Agraphia or impairment in producing written language can occur in many ways and many forms because writing involves many cognitive processes (language processing, spelling, visual perception, visuospatial orientation for graphic symbols, motor planning, and motor control of handwriting).

Agraphia has two main subgroupings: central ("aphasic") agraphia and peripheral ("nonaphasic") agraphia. Central agraphias include , phonological, deep, and semantic agraphia. Peripheral agraphias include allographic, apraxic, motor execution, hemianoptic and afferent agraphia.

Central agraphia occurs when there are both impairments in spoken language and impairments to the various motor and visualization skills involved in writing. Individuals who have agraphia with fluent aphasia write a normal quantity of well-formed letters, but lack the ability to write meaningful words. Receptive aphasia is an example of fluent aphasia. Those who have agraphia with nonfluent aphasia can write brief sentences but their writing is difficult to read. Their writing requires great physical effort but lacks proper syntax and often has poor spelling. Expressive aphasia is an example of nonfluent aphasia. Individuals who have Alexia with agraphia have difficulty with both the production and comprehension of written language. This form of agraphia does not impair spoken language.

- Deep agraphia affects an individuals' phonological ability and orthographic memory. Deep agraphia is often the result of a lesion involving the left parietal region (supramarginal gyrus or insula). Individuals can neither remember how words look when spelled correctly, nor sound them out to determine spelling. Individuals typically rely on their damaged orthographic memory to spell; this results in frequent errors, usually semantic in nature. Individuals have more difficulty with abstract concepts and uncommon words. Reading and spoken language are often impaired as well.

- Gerstmann syndrome agraphia is the impairment of written language production associated with the following structural symptoms: difficulty discriminating between one's own fingers, difficulty distinguishing left from right, and difficulty performing calculations. All four of these symptoms result from pathway lesions. Gerstmann's syndrome may additionally be present with alexia and mild aphasia.

- Global agraphia also impairs an individuals' orthographic memory although to a greater extent than deep agraphia. In global apraxia, spelling knowledge is lost to such a degree that the individual can only write very few meaningful words, or cannot write any words at all. Reading and spoken language are also markedly impaired.

- Lexical and structural agraphia are caused by damage to the orthographic memory; these individuals cannot visualize the spelling of a word, though they do retain the ability to sound them out. This impaired spelling memory can imply the loss or degradation of the knowledge or just an inability to efficiently access it. There is a regularity effect associated with lexical agraphia in that individuals are less likely to correctly spell words without regular, predictable spellings. Additionally, spelling ability tends to be less impaired for common words. Individuals also have difficulty with homophones. Language competence in terms of grammar and sentence writing tends to be preserved.

- Phonological agraphia is the opposite of lexical agraphia in that the ability to sound out words is impaired, but the orthographical memory of words may be intact. It is associated with a lexicality effect by a difference in the ability to spell words versus nonwords; individuals with this form of agraphia are depending on their orthographic memory. Additionally, it is often harder for these individuals to access more abstract words without strong semantic representations (i.e., it is more difficult for them to spell prepositions than concrete nouns).

- Pure agraphia is the impairment in written language production without any other language or cognitive disorder.

Agraphia can occur separately or co-occur and can be caused by damage to the angular gyrus

Deep dyslexia is usually classified as an "acquired reading disorder", as opposed to a "developmental dyslexia", in previously literate adults as a consequence of a brain injury. However, recently, developmental deep dyslexia has also been reported in children with Williams syndrome.

Deep dyslexia is considered to be a "central dyslexia" as compared to a "peripheral dyslexia". Peripheral dyslexics have difficulty matching the visual characteristics of letters that comprise a word to a stored memory of this word from prior encounters. Central dyslexics are unable to properly match the visual word to the word's meaning. They may also be incapable of speaking, or phonating, the sequence of written letters that they see into the word these letters represent. Deep dyslexia differs from other forms of central dyslexia (phonological dyslexia and surface dyslexia) in that deep dyslexics have many more symptoms and these symptoms are generally more severe. According to the "continuum" hypothesis, deep dyslexia is a more severe form of phonological dyslexia.

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.

There are three main types of anomia:

- Word selection anomia occurs when the patient knows how to use an object and can correctly select the target object from a group of objects, and yet cannot name the object. Some patients with word selection anomia may exhibit selective impairment in naming particular types of objects, such as animals or colors. In the subtype known as color anomia, the patient can distinguish between colors but cannot identify them by name or name the color of an object. The patients can separate colors into categories, but they cannot name them.

- Semantic anomia is a disorder in which the meaning of words becomes lost. In patients with semantic anomia, a naming deficit is accompanied by a recognition deficit. Thus, unlike patients with word selection anomia, patients with semantic anomia are unable to select the correct object from a group of objects, even when provided with the name of the target object.

- Disconnection anomia results from the severing of connections between sensory and language cortices. Patients with disconnection anomia may exhibit modality-specific anomia, where the anomia is limited to a specific sensory modality, such as hearing. For example, a patient who is perfectly capable of naming a target object when it is presented via certain sensory modalities like audition or touch, may be unable to name the same object when the object is presented visually. Thus, in such a case, the patient's anomia arises as a consequence of a disconnect between his/her visual cortex and language cortices.

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.

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.

Anomic aphasia (anomia) is a type of aphasia characterized by problems recalling words, names, and numbers. Speech is fluent and receptive language is not impaired in someone with anomic aphasia. Subjects often use circumlocutions (speaking in a roundabout way) in order to avoid a name they cannot recall or to express a certain word they cannot remember. Sometimes the subject can recall the name when given clues. Additionally, patients are able to speak with correct grammar; the main problem is finding the appropriate word to identify an object or person.

Sometimes subjects may know what to do with an object, but still not be able to give a name to the object. For example, if a subject is shown an orange and asked what it is called, the subject may be well aware that the object can be peeled and eaten, and may even be able to demonstrate this by actions or even verbal responses – however, they cannot recall that the object is called an "orange". Sometimes, when a person with this condition is multilingual, they might confuse the language they are speaking in trying to find the right word (inadvertent code-switching).

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.

Studies show that low receptive and expressive language at young ages was correlated to increased autism symptom severity in children in their early school years. Below is a chart depicting language deficits of children on the Autistic Spectrum. This table indicates the lower levels of language processing, receptive/expressive disorders, which is more severe in children with autism. When autistic children speak, they are often difficult to understand, their language is sparse and dysfluent, they speak in single, uninflected words or short phrases, and their supply of words is severely depleted. This leads to limited vocabulary while also having deficits in verbal short term memory.

Conduction aphasics will show relatively well-preserved auditory comprehension, which may even be completely functional. Spontaneous speech production will be fluent and generally grammatically and syntactically correct. Intonation and articulation will also be preserved. Speech will often contain paraphasic errors: phonemes and syllables will be dropped or transposed (e.g., "snowball" → "snowall", "television" → "vellitision", "ninety-five percent" → "ninety-twenty percent"). The hallmark deficit of this disorder, however, is in repetition. Patients will show a marked inability to repeat words or sentences when prompted by an examiner. After saying a sentence to a person with conduction aphasia, he or she will be able to paraphrase the sentence accurately but will not be able to repeat it, possibly because their "motor speech error processing is disrupted by inaccurate forward predictions, or because detected errors are not translated into corrective commands due to damage to the auditory-motor interface". When prompted to repeat words, patients will be unable to do so, and produce many paraphasic errors. For example, when prompted with "bagger", a patient may respond with, "gabber". Oral reading can also be poor.

However, patients recognize their paraphasias and errors and will try to correct them, with multiple attempts often necessary for success. This recognition is due to preserved auditory error detection mechanisms. Error sequences frequently fit a pattern of incorrect approximations featuring known morphemes that "a") share one or more similarly located phonemes but "b") differ in at least one aspect that makes the substituted morpheme(s) semantically distinct. This repetitive effort to approximate the appropriate word or phrase is known as "conduite d’approche". For example, when prompted to repeat "Rosenkranz", a German-speaking patient may respond with, "rosenbrau... rosenbrauch... rosengrau... bro... grosenbrau... grossenlau, rosenkranz... kranz... rosenkranz".

Conduction aphasia is a relatively mild language impairment, and most patients return to day-to-day life. Symptoms of conduction aphasia, as with other aphasias, can be transient, lasting only several hours or a few days. As aphasias and other language disorders are frequently due to stroke, their symptoms can change and evolve over time, or simply disappear. This is due to healing in the brain after inflammation or hemorrhage, which leads to decreased local impairment. Furthermore, plastic changes in the brain may lead to the recruitment of new pathways to restore lost function. For example, the right hemisphere speech systems may learn to correct for left-hemisphere damage. However, chronic conduction aphasia is possible, without transformation to other aphasias. These patients show prolonged, profound deficits in repetition, frequent phonemic paraphasias, and "conduite d'approche" during spontaneous speech.

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.

Language disorders or language impairments are disorders that involve the processing of linguistic information. Problems that may be experienced can involve grammar (syntax and/or morphology), semantics (meaning), or other aspects of language. These problems may be receptive (involving impaired language comprehension), expressive (involving language production), or a combination of both. Examples include specific language impairment and aphasia, among others. Language disorders can affect both spoken and written language, and can also affect sign language; typically, all forms of language will be impaired.

Current data indicates that 7% of young children display language disorder, with boys being diagnosed twice as much as girls.

Preliminary research on potential risk factors have suggested biological components, such as low-birth weight, prematurity, general birth complications, and male gender, as well as family history and low parental education can increase the chance of developing language disorders.

For children with phonological and expressive language difficulties, there is evidence supporting speech and language therapy. However, the same therapy is shown to be much less effective for receptive language difficulties. These results are consistent with the poorer prognosis for receptive language impairments that are generally accompanied with problems in reading comprehension.

Note that these are distinct from speech disorders, which involve difficulty with the act of speech production, but not with language.

Language disorders tend to manifest in two different ways: receptive language disorders (where one cannot properly comprehend language) and expressive language disorders (where one cannot properly communicate their intended message).

Auditory verbal agnosia can be referred to as a pure aphasia because it has a high degree of specificity. Despite an inability to comprehend speech, patients with auditory verbal agnosia typically retain the ability to hear and process non-speech auditory information, speak, read and write. This specificity suggests that there is a separation between speech perception, non-speech auditory processing, and central language processing. In support of this theory, there are cases in which speech and non-speech processing impairments have responded differentially to treatment. For example, some therapies have improved writing comprehension in patients over time, while speech remained critically impaired in those same patients.

The term "pure word deafness" is something of a misnomer. By definition, individuals with pure word deafness are not deaf – in the absence of other impairments, these individuals have normal hearing for all sounds, including speech. The term "deafness" originates from the fact that individuals with AVA are unable to "comprehend" speech that they hear. The term "pure word" refers to the fact that comprehension of verbal information is selectively impaired in AVA. For this reason, AVA is distinct from other auditory agnosias in which the recognition of nonspeech sounds is impaired. Classical (or pure) auditory agnosia is an inability to process environmental sounds. Interpretive or receptive agnosia (amusia) is an inability to understand music.

Patients with pure word deafness complain that speech sounds simply do not register, or that they tend not to come up. Other claims include speech sounding as if it were in a foreign language, the words having a tendency to run together, or the feeling that speech was simply not connected to the patient's voice.

Dysgraphia is nearly always accompanied by other learning differences such as dyslexia or attention deficit disorder, and this can impact the type of dysgraphia a person might have. There are three principal subtypes of dysgraphia that are recognized. There is little information available about different types of dysgraphia and there are likely more subtypes than the ones listed below. Some children may have a combination of two or more of these, and individual symptoms may vary in presentation from what is described here. Most common presentation is a motor dysgraphia/agraphia resulting from damage to some part of the motor cortex in the parietal lobes.

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.

Aphasia is loss of the ability to produce or comprehend language. There are acute aphasias which result from stroke or brain injury, and primary progressive aphasias caused by progressive illnesses such as dementia.

- Acute aphasias

- Expressive aphasia also known as Broca's aphasia, expressive aphasia is a non-fluent aphasia that is characterized by damage to the frontal lobe region of the brain. A person with expressive aphasia usually speaks in short sentences that make sense but take great effort to produce. Also, a person with expressive aphasia understands another person's speech but has trouble responding quickly.

- Receptive aphasia also known as Wernicke's aphasia, receptive aphasia is a fluent aphasia that is categorized by damage to the temporal lobe region of the brain. A person with receptive aphasia usually speaks in long sentences that have no meaning or content. People with this type of aphasia often have trouble understanding other's speech and generally do not realize that they are not making any sense.

- Conduction aphasia

- Anomic aphasia

- Global aphasia

- Primary progressive aphasias

- Progressive nonfluent aphasia

- Semantic dementia

- Logopenic progressive aphasia

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

In all of these ways, TSA is very similar to a more commonly known language disorder, receptive aphasia. However, transcortical sensory aphasia differs from receptive aphasia in that patients still have intact repetition and exhibit echolalia, or the compulsive repetition of words. Transcortical sensory aphasia cannot be diagnosed through brain imaging techniques such as functional magnetic resonance imaging (fMRI), as the results are often difficult to interpret. Therefore, clinicians rely on language assessments and observations to determine if a patient presents with the characteristics of TSA. Patients diagnosed with TSA have shown partial recovery of speech and comprehension after beginning speech therapy. Speech therapy methods for patients with any subtype of aphasia are based on the principles of learning and neuroplasticity. Clinical research on TSA is limited because it occurs so infrequently in patients with aphasia that it is very difficult to perform systematic studies.

TSA should not be confused with transcortical motor aphasia (TMA), which is characterized by nonfluent speech output, with good comprehension and repetition. Patients with TMA have impaired writing skills, difficulty speaking and difficulty maintaining a clear thought process. Furthermore, TMA is caused by lesions in cortical motor areas of the brain as well as lesions in the anterior portion of the basal ganglia, and can be seen in patients with expressive aphasia.

The word hyperlexia is derived from the Greek terms "hyper" ("over") and "léxis" ("diction", "word").

Peripheral dyslexias have been described as affecting the visual analysis of letters as a result of brain injury. Hemianopsia, a visual field loss on the left/right side of the vertical midline, is associated with this condition.

Central dyslexias include surface dyslexia, semantic dyslexia, phonological dyslexia, and deep dyslexia. ICD-10 reclassified the previous distinction between dyslexia (315.02 in ICD-9) and alexia (315.01 in ICD-9) into a single classification as R48.0. The terms are applied to developmental dyslexia and inherited dyslexia along with developmental aphasia and inherited alexia, which are considered synonymous.

Impaired verbal comprehension can be the result a number of causes such as failure of speech sound discrimination, word recognition, auditory working memory, or syntactic structure building. When clinically examined, patients with TSA will exhibit poor comprehension of verbal commands. Based on the extent of the comprehension deficiency, patients will have difficulty following simple commands, e.g. “close your eyes.” Depending on the extent of affected brain area, patients are able to follow simple commands but may not be able to comprehend more difficult, multistep commands, e.g. “point to the ceiling, then touch your left ear with your right hand." Verbal commands as such, that require the patient to cross over the midline of their body are typically more taxing than commands that involve solely the right or left side. When increasing the complexity of verbal commands comprehension is often tested by varying the grammatical structure of the command to determine whether or not the patient understands different grammatical variations of the same sentence. Commands involving the passive voice or possessive, e.g. "If the snake killed the mouse, which one is still alive," usually result in comprehension problems in those who can understand simple questions.

Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia. An acquired language disorder, it is characterized by intact auditory comprehension, fluent (yet paraphasic) speech production, but poor speech repetition. They are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as patients show significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. Patients will display frequent errors during spontaneous speech, such as substituting or transposing sounds. They will also be aware of their errors, and will show significant difficulty correcting them. For example: "Clinician: Now, I want you to say some words after me. Say ‘boy’. Patient: Boy. Clinician: Home. Patient: Home. Clinician: Seventy-nine. Patient: Ninety-seven. No … sevinty-sine … siventy-nice…. Clinician: Let’s try another one. Say ‘refrigerator’. Patient: Frigilator … no? how about … frerigilator … no frigaliterlater … aahh! It’s all mixed up!"

Shallice and Warrington (1970) were able to differentiate two variants of

this constellation: the reproduction and the repetition type. These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, afflicting confrontation tasks such as repetition, reading and naming in a similar manner.

Left-hemisphere damage involving auditory regions often result in speech deficits. Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech. Studies have suggested that conduction aphasia is a result of damage specifically to the left superior temporal gyrus and/or the left supra marginal gyrus. The classical explanation for conduction aphasia is that of a disconnection between the brain areas responsible for speech comprehension (Wernicke's area) and speech production (Broca's area), due specifically to damage to the arcuate fasciculus, a deep white matter tract. Patients are still able to comprehend speech because the lesion does not disrupt the ventral stream pathway.

Two areas of the brain, Broca’s area and Wernicke’s area, are responsible for various disruptions in speech when damaged. Each is defined by their distinct characteristics. Broca’s aphasia is characterized by non-fluent or telegraphic-type speech - where articles, conjunctions, prepositions, auxiliary verbs, pronouns and morphological inflections (plurals, past tense) are omitted. The word substitutions are infrequent and distortion of consonants and simplification of consonant clusters is frequent. Content words such as nouns, verbs and adjectives may be preserved. Subjects of this aphasia are aware of their errors in speech. Damage to the Broca’s area does not affect comprehension of speech.

Wernicke’s aphasia is characterized by fluent language with made up or unnecessary words with little or no meaning to speech. Those who suffer from this type of aphasia have difficulty understanding others speech and are unaware of their own mistakes. When corrected they will repeat their verbal paraphasias and have trouble finding the correct word. Wernicke’s aphasia is found in the dominant hemisphere of the posterior gyrus of the first temporal convolution of the brain, whereas Broca’s aphasia is found anterior to the Wernicke’s area.