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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain (with loss of word meaning). SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD), with the other two being frontotemporal dementia and progressive nonfluent aphasia. SD is a clinically defined syndrome, but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). SD is one of the three variants of Primary Progressive Aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease. It is important to note the distinctions between Alzheimer’s Disease and Semantic dementia with regard to types of memory affected. In general, Alzheimer’s Disease is referred to as disorder affecting mainly episodic memory, defined as the memory related to specific, personal events distinct for each individual. Semantic dementia generally affects semantic memory, which refers to long-term memory that deals with common knowledge and facts.3

It was first described by Arnold Pick in 1904 and in modern times was characterized by Professor Elizabeth Warrington in 1975, but it was not given the name semantic dementia until 1989. The clinical and neuropsychological features, and their association with temporal lobe atrophy were described by Professor John Hodges and colleagues in 1992.

Autotopagnosia from the Greek "a" and "gnosis," meaning "without knowledge", "topos" meaning "place", and "auto" meaning "oneself", autotopagnosia virtually translates to the "lack of knowledge about one's own space," and is clinically described as such.

Autotopagnosia is a form of agnosia, characterized by an inability to localize and orient different parts of the body. The psychoneurological disorder has also been referred to as "body-image agnosia" or "somatotopagnosia." "Somatotopagnosia" has been argued to be a better suited term to describe the condition. While autotopagnosia emphasizes the deficiencies in localizing only one's own body parts and orientation, "somatotopagnosia" also considers the inability to orient and recognize the body parts of others or representations of the body (e.g., manikins, diagrams).

Typically, the cause of autotopagnosia is a lesion found in the parietal lobe of the left hemisphere of the brain. However, it as also been noted that patients with generalized brain damage present with similar symptoms of autotopagnosia.

As a concept, autotopagnosia has been criticized as nonspecific; some claim that this is a manifestation of a greater symptomatic complex of anomia, marked by an inability to name things in general—not just parts of the human body.

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.

There is no curative treatment for this condition. Supportive management is helpful.

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

There is currently no known curative treatment for SD. The average duration of illness is 8–10 years, and its progression cannot be slowed. Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible.

Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.

SD has no known preventative measures.

The main clinical features are signature language progressive difficulties with speech production. There can be problems in different parts of the speech production system, hence patients can present with articulatory breakdown, phonemic breakdown (difficulties with sounds) and other problems. However, it is rare for patients to have just one of these problems and most people will present with more than one problem. Features include:

- Hesitant, effortful speech

- Speech 'apraxia'

- Stutter (including return of a childhood stutter)

- Anomia

- Phonemic paraphasia (sound errors in speech e.g. 'gat' for 'cat')

- Agrammatism (using the wrong tense or word order)

As the disease develops, speech quantity decreases and many patients will become mute.

Cognitive domains other than language are rarely affected early on. However, as the disease progresses other domains can be affected. Problems with writing, reading and speech comprehension can occur as can behavioural features similar to frontotemporal dementia.

While most cases of visual agnosia are seen in older adults who have experienced extensive brain damage, there are also cases of young children with less brain damage during developmental years acquiring the symptoms. Commonly, visual agnosia presents as an inability to recognize an object in the absence of other explanations, such as blindness or partial blindness, anomia, memory loss, etc.. Other common manifestations of visual agnosia that are generally tested for include difficulty identifying objects that look similar in shape, difficulty with identifying line drawings of objects, and recognizing objects that are shown from less common views, such as a horse from a top-down view.

Within any given patient, a variety of symptoms can occur, and the impairment of ability is not only binary but can range in severity. For example, Patient SM is a prosopagnosic with a unilateral lesion to left extrastriate cortex due to an accident in his twenties who displays behavior similar to congenital prosopagnosia. Although he can recognize facial features and emotions – indeed he sometimes uses a standout feature to recognize a face – face recognition is almost impossible purely from visual stimuli, even for faces of friends, family, and himself. The disorder also affects his memory of faces, both in storing new memories of faces and recalling stored memories.

Nevertheless, it is important to note the reach of symptoms to other domains. SM’s object recognition is similarly impaired though not entirely; when given line drawings to identify, he was able to give names of objects with properties similar to the drawing, implying that he is able to see the features of the drawing. Similarly, copying a line drawing of a beach scene led to a simplified version of the drawing, though the main features were accounted for. For recognition of places, he is still impaired but familiar places are remembered and new places can be stored into memory.

In adults, many of the symptoms diminish over time. Although it has been suggested that a similar diminishing of symptoms occurs in children as well, it appears more likely that most do not overcome their deficits, but instead simply learn to adjust.

Gerstmann syndrome is a neuropsychiatric disorder that is characterized by a constellation of symptoms that suggests the presence of a lesion in a particular area of the brain. (It should not be confused with Gerstmann-Sträussler-Scheinker syndrome, which is a transmissible spongiform encephalopathy.) Damage to the inferior parietal lobule of the dominant hemisphere results in Gerstmann's syndrome.

It is named for Josef Gerstmann.

Many studies have shown that disconnection syndromes such as aphasia, agnosia, apraxia, pure alexia and many others are not caused by direct damage to functional neocortical regions. They can also be present on only one side of the body which is why these are categorized as hemispheric disconnections. The cause for hemispheric disconnection is if the interhemispheric fibers, as mentioned earlier, are cut or reduced.

An example is commissural disconnect in adults which usually results from surgical intervention, tumor, or interruption of the blood supply to the corpus callosum or the immediately adjacent structures. Callosal disconnection syndrome is characterized by left ideomotor apraxia and left-hand agraphia and/or tactile anomia, and is relatively rare.

Other examples include commissurotomy, the surgical cutting of cerebral commissures to treat epilepsy and callosal agenesis which is when individuals are born without a corpus callosum. Those with callosal agenesis can still perform interhemispheric comparisons of visual and tactile information but with deficits in processing complex information when performing the respective tasks.

Cerebellar cognitive affective syndrome (CCAS), also called "Schmahmann's syndrome" is a condition that follows from lesions (damage) to the cerebellum of the brain. This syndrome, described by Dr. Jeremy Schmahmann and his colleagues refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.