Social-emotional agnosia is mainly caused by abnormal functioning in a particular brain area called the amygdala. Typically this agnosia is only found in people with bilateral amygdala damage; that is damage to amygdala regions in both hemispheres of the brain. It can be accompanied by right or bilateral temporal lobe damage. The amygdala dysfunction causes the inability to select appropriate behaviors in a specific social context. Symptoms can include reduced aggression, fearfulness, competitiveness, and social dominance. Those with social-emotional agnosia have difficulty discerning the emotional meaning and significance behind objects, which causes a loss of fondness and familiarity. Bilateral amygdala damage has also been associated with social unresponsiveness, leading to an avoidance of social interactions and a preference for isolation from their own species. Evidence suggests that damage to the amygdala and the limbic system (specifically the amygdala-hypothalamus pathway) results in the loss of the core ability to recognize and interpret the mental states of others, a vital ability in social interactions. The amygdala evokes highly personal emotional memories and the loss of this function causes hypo-emotionality, a general lack of emotion when presented with different stimuli. Hypersexuality has also been observed in those with disconnection in the amygdala-hypothalamus pathway. Temporal lobe epilepsy has been shown to cause bilateral amygdala damage which could result in symptoms similar to social-emotional agnosia, but the precise relationship between the two disorders is unknown.

Longitudinal studies indicate that problems are largely resolved by 5 years of age in around 40% of 4-year-olds with early language delays who have no other presenting risk factors. However, for children who still have significant language difficulties at school entry, reading problems are common, even for children who receive specialist help, and educational attainments are typically poor. Poor outcomes are most common in cases where comprehension as well as expressive language is affected. There is also evidence that scores on tests of nonverbal ability of children with DLD decrease over the course of development.

DLD is associated with an elevated risk of social, emotional and mental health concerns. For instance, in a UK survey, 64% of a sample of 11-year-olds with DLD scored above a clinical threshold on a questionnaire for psychiatric difficulties, and 36% were regularly bullied, compared with 12% of comparison children. In the longer-term, studies of adult outcomes of children with DLD have found elevated rates of unemployment, social isolation and psychiatric disorder among those with early comprehension difficulties. However, better outcomes are found for children who have milder difficulties and do not require special educational provision.

Social-emotional agnosia, also known as emotional agnosia or expressive agnosia, is the inability to perceive facial expressions, body language, and voice intonation. A person with this disorder is unable to non-verbally perceive others' emotions in social situations, limiting normal social interactions. The condition causes a functional blindness to subtle non-verbal social-emotional cues in voice, gesture, and facial expression. People with this form of agnosia have difficulty in determining and identifying the motivational and emotional significance of external social events, and may appear emotionless or agnostic (uncertainty or general indecisiveness about a particular thing). Symptoms of this agnosia can vary depending on the area of the brain affected. Social-emotional agnosia often occurs in individuals with schizophrenia and autism. It is difficult to distinguish from, and has been found to co-occur with, alexithymia.

"Developmental prosopagnosia" (DP), also called "Congenital prosopagnosia" (CP), is a face-recognition deficit that is lifelong, manifesting in early childhood, and that cannot be attributed to acquired brain damage. A number of studies have found functional deficits in DP both on the basis of EEG measures and fMRI. It has been suggested that a genetic factor is responsible for the condition. The term "hereditary prosopagnosia" was introduced if DP affected more than one family member, essentially accenting the possible genetic contribution of this condition. To examine this possible genetic factor, 689 randomly selected students were administered a survey in which seventeen developmental prosopagnosics were quantifiably identified. Family members of fourteen of the DP individuals were interviewed to determine prosopagnosia-like characteristics, and in all fourteen families, at least one other affected family member was found.

In 2005, a study led by Ingo Kennerknecht showed support for the proposed congenital disorder form of prosopagnosia. This study provides epidemiological evidence that congenital prosopagnosia is a frequently occurring cognitive disorder that often runs in families. The analysis of pedigree trees formed within the study also indicates that the segregation pattern of hereditary prosopagnosia (HPA) is fully compatible with autosomal dominant inheritance. This mode of inheritance explains why HPA is so common among certain families (Kennerknecht et al. 2006).

There are many developmental disorders associated with an increased likelihood that the person will have difficulties in face perception, of which the person may or may not be aware. The mechanism by which these perceptual deficits take place is largely unknown. A partial list of some disorders that often have prosopagnosiac components would include nonverbal learning disorder, Alzheimer's disease, and autism in general. However, these types of disorders are very complicated, so arbitrary assumptions should be avoided.

In 2012, it was shown that developmental prosopagnosia cases show poor integration of low and high spatial frequency information.

Epidemiological surveys, in the US and the UK converge in estimating the prevalence of DLD in 5-year-olds at around 7 percent.

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.

One cause of aprosodia is suffering brain trauma to one of several specific areas of the brain, resulting in the inability to properly process or convey

emotional cues. This brain damage can occur in the form of ischemic damage from stroke, removal during surgery, brain lesions, or trauma such as a localized bullet wound. It is worth noting however, that this localization occurs over a range of areas that can vary from person to person and more research is required to further define these areas. Diagnostic confirmation of aprosodia using brain scanning techniques is a relatively recent occurrence, at least with respect to quantitative specificity. As brain imaging techniques are refined to allow for greater temporal and spatial resolution, it is hoped that more will be able to be learned about aprosodias at a functional anatomical level.

Neuroscientists have learned a lot about the role of the brain in numerous cognitive mechanisms by understanding corresponding disorders. Similarly, neuroscientists have come to learn a lot about music cognition by studying music-specific disorders. Even though music is most often viewed from a "historical perspective rather than a biological one" music has significantly gained the attention of neuroscientists all around the world. For many centuries music has been strongly associated with art and culture. The reason for this increased interest in music is because it "provides a tool to study numerous aspects of neuroscience, from motor skill learning to emotion".

It is now generally accepted that SLI is a strongly genetic disorder. The best evidence comes from studies of twins. Two twins growing up together are exposed to the same home environment, yet may differ radically in their language skills. Such different outcomes are, however, seen almost exclusively in fraternal (non-identical) twins, who are genetically different. Identical twins share the same genes and tend to be much more similar in language ability.

There can be some variation in the severity and persistence of SLI in identical twins, indicating that environmental factors affect the course of disorder, but it is unusual to find a child with SLI who has an identical twin with normal language.

SLI is not usually caused by a mutation in a single gene. Current evidence suggests that there are many different genes that can influence language learning, and SLI results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. It has been hypothesized, however, that a mutation of the FOXP2 gene may have an influence on the development on SLI to a certain degree, as it regulates genes pertinent to neural pathways related to language.

Only a handful of non-genetic factors have been found selectively to impact on language development in children. Later-born children in large families are at greater risk than earlier born.

Overall, genetic mutation, hereditary influences, and environmental factors may all have a role in the development and manifestation of SLI. It is important, therefore, to not associate the development to a single factor, but recognize that it is oftentimes the result of complex interactions between any or all of these factors.

Aprosodia is a neurological condition characterized by the inability of a person to properly convey or interpret emotional prosody. Prosody in language refers to the ranges of rhythm, pitch, stress, intonation, etc. These neurological deficits can be the result of damage of some form to the non-dominant hemisphere areas of language production. The prevalence of aprosodias in individuals is currently unknown, as testing for aprosodia secondary to other brain injury is only a recent occurrence.

Longitudinal studies indicate that problems are largely resolved by 5 years in around 40% of 4-year-olds with SLI. However, for children who still have significant language difficulties at school entry low levels of literacy are common, even for children who receive specialist help,

and educational attainments are typically poor. Poor outcomes are most common in cases where comprehension as well as expressive language is affected. There is also evidence that the nonverbal IQ of children with SLI decreases over the course of development.

SLI is associated with a high rate of psychiatric disorder. For instance, Conti-Ramsden and Botting (2004) found that 64% of a sample of 11-year-olds with SLI scored above a clinical threshold on a questionnaire for psychiatric difficulties, and 36% were regularly bullied, compared with 12% of comparison children. In the longer-term, studies of adult outcomes of children with SLI find elevated rates of unemployment, social isolation and psychiatric disorder. However, most studies focused on children with severe problems, where comprehension as well as expressive language was affected. Better outcomes are found for children who have milder difficulties and do not require special educational provision.

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.

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.

Prosopagnosia can be caused by lesions in various parts of the inferior occipital areas (occipital face area), fusiform gyrus (fusiform face area), and the anterior temporal cortex. Positron emission tomography (PET) and fMRI scans have shown that, in individuals without prosopagnosia, these areas are activated specifically in response to face stimuli. The inferior occipital areas are mainly involved in the early stages of face perception and the anterior temporal structures integrate specific information about the face, voice, and name of a familiar person.

Acquired prosopagnosia can develop as the result of several neurologically damaging causes. Vascular causes of prosopagnosia include posterior cerebral artery infarcts (PCAIs) and hemorrhages in the infero-medial part of the temporo-occipital area. These can be either bilateral or unilateral, but if they are unilateral, they are almost always in the right hemisphere. Recent studies have confirmed that right hemisphere damage to the specific temporo-occipital areas mentioned above is sufficient to induce prosopagnosia. MRI scans of patients with prosopagnosia showed lesions isolated to the right hemisphere, while fMRI scans showed that the left hemisphere was functioning normally. Unilateral left temporo-occipital lesions result in object agnosia, but spare face recognition processes, although a few cases have been documented where left unilateral damage resulted in prosopagnosia. It has been suggested that these face recognition impairments caused by left hemisphere damage are due to a semantic defect blocking retrieval processes that are involved in obtaining person-specific semantic information from the visual modality.

Other less common etiologies include carbon monoxide poisoning, temporal lobectomy, encephalitis, neoplasm, right temporal lobe atrophy, trauma, Parkinson's disease, and Alzheimer's 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.

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.

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.

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.

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

Integrative agnosia is a sub-disease of agnosia, meaning the lack of integrating perceptual wholes within

knowledge. Integrative agnosia can be assessed by several experimental tests such as the Efron shape test, which

determines the specificity of the disease being Integrative.

This disease is often caused by brain trauma, producing medial ventral lesions to the extrastriate cortex. Affecting this region of the brain produces learning impairments: the inability to

integrate parts such as spatial distances or producing visual images from short or long-term memory.

Mixed receptive-expressive language disorder (DSM-IV 315.32) is a communication disorder in which both the receptive and expressive areas of communication may be affected in any degree, from mild to severe. Children with this disorder have difficulty understanding words and sentences. This impairment is classified by deficiencies in expressive and receptive language development that is not attributed to sensory deficits, nonverbal intellectual deficits, a neurological condition, environmental deprivation or psychiatric impairments. Research illustrates that 2% to 4% of 5 year olds have mixed receptive-expressive language disorder. This distinction is made when children have issues in expressive language skills, the production of language, and when children also have issues in receptive language skills, the understanding of language. Those with mixed receptive-language disorder have a normal left-right anatomical asymmetry of the planum temporale and parietale. This is attributed to a reduced left hemisphere functional specialization for language. Taken from a measure of cerebral blood flow (SPECT) in phonemic discrimination tasks, children with mixed receptive-expressive language disorder do not exhibit the expected predominant left hemisphere activation. Mixed receptive-expressive language disorder is also known as receptive-expressive language impairment (RELI) or receptive language disorder.

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.

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.

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

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

Some of the causes of integrative agnosia include stroke, traumatic brain injury, Alzheimer's disease, an anoxic episode following myocardial infarction, and progressive multifocal leukoencephalopathy.