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.

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

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.

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.

The most common cause of asemia is brain damage, such as a stroke or a brain tumor. Other possible causes include Alzheimer's disease and infection. Roger Wolcott Sperry, through his research of split-brain patients, had found out that the human brain lateralizes functions, meaning that the two hemispheres of the brain have different functions. Brain damage, specifically to the left hemisphere, can impair our ability to speak or understand language. This led Sperry to conclude that due to the lateralization of brain function, language is based in the left hemisphere. Therefore, any kind of brain damage to the left hemisphere will greatly impact language, whether it is expressive or receptive.

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.

Logopenic progressive aphasia (LPA) is a form of primary progressive aphasia. It is defined clinically by impairments in naming and sentence repetition. It is similar to conduction aphasia and is associated with atrophy to the left posterior temporal cortex and inferior parietal lobule. It is suspected that an atypical form of Alzheimer's disease is the most common cause of logopenic progressive aphasia.

Although patients with the logopenic variant of PPA are still able to produce speech, their speech rate may be significantly slowed down due to word retrieval difficulty. Over time, they may experience the inability to retain lengthy information, causing problems with understanding complex verbal information. Some additional behavioral features include irritability, anxiety and agitation.

Compared to other forms of primary progressive aphasia, the logopenic variant has been found to be associated with cognitive and behavioral characteristics. Studies have shown that patients with the logopenic variant perform significantly worse on tests of calculation than other primary progressive aphasia patients. Several logopenic variant patients, especially those with Alzheimer’s disease pathology, have also been found to perform poorly on memory tasks.

Logopenic progressive aphasia is caused by damage to segregated brain regions, specifically the inferior parietal lobe and superior temporal regions. Difficulties in naming are produced from the thinning of the inferior parietal lobe. Damage to the dorsal pathways creates language deficiency in patients that is characteristic of logopenic progressive aphasia.

There are many potential causes of dysarthria. They include toxic, metabolic, degenerative diseases, traumatic brain injury, or thrombotic or embolic stroke.

Degenerative diseases include parkinsonism, amyotrophic lateral sclerosis (ALS), multiple sclerosis, Huntington's disease, Niemann-Pick disease, and Friedreich ataxia.

Toxic and metabolic conditions include: Wilson's disease, hypoxic encephalopathy such as in drowning, and central pontine myelinolysis.

These result in lesions to key areas of the brain involved in planning, executing, or regulating motor operations in skeletal muscles (i.e. muscles of the limbs), including muscles of the head and neck (dysfunction of which characterises dysarthria). These can result in dysfunction, or failure of: the motor or somatosensory cortex of the brain, corticobulbar pathways, the cerebellum, basal nuclei (consisting of the putamen, globus pallidus, caudate nucleus, substantia nigra etc.), brainstem (from which the cranial nerves originate), or the neuro-muscular junction (in diseases such as myasthenia gravis) which block the nervous system's ability to activate motor units and effect correct range and strength of movements.

Causes:

- Brain tumor

- Cerebral palsy

- Guillain–Barré syndrome

- Hypothermia

- Lyme disease

- Stroke

- Intracranial hypertension (formerly known as pseudotumor cerebri)

- Tay-Sachs, and late onset Tay-Sachs (LOTS), disease

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.

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.

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].

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.

Progressive nonfluent aphasia (PNFA) is one of three clinical syndromes associated with frontotemporal lobar degeneration. PNFA has an insidious onset of language deficits over time as opposed to other stroke-based aphasias, which occur acutely following trauma to the brain. The specific degeneration of the frontal and temporal lobes in PNFA creates hallmark language deficits differentiating this disorder from other Alzheimer-type disorders by the initial absence of other cognitive and memory deficits. This disorder commonly has a primary effect on the left hemisphere, causing the symptomatic display of expressive language deficits (production difficulties) and sometimes may disrupt receptive abilities in comprehending grammatically complex language.

In relation to other types of aphasia, TMoA occurs less frequently, so there is less information on its prognosis. In general, for individuals with aphasia, most recovery is seen within 6 months of the stroke or injury although more recovery may continue in the following months or years. The timeline of recovery may look different depending on the type of stroke that caused the aphasia. With an ischemic stroke, recovery is greatest within the first two weeks and then diminishes overtime until the progress stabilizes. With a hemorrhagic stroke, the patient often shows little improvement in the first few weeks and then has relatively rapid recovery until they stabilize.

In a study involving eight patients with border zone lesions, all patients presented with transcortical mixed aphasia initially after the stroke. Three of these patients made a complete recovery within a few days post-stroke. For three other patients with more anterior lesions, their aphasia transitioned to TMoA. All participants in the study regained full language abilities within 18 months following their stroke. This suggests a positive long-term prognosis for patients with TMoA. However, this might not be the case for all patients and more research is needed in order to solidify these findings. Another study found that prognosis of TMoA is affected by lesion size. Smaller lesions typically cause delays in speech initiation; whereas, larger lesions lead to more profound language abnormalities and difficulty with abstract language abilities.

Research has shown that treatment has a direct effect on aphasia outcomes. Intensity, duration and timing of treatment all need to be taken in to consideration when choosing a course of treatment and determining a prognosis. In general, greater intensity leads to greater improvement. For duration, longer-term treatment produces more permanent changes. As for timing, beginning treatment too early may be difficult for the system which has not recovered enough to do intensive therapy, but beginning too late may result missing the window of the opportunity in which the most change can occur. Neuroplasticity, the brain's natural ability to reorganize itself following a traumatic event, occurs best when treatment connects simultaneous events, maintains attention, taps into positive emotion, utilizes repetition tasks, and is specific to the individual's needs.

Other factors affecting prognosis includes location and site of lesion. Since the lesion that results in TMoA usually occurs in the watershed area and does not directly involve the areas of the brain responsible for general language abilities, prognosis for these patients is good overall. Other factors that determine a patient’s prognosis include age, education prior to the stroke, gender, motivation, and support.

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.

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.

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".

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

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 prognosis for individuals with apraxia varies. With therapy, some patients improve significantly, while others may show very little improvement. Some individuals with apraxia may benefit from the use of a communication aid.

However, many people with apraxia are no longer able to be independent. Those with limb-kinetic and/or gait apraxia should avoid activities in which they might injure themselves or others.

Occupational therapy, physical therapy, and play therapy may be considered as other references to support patients with apraxia. These team members could work along with the SLP to provide the best therapy for people with apraxia. However, because people with limb apraxia may have trouble directing their motor movements, occupational therapy for stroke or other brain injury can be difficult.

No medication has been shown useful for treating apraxia.

Asemia is a more severe condition than aphasia, so it does have some similarities with the disease. People who have asemia have the inability to comprehend signs, symbols, and even language. They also have the inability to use signs, symbols, and language. People with asemia sometimes may take up asemic writing, which is "wordless" writing. What wordless writing could mean is that the writing looks like regular or traditional writing, but there is no content that makes sense. The concept of syntax, semantics, or even communication does not exist in asemic writing.

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.

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.

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.

Conduction aphasia is caused by damage to the parietal lobe of the brain, especially in regards to the area associated with the left-hemisphere dominant dorsal stream network. The arcuate fasciculus, which connects Broca's area and Wernicke's area (important for speech and language production and comprehension, respectively), is affected. These two areas control speech and language in the brain. The arcuate fasciculus is a thick band of fiber that connects the two areas and carries messages between them. When this area is damaged, the patient experiences damage to the auditory-motor integration system. This results in disruption to the delayed auditory feedback network, causing the individual to have difficulty correcting themselves on speech repetition tasks. Additionally, recent evidence suggests that conduction aphasia can also be caused by lesions in the left superior temporal gyrus and/or the left supramarginal gyrus.

The brain damage causing conduction aphasia is often from a stroke, which can produce both localized and widespread damage. Traumatic brain injury and tumors can also lead to localized lesions, with potential to cause conduction aphasia. Conduction aphasia can also be seen in cases of cortical damage without subcortical extensions.