Specific language impairment (SLI) is diagnosed when a child has delayed or disordered language development for no apparent reason. Usually the first indication of SLI is that the child is later than usual in starting to speak and subsequently is delayed in putting words together to form sentences. Spoken language may be immature. In many children with SLI, understanding of language, or "receptive" language, is also impaired, though this may not be obvious unless the child is given a formal assessment.

Although difficulties with use and understanding of complex sentences are a common feature of SLI, the diagnostic criteria encompass a wide range of problems, and for some children other aspects of language are problematic (see below). In general, the term SLI is reserved for children whose language difficulties persist into school age, and so it would not be applied to toddlers who are late to start talking, most of whom catch up with their peer group after a late start.

Specific language impairment (SLI) is diagnosed when a child's language does not develop normally and the difficulties cannot be accounted for by generally slow development, physical abnormality of the speech apparatus, autism spectrum disorder, apraxia, acquired brain damage or hearing loss. Twin studies have shown that it is under genetic

influence. Although language impairment can result from a single-gene mutation, this is unusual. More commonly SLI results from the combined influence of multiple genetic variants, each of which is found in the general population, as well as environmental influences.

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.

In 2006, the U.S. Department of Education indicated that more than 1.4 million students were served in the public schools' special education programs under the speech or language impairment category of IDEA 2004. This estimate does not include children who have speech/language problems secondary to other conditions such as deafness; this means that if all cases of speech or language impairments were included in the estimates, this category of impairment would be the largest. Another source has estimated that communication disorders—a larger category, which also includes hearing disorders—affect one of every 10 people in the United States.

ASHA has cited that 24.1% of children in school in the fall of 2003 received services for speech or language disorders—this amounts to a total of 1,460,583 children between 3 –21 years of age. Again, this estimate does not include children who have speech/language problems secondary to other conditions. Additional ASHA prevalence figures have suggested the following:

- Stuttering affects approximately 4% to 5% of children between the ages of 2 and 4.

- ASHA has indicated that in 2006:

- Almost 69% of SLPs served individuals with fluency problems.

- Almost 29% of SLPs served individuals with voice or resonance disorders.

- Approximately 61% of speech-language pathologists in schools indicated that they served individuals with SLI

- Almost 91% of SLPs in schools indicated that they servedindividuals with phonological/articulation disorder

- Estimates for language difficulty in preschool children range from 2% to 19%.

- Specific Language Impairment (SLI) is extremely common in children, and affects about 7% of the childhood population.

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.

A communication disorder is any disorder that affects an individual's ability to comprehend, detect, or apply language and speech to engage in discourse effectively with others. The delays and disorders can range from simple sound substitution to the inability to understand or use one's native language.

A speech sound disorder is a speech disorder in which some speech sounds (called phonemes) in a child's (or, sometimes, an adult's) language are either not produced, not produced correctly, or are not used correctly. The term protracted phonological development is sometimes preferred when describing children's speech to emphasize the continuing development while acknowledging the delay.

Expressive language disorder is a communication disorder in which there are difficulties with verbal and written expression. It is a specific language impairment characterized by an ability to use expressive spoken language that is markedly below the appropriate level for the mental age, but with a language comprehension that is within normal limits. There can be problems with vocabulary, producing complex sentences, and remembering words, and there may or may not be abnormalities in articulation.

As well as present speech production, very often, someone will have difficulty remembering things. This memory problem is only disturbing for speech; non-verbal or non-linguistically based memory will be unimpaired. An example of a child with expressive language disorder can be seen here.

Expressive language disorder affects work and schooling in many ways. It is usually treated by specific speech therapy, and usually cannot be expected to go away on its own.

Expressive language disorder can be further classified into two groups: developmental expressive language disorder and acquired expressive language disorder. Developmental expressive language disorder currently has no known cause, is first observed when a child is learning to talk, is more common in boys than girls, and is much more common than the acquired form of the disorder. Acquired expressive language disorder is caused by specific damage to the brain by a stroke, traumatic brain injury, or seizures.

Care must be taken to distinguish expressive language disorder from other communication disorders, sensory-motor disturbances, intellectual disability and/or environmental deprivation (see DSM-IV-TR criterion D). These factors affect a person's speech and writing to certain predictable extents, and with certain differences.

Careful diagnosis is also important because "atypical language development can be a secondary characteristic of other physical and developmental problems that may first manifest as language problems".

Language disorders or language impairments are disorders that involve the processing of linguistic information. Problems that may be experienced can involve grammar (syntax and/or morphology), semantics (meaning), or other aspects of language. These problems may be receptive (involving impaired language comprehension), expressive (involving language production), or a combination of both. Examples include specific language impairment and aphasia, among others. Language disorders can affect both spoken and written language, and can also affect sign language; typically, all forms of language will be impaired.

Current data indicates that 7% of young children display language disorder, with boys being diagnosed twice as much as girls.

Preliminary research on potential risk factors have suggested biological components, such as low-birth weight, prematurity, general birth complications, and male gender, as well as family history and low parental education can increase the chance of developing language disorders.

For children with phonological and expressive language difficulties, there is evidence supporting speech and language therapy. However, the same therapy is shown to be much less effective for receptive language difficulties. These results are consistent with the poorer prognosis for receptive language impairments that are generally accompanied with problems in reading comprehension.

Note that these are distinct from speech disorders, which involve difficulty with the act of speech production, but not with language.

Language disorders tend to manifest in two different ways: receptive language disorders (where one cannot properly comprehend language) and expressive language disorders (where one cannot properly communicate their intended message).

Disorders and tendencies included and excluded under the category of communication disorders may vary by source. For example, the definitions offered by the American Speech–Language–Hearing Association differ from that of the Diagnostic Statistical Manual 4th edition (DSM-IV).

Gleanson (2001) defines a communication disorder as a speech and language disorder which refers to problems in communication and in related areas such as oral motor function. The delays and disorders can range from simple sound substitution to the inability to understand or use their native language.

In general, communications disorders commonly refer to problems in speech (comprehension and/or expression) that significantly interfere with an individual’s achievement and/or quality of life. Knowing the operational definition of the agency performing an assessment or giving a diagnosis may help.

Persons who speak more than one language or are considered to have an accent in their location of residence do not have speech disorders if they are speaking in a manner consistent with their home environment or a blending of their home and foreign environment.

Most speech sound disorders occur without a known cause. A child may not learn how to produce sounds correctly or may not learn the rules of speech sounds on his or her own. These children may have a problem with speech development, which does not always mean that they will simply outgrow it by themselves. Many children do develop speech sounds over time but those who do not often need the services of a Speech-Language Pathologist to learn correct speech sounds.

Some speech sound errors can result from other syndromes or disorders such as:

- developmental disorders (e.g. autism)

- genetic disorders (e.g. Down syndrome)

- hearing loss, including temporary hearing loss, such as from ear infections

- cleft palate or other physical anomalies of the mouth

- illness

- neurological disorders (e.g. cerebral palsy)

Acquired disorders result from brain injury, stroke or atrophy, many of these issues are included under the Aphasia umbrella.

Brain damage, for example, may result in various forms of aphasia if critical areas of the brain such as Broca's or Wernicke's area are damaged by lesions or atrophy as part of a dementia.

Developmental verbal dyspraxia is a developmental inability to motor plan volitional movement for the production of speech in the absence of muscular weakness. Research has suggested links to the FOXP2 gene.

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.

Aphasia is an inability to comprehend and formulate language because of damage to specific brain regions. This damage is typically caused by a cerebral vascular accident (stroke), or head trauma, however these are not the only possible causes. To be diagnosed with aphasia, a person's speech or language must be significantly impaired in one (or several) of the four communication modalities following acquired brain injury or have significant decline over a short time period (progressive aphasia). The four communication modalities are auditory comprehension, verbal expression, reading and writing, and functional communication.

The difficulties of people with aphasia can range from occasional trouble finding words to losing the ability to speak, read, or write; intelligence, however, is unaffected. Expressive language and receptive language can both be affected as well. Aphasia also affects visual language such as sign language. In contrast, the use of formulaic expressions in everyday communication is often preserved. One prevalent deficit in the aphasias is anomia, which is a deficit in word finding ability.

The term "aphasia" implies that one or more communication modalities in the brain have been damaged and are therefore functioning incorrectly. Aphasia does not refer to damage to the brain that results in motor or sensory deficits, which produces abnormal speech; that is, aphasia is not related to the mechanics of speech but rather the individual's language cognition (although a person can have both problems). An individual's "language" is the socially shared set of rules as well as the thought processes that go behind verbalized speech. It is not a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment.

Aphasia affects about 2 million people in the US and 250,000 people in Great Britain. Nearly 180,000 people in the US acquire the disorder a year. 84.5% of people have never heard of the condition.

Stuttering, also known as stammering, is a speech disorder in which the flow of speech is disrupted by involuntary repetitions and prolongations of sounds, syllables, words or phrases as well as involuntary silent pauses or blocks in which the person who stutters is unable to produce sounds. The term "stuttering" is most commonly associated with involuntary sound repetition, but it also encompasses the abnormal hesitation or pausing before speech, referred to by people who stutter as "blocks", and the prolongation of certain sounds, usually vowels or semivowels. According to Watkins et al., stuttering is a disorder of "selection, initiation, and execution of motor sequences necessary for fluent speech production." For many people who stutter, repetition is the primary problem. The term "stuttering" covers a wide range of severity, encompassing barely perceptible impediments that are largely cosmetic to severe symptoms that effectively prevent oral communication. In the world, approximately four times as many men as women stutter, encompassing 70 million people worldwide, or about 1% of the world's population.

The impact of stuttering on a person's functioning and emotional state can be severe. This may include fears of having to enunciate specific vowels or consonants, fears of being caught stuttering in social situations, self-imposed isolation, anxiety, stress, shame, being a possible target of bullying (especially in children), having to use word substitution and rearrange words in a sentence to hide stuttering, or a feeling of "loss of control" during speech. Stuttering is sometimes popularly seen as a symptom of anxiety, but there is actually no direct correlation in that direction (though as mentioned the inverse can be true, as social anxiety may actually develop in individuals as a result of their stuttering).

Stuttering is generally not a problem with the physical production of speech sounds or putting thoughts into words. Acute nervousness and stress do not cause stuttering, but they can trigger stuttering in people who have the speech disorder, and living with a stigmatized disability can result in anxiety and high allostatic stress load (chronic nervousness and stress) that reduce the amount of acute stress necessary to trigger stuttering in any given person who stutters, exacerbating the problem in the manner of a positive feedback system; the name 'stuttered speech syndrome' has been proposed for this condition. Neither acute nor chronic stress, however, itself creates any predisposition to stuttering.

The disorder is also "variable", which means that in certain situations, such as talking on the telephone or in a large group, the stuttering might be more severe or less, depending on whether or not the stutterer is self-conscious about their stuttering. Stutterers often find that their stuttering fluctuates and that they have "good" days, "bad" days and "stutter-free" days. The times in which their stuttering fluctuates can be random. Although the exact etiology, or cause, of stuttering is unknown, both genetics and neurophysiology are thought to contribute. There are many treatments and speech therapy techniques available that may help decrease speech disfluency in some people who stutter to the point where an untrained ear cannot identify a problem; however, there is essentially no cure for the disorder at present. The severity of the person's stuttering would correspond to the amount of speech therapy needed to decrease disfluency. For severe stuttering, long-term therapy and hard work is required to decrease disfluency.

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.

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.

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.

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.

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.

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

Among preschoolers, the prognosis for recovery is good. Based on research, about 65% of preschoolers who stutter recover spontaneously in the first two years of stuttering, and about 74% recover by their early teens. In particular, girls seem to recover well. For others, early intervention is effective in helping the child overcome disfluency.

Once stuttering has become established, and the child has developed secondary behaviors, the prognosis is more guarded, and only 18% of children who stutter after five years recover spontaneously. However, with treatment young children may be left with little evidence of stuttering.

With adult people who stutter, there is no known cure, though they may make partial recovery or even complete recovery with intervention. People who stutter often learn to stutter less severely, though others may make no progress with therapy.

Emotional sequelae associated with stuttering primarily relates to state-dependent anxiety related to the speech disorder itself. However, this is typically isolated to social contexts that require speaking, is not a trait anxiety, and this anxiety does not persist if stuttering remits spontaneously. Research attempting to correlate stuttering with generalized or state anxiety, personality profiles, trauma history, or decreased IQ have failed to find adequate empirical support for any of these claims.

Motor speech disorders are a class of speech disorders that disturb the body's natural ability to speak due to neurologic impairments. These neurologic impairments make it difficult for individuals with motor speech disorders to plan, program, control, coordinate, and execute speech productions. Disturbances to the individual's natural ability to speak vary in their etiology based on the integrity and integration of cognitive, neuromuscular, and musculoskeletal activities. Speaking is an act dependent on thought and timed execution of airflow and oral motor / oral placement of the lips, tongue, and jaw that can be disrupted by weakness in oral musculature (dysarthria) or an inability to execute the motor movements needed for specific speech sound production (apraxia of speech or developmental verbal dyspraxia). Such deficits can be related to pathology of the nervous system (central and /or peripheral systems involved in motor planning) that affect the timing of respiration, phonation, prosody, and articulation in isolation or in conjunction.

Receptive language disorders can be acquired or developmental (most often the latter). When developmental, difficulties in spoken language tend to occur before three years of age. Usually such disorders are accompanied by expressive language disorders.

However, unique symptoms and signs of a receptive language disorder include: struggling to understand meanings of words and sentences, struggling to put words in proper order, and inability to follow verbal instruction.

Treatment options include: language therapy, special education classes for children at school, and a psychologist if accompanying behavioral problems are present.