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.

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.

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 most common cause of Wernicke's aphasia is stroke. Strokes may occur when blood flow to the brain is completely interrupted or severely reduced. This has a direct effect on the amount of oxygen and nutrients being able to supply the brain, which causes brain cells to die within minutes. The primary classifications of stroke are hemorrhagic (ruptured blood vessel), or ischemic (blood clot reduces or completely stops blood flow). Two of the most common types of hemorrhagic stroke are subarachnoid hemorrhage and intracerebral hemorrhage. Subarachnoid hemorrhage is when an artery near the surface of the brain bursts causing blood to leak into the space between the brain and skull. Meanwhile intracerebral hemorrhage occurs when a blood vessel inside the brain bursts, causing spillage into surrounding brain tissue. Three main causes of these hemorrhagic strokes are hypertension (uncontrolled high blood pressure), aneurisms (weak spots in blood vessel walls), and arteriovenous malformations (rupture of abnormal tangle of thin-walled blood vessels). As previously noted the other major classification for a stroke is an ischemic stroke. The ischemic strokes, which are the most common form of stroke, are further broken down and can be classified as embolic or thrombotic. Embolic strokes occur when a blood clot forms away from the brain, typically in the heart. A small portion of this clot breaks away and travels through the blood vessels until eventually reaching a small enough vessel in the brain that it can no longer pass through, causing a blockage. Thrombotic strokes on the other hand are due to the formation of a blood clot directly formed in one of the arteries that supply the brain. In general, stroke is the number one leading cause of disability worldwide.,

"The middle cerebral arteries supply blood to the cortical areas involved in speech, language and swallowing. The left middle cerebral artery provides Broca's area, Wernicke's area, Heschl's gyrus, and the angular gyrus with blood". Therefore, in patients with Wernicke's aphasia, there is typically an occlusion to the left middle cerebral artery.

As a result of the occlusion in the left middle cerebral artery, Wernicke's aphasia is most commonly caused by a lesion in the posterior superior temporal gyrus (Wernicke's area). This area is posterior to the primary auditory cortex (PAC) which is responsible for decoding individual speech sounds. Wernicke's primary responsibility is to assign meaning to these speech sounds. The extent of the lesion will determine the severity of the patients deficits related to language. Damage to the surrounding areas (perisylvian region) may also result in Wernicke's aphasia symptoms due to variation in individual neuroanatomical structure and any co-occurring damage in adjacent areas of the brain.

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.

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].

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.

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.

"Developmental prosopagnosia" (DP), also called "Congenital prosopagnosia" (CP), is a face-recognition deficit that is lifelong, manifesting in early childhood, and that cannot be attributed to acquired brain damage. A number of studies have found functional deficits in DP both on the basis of EEG measures and fMRI. It has been suggested that a genetic factor is responsible for the condition. The term "hereditary prosopagnosia" was introduced if DP affected more than one family member, essentially accenting the possible genetic contribution of this condition. To examine this possible genetic factor, 689 randomly selected students were administered a survey in which seventeen developmental prosopagnosics were quantifiably identified. Family members of fourteen of the DP individuals were interviewed to determine prosopagnosia-like characteristics, and in all fourteen families, at least one other affected family member was found.

In 2005, a study led by Ingo Kennerknecht showed support for the proposed congenital disorder form of prosopagnosia. This study provides epidemiological evidence that congenital prosopagnosia is a frequently occurring cognitive disorder that often runs in families. The analysis of pedigree trees formed within the study also indicates that the segregation pattern of hereditary prosopagnosia (HPA) is fully compatible with autosomal dominant inheritance. This mode of inheritance explains why HPA is so common among certain families (Kennerknecht et al. 2006).

There are many developmental disorders associated with an increased likelihood that the person will have difficulties in face perception, of which the person may or may not be aware. The mechanism by which these perceptual deficits take place is largely unknown. A partial list of some disorders that often have prosopagnosiac components would include nonverbal learning disorder, Alzheimer's disease, and autism in general. However, these types of disorders are very complicated, so arbitrary assumptions should be avoided.

In 2012, it was shown that developmental prosopagnosia cases show poor integration of low and high spatial frequency information.

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.

Wernicke's aphasia, also known as receptive aphasia, sensory aphasia, or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernicke's aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities, and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits (i.e. hemiparesis) do not occur in individuals with Wernicke's aphasia. Therefore, they may produce a large amount of speech without much meaning. Wernicke's aphasia was named after Carl Wernicke who is credited with discovering the area of the brain responsible for language comprehension. Individuals with Wernicke's aphasia are typically unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.

Like many acquired language disorders, Wernicke's aphasia can be experienced in many different ways and to many different degrees. Patients diagnosed with Wernicke's aphasia can show severe language comprehension deficits; however, this is dependent on the severity and extent of the lesion. Severity levels may range from being unable to understand even the simplest spoken and/or written information to missing minor details of a conversation. Many diagnosed with Wernicke's aphasia have difficulty with repetition in words and sentences, and or working memory.

There have been no large epidemiological studies on the incidence and prevalence of the PPA variants. Though it most likely has been underestimated, onset of PPA has been found to occur in the sixth or seventh decade.

There are no known environmental risk factors for the progressive aphasias. However, one observational, retrospective study suggested that vasectomy could be a risk factor for PPA in men. These results have yet to be replicated or demonstrated by prospective studies.

PPA is not considered a hereditary disease. However, relatives of a person with any form of frontotemporal lobar degeneration, including PPA, are at slightly greater risk of developing PPA or another form of the condition. In a quarter of patients diagnosed with PPA, there is a family history of PPA or one of the other disorders in the FTLD spectrum of disorders. It has been found that genetic predisposition varies among the different PPA variants, with PNFA being more commonly familial in nature than LPA or SD.

The most convincing genetic basis of PPA has been found to be a mutation in the GRN gene. Most patients with observed GRN mutations present clinical features of PNFA, but the phenotype can be atypical.

Agraphia has a multitude of causes ranging from strokes, lesions, traumatic brain injury, and dementia. Twelve regions of the brain are associated with handwriting. The four distinct functional areas are the left superior frontal area composed of the middle frontal gyrus and the superior frontal sulcus, the left superior parietal area composed of the inferior parietal lobule, the superior parietal lobule and the intraparietal sulcus and lastly the primary motor cortex and the somatosensory cortex. The eight other areas are considered associative areas and are the right anterior cerebellum, the left posterior nucleus of the thalamus, the left inferior frontal gyrus, the right posterior cerebellum, the right superior frontal cortex, the right inferior parietal lobule, the left fusiform gyrus and the left putamen. The specific type of agraphia resulting from brain damage will depend on which area of the brain was damaged.

Phonological agraphia is linked to damage in areas of the brain involved in phonological processing skills (sounding out words), specifically the language areas around the sylvian fissure, such as Broca's area, Wernicke's area, and the supramarginal gyrus.

Lexical agraphia is associated with damage to the left angular gyrus and/or posterior temporal cortex. The damage is typically posterior and inferior to the perisylvian language areas.

Deep agraphia involves damage to the same areas of the brain as lexical agraphia plus some damage to the perisylvian language areas as well. More extensive left hemisphere damage can lead to global agraphia.

Gerstmann's syndrome is caused by a lesion of the dominant (usually the left) parietal lobe, usually an angular gyrus lesion.

Apraxic agraphia with ideomotor apraxia is typically caused by damage to the superior parietal lobe (where graphomotor plans are stored) or the premotor cortex (where the plans are converted into motor commands). Additionally, some individuals with cerebellar lesions (more typically associated with non-apraxic motor dysfunction) develop apraxic agraphia. Apraxic agraphia without ideomotor apraxia may be caused by damage to either of the parietal lobes, the dominant frontal lobe, or to the dominant thalamus.

Visuospatial agraphia typically has a right hemisphere pathology. Damage to the right frontal area of the brain may cause more motor defects, whereas damage to the posterior part of the right hemisphere leads predominantly to spatial defects in writing.

Currently, the specific causes for PPA and other degenerative brain disease similar to PPA are unknown. Autopsies have revealed a variety of brain abnormalities in people who had PPA. These autopsies, as well as imaging techniques such as CT scans, MRI, EEG, single photon emission computed tomography (SPECT), and positron emission tomography (PET), have generally revealed abnormalities to be almost exclusively in the left hemisphere.

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.

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.

Prosopagnosia can be caused by lesions in various parts of the inferior occipital areas (occipital face area), fusiform gyrus (fusiform face area), and the anterior temporal cortex. Positron emission tomography (PET) and fMRI scans have shown that, in individuals without prosopagnosia, these areas are activated specifically in response to face stimuli. The inferior occipital areas are mainly involved in the early stages of face perception and the anterior temporal structures integrate specific information about the face, voice, and name of a familiar person.

Acquired prosopagnosia can develop as the result of several neurologically damaging causes. Vascular causes of prosopagnosia include posterior cerebral artery infarcts (PCAIs) and hemorrhages in the infero-medial part of the temporo-occipital area. These can be either bilateral or unilateral, but if they are unilateral, they are almost always in the right hemisphere. Recent studies have confirmed that right hemisphere damage to the specific temporo-occipital areas mentioned above is sufficient to induce prosopagnosia. MRI scans of patients with prosopagnosia showed lesions isolated to the right hemisphere, while fMRI scans showed that the left hemisphere was functioning normally. Unilateral left temporo-occipital lesions result in object agnosia, but spare face recognition processes, although a few cases have been documented where left unilateral damage resulted in prosopagnosia. It has been suggested that these face recognition impairments caused by left hemisphere damage are due to a semantic defect blocking retrieval processes that are involved in obtaining person-specific semantic information from the visual modality.

Other less common etiologies include carbon monoxide poisoning, temporal lobectomy, encephalitis, neoplasm, right temporal lobe atrophy, trauma, Parkinson's disease, and Alzheimer's disease.

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.

Jargon aphasia is a type of fluent aphasia in which an individual's speech is incomprehensible, but appears to make sense to the individual. Persons experiencing this condition will either replace a desired word with another that sounds or looks like the original one, or has some other connection to it, or they will replace it with random sounds. Accordingly, persons with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they can't find with sounds.

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.

Paragrammatism is the confused or incomplete use of grammatical structures, found in certain forms of speech disturbance. Paragrammatism is the inability to form grammatically correct sentences. It is characteristic of fluent aphasia, most commonly Receptive aphasia. Paragrammatism is sometimes called "extended paraphasia," although it is different from paraphasia. Paragrammatism is roughly synonymous with "word salad," which concerns the semantic coherence of speech rather than its production.

Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues.

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.