Instruct: Given a question, retrieve documents that answer the question.
Query: How does agnosia affect the brain?
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.
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.
Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma. Amnesia can also be caused temporarily by the use of various sedatives and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that was caused. There are two main types of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation. In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.
Language processing has been linked to Broca's area since Pierre Paul Broca reported impairments in two patients. They had lost the ability to speak after injury to the posterior inferior frontal gyrus (pars triangularis) (BA45) of the brain. Since then, the approximate region he identified has become known as Broca's area, and the deficit in language production as Broca's aphasia, also called expressive aphasia. Broca's area is now typically defined in terms of the pars opercularis and pars triangularis of the inferior frontal gyrus, represented in Brodmann's cytoarchitectonic map as Brodmann area 44 and Brodmann area 45 of the dominant hemisphere.
Studies were completed consistently throughout Molaison's lifetime to discover more about amnesia. Researchers did a 14-year follow-up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that had happened since his surgery. However, he could still remember things that had happened prior to the operation. Researchers also found that, when asked, Molaison could answer questions about national or international events, but he could not remember his own personal memories. After his death Molaison donated his brain to science, where they were able to discover the areas of the brain that had the lesions which caused his amnesia. This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works.
Studies on specific cases demonstrate how particular impaired areas of the hippocampus are associated with the severity of RA. Damage can be limited to the CA1 field of the hippocampus, causing very limited RA for about 1 to 2 years. More extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years. Another study also suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive RA, covering 40 to 50 years. These findings suggest that density of RA becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures.
Broca's aphasia is a specific type of expressive aphasia and is so named due to the aphasia that results from damage or lesions to the Broca's area of the brain, that exists most commonly in the left inferior frontal hemisphere. Thus, the aphasia that develops from the lack of functioning of the Broca's area is an expressive and non-fluent aphasia. It is called 'non-fluent' due the issues that arise because Broca's area is critical for language pronunciation and production. The area controls some motor aspects of speech production and articulation of thoughts to words and as such lesions to the area result in the specific non-fluent aphasia.
The term "agnotology" was first coined in a footnote in Proctor's 1995 book, "The Cancer Wars: How Politics Shapes What We Know and Don't Know About Cancer": "Historians and philosophers of science have tended to treat ignorance as an ever-expanding vacuum into which knowledge is sucked – or even, as Johannes Kepler once put it, as the mother who must die for science to be born. Ignorance, though, is more complex than this. It has a distinct and changing political geography that is often an excellent indicator of the politics of knowledge. We need a political agnotology to complement our political epistemologies".
Eloquent cortex is a name used by neurologists for areas of cortex that—if removed—will result in loss of sensory processing or linguistic ability, minor paralysis, or paralysis. The most common areas of eloquent cortex are in the left temporal and frontal lobes for speech and language, bilateral occipital lobes for vision, bilateral parietal lobes for sensation, and bilateral motor cortex for movement.
The optic nerve hypoplasia is generally manifested by nystagmus (involuntary eye movements, often side-to-side) and a smaller-than-usual optic disc. The degree of visual impairment is variable, and ranges from normal vision to complete blindness. When nystagmus develops, it typically appears by 1–8 months of age, and usually indicates that there will be a significant degree of visual impairment, but the severity is difficult to predict in infancy. Although there are many measures to compensate for visual impairment, there are few treatments available to induce normal optic nerve function.
It has been stated that "The cognitive consequences of anterior cingulate lesions remain rather equivocal, with a number of case reports of intact general neuropsychological and executive function in the presence of large anterior dorsal cingulate lesions. For an alternative view of anterior cingulate, see Rushworth's review (2007).
Priming studies on Cochrane revealed that individuals with severe amnesia can display intact priming capabilities regardless of episodic memory damage. Priming involves initially exposing a subject to a word or image so that a memory of that word or image can be formed. This is meant to improve a subject's recall of that word or image when that word or image is shown at a later time. Cochrane additionally showed that priming effects can last for long periods of time; in one study, researchers presented Cochrane with a list of words, and after 12 months showed him the same words with letters missing. Cochrane was able to complete these fragmented words as successfully as a person with normal brain function who was shown the same list initially. This challenged the previous opinion that patients with anterograde amnesia are incapable of adding information to their declarative memory.
Research has discovered dystrophic (defective development) human microglia. "These cells are characterized by abnormalities in their cytoplasmic structure, such as deramified, atrophic, fragmented or unusually tortuous processes, frequently bearing spheroidal or bulbous swellings." The incidence of dystrophic microglia increases with aging. Microglial degeneration and death have been reported in research on Prion disease, Schizophrenia and Alzheimer's disease, indicating that microglial deterioration might be involved in neurodegenerative diseases. A complication of this theory is the fact that it is difficult to distinguish between "activated" and "dystrophic" microglia in the human brain.
Neuroplasticity is defined as the brain's ability to reorganize itself, lay new pathways, and rearrange existing ones, as a result of experience. Neuronal changes after damage to the brain such as collateral sprouting, increased activation of the homologous areas, and map extension demonstrate the brain's neuroplastic abilities. According to Thomson, "Portions of the right hemisphere, extended left brain sites, or both have been shown to be recruited to perform language functions after brain damage. All of the neuronal changes recruit areas not originally or directly responsible for large portions of linguistic processing. Principles of neuroplasticity have been proven effective in neurorehabilitation after damage to the brain. These principles include: incorporating multiple modalities into treatment to create stronger neural connections, using stimuli that evoke positive emotion, linking concepts with simultaneous and related presentations, and finding the appropriate intensity and duration of treatment for each individual patient.
This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, "If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic." Merzenich received the 2016 Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."
Post-concussion syndrome, also known as postconcussive syndrome or PCS, is a set of symptoms that may continue for weeks, months, or a year or more after a concussion – a mild form of traumatic brain injury (TBI). The rates of PCS vary, but most studies report that about 15% of individuals with a history of a single concussion develop persistent symptoms associated with the injury. A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury. Loss of consciousness is not required for a diagnosis of concussion or post-concussion syndrome.
Studies in patients that were a subject to bilateral cingulotomy, that involved fMRI analyses, showed that the anterior cingulate cortex has a key role in cognitive control and is highly likely to be involved in the control of attentional response, whereas the dorsal part of that region of the brain was not identified to be involved in such a process, although this is still under dispute. The function of the dorsal part of the cingulate cortex was connected to the sorting out and processing of conflicting information signals. In addition, neuroimaging studies also indicated that the anterior cingulate cortex participates in the modulation of cortical regions that are of higher order as well as sensory processing areas.
Functional MRI analyses of the anterior cingulate cortex have also led to the introduction of bilateral cingulotomy for the treatment of chronic pain. Such application was introduced since the anterior cingulate cortex has been found to be related to the processing nociceptive information input. In particular the role of the anterior cingulate cortex is in the interpretation of how a stimulus affects a person rather than its actual physical intensity.
Short-term memory is supported by transient patterns of neuronal communication, dependent on regions of the frontal lobe (especially dorsolateral prefrontal cortex) and the parietal lobe. Long-term memory, on the other hand, is maintained by more stable and permanent changes in neural connections widely spread throughout the brain. The hippocampus is essential (for learning new information) to the consolidation of information from short-term to long-term memory, although it does not seem to store information itself. It was thought that without the hippocampus new memories were unable to be stored into long-term memory and that there would be a very short attention span, as first gleaned from patient Henry Molaison after what was thought to be the full removal of both his hippocampi. More recent examination of his brain, post-mortem, shows that the hippocampus was more intact than first thought, throwing theories drawn from the initial data into question. The hippocampus may be involved in changing neural connections for a period of three months or more after the initial learning.
FI is a sign or a symptom, not a diagnosis, and represents an extensive list of causes. Usually, it is the result of a complex interplay of several coexisting factors, many of which may be simple to correct. Up to 80% of people may have more than one abnormality that is contributing. Deficits of individual functional components of the continence mechanism can be partially compensated for a certain period of time, until the compensating components themselves fail. For example, obstetric injury may precede onset by decades, but postmenopausal changes in the tissue strength reduce in turn the competence of the compensatory mechanisms. The most common factors in the development are thought to be obstetric injury and after effects of anorectal surgery, especially those involving the anal sphincters and hemorrhoidal vascular cushions. The majority of incontinent persons over the age of 18 fall into one of several groups: those with structural anorectal abnormalities (sphincter trauma, sphincter degeneration, perianal fistula, rectal prolapse), neurological disorders (multiple sclerosis, spinal cord injury, spina bifida, stroke, etc.), constipation/fecal loading (presence of a large amount of feces in the rectum with stool of any consistency), cognitive and/or behavioral dysfunction (dementia, learning disabilities), diarrhea, inflammatory bowel diseases (e.g. ulcerative colitis, Crohn's disease), irritable bowel syndrome, disability related (people who are frail, acutely unwell, or have chronic/acute disabilities), and those cases which are idiopathic (of unknown cause). Diabetes mellitus is also known to be a cause, but the mechanism of this relationship is not well understood.
Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may also vary by age, by severity of the hypoglycemia and the speed of the decline. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, as well as previous incidents.
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.
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. 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.
The affected individual may not realize that they have a visual problem and may complain of becoming "clumsy" or "muddled" when performing familiar tasks such as setting the table or simple DIY.
Anosognosia, a lack of awareness of the deficit, is common and can cause therapeutic resistance. In some agnosias, such as prosopagnosia, awareness of the deficit is often present; however shame and embarrassment regarding the symptoms can be a barrier in admission of a deficiency. Because agnosias result from brain lesions, no direct treatment for them currently exists, and intervention is aimed at utilization of coping strategies by patients and those around them. Sensory compensation can also develop after one modality is impaired in agnostics
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.