Instruct: Given a question, retrieve documents that can help answer the question.
Query: What causes agnosia?
Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders.[4] Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved.[4]
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.
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.
The term auditory agnosia was originally coined by Freud (1891) to describe patients with selective impairment of environmental sounds. In a review of the auditory agnosia literature, Ulrich re-named this disorder as non-verbal auditory agnosia (although sound auditory agnosia and environmental sound auditory agnosia are also commonly used). This disorder is very rare and only 18 cases have been documented. In contradiction to pure word deafness and general auditory agnosia, this disorder is likely under-diagnosed because patients are often not aware of their disorder, and thus don’t seek medical intervention.
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.
Lesions to the left angular gyrus are associated with finger agnosia, as well as the other symptoms of Gerstmann Syndrome, also known as Angular Gyrus Syndrome. In a study by Rusconi et al., repetitive transcranial magnetic stimulation was used in healthy individuals to simulate finger agnosia. Stimulation to the intraparietal sulcus, supramarginal gyrus, as well as the left and right angular gyrus and posterior parietal areas caused difficulties in naming, recognizing, and distinguishing fingers.
Auerbach et al considered word deafness and general auditory agnosia as two separate disorders, and labelled general auditory agnosia as pre-phonemic auditory agnosia and word deafness as post-phonemic auditory agnosia. They suggested that pre-phonemic auditory agnosia manifests because of general damage to the auditory cortex of both hemispheres, and that post-phonemic auditory agnosia manifests because of damage to a spoken word recognition center in the left hemisphere. Recent evidence, possibly verified Auerbach hypothesis, since an epileptic patient who undergone electro-stimulation to the anterior superior temporal gyrus was demonstrated a transient loss of speech comprehension, but with intact perception of environmental sounds and music.
For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.
Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway . Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it "was" a lion creating the noise. All auditory agnosia patients read lips in order to enhance the speech comprehension. It is yet unclear whether auditory agnosia (also called general auditory agnosia) is a combination of milder disorders, such auditory verbal agnosia (pure word deafness), non-verbal auditory agnosia, amusia and word meaning deafness), or a mild case of the more severe disorder, cerebral deafness. So far, 203 patients with auditory perceptual deficits due to CNS damage were reported in the medical literature, of which 183 diagnosed with general auditory agnosia or word deafness, 34 with cerebral deafness, 51 with non-verbal auditory agnosia-amusia and 8 word meaning deafness (for a list of patients see).
According to Denny-Brown’s 1954 article lesions of the parieto-occipital region cause disturbance of recognition in a patient – left-sided lesions usually cause agnosia, while right-sided lesions usually cause lack of recognition of the person’s left side and extrapersonal space. Denny-Brown defines agnosia as a disorder in formation or use of symbolic concepts, such as recognizing body parts; in naming objects; in understanding numbers; or in understanding geographic and/or spatial location. It applies to both sides of a person, even though a lesion in only one side of the parietal lobe – the dominant one – causes it. He argues that amorphosynthesis, on the other hand, is usually caused by a lesion in the non-dominant parieto-occipital lobe and results in lack of awareness on the opposite side of the body.
Agnosia is a rare occurrence and can be the result of a stroke, dementia, head injury, brain infection, or hereditary.
Apperceptive agnosia is a deficit in object perception creating an inability to understand the significance of objects.
Similarly, associative visual agnosia is the inability to understand the significance of objects; however, this time the deficit is in semantic memory. Both of these agnosias can affect the pathway to object recognition, like Marr's Theory of Vision. More specifically unlike apperceptive agnosia, associative agnosic patients are more successful at drawing, copying, and matching tasks; however, these patients demonstrate that they can perceive but not recognize.
Integrative agnosia(a subtype of associative agnosia) is the inability to integrate separate parts to form a whole image. With these types of agnosias there is damage to the ventral (what) stream of the visual processing pathway.
Object orientation agnosia is the inability to extract the orientation of an object despite adequate object recognition. With this type of agnosia there is damage to the dorsal (where) stream of the visual processing pathway.
This can affect object recognition in terms of familiarity and even more so in unfamiliar objects and viewpoints.
A difficulty in recognizing faces can be explained by prosopagnosia. Someone with prosopagnosia cannot identify the face but is still able to perceive age, gender, and emotional expression. The brain region that specifies in facial recognition is the fusiform face area. Prosopagnosia can also be divided into apperceptive and associative subtypes. Recognition of individual chairs, cars, animals can also be impaired; therefore, these object share similar perceptual features with the face that are recognized in the fusiform face area.
Visual agnosia occurs after damage to visual association cortex or to parts of the ventral stream of vision, known as the "what pathway" of vision for its role in object recognition. This occurs even when no damage has been done to the eyes or optic tract that leads visual information into the brain; in fact, visual agnosia occurs when symptoms cannot be explained by such damage. Damage to specific areas of the ventral stream impair the ability to recognize certain categories of visual information, such as the case of prospagnosia. Patients with visual agnosia generally do not have damage to the dorsal stream of vision, known as the "where pathway" of vision because of its role determining object's position in space, allowing individuals with visual agnosia to show relatively normal visually guided behavior.
Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.[22]
An agnosia that affects hearing, "auditory sound agnosia", is broken into subdivisions based on level of processing impaired, and a "semantic-associative" form is investigated within the auditory agnosias.
In childhood, auditory verbal agnosia can also be caused by Landau-Kleffner syndrome, also called acquired epileptic aphasia. It is often the first symptom of this disease. A review of 45 cases suggested a relationship between prognosis and age of onset with poorer prognosis for those with earlier onset. In extremely rare cases, auditory verbal agnosia has been known to present as a symptom of neurodegenerative disease, such as Alzheimer's disease. In such cases auditory verbal agnosia is a symptom that is typically followed by more severe neurological symptoms typical of Alzheimer's disease.
Apperceptive agnosia is a failure in recognition that is due to a failure of perception. In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur. When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; This occurs because apperceptive agnosia is most likely to present visual impairments. However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas.
Damage to the left hemisphere of the brain has been explicitly implicated in the associative form of visual agnosia. Goldberg suggested that the associative visual form of agnosia results from damage to the ventral stream of the brain, the occipito-temporal stream, which plays a key role in object recognition as the so-called "what" region of the brain, as opposed to the "where," dorsal stream.
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.
Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. There are two types of visual agnosia: apperceptive agnosia and associative agnosia.
No two apperceptive agnosic patients are the same, but case studies have been used to make theories on what causes the object recognition deficits. While it is established that semantics plays a large role in apperceptive agnosia deficits, it is not agreed upon how semantics alter recognition processes. One theory proposes that semantic memories are divided into differential semantic categories. Brain damage leads to apperceptive agnosia because there is damage to a particular semantic category. Another theory, referred to as functional specialization, states that individual parts of the brain specialize in different tasks. According to this theory, if an area of the brain is damaged, the function that the area is responsible for may decline as well. Yet another theory suggests that the pattern of deficit arise from independent impairments to a particular input modality and a single non perceptual semantic system that is organized by category. Deficits are largely due to semantics, however many categories are related perceptually as well. Objects that are biologically similar are likely to have physical resemblance to each other as well. Evidence for this arises in the finding that perceptual confusion arises because of structural similarity contributes or accounts for some modality specific deficit.
In analyzing W.F., Denny-Brown raises the question of why the patient’s left-sided lesion caused amorphosynthesis rather than agnosia. In general, as Denny-Brown explains in his introduction, left-sided lesions cause agnosia while right-sided lesions cause amorphosynthesis. He gives two possible explanations – first, that the right hemisphere might be dominant in the patient, not the left. This would suggest that just as right-handed and left-handedness differ among the population, so too does the dominance of the parieto-occipital lobe. While Denny-Brown notes that he cannot refute this explanation, he sees it as more likely that the patient’s lesion simply did not extend posteriorly to produce agnosia. Therefore, he argues that the difference between causes of amorphosynthesis and agnosia is directly related to the size and extension of the parieto-occipital lesion. As a whole, he concludes that amorphosynthesis of the opposite side of the body from a parieto-occipital lesion can occur on as a result of either left or right-sided lesion, even though amorphosynthesis from right parietal lesion is more commonly observed.
Visual object agnosia (or semantic agnosia) is the most commonly encountered form of agnosia. The clinical "definition" of the disorder is when an affected person is able to copy/draw things that they cannot recognize. Individuals afflicted with the associative type often cannot identify, describe or mimic functions of items, though perception is intact, since images of objects can be copied or drawn. Individuals may retain semantic knowledge of the items, as exemplified during tasks where objects are presented through alternate modalities, through touch or verbal naming or description. Some associative visual object agnostics retain the ability to categorize items by context or general category, though unable to name or describe them. Diffuse hypoxic damage is the most common cause of visual object agnosias.
There is a strong link between acalculia and finger agnosia. Early in development, calculation begins with our fingers. The order that we use when we count with our finger is very specific and it is found in a variety of different cultures. The use of a base ten number system is also found in many cultures. Gerstmann believed that it was no coincidence the word digit means both a finger and any numeral.
Rusconi et al. suggested that these two conditions co-occur because they are close in cortical territory. In their 2005 study with repetitive transcranial magnetic stimulation (rTMS), they noted both finger agnosia and acalculia in the test subjects when areas of the intraparietal sulcus were stimulated. They concluded that the areas underlying finger agnosia and acalculia are extremely close to one another, but distinct. These areas receive blood from the same branch of the middle cerebral artery. Any damage to that blood supply would cause symptoms of both acalculia and finger agnosia.
Factor 1 is responsible for identifying why the delusional idea developed. In monothematic delusions, some neuropsychological abnormality typically causes the delusion. In mirrored-self misidentification, this abnormality can be either impaired facial processing or mirror agnosia. Patients with impaired facial processing cannot pair the reflected face in the mirror to a memory of one's own face, thus leading to the conclusion that the person in the mirror must be someone other than one's self. Patients with mirror agnosia are unable to understand how mirrors work; they believe the mirror represents a separate space, typically either the other side of a window or another room due to the presence of a hole in the wall. However, not all patients with impaired facial processing or mirror agnosia develop the delusion; there therefore needs to be a second factor that accounts for why some patients with impaired facial processing or mirror agnosia develop the delusion and others with the same conditions do not.
Auditory verbal agnosia (AVA) is not the same as auditory agnosia; patients with (nonverbal) auditory agnosia have a relatively more intact speech comprehension system despite their impaired recognition of nonspeech sounds.