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.

Constructional apraxia is characterized by an inability or difficulty to build, assemble, or draw objects. Apraxia is a neurological disorder in which people are unable to perform tasks or movements even though they understand the task, are willing to complete it, and have the physical ability to perform the movements. Constructional apraxia may be caused by lesions in the parietal lobe following stroke or it may serve as an indicator for Alzheimer's disease.

A key deficit in constructional apraxia patients is the inability to correctly copy or draw an image. There are qualitative differences between patients with left hemisphere damage, right hemisphere damage, and Alzheimer's Disease.

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.

In most individuals with expressive aphasia, the majority of recovery is seen within the first year following a stroke or injury. The majority of this improvement is seen in the first four weeks in therapy following a stroke and slows thereafter. However, this timeline will vary depending upon the type of stroke experienced by the patient. Patients who experienced an ischemic stroke may recover in the days and weeks following the stroke, and then experience a plateau and gradual slowing of recovery. On the contrary, patients who experienced a hemorrhagic stroke experience a slower recovery in the first 4–8 weeks, followed by a faster recovery which eventually stabilizes.

Numerous factors impact the recovery process and outcomes. Site and extent of lesion greatly impacts recovery. Other factors that may affect prognosis are age, education, gender, and motivation. Occupation, handedness, personality, and emotional state may also be associated with recovery outcomes.

Studies have also found that prognosis of expressive aphasia correlates strongly with the initial severity of impairment. However, it has been seen that continued recovery is possible years after a stroke with effective treatment. Timing and intensity of treatment is another factor that impacts outcomes. Research suggests that even in later stages of recovery, intervention is effective at improving function, as well as, preventing loss of function.

Unlike receptive aphasia, patients with expressive aphasia are aware of their errors in language production. This may further motivate a person with expressive aphasia to progress in treatment, which would affect treatment outcomes. On the other hand, awareness of impairment may lead to higher levels of frustration, depression, anxiety, or social withdrawal, which have been proven to negatively affect a person's chance of recovery.

The cause of IA is still somewhat of a mystery to most researchers. That is because there is no localized focal point in the brain that shows where this deficit will occur. Since 1905 Liepmann proposed a hypothesis of an action processing system that is found in the left hemisphere of the brain, which is dedicated to skilled, motor planning that guides the movement of the body. Yet, he still was never able to produce two patients with the same brain damage that showed ideational apraxia. The major ideas of where IA is found are in the left posterior temporal-parietal junction. Possibly damage to the lateral sulcus also known as Sylvian fissure may contribute to an individual’s deterioration of object recognition. Another possible area of damage leading to IA is the submarginal gyrus, which is located in the parietal lobe of the brain. Overall, IA is an autonomous syndrome, linked to damage in the left hemisphere involving semantic memory disorders rather than a defect in motor control.

Several severe injuries or diseases can cause IA in a wide range of patients. Alzheimer's patients are the largest cohort groups that express IA. Other groups that are often seen with this dysfunction are stroke victims, traumatic brain injuries, and dementia. Interestingly, the damage is almost always found in the dominant hemisphere (i.e. usually the left hemisphere) of the patient.

The most common cause of expressive aphasia is stroke. A stroke is caused by hypoperfusion (lack of oxygen) to an area of the brain, which is commonly caused by thrombosis or embolism. Some form of aphasia occurs in 34 to 38% of stroke patients. Expressive aphasia occurs in approximately 12% of new cases of aphasia caused by stroke.

In most cases, expressive aphasia is caused by a stroke in Broca's area or the surrounding vicinity. Broca's area is in the lower part of the premotor cortex in the language dominant hemisphere and is responsible for planning motor speech movements. However, cases of expressive aphasia have been seen in patients with strokes in other areas of the brain. Patients with classic symptoms of expressive aphasia in general have more acute brain lesions, whereas patients with larger, widespread lesions exhibit a variety of symptoms that may be classified as global aphasia or left unclassified.

Expressive aphasia can also be caused by trauma to the brain, tumor, cerebral hemorrhage by extradural hematoma.

Understanding lateralization of brain function is important for understanding what areas of the brain cause expressive aphasia when damaged. In the past, it has been believed that the area for language production differs between left and right-handed individuals. If this were true, damage to the homologous region of Broca's area in the right hemisphere should cause aphasia in a left-handed individual. More recent studies have shown that even left-handed individuals typically have language functions only in the left hemisphere. However, left-handed individuals are more likely to have a dominance of language in the right hemisphere.

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.

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.

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.

Ideational apraxia (IA) is a neurological disorder which explains the loss of ability to conceptualize, plan, and execute the complex sequences of motor actions involved in the use of tools or otherwise interacting with objects in everyday life. Ideational apraxia is a condition in which an individual is unable to plan movements related to interaction with objects, because he has lost the perception of the object's purpose. Characteristics of this disorder include a disturbance in the concept of the sequential organization of voluntary actions. The patient appears to have lost the knowledge or thought of what an object represents. This disorder was first seen 100 years ago by Doctor Arnold Pick, who described a patient who appeared to have lost their ability to use objects. The patient would make errors such as combing their hair with the wrong side of the comb or placing a pistol in his mouth. From that point on, several other

researchers and doctors have stumbled upon this unique disorder. IA has been described under several names such as, agnosia of utilization, conceptual apraxia or loss of knowledge about the use of tools, or semantic amnesia of tool usage. The term apraxia was first created by Steinthal in 1871 and was then applied by Gogol, Kusmaul, Star, and Pick to patients who failed to pantomime the use of tools. It was not until the 1900s, when Liepmann refined the definition, that it specifically described disorders that involved motor planning, rather than disturbances in the patient’s visual perception, language, or symbolism.

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.

The most common cause of ideomotor apraxia is a unilateral ischemic lesion to the brain, which is damage to one hemisphere of the brain due to a disruption of the blood supply, as in a stroke. There are a variety of brain areas where lesions have been correlated to ideomotor apraxia. Initially it was believed that damage to the subcortical white matter tracts, the axons that extend down from the cells bodies in the cerebral cortex, was the main area responsible for this form of apraxia. Lesions to the basal ganglia may also be responsible, although there is considerable debate as to whether damage to the basal ganglia alone would be sufficient to induce apraxia. Lesions to these lower brain structures has not, however, been shown to be more prevalent in apraxic patients. In fact, these types of lesions are more common in nonapraxic patients. The lesions most associated with ideomotor apraxia are to the left parietal and premotor areas. Patients with lesions to the supplementary motor area have also presented with ideomotor apraxia. Lesions to the corpus callosum can also induce apraxic-like symptoms, with varying effects on the two hands, although this has not been thoroughly studied. In addition to ischemic lesions to the brain, ideomotor apraxia has also been seen in neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease, Huntington's disease, corticobasal degeneration, and progressive supranuclear palsy.

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.

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".

Bálint's syndrome has been found in patients with bilateral damage to the posterior parietal cortex. The primary cause of the damage and the syndrome can originate from multiple strokes, Alzheimer's disease, intracranial tumors, or brain injury. Progressive multifocal leukoencephalopathy and Creutzfeldt–Jakob disease have also been found to cause this kind of damage. This syndrome is caused by damage to the posterior superior watershed areas, also known as the parietal-occipital vascular border zone (Brodmann's areas 19 and 7).

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.

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.

Apraxia is most often due to a lesion located in the dominant (usually left) hemisphere of the brain, typically in the frontal and parietal lobes. Lesions may be due to stroke, acquired brain injuries, or neurodegenerative diseases such as Alzheimer's disease or other dementias, Parkinson's disease, or Huntington's disease. It is also possible for apraxia to be caused by lesions in other areas of the brain including the non-dominant (usually right) hemisphere.

Ideomotor apraxia is typically due to a decrease in blood flow to the dominant hemisphere of the brain and particularly the parietal and premotor areas. It is frequently seen in patients with corticobasal degeneration.

Ideational apraxia has been observed in patients with lesions in the dominant hemisphere near areas associated with aphasia; however, more research is needed on ideational apraxia due to brain lesions. The localization of lesions in areas of the frontal and temporal lobes would provide explanation for the difficulty in motor planning seen in ideational apraxia as well as its difficulty to distinguish it from certain aphasias.

Constructional apraxia is often caused by lesions of the inferior non-dominant parietal lobe, and can be caused by brain injury, illness, tumor or other condition that can result in a brain lesion.

Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills (needed for both written and oral language) as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.

Lack of awareness of the syndrome may lead to misdiagnosis such as blindness, psychosis, or dementia. Symptoms of Bálint's syndrome are most likely to be noticed first by therapists providing rehabilitation following brain lesions. However, due to the scarcity among practitioners of familiarity with the syndrome, the symptoms are often explained away incorrectly without being considered as a possibility and followed by medical confirmation of clinical and neuroradiological findings. Any severe disturbance of space representation, spontaneously appearing following bilateral parietal damage, strongly suggests the presence of Bálint's syndrome and should be investigated as such. One study reports that damage to the bilateral dorsal occipitoparietal regions appeared to be involved in Bálint's syndrome.

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.

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.

Recent research has established the existence of primary progressive apraxia of speech caused by neuroanatomic motor atrophy. For a long time, this disorder was not distinguished from other motor speech disorders such as dysarthria and in particular primary progressive aphasia. Many studies have been done trying to identify areas in the brain in which this particular disorder occurs or at least to show that it occurs in different areas of the brain than other disorders. One study observed 37 patients with neurodegenerative speech disorders to determine whether or not it is distinguishable from other disorders, and if so where in the brain it can be found. Using speech and language, neurological, neuropsychological and neuroimaging testing, the researchers came to the conclusion that PAS does exist and that it correlates to superior lateral premotor and supplementary motor atrophy. However, because PAS is such a rare and recently discovered disorder, many studies do not have enough subjects to observe to make data entirely conclusive.