language. ACT helps in this by facilitating the relearning of a set of personally relevant written words for use in communication.

- Copy and Recall Treatment (CART) method helps to reestablish the ability to spell specific words that are learned through repeated copying and recall of target words. CART is more likely to be successful in treating lexical agraphia when a few words are trained to mastery than when a large group of unrelated words is trained. Words chosen can be individualized to the patient, which makes treatment more personalized.

- Graphemic buffer uses the training of specific words to improve spelling. Cueing hierarchies and copy and recall method of specific words are used, to work the words into the short-term memory loop, or graphemic buffer. The segmentation of longer words into shorter syllables helps bring words into short-term memory.

- Problem solving approach is used as a self-correcting method for phonological errors. The individual sounds out the word and attempts to spell it, typically using an electronic dictionary-type device that indicates correct spelling. This method takes advantage of the preserved sound-to-letter correspondences when they are intact. This approach may improve access to spelling memory, strengthen orthographic representations, or both.

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.

The syndrome can be difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory/verbal processing disorder, attention deficit hyperactivity disorder, intellectual disability, childhood schizophrenia, or emotional/behavioral problems. An EEG (electroencephalogram) test is imperative to a diagnosis. Many cases of patients exhibiting LKS will show abnormal electrical brain activity in both the right and left hemispheres of the brain; this is exhibited frequently during sleep. Even though an abnormal EEG reading is common in LKS patients, a relationship has not been identified between EEG abnormalities and the presence and intensity of language problems. In many cases however, abnormalities in the EEG test has preceded language deterioration and improvement in the EEG tracing has preceded language improvement (this occurs in about half of all affected children). Many factors inhibit the reliability of the EEG data: neurologic deficits do not closely follow the maximal EEG changes in time.

The most effective way of confirming LKS is by obtaining overnight sleep EEGs, including EEGs in all stages of sleep. Many conditions like demyelination and brain tumors can be ruled out by using magnetic resonance imaging (MRI). In LKS, fluorodeoxyglucose (FDG) and positron emission tomography (PET) scanning can show decreased metabolism in one or both temporal lobes - hypermetabolism has been seen in patients with acquired epileptic aphasia.

Most cases of LKS do not have a known cause. Occasionally, the condition may be induced secondary to other diagnoses such as low-grade brain tumors, closed-head injury, neurocysticercosis, and demyelinating disease. Central Nervous System vasculitis may be associated with this condition as well.

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.

If a suspected brain injury has occurred, the patient undergoes a series of medical imaging, which could include MRI(magnetic resonance imaging) or CT (computed tomography) scan. After the diagnosis of a brain injury, a speech and language pathologist will perform a variety of tests to determine the classification of aphasia. Additionally, the Boston Assessment of Severe Aphasia (BASA) is a commonly used assessment for diagnosing aphasia. BASA is used to determine treatment plans after strokes lead to symptoms of aphasia and tests both gestural and verbal responses. Cognitive functions can be assessed using the Cognitive Test Battery for Global Aphasia (CoBaGa). The CoBaGa is an appropriate measure to assess a person with severe aphasia because it does not require verbal responses, rather manipulative answers. The CoBaGa assesses cognitive functions such as attention, executive functions, logical reasoning, memory, visual-auditory recognition, and visual-spatial ability. Van Mourik et al. conducted a study in which they assessed the cognitive abilities of people with global aphasia using the Global Aphasic Neuropsychological Battery. This test assesses attention/concentration, memory, intelligence, and visual and auditory nonverbal recognition. The results of this study helped the researchers determine there were varying levels of severity among individuals with global aphasia.

Speech and language therapy is typically the primary treatment for individuals with aphasia. The goal of speech and language therapy is to increase the person’s communication abilities to a level functional for daily life. Goals are chosen based on collaboration between speech language pathologists, patients, and their family/caregivers. Goals should be individualized based on the person’s aphasia symptoms and communicative needs. In 2016, Wallace et al. found the following outcomes were commonly prioritized in therapy: communication, life participation, physical and emotional well-being, normalcy, and health and support services. However, available research is inconclusive about which specific approach to speech and language therapy is most effective in treating global aphasia.

Therapy can be either group or individual. Group therapies that integrate the use of visual aids allow for enhanced social and communication-skill development. Group therapy sessions typically revolve around simple, preplanned activities or games, and aim to facilitate social communication.

One particular therapy designed specifically for treatment of aphasia is Visual Action Therapy (VAT). VAT is a non-verbal gestural output program with 3 phases and 30 total steps. The program teaches unilateral gestures as symbolic representations of real life objects. Research on the effectiveness of VAT is limited and inconclusive.

One important therapy technique includes teaching family members and caregivers strategies for more effectively communicating with their loved ones. Research offers such strategies including, simplifying sentences and using common words, gaining the person's attention before speaking, using pointing and visual cues, allowing for adequate response time, and creating a quiet environment free of distractions.

Another approach to speech and language treatment is constraint-induced language therapy (CILT). CILT involves teaching the patient to use speech in small segments but avoid using gestures and familiar words . The speech language pathologist provides positive feedback throughout and ignores any mistakes made by the patient. The intensity with which this treatment is provided has been debated in the literature. One study, performed in 2015, compared the outcomes of patients with aphasia who received CILT for either 30 hours total over 2 weeks or 30 hours distributed over 10 weeks. Results showed that both groups made significant speech and language improvements. Overall, CILT is an effective treatment at a variety of intensities.

Research supporting the efficacy of pharmacological treatments for aphasia is limited. To date, no large scale clinical trials have proven benefits of pharmacological treatment.

Many researchers are investigating the characteristics of apraxia of speech and the most effective treatment methods. Below are a couple of the recent findings:

Sound Production Treatment:

Articulatory-kinematic treatments have the strongest evidence of their use in treating Acquired Apraxia of Speech. These treatments use the facilitation of movement, positioning, timing, and articulators to improve speech production. Sound Production Treatment (SPT) is an articulatory-kinematic treatment that has received more research than many other methods. It combines modeling, repetition, minimal pair contrast, integral stimulation, articulatory placement cueing, and verbal feedback. It was developed to improve the articulation of targeted sounds in the mid-1990s. SPT shows consistent improvement of trained sounds in trained and untrained words. The best results occur with eight to ten exemplars of the targeted sound to promote generalization to untrained exemplars of trained sounds. In addition, maintenance effects are the strongest with 1–2 months post-treatment with sounds that reached high accuracy during treatment. Therefore, the termination of treatment should not be determined by performance criteria, and not by the number of sessions the client completes, in order to have the greatest long-term effects. While there are many parts of SPT that should receive further investigation, it can be expected that it will improve the production of targeted sounds for speakers with apraxia of Speech.

Repeated Practice & Rate/Rhythm Control Treatments:

Julie Wambaugh’s research focuses on clinically applicable treatments for acquired apraxia of speech. She recently published an article examining the effects of repeated practice and rate/rhythm control on sound production accuracy. Wambaugh and colleagues studied the effects of such treatment for 10 individuals with acquired apraxia of speech. The results indicate that repeated practice treatment results in significant improvements in articulation for most clients. In addition, rate/rhythm control helped some clients, but not others. Thus, incorporating repeated practice treatment into therapy would likely help individuals with AOS.

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.

Apraxia of speech can be diagnosed by a speech language pathologist (SLP) through specific exams that measure oral mechanisms of speech. The oral mechanisms exam involves tasks such as pursing lips, blowing, licking lips, elevating the tongue, and also involves an examination of the mouth. A complete exam also involves observation of the patient eating and talking. SLPs do not agree on a specific set of characteristics that make up the apraxia of speech diagnosis, so any of the characteristics from the section above could be used to form a diagnosis. Patients may be asked to perform other daily tasks such as reading, writing, and conversing with others. In situations involving brain damage, an MRI brain scan also helps identify damaged areas of the brain.

A differential diagnosis must be used in order to rule out other similar or alternative disorders. Although disorders such as expressive aphasia, conduction aphasia, and dysarthria involve similar symptoms as apraxia of speech, the disorders must be distinguished in order to correctly treat the patients. While AOS involves the motor planning or processing stage of speech, aphasic disorders can involve other language processes.

According to Ziegler et al., this difficulty in diagnosis derives from the unknown causes and function of the disorder, making it hard to set definite parameters for AOS identification. Specifically, he explains that oral-facial apraxia, dysarthria, and aphasic phonological impairment are the three distinctly different disorders that cause individuals to display symptoms that are often similar to those of someone with AOS, and that these close relatives must be correctly ruled out by a Speech Language Pathologist before AOS can be given as a diagnosis. In this way, AOS is a diagnosis of exclusion, and is generally recognized when all other similar speech sound production disorders are eliminated.

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".

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.