question: why do people not forget their language when they get amnesia?
comment: There are forms of loss of function that do uniquely impact language ability and that also hints at the reason one can get amnesia and remember language. The brain develops to have specialized areas for certain functions and while it's capable of "remapping" in some circumstances, language is largely controlled by what are known as the Broca area and the Wernicke's area. Long term memory is much more distributed in how it's controlled. & #x200B; Additionally, amnesia is a non-specific diagnosis - it's not a "cause" it is a symptom of many possible causes that range from emotion to physical. Generally when people talk about temporary amnesia it's physical (e.g. the television version) and when that happens it suggest damage to the memory centers of the brain but not the language centers. It's also common for lots and lots of capabilities to be retained in amnesia - e.g. you remember how to walk, you retain general motor skills and even highly developed coordination and so on - all subject to some element of what we crudely call "memory".
passages: Ten years later, Paul Broca examined two patients exhibiting impaired speech due to frontal lobe injuries. Broca’s first patient lacked productive speech. He saw this as an opportunity to address language localization. It wasn't until Leborgne, formally known as "tan", died when Broca confirmed the frontal lobe lesion from an autopsy. The second patient had similar speech impairments, supporting his findings on language localization. The results of both cases became a vital verification of the relationship between speech and the left cerebral hemisphere. The affected areas are known today as Broca’s area and Broca’s Aphasia.
   An impairment following damage to a region of the brain does not necessarily imply that the damaged area is wholly responsible for the cognitive process which is impaired, however. For example, in pure alexia, the ability to read is destroyed by a lesion damaging both the left visual field and the connection between the right visual field and the language areas (Broca's area and Wernicke's area). However, this does not mean one suffering from pure alexia is incapable of comprehending speech—merely that there is no connection between their working visual cortex and language areas—as is demonstrated by the fact that pure alexics can still write, speak, and even transcribe letters without understanding their meaning.
   Patients suffering from frontal lobe dysfunction and ultimately source amnesia, will have much greater difficulty finishing this task successfully through method of strategy.
  
  Section::::Diagnostic tests.:Verbal fluency test.
  
  The verbal fluency test is a widely and commonly used test to assess for frontal lobe dysfunction in patients.
  
  BULLET::::- Procedure:
  
  Participants are asked to generate words beginning with letters that had previously been introduced to them (e.g.: generate a word beginning with 'A' or 'R'). They are given three 1-min trials (one trial per letter). The goal is to say as many different words possible that begin with the given letter.
   Bilingual patients typically experience anomia to a greater degree in just one of their fluent languages. However, evidence conflicts as to which language – first or second – suffers more.
  
  Research on children with anomia has indicated that children who undergo treatment are, for the most part, able to gain back normal language abilities, aided by brain plasticity. However, longitudinal research on children with anomic aphasia due to head injury shows that even several years after the injury, some signs of deficient word retrieval are still observed. These remaining symptoms can sometimes cause academic difficulties later on.
  
  Section::::Patients.
   how memory and learning were affected by morphine. They found that when mice learned a response under the influence of morphine, they later performed it most efficiently under the influence of morphine. When mice learned the response free of morphine, they recalled it best when similarly sober. And for mice that were taught the response under the
  
  influence of morphine, once the drug wore off, they suffered amnestic effects; they could no longer remember the learned response.
   Mechanisms for recovery differ from patient to patient. Some mechanisms for recovery occur spontaneously after damage to the brain, whereas others are caused by the effects of language therapy. FMRI studies have shown that recovery can be partially attributed to the activation of tissue around the damaged area and the recruitment of new neurons in these areas to compensate for the lost function. Recovery may also be caused in very acute lesions by a return of blood flow and function to damaged tissue that has not died around an injured area. It has been stated by some researchers that the recruitment and recovery of neurons in the left hemisphere opposed to the recruitment of similar neurons in the right hemisphere is superior for long-term recovery and continued rehabilitation. It is thought that, because the right hemisphere is not intended for full language function, using the right hemisphere as a mechanism of recovery is effectively a "dead-end" and can lead only to partial recovery.
   Ten years later, Paul Broca examined two patients exhibiting impaired speech due to frontal lobe injuries. Broca’s first patient lacked productive speech. He saw this as an opportunity to address language localization. It wasn’t until Leborgne, formally known as "tan", died when Broca confirmed the frontal lobe lesion from an autopsy. The second patient had similar speech impairments, supporting his findings on language localization. The results of both cases became a vital verification of the relationship between speech and the left cerebral hemisphere. The affected areas are known today as Broca’s area and Broca’s Aphasia.
   An important finding in amnesic patients with MTL damage is the impairment of memory in all sensory modalities – sound, touch, smell, taste, and sight. This reflects the fact that the MTL is a processor for all of the sensory modalities, and helps store these kind of thoughts into memory. In addition, subjects can often remember how to perform relatively simple tasks immediately (on the order of 10 seconds), but when the task becomes more difficult, even on the same time scale, subjects tend to forget. This demonstrates the difficulty of separating procedural memory tasks from declarative memory; some elements of declarative memory may be used in learning procedural tasks.
   Lesions to the thalamus have been found to impair the recognition memory of monkeys. In a study conducted by Aggleton and Mishkin, they found that monkeys with lesions to the anterior thalamus and the posterior thalamus had an impaired ability for recognition and associative memory on matching tests. The researchers also suggested that combined damage to both regions of the thalamus can lead to amnesia.
  
  Section::::Neuroanatomy.:Amygdala.
   Section::::In fiction.
  
  Global amnesia is a common motif in fiction despite being extraordinarily rare in reality. In the introduction to his anthology "The Vintage Book of Amnesia", Jonathan Lethem writes:
   Research suggests there are also context-dependent cues which are dependent on environment and situation. In an experiment conducted in 1975 deep sea divers were divided into two groups. Each group had the same list of 36 unrelated words to learn. But one of the groups learned it 15 feet underwater, and the other on land. Both groups then had recall those words underwater as well as on land. The divers who had learnt the words on land recalled 38% when tested on land and 21% when under water. Those who had learnt the words under water recalled 21% on the beach and 32% when under water.
   BULLET::::- The hippocampus deals largely with memory consolidation, where information from the working memory and short-term memory is encoded into long-term storage for future retrieval. Amnesic patients with damage to the hippocampus are able to demonstrate some degree of unimpaired semantic memory, despite a loss of episodic memory, due to spared parahippocampal cortex. In other words, retrograde amnesics "know" an information or skill, but cannot "remember" how they do.
  
  BULLET::::- The diencephalon and the surrounding areas' role in memory is not well understood. However, this structure appears to be involved in episodic memory recall.
   Section::::Against amnesia.
   Poreh et al. describe a case study of patient A.D., whose damage to the fornix rendered the hippocampus useless, but spared adjacent cortical areas – a fairly rare injury. When the patient was given a test with something with which he had some familiarity, the patient was able to score well. In general, however, A.D. had severely impaired episodic memory, but had some ability to learn semantic knowledge. Other studies show animals with similar injuries can recognize objects with which they are familiar, but, when the objects are presented in an unexpected context, they do not score well on recognition tests.
   Studies on Cochrane also illuminated the relationship between semantic learning and episodic memory, showing that patients with severe amnesia are capable of retaining new semantic knowledge in the absence of episodic memory. Researchers found that Cochrane was able to learn new semantic knowledge and retain it over a long period of time. In one study, researchers taught Cochrane 64 three-word sentences over multiple testing trials, and after 12 months, presented the same sentences to him with the last of the three words missing. Cochrane showed significant retention of this semantic knowledge, completing 25 of the 64 sentences. This showed that amnesic patients can learn new semantic information, although slower than normal test subjects.
   Section::::Analysis.
   A common way to demonstrate modularity is to find a double dissociation. That is two groups: First, people for whom language is severely damaged and yet have normal cognitive abilities and, second, persons for whom normal cognitive abilities are grossly impaired and yet language remains intact. Whilst extensive lesions in the left hemisphere perisylvian area can render persons unable to produce or perceive language (global aphasia), there is no known acquired case where language is completely intact in the face of severe non-linguistic deterioration. Thus, functional module status cannot be granted to language processing based on this evidence.
   The most famous case reported is that of patient Henry Molaison, known as H.M., in March 1953. Molaison's chief complaint was the persistence of severe seizures and therefore had a bilateral lobectomy (both of his MTLs were removed). As a result, Molaison had bilateral damage to both the hippocampal formation and the perirhinal cortex. Molaison had average intelligence and perceptual ability and a decent vocabulary. However, he could not learn new words or remember things that had happened more than a few minutes earlier. He could remember anything from his childhood. If the memory was created from before his lobectomy, he still had the ability to retrieve it and remember. However, he was able to learn some new skills. He was the first well-documented case of severe anterograde amnesia, and was studied until his death in 2008.
   Further studies on Cochrane tested the possibility of amnesia patients to learn information that was more complex than information acquired with priming. Researchers also examined if patients could learn information applicable to completing daily tasks. One study showed that Cochrane could learn vocabulary associated with operating a desktop computer; further studies revealed that Cochrane could actually learn commands related to computers to the extent that he was able to perform basic programming tasks on a microcomputer.
   The term is ; .
  
  Section::::Signs and symptoms.
  
  People with amnesia can learn new information, particularly non-declarative knowledge. However, some people with dense anterograde amnesia do not remember the episodes during which they previously learned or observed the information.
  
  Section::::Signs and symptoms.:Declarative information.
   An example of a case study of transient semantic amnesia involves a patient who was admitted into hospital with an acute loss of memory for common words and their meanings. For example, he was unable to understand and differentiate between a "car" and an "engine". His speech was fluent, he could perform quick mental maths, and when reviewed by the doctor, his orientation and verbal anterograde memory was normal. However he had been suffering from migraine for a long time. When reviewed after a month, the patient was back to normal based on a cognitive assessment as well as CT scans. He was also able to remember the sequence of events that led to his admission into the hospital.
   While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain. Wernicke–Korsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole-grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast. Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.
   Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. The reason patients could not form new episodic memories is likely because the CA1 region of the hippocampus was a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.
   Section::::Prevention.:Older adults.
   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.
  
presuppositions: Amnesia is a specific diagnosis.  Because amnesia causes memory loss, people should not remember their language after being effected by amnesia. 
corrections: Amnesia is a symptom of many possible causes and does not a specific diagnosis.  Amnesia is a non-specific diagnosis and can block memories from specific areas of the brain, however many general motor skills such as walking and talking are retained. 
raw_presuppositions: Amnesia is a specific diagnosis.  Because amnesia causes memory loss, people should not remember their language after being effected by amnesia.  Amnesia erases all memory
raw_corrections: Amnesia is a symptom of many possible causes and does not a specific diagnosis.  Amnesia is a non-specific diagnosis and can block memories from specific areas of the brain, however many general motor skills such as walking and talking are retained.  Amnesia is a non-specific diagnosis and can block memories from specific areas of the brain.