Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

- Exercising regularly

- Eating a healthy diet

- Keeping alcohol consumption low and avoiding tobacco use

- Controlling blood pressure

If the symptoms of aphasia last longer than two or three months after a stroke, a complete recovery is unlikely. However, it is important to note that some people continue to improve over a period of years and even decades. Improvement is a slow process that usually involves both helping the individual and family understand the nature of aphasia and learning compensatory strategies for communicating.

After a traumatic brain injury (TBI) or cerebrovascular accident (CVA), the brain undergoes several healing and re-organization processes, which may result in improved language function. This is referred to as spontaneous recovery. Spontaneous recovery is the natural recovery the brain makes without treatment, and the brain begins to reorganize and change in order to recover. There are several factors that contribute to a person's chance of recovery caused by stroke, including stroke size and location. Age, sex, and education have not been found to be very predictive.

Specific to aphasia, spontaneous recovery varies among affected people and may not look the same in everyone, making it difficult to predict recovery.

Though some cases of Wernicke’s aphasia have shown greater improvements than more mild forms of aphasia, people with Wernicke’s aphasia may not reach as high a level of speech abilities as those with mild forms of aphasia.

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.

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.

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

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.

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.

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.

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

Simultanagnosia (or simultagnosia) is a rare neurological disorder characterized by the inability of an individual to perceive more than a single object at a time. This type of visual attention problem is one of three major components (the others being optic ataxia and optic apraxia) of Bálint's syndrome, an uncommon and incompletely understood variety of severe neuropsychological impairments involving space representation (visuospatial processing). The term "simultanagnosia" was first coined in 1924 by Wolpert to describe a condition where the affected individual could see individual details of a complex scene but failed to grasp the overall meaning of the image.

Simultanagnosia can be divided into two different categories: dorsal and ventral. Ventral occipito-temporal lesions cause a mild form of the disorder, while dorsal occipito-parietal lesions cause a more severe form of the disorder.

When evaluating the prognosis of a patient, the main contributing participant factors that influence the extent of neuroplasticity, or the brain's ability to change are: age, lesion location, pre-existing cognitive status, motivation, age, overall health, and interaction amongst these. After brain damage, initial signs of global aphasia may appear within the first two days due to brain swelling (cerebral edema). With some time and natural recovery, impairment presentation may progress into expressive aphasia (most commonly) or receptive aphasia. Due to the size and location of the lesion associated with global aphasia, the prognosis for language abilities is poor. Research has shown that the prognosis of long-term language abilities is determined by the initial severity level of aphasia within the first four weeks after a stroke. As a result, there is a poor prognosis for persons who retain a diagnosis of aphasia after one month due to limited initial language abilities. Nonetheless, in the first year post-stroke, patients with global aphasia showed improvement in their Western Aphasia Battery (WAB) scores from baseline. When compared to individuals with Broca’s, Wernicke’s, anomic, and conduction types of aphasia, those with Broca’s aphasia showed the best rate and extent of improvement followed by global aphasia. The rate of improvement in language function was highest in the first four weeks after stroke.

Although the prognosis for persons diagnosed with global aphasia is poor, improvement in varying aspects of language is possible. For example, in 1992, Ferro performed research in which he studied the recovery of individuals with acute global aphasia, resulting from the five different lesion sites. The first lesion site was in the fronto-tempo-parietal region of the brain; patients with lesions in this location saw the least amount of gains out of all of the participants in the study, and they often never recovered from global aphasia. However, the second lesion site was the anterior, suprasylvian, frontal part of the brain; the third lesion site was the subcortical infarcts; and the fourth lesion site was the posterior, suprasylvian, parietal infarcts. Participants with lesions two, three, and four often recovered to a less severe form of aphasia, such as Broca's or transcortical. The fifth lesion site was a double lesion in both the frontal and temporal infarcts; patients with lesions at this site showed slight improvement. However, studies show that spontaneous improvement, if it happens, occurs within six months, but complete recovery is rare.

Studies have shown that persons with global aphasia have improved their verbal and nonverbal speech and language skills through speech and language therapy. One study examined the recovery of a group of individuals who were classified as having global aphasia at 3 months poststroke. The individuals received intensive speech and language intervention. The results of the study illustrated that all of the patients showed improvement. The greatest area of improvement was in auditory comprehension, and the least in the use of propositional speech. After 6 months poststroke, the individuals showed an increased use of gestures to communicate, as their communication skills remained severely impaired.

During therapy, most progress is seen within the first 3 years, but it is possible for language abilities to continuously improve at a steady rate due to long-term intensive language intervention. While improvement in language abilities is possible with intervention, only 20 percent of persons diagnosed with global aphasia achieve functional use of language. Communication of basic needs and the comprehension of simple conversations on highly familiar topics, are examples of common functional language use for this population.

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

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

General principles of treatment:

- restitution

- repetitive training of impaired ability

- development of compensatory strategies utilizing retained cognitive functions

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

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.

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.

Due to the subjective nature of autotopagnosia, there are many hypotheses presented as to the underlying causation. Since the condition by definition is an inability to recognize the human body and its parts, the disorder could stem from a language deficit specific to body parts. On the other hand, the patient could suffer from a disrupted body image or a variation of the inability to separate parts from whole. It is also believed that autotopagnosia has multiple underlying causes that cannot be categorized as either language-specific or body-image-specific. The rarity of autotopagnosia, frequently combined with the manifestation of other psychoneurological disorders, makes the prime cause extremely difficult to study. In many cases, one of these accompanying conditions—often aphasia—could be masking the patient’s autotopagnosia altogether.

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

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

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.

Auditory verbal agnosia has been shown to form as a result of tumor formation, especially in the posterior third ventricle, trauma, lesions, cerebral infarction, encephalitis as a result of herpes simplex, and Landaui-Kleffner syndrome. The exact location of damage which results in pure word deafness is still under debate, but the planum temporale, posterior STG, and white matter damage to the acoustic radiations (AR) have all been implicated.

Auditory verbal agnosia is rarely diagnosed in its pure form. Auditory verbal agnosia can both present as the result of acute damage or as chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. In contrast, auditory verbal agnosia has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. MRIs showed cortical atrophy in the left superior temporal lobe region.

In childhood, auditory verbal agnosia can also be caused by Landau-Kleffner syndrome, also called acquired epileptic aphasia. It is often the first symptom of this disease. A review of 45 cases suggested a relationship between prognosis and age of onset with poorer prognosis for those with earlier onset. In extremely rare cases, auditory verbal agnosia has been known to present as a symptom of neurodegenerative disease, such as Alzheimer's disease. In such cases auditory verbal agnosia is a symptom that is typically followed by more severe neurological symptoms typical of Alzheimer's disease.

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.

Auditory verbal agnosia (AVA), also known as pure word deafness, is the inability to comprehend speech. Individuals with this disorder lose the ability to understand language, repeat words, and write from dictation. Some patients with AVA describe hearing spoken language as meaningless noise, often as though the person speaking was doing so in a foreign language. However, spontaneous speaking, reading, and writing are preserved. The maintenance of the ability to process non-speech auditory information, including music, also remains relatively more intact than spoken language comprehension. Individuals who exhibit pure word deafness are also still able to recognize non-verbal sounds. The ability to interpret language via lip reading, hand gestures, and context clues is preserved as well. Sometimes, this agnosia is preceded by cortical deafness; however, this is not always the case. Researchers have documented that in most patients exhibiting auditory verbal agnosia, the discrimination of consonants is more difficult than that of vowels, but as with most neurological disorders, there is variation among patients.

Auditory verbal agnosia (AVA) is not the same as Auditory agnosia; patients with (nonverbal) auditory agnosia have a relatively more intact speech comprehension system despite their impaired recognition of nonspeech sounds.

Patients with simultanagnosia, a component of Bálint's syndrome, have a restricted spatial window of visual attention and cannot see more than one object at a time in a scene that contains more than one object. For instance, if presented with an image of a table containing both food and various utensils, a patient will report seeing only one item, such as a spoon. If the patient's attention is redirected to another object in the scene, such as a glass, the patient will report that they see the glass but no longer see the spoon. As a result of this impairment, simultanagnosic patients often fail to comprehend the overall meaning of a scene.

In addition, patients note that one stationary object may spontaneously disappear from view as they become aware of another object in the scene.

Simultanagnosic patients often exhibit a phenomenon known as "local capture" where they only identify the local elements of stimuli containing local and global features. However, recent studies have demonstrated that implicit processing of the global structure can occur. With the appropriate stimulus conditions, explicit processing of the global form may occur. For example, a study performed with Navon hierarchical letters, which are large letters composed of smaller ones, revealed that the use of smaller and denser Navon letters biased the patient towards global processing.

Disconnection syndrome is a general term for a number of neurological symptoms caused by damage to the white matter axons of communication pathways—via lesions to association fibers or commissural fibers—in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

Callosal syndrome, or split-brain, is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms. Other types of disconnection syndrome include conduction aphasia (lesion of the association tract connecting Broca’s area and Wernicke’s), agnosia, apraxia, pure alexia, etc.

Although it is still unclear what precise deficits in brain function cause the symptoms of autotopagnosia, the location of brain damage is not as ambiguous. Autotopagnosia is most often attributed to lesions in the parietal lobe of the left hemisphere of the brain. However, it is also believed that the disorder can be caused by general brain damage as well. Many different types of brain lesions can cause autotopagnosia; however, neoplastic lesions seem to be the most common. “Pure” autotopagnosia is often seen with smaller lesions, as larger lesions tend to create other unseen deficits that can confuse or mask the appearance of the symptoms of autotopagnosia—such as aphasia, as discussed above.

The parietal lobe is involved in the integration of sensory information and visuospatial processing. The left parietal lobe, specifically, is important to the understanding of language and mathematics, and has a more prominent role for right handed people.

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.

The syndrome rarely presents itself the same way in every patient. Some symptoms that occur may be:

- Constructional apraxia: difficulty in constructing: drawing, copying, designs, copying 3D models

- Topographical disorientation: difficulty finding one's way in the environment

- Optic ataxia: deficit in visually-guided reaching

- Ocular motor apraxia: inability to direct gaze, a breakdown (failure) in starting (initiating) fast eye movements

- Dressing apraxia: difficulty in dressing usually related to inability to orient clothing spatially, and to a disrupted awareness of body parts and the position of the body and its parts in relation to themselves and objects in the environment

- Right-left confusion: difficulty in distinguishing the difference between the directions left and right