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.

It is generally accepted that DLD is strongly influenced by genetic factors. The best evidence comes from the Twin study method. Two twins growing up together are exposed to the same home environment, yet may differ radically in their language skills. Such different outcomes are, however, much more common in fraternal (non-identical) twins, who are genetically different. Identical twins share the same genes and tend to be much more similar in language ability. There can be some variation in the severity and persistence of DLD in identical twins, indicating that non-genetic factors affect the course of disorder, but it is unusual to find a child with DLD who has an identical twin with typical language.

There was considerable excitement when a large, multigenerational family with a high rate of DLD were found to have a mutation of the FOXP2 gene just in the affected family members. However, subsequent studies have found that, though DLD runs in families, it is not usually caused by a mutation in FOXP2 or another specific gene. Current evidence suggests that there are many different genes that can influence language learning, and DLD results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. Nevertheless, study of the mode of action of the FOXP2 gene has helped identify other common genetic variants involved in the same neural pathways that may play a part in causing DLD.

Language disorders are associated with aspects of home environment, and it is often assumed that this is a causal link, with poor language stimulation leading to weak language skills. Twin studies, however, show that two children in the same home environment can have very different language outcomes, suggesting we should consider other explanations for the link. Children with DLD often grow up into adults who have relatively low educational attainments, and their children may share a genetic risk for language disorder.

One non-genetic factor that is known to have a specific impact on language development is being a younger sibling in a large family.

Longitudinal studies indicate that problems are largely resolved by 5 years of age in around 40% of 4-year-olds with early language delays who have no other presenting risk factors. However, for children who still have significant language difficulties at school entry, reading problems are common, even for children who receive specialist help, and educational attainments are typically poor. Poor outcomes are most common in cases where comprehension as well as expressive language is affected. There is also evidence that scores on tests of nonverbal ability of children with DLD decrease over the course of development.

DLD is associated with an elevated risk of social, emotional and mental health concerns. For instance, in a UK survey, 64% of a sample of 11-year-olds with DLD scored above a clinical threshold on a questionnaire for psychiatric difficulties, and 36% were regularly bullied, compared with 12% of comparison children. In the longer-term, studies of adult outcomes of children with DLD have found elevated rates of unemployment, social isolation and psychiatric disorder among those with early comprehension difficulties. However, better outcomes are found for children who have milder difficulties and do not require special educational provision.

It is now generally accepted that SLI is a strongly genetic disorder. The best evidence comes from studies of twins. Two twins growing up together are exposed to the same home environment, yet may differ radically in their language skills. Such different outcomes are, however, seen almost exclusively in fraternal (non-identical) twins, who are genetically different. Identical twins share the same genes and tend to be much more similar in language ability.

There can be some variation in the severity and persistence of SLI in identical twins, indicating that environmental factors affect the course of disorder, but it is unusual to find a child with SLI who has an identical twin with normal language.

SLI is not usually caused by a mutation in a single gene. Current evidence suggests that there are many different genes that can influence language learning, and SLI results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. It has been hypothesized, however, that a mutation of the FOXP2 gene may have an influence on the development on SLI to a certain degree, as it regulates genes pertinent to neural pathways related to language.

Only a handful of non-genetic factors have been found selectively to impact on language development in children. Later-born children in large families are at greater risk than earlier born.

Overall, genetic mutation, hereditary influences, and environmental factors may all have a role in the development and manifestation of SLI. It is important, therefore, to not associate the development to a single factor, but recognize that it is oftentimes the result of complex interactions between any or all of these factors.

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.

Deep dyslexia is a form of dyslexia that disrupts reading processes. Deep dyslexia may occur as a result of a head injury, stroke, disease, or operation. This injury results in the occurrence of semantic errors during reading and the impairment of nonword reading.

The term dyslexia comes from the Greek words 'dys' meaning 'impaired', and 'lexis' meaning 'word' and is used to describe disorders of language concerning reading and spelling.

Numerous models and hypotheses have been proposed in attempt to explain the broad range of symptoms experienced by deep dyslexics, but a definite consensus has yet to be reached. The proposed models and hypotheses have helped in treatment of some suffering patients, but only with certain specific symptoms. Additionally, the recovery seen is not experienced equally in all patients.

Surface dyslexia is a type of dyslexia, or reading disorder. According to Marshall & Newcombe's (1973) and McCarthy & Warrington's study (1990), patients with this kind of disorder cannot recognize a word as a whole due to the damage of the left parietal or temporal lobe. Individuals with surface dyslexia are unable to recognize a word as a whole word and retrieve its pronunciation from memory. Rather, individuals with surface dyslexia rely on pronunciation rules. Thus, patients with this particular type of reading disorder read non-words fluently, like "yatchet", but struggle with words that defy pronunciation rules (i.e. exception words). For example, a patient with surface dyslexia can correctly read regular words like "mint", but will err when presented a word that disobeys typical pronunciation rules, like "pint". Often, semantic knowledge is preserved in individuals with surface dyslexia.

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.

Epidemiological surveys, in the US and Canada, estimated the prevalence of SLI in 5-year-olds at around 7 percent. However, neither study adopted the stringent 'discrepancy' criteria of the Diagnostic and Statistical Manual of Mental Disorders or ICD-10; SLI was diagnosed if the child scored below cut-off on standardized language tests, but had a nonverbal IQ of 90 or above and no other exclusionary criteria.

Anomia can be genetic or caused by damage to various parts of the parietal lobe or the temporal lobe of the brain by an accident or stroke, or a brain tumor.

Although the main causes are not specifically known, many researchers have found factors contributing to anomic aphasia. It is known that people with damage to the left hemisphere of the brain are more likely to have anomic aphasia. Broca's area, the speech production center in the brain, was linked to being the source for speech execution problems, with the use of functional magnetic resonance imaging (fMRI), now commonly used to study anomic patients. Other experts believe that damage to Wernicke's area, which is the speech comprehension area of the brain, is connected to anomia because the patients cannot comprehend the words that they are hearing.

Although many experts have believed that damage to Broca's area or Wernicke's area are the main causes of anomia, current studies have shown that damage in the left parietal lobe is the epicenter of anomic aphasia. One study was conducted using a word repetition test as well as fMRI in order to see the highest level of activity as well as where the lesions are in the brain tissue. Fridrikkson, et al. saw that damage to neither Broca's area nor Wernicke's area were the sole sources of anomia in the subjects. Therefore, the original anomia model, which theorized that damage occurred on the surface of the brain in the grey matter was debunked, and it was found that the damage was in the white matter deeper in the brain, on the left hemisphere. More specifically, the damage was in a part of the nerve tract called the arcuate fasciculus, for which the mechanism of action is unknown, though it is known to connect the posterior (back) of the brain to the anterior (front) and vice versa.

New data has shown that although the arcuate fascicles' main function does not include connecting Wernicke's area and Broca's area, damage to the tract does create speech problems because the speech comprehension and speech production areas are connected by this tract. Some studies have found that in right-handed people the language center is 99% in the left hemisphere; therefore, anomic aphasia almost exclusively occurs with damage to the left hemisphere. However, in left-handed people the language center is about 60% in the left hemisphere; thus, anomic aphasia can occur with damage to the right hemisphere in left-handed people.

People affected by jargon aphasia usually are elderly and/or people who have damage to the neural pathways of certain parts of the brain. This is usually the result of the following conditions[2]:

- Stroke

- Traumatic Brain Injury

- Epilepsy

- Migraine

- Brain Tumor

- Alzheimer's Disease

- Parkinson's Disease

Since jargon is associated with fluent (Wernicke’s) aphasia, it is usually caused by damage of the temporal lobe, and more specifically, Wernicke’s area. After the condition is diagnosed, a Computerized Tomography (CT) or Magnetic Resonance Imaging (MRI) scan is typically used to determine the location and severity of the brain damage that has caused the aphasia[2].

There have been cases in which aphasia has developed after damage to only the right hemisphere of the brain. These cases are few and far between, and usually involve unique circumstances for the individual. Most commonly, these results can stem from brain organization that is different than the general population, or a heavier than normal reliance on the right hemisphere of the brain[7].

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.

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.

Dyscalculia is thought to be present in 3–6% of the general population, but estimates by country and sample vary somewhat. Many studies have found prevalence rates by gender to be equivalent. Those that find gender difference in prevalence rates often find dyscalculia higher in females, but some few studies have found prevalence rates higher in males.

Mixed receptive-expressive language disorder (DSM-IV 315.32) is a communication disorder in which both the receptive and expressive areas of communication may be affected in any degree, from mild to severe. Children with this disorder have difficulty understanding words and sentences. This impairment is classified by deficiencies in expressive and receptive language development that is not attributed to sensory deficits, nonverbal intellectual deficits, a neurological condition, environmental deprivation or psychiatric impairments. Research illustrates that 2% to 4% of 5 year olds have mixed receptive-expressive language disorder. This distinction is made when children have issues in expressive language skills, the production of language, and when children also have issues in receptive language skills, the understanding of language. Those with mixed receptive-language disorder have a normal left-right anatomical asymmetry of the planum temporale and parietale. This is attributed to a reduced left hemisphere functional specialization for language. Taken from a measure of cerebral blood flow (SPECT) in phonemic discrimination tasks, children with mixed receptive-expressive language disorder do not exhibit the expected predominant left hemisphere activation. Mixed receptive-expressive language disorder is also known as receptive-expressive language impairment (RELI) or receptive language disorder.

Dysgraphia is a biologically based disorder with genetic and brain bases. More specifically, it is a working memory problem. In dysgraphia, individuals fail to develop normal connections among different brain regions needed for writing. People with dysgraphia have difficulty in automatically remembering and mastering the sequence of motor movements required to write letters or numbers. Dysgraphia is also in part due to underlying problems in orthographic coding, the orthographic loop, and graphmotor output (the movements that result in writing) by one’s hands, fingers and executive functions involved in letter writing. The orthographic loop is when written words are stored in the mind’s eye, connected through sequential finger movement for motor output through the hand with feedback from the eye.

Anomic aphasia (also known as dysnomia, nominal aphasia, and amnesic aphasia) is a mild, fluent type of aphasia where an individual has word retrieval failures and cannot express the words they want to say (particularly nouns and verbs). Anomia is a deficit of expressive language. The most pervasive deficit in the aphasias is anomia. Some level of anomia is seen in all of the aphasias. Individuals with aphasia who display anomia can often describe an object in detail and maybe even use hand gestures to demonstrate how the object is used but cannot find the appropriate word to name the object.

In 2006, the U.S. Department of Education indicated that more than 1.4 million students were served in the public schools' special education programs under the speech or language impairment category of IDEA 2004. This estimate does not include children who have speech/language problems secondary to other conditions such as deafness; this means that if all cases of speech or language impairments were included in the estimates, this category of impairment would be the largest. Another source has estimated that communication disorders—a larger category, which also includes hearing disorders—affect one of every 10 people in the United States.

ASHA has cited that 24.1% of children in school in the fall of 2003 received services for speech or language disorders—this amounts to a total of 1,460,583 children between 3 –21 years of age. Again, this estimate does not include children who have speech/language problems secondary to other conditions. Additional ASHA prevalence figures have suggested the following:

- Stuttering affects approximately 4% to 5% of children between the ages of 2 and 4.

- ASHA has indicated that in 2006:

- Almost 69% of SLPs served individuals with fluency problems.

- Almost 29% of SLPs served individuals with voice or resonance disorders.

- Approximately 61% of speech-language pathologists in schools indicated that they served individuals with SLI

- Almost 91% of SLPs in schools indicated that they servedindividuals with phonological/articulation disorder

- Estimates for language difficulty in preschool children range from 2% to 19%.

- Specific Language Impairment (SLI) is extremely common in children, and affects about 7% of the childhood population.

Perseverative paraphasia is a type of paraphasia in which the previous response persists and interferes with retrieval of new responses. (See the experimental case study D.L.A published by Dennis in 1976.) It is associated with lesions in the left caudate nucleus.

Dyscalculia is difficulty in learning or comprehending arithmetic, such as difficulty in understanding numbers, learning how to manipulate numbers, and learning facts in mathematics. It is generally seen as a specific developmental disorder.

Dyscalculia can occur in people from across the whole IQ range – often higher than average – along with difficulties with time, measurement, and spatial reasoning. Estimates of the prevalence of dyscalculia range between 3 and 6% of the population. In 2004, it was reported that a quarter of children with dyscalculia had ADHD.

In 2015, it was established that 11% of children with dyscalculia also have ADHD. Dyscalculia has also been associated with people who have Turner syndrome and people who have spina bifida.

Mathematical disabilities can occur as the result of some types of brain injury, in which case the proper term, acalculia, is to distinguish it from dyscalculia which is of innate, genetic or developmental origin.

Language-based learning disabilities or LBLD are "heterogeneous" neurological differences that can affect skills such as listening, reasoning, speaking, reading, writing, and maths calculations. It is also associated with movement, coordination, and direct attention. LBLD is not usually identified until the child reaches school age. Most people with this disability find it hard to communicate, to express ideas efficiently and what they say may be ambiguous and hard to understand

It is a neurological difference. It is often hereditary, and is frequently associated to specific language problems.

There are two types of learning disabilities: non-verbal, which includes disabilities from psychomotor difficulties to dyscalculia, and verbal, language based.

There are some common problems not related to dysgraphia but often associated with dysgraphia, the most common of which is stress. Often children (and adults) with dysgraphia will become extremely frustrated with the task of writing (and spelling); younger children may cry, pout, or refuse to complete written assignments. This frustration can cause the child (or adult) a great deal of stress and can lead to stress-related illnesses. This can be a result of any symptom of dysgraphia.

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.

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.

If assessed on the Wechsler Adult Intelligence Scale, for instance, symptoms of mixed receptive-expressive language disorder may show as relatively low scores for Information, Vocabulary and Comprehension (perhaps below the 25th percentile). If a person has difficulty with specific types of concepts, for example spatial terms, such as 'over', 'under', 'here' and 'there', they may also have difficulties with arithmetic, understanding word problems and instructions, or difficulties using words at all.

They may also have a more general problem with words or sentences, both comprehension and orally. Some children will have issues with pragmatics - the use of language in social contexts as well; and therefore, will have difficulty with inferring meaning. Furthermore, they have severe impairment of spontaneous language production and for this reason, they have difficulty in formulating questions. Generally, children will have trouble with morphosyntax, which is word inflections. These children have difficulty understanding and applying grammatical rules, such as endings that mark verb tenses (e.g. -"ed"), third-person singular verbs (e.g. I "think", he "thinks"), plurals (e.g. -"s"), auxiliary verbs that denote tenses (e.g. "was" running, "is" running), and with determiners ("the, a"). Moreover, children with mixed receptive-expressive language disorders have deficits in completing two cognitive operations at the same time and learning new words or morphemes under time pressure or when processing demands are high. These children also have auditory processing deficits in which they process auditory information at a slower rate and as a result, require more time for processing.