Anterograde amnesia is a loss of the ability to create new memories after the event that caused the amnesia,

leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where most memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.
Contents [hide]

1 Causes

1.1 Alcohol intoxication

2 Symptoms 3 Pathophysiology

o o

3.1 Medial temporal lobe 3.2 Other memory systems

4 Reorganization of memory 5 Notable cases 6 Controversies

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6.1 Episodic versus semantic memory 6.2 Familiarity and the fractionation of memory 6.3 Islands of memory

7 References 8 Other sources

[edit]Causes This disorder is usually acquired in one of few ways: One cause is benzodiazepine drugs, such as midazolam, flunitrazepam, lorazepam, temazepam, nitrazepam, triazolam, andnimetazepam, which are known to have powerful amnesic effects. This has also been recorded in non-benzodiazapine sedatives which act on the same set of receptors, such as Zopiclone (also known by brand names Imovane and Zimovane).[1] Another cause is a traumatic brain injury in which damage is usually done to the hippocampus or surrounding cortices. It can also be caused by shock or an emotional disorder. Illness, though much rarer, can also cause anterograde amnesia if it causes encephalitis, which is the inflammation of brain tissue. For example, herpes encephalitis, when left untreated for over 96 hours, may lead to permanent damage in hippocampal regions and a permanently reduced or eliminated ability to encode new explicit memory (also known as declarative memory), which consists of two main subdivisions: episodic memory and semantic memory. If the damage due to encephalitis is over a certain threshold, encoding new episodic and/or semantic memory becomes impossible for the patient, leading to anterograde amnesia. Patients suffering from

anterograde amnesia may have either episodic, semantic, or both types of explicit memory impaired for events after the trauma that caused the amnesia. This suggests memory consolidation for different types of memory takes place in different regions of the brain. Despite this, current knowledge on human memory is still insufficient to map out the wiring of a human brain to discover which parts of which lobe are responsible for the various episodic and semantic knowledge within a persons memory. Amnesia is seen in patients who, for the reason of preventing another more serious disorder, have parts of their brain known to be involved in memory circuits removed, the most notable of which is known as the medial temporal lobe (MTL) memory system, described below. Patients with seizures originating in the MTL may have either side or both structures removed (there is one structure per hemisphere). In addition, patients with tumors who undergo surgery will often sustain damage to these structures, as is described in a case below. Damage to any part of this system, including the hippocampus and surrounding cortices, results in amnesic syndromes.[2] This is why people who suffer from strokes have a chance of developing cognitive deficits that result in anterograde amnesia, since strokes can involve the temporal lobe and the temporal cortex, and the temporal cortex houses the hippocampus. [edit]Alcohol

intoxication

See also: Blackout Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brain's ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy people's long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for inexperienced drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.[3] Chronic and severe alcohol abuse often results in thiamine deficiency and causes confusion, ataxia, and opthalmoplegia; characteristic symptoms of Wernickes encephalopathy. All of these are symptoms of alcohol -related anterograde amnesia.[citation needed] Another common cause of anterograde amnesia related to consumption of alcohol is the effects of Korsakoff's syndrome, a neurological disorder caused by the lack of thiamine (vitamin B1) in the brain. Chronic alcoholism causes this malnutrition, resulting in the syndrome, and among the symptoms of Korsakoffs syndrome are apathy, confabulation (delusions that result in invented memories), and anterograde amnesia. [edit]Symptoms Patients who suffer from anterograde amnesic syndromes may present with widely varying degrees of forgetfulness. Some patients with severe cases have a combined form of anterograde and retrograde amnesia, sometimes called global amnesia.

In the case of drug-induced amnesia, it may be short-lived and patients can recover from it. In the other case, which has been studied extensively since the early 1970s, patients often have permanent damage, although some recovery is possible, depending on the nature of the pathophysiology. Usually, some capacity for learning remains, although it may be very elementary. In cases of pure anterograde amnesia, patients have recollections of events prior to the injury, but cannot recall day-to-day information or new facts presented to them after the injury occurred.[2] In most cases of anterograde amnesia, patients lose declarative memory, or the recollection of facts, but they retain nondeclarative memory, often called procedural memory. For instance, they are able to remember and in some cases learn how to do things such as talking on the phone or riding a bicycle, but they may not remember what they had eaten earlier that day for lunch.[2] One extensively studied anterograde amnesiac patient, codenamed H.M., demonstrated that despite his amnesia preventing him from learning new declarative information, procedural memory consolidation was still possible, albeit severely reduced in power. He, along with other patients with anterograde amnesia, were given the same maze to complete day after day. Despite having no memory of having completed the maze the day before, unconscious practice of completing the same maze over and over reduced the amount of time needed to complete it in subsequent trials. From these results, Corkin et al. concluded despite having no declarative memory (i.e. no conscious memory of completing the maze exists), the patients still had a working procedural memory (learning done unconsciously through practice). This supports the notion that declarative and procedural memory are consolidated in different areas of the brain. In addition, patients have a diminished ability to remember the temporal context in which objects were presented. Certain authors claim the deficit in temporal context memory is more significant than the deficit in semantic learning ability (described below).[4] [edit]Pathophysiology The pathophysiology of anterograde amnesic syndromes varies with the extent of damage and the regions of the brains that were damaged. The most well-described regions indicated in this disorder are the medial temporal lobe (MTL), basal forebrain, and fornix. Beyond the details described below, the precise process of how we remember on a micro scale remains a mystery. Neuropsychologists and scientists are still not in total agreement over whether forgetting is due to faulty encoding, accelerated forgetting, or faulty retrieval, although a great deal of data seem to point to the encoding hypothesis.[5] In addition, neuroscientists are also in disagreement about the length of time involved in memory consolidation. Though most researchers, including Hasselmo et al., have found the consolidation process is spread out over several hours before transitioning from a fragile to a more permanent state, others, including Brown et al., posit that memory consolidation can take months or even years in a drawn-out process of consolidation and reinforcement. Further research into the length of time of memory consolidation will shed more light on why anterograde amnesia sometimes affects some memories gained after the event(s) that caused the amnesia, but does not affect other such memories. [edit]Medial

temporal lobe

The MTL memory system includes the hippocampal formation (CA fields, dentate gyrus, subicular complex), perirhinal, entorhinal, and parahippocampal cortices. It is known to be important for the storage and processing of declarative memory, which allows for factual recall. It is also known to communicate with the neocortex in the establishment and maintenance of long-term memories, although its known functions are independent of long-term memory. Nondeclarative memory, on the other hand, which allows for the performance of different skills and habits, is not part of the MTL memory system. Most data point to a "division of labor" among the parts of this system, although this is still being debated and is described in detail below. [2]

In animal models, researchers have shown monkeys with damage to both the hippocampus and its adjacent cortical regions were more severely impaired in terms of anterograde amnesia than monkeys with damage localized to hippocampal structures.[2] However, conflicting data in another primate study point to the observation that the amount of tissue damaged does not necessarily correlate with the severity of the memory loss.[6] Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic memory and semantic memory (described below).[2] 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.[7] MTL amnesic patients with localized damage to the hippocampus retain other perceptual abilities, such as the ability to intelligently function in society, to make conversation, to make ones bed, etc. Additionally, anterograde amnesics without combined retrograde disorders (localized damage to the MTL system) have memories prior to the traumatic event. For this reason, the MTL is not the storage place of all memories; other regions in the brain also store memories. The key is the MTL is responsible for the learning of new materials. [2] [edit]Other

memory systems

A limited number of cases have been described in which patients with damage to other parts of the brain acquired anterograde amnesia. Easton and Parker observed damage to either the hippocampus or the surrounding cortices does not seem to result in severe amnesia in primate models. They suggested damage to the hippocampus and surrounding structures alone does not explain the amnesia they saw in patients, or increasing damage does not correlate with the degree of impairment.[6] Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic and semantic memory. To demonstrate their hypothesis, they used a primate model with damage to the basal forebrain. They proposed that the disruption of neurons that project from the basal forebrain to the MTL are responsible for some of the impairment in anterograde amnesia. Easton and Parker also reported MRI scans of patients with severe anterograde amnesia showed damage beyond to cortical areas around the hippocampus and amygdala (a region of brain involved in emotions) and to surrounding white matter (white matter in the brain consists of axons, long projections of neuronal cell bodies). Another case described the onset of anterograde amnesia as a result of cell death in the fornix, another structure that carries information from the hippocampus to the structures of the limbic system and the diencephalon. The patient in this case did not show any disconnection syndrome, which is unexpected since the structures involved divide the brain hemispheres (both sides of her brain were able to communicate). Instead, she showed signs of amnesia. The final diagnosis was made by MRI. This particular amnesic syndrome is difficult to diagnose and often is misdiagnosed by physicians as an acute psychiatric disorder. [8] [edit]Reorganization

of memory

When there is damage to just one side of the MTL, there is opportunity for normal functioning or near-normal function for memories. Neuroplasticity describes the ability of the cortex to remap when necessary. Remapping can occur in cases like the one above, and, with time, the patient can recover and become more skilled at

remembering. A case report describing a patient who had two lobectomies - in the first, doctors removed part of her right MTL first because of seizures originating from the region, and later her left because she developed a tumor demonstrates this. This case is unique because it is the only one in which both sides of the MTL were removed at different times. The authors observed that the patient was able to recover some ability to learn when she had only one MTL, but observed the deterioration of function when both sides of the MTL were afflicted. The reorganization of brain function for epileptic patients has not been investigated much, but imaging results show that it is likely.[9] [edit]Notable

cases

The most famous case reported is that of patient Henry Molaison, known as H.M., in March 1953.[10] 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 also 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[2] until his death in 2008.[11] A similar case involved Clive Wearing, an accomplished musicologist who contracted a cold virus that attacked his brain, causing herpes simplex encephalitis. As a result, Wearing developed anterograde amnesia, as well as retrograde amnesia, so he has little memory of what happened before the virus struck him in 1985, and cannot learn new declarative knowledge after the virus struck him, either. As a result of anterograde amnesia, Wearing repeatedly wakes up every day in 30-second intervals until his wife stops him, because his episodic memory is nonfunctional (so he does not consciously recall having woken up 30 seconds prior). Despite this, however, Wearing maintained his ability to play the piano and conduct choirs. This case is significant because it demonstrates declarative and procedural memory are separate. Therefore, despite anterograde amnesia preventing Wearing from learning new bits of information that can be explained in words (declarative memory), and also preventing him from storing new memories of events or episodes (also part of declarative memory), he has little trouble in retaining his musical abilities (procedural memory), though he has no conscious memory of having learned music. Another case in the literature is E.P., a severely amnesic patient who was able to learn three-word sentences. He performed better on consecutive tests over a 12-week period (24 study sessions). However, when asked how confident he was about the answers, his confidence did not appear to increase. Bayley and Squire proposed his learning was similar to the process required by procedural memory tasks; E.P. could not get the answers right when one word in the three-word sentence was changed or the order of words was changed, and his ability to answer correctly, thus, became more of a "habit". Bayley and Squire claim the learning may have happened in the neocortex, and it happened without the conscious knowledge of E.P. They hypothesized the information may be acquired directly by the neocortex (to which the hippocampus projects) when there is repetition.[12] This case illustrates the difficulty in separating procedural from declarative tasks; this adds another dimension to the complexity of anterograde amnesia. [edit]Controversies [edit]Episodic

versus semantic memory

As described above, patients with anterograde amnesia have a wide range of forgetfulness. Declarative memory can be further subdivided into episodic and semantic memory. Episodic memory is described as the recollection of autobiographical information with a temporal and/or spatial context, whereas semantic memory involves recall of factual information with no such association (language, history, geography, etc.) In a case study of a girl who developed anterograde amnesia during childhood, it was determined that the patient C.L. retained semantic memory while suffering an extreme impairment of episodic memory.[13] One patient known by the codename Gene was involved in a motorcycle accident that damaged significant portions of his frontal and temporal lobes, including his left hippocampus. As a result, he cannot remember any specific episode in his life, such as a train derailment near his house. However, his semantic memory is intact; he remembers that he owns a car and two motorcycles, and he can even remember the names of his classmates in a school photograph. In stark contrast, a woman whose temporal lobes were damaged in the front due to encephalitis lost her semantic memory; she lost her memory of many simple words, historical events, and other trivial information categorized under semantic memory. However, her episodic memory was left intact; she can recall episodes such as her wedding and her fathers death with great detail. Vicari et al. describe that it remains unclear whether or not neural circuits involved in semantic and episodic memory overlap partially or completely, and this case seems to suggest that the two systems are independent. Both of the patient's hippocampal and diencephalic structures on the right and left sides were disconnected. When she came to Vicari et al.s office, the patient C.L.s chief complaint was forgetfulness involving both semantic and episodic memory. After administering a battery of neuropsychological tests, Vicari determined that C.L. performed well in tests of visual naming and sentence comprehension, visual-spatial ability, and general semantic knowledge about the world. They also noted an improved vocabulary and general knowledge base after 18 months. C.L.s episodic memory, on the other hand, was far below expectations: She could not retain daily events, where she had gone on vacation, the names of places she had been, and other such information. However, this study and others like it are susceptible to subjectivity, since it is not always clear to distinguish between episodic and semantic memory. For this reason, the topic remains controversial and debated. [edit]Familiarity

and the fractionation of memory

The right hippocampus is clearly necessary for familiarity in spatial tasks, whereas the left hippocampus is necessary for familiarity-based recollection in verbal tasks.[14] Some researchers claim the hippocampus is important for the retrieval of memories, whereas adjacent cortical regions can support familiarity-based memories. These memory decisions are made based on matching already-existing memories (before the onset of pathology) to the current situation. According to Gilboa et al., patients with localized hippocampal damage can score well on a test if it is based on familiarity.[15] Poreh et al.[16] 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. [edit]Islands

of memory

Patients with anterograde amnesia have trouble recalling new information and new autobiographical events, but the data are less consistent in regards to the latter. Medveds and Hirst recorded the presence of islands of memory detailed accounts that were described by such patients. The island memories were a combination of semantic and episodic memories. The researchers recorded patients giving long narratives with a fair amount of detail that resembled memories that the patients had prior to the trauma. The appearance of islands of memory could have something to do with the functioning of adjacent cortical areas and the neocortex. In addition, the researchers suspect that the amygdala played a role in the narratives. [17]

Anterograde Amnesia Anterograde amnesia is one of the many types of memory loss that take place among those who suffer from this condition. Learn more about the causes, symptoms and treatment methods involved for this condition. Ads by Google Liver symptoms test Wonder if you have liver disorder. Take a simple liver questionnaire www.essentiale-asia.com The term 'amnesia', takes root for many other forms of memory loss, that occur due to problems that target the brain, crippling it in a way where it cannot retain information, sometimes old, or new. It is one of many types of amnesia that occur in those who cannot remember new events for more than a couple of minutes. Those who suffer from a condition of 'pure' anterograde amnesia, will be able to still remember past events, but anything that should happen at a given time in the present, is forgotten in a span of a couple of seconds or minutes, and isn't recorded by one's long-term memory. If you were to ask him / her what they ate a couple of hours ago, or the directions to a place they'd been to the previous day, you'll find their expressions blank and confused. It isn't an easy condition to live with, especially when dealing with family and friends, and of course colleagues or peers. Even simple details like what day it is or which year is currently running, are foreign to the one suffering from this form of memory loss. Types of Amnesia We first try to understand some of the other forms of common memory loss that exist among us. Transient Global Amnesia: This is a severe case of anterograde amnesia, where patients aren't able to recollect new memories at all, where older memories are somewhat remembered, but not completely. Although rare, this is a very possible case among people. Childhood / Infantile Amnesia: This form of memory loss takes place among those who have no strong memories of their childhood. Doctors say that this may be due to the cause of incomplete maturity of the brain during one's younger days. Retrograde Amnesia: This kind of memory loss is the complete opposite as that of anterograde, wherein patients remember all events that are new and happening in the present, but cannot remember details of his / her past.

Hysterical / Fugue Amnesia: This form of amnesia takes form when one is put through a traumatic event in his / her life, where the brain cannot handle the devastating effects of this. The person then wakes up one day and has no clue as to who he / she is, including what their name is. He / she has no idea what they look like, since their reflections look alien to them. Sometimes it comes back out of the blue in a couple of days, but in some cases this is permanent. The event that caused such a traumatic effect on the brain is not remembered in its entirety. Traumatic Amnesia: This comes about when one has been through a car accident, or experienced a hard blow to the head. Memory can come back depending on how severe the brain damage is. In some cases, people can slip into comas and lose their consciousness abruptly. Blackout Phenomenon: This takes place when one has drunk more than the body can handle. There is no recollection whatsoever of the previous day's events, where he / she has no idea what took place in previous events before they went on the binge. Wernike-Korsakoff's Psychosis: This kind of amnesia is also linked to malnutrition, where the main reason is drinking on a regular basis in heavy doses. This condition gets worse as time lapses, where one ultimately goes numb in his / her toes and fingers, with a lack of coordination as a result of neurological problems. Anterograde Amnesia Causes These can take form as a result of many underlying factors, or severe ones, which subject the person to memory loss in varying degrees - either mild or severe in nature. The damage is seen to affect either or more parts of the brain like the basal forebrain, hippocampus, abd diencephalon. Tumor formation in the brain. Result of strokes. Certain drugs can have powerful amnesiac effects on the brain, like midazolam, lorazepam, nimetazepam, flunitrazepam, and triazolam to name a few. These drugs collectively are known as benzodiazepine drugs. Lack of oxygen supply to the brain. Some people who suffer from celiac disease, experience amnesia-like symptoms. The medication 'ambien', can bring about memory loss in some patients. Inflammation in the brain (encephalitis). Electroshock therapy Regular alcohol abuse, leading to thiamine deficiency. Bleeding that takes place within the skull and brain (subarachnoid hemorrhage). Alzheimer's disease Head injuries caused by traumatic accident. Dementia Seizure disorders

Anterograde Amnesia Symptoms The memory loss symptoms that take place can occur suddenly and without warning among those who experience the onset of amnesia, or can occur when one regains consciousness after an accident. Loss of memory is partial. Memories aren't remembered on specific dates. Not easy remembering faces of close family / friends. Feeling confused and out of sorts.

Difficulty retaining new information. Places that one has frequented to, are not familiar anymore. Memory loss of the past is absolute. Movement is haphazard, sometimes bringing on tremors.

Treatment for Anterograde Amnesia We now look into the options available for those who suffer from this condition, with memory loss treatment methods. Using Reminders People who've suffered from anterograde amnesia, will have recalled how to use a phone, and how the different applications function. He / she can immediately make a record of events that they need to remember in the future, and keep reminders that can alarm one of stored data on the event date. Even tasks that need to be recorded and remembered, can be fed to these devices to help with chores and important work. Even medications that one needs to take can be kept on alert using these devices as a helping source. Patients can make use of calendars, post-its and event book logs to keep track of social gatherings, meetings, and important dates. Using Family and Friends for Help Sit down with family and friends and explain how you will need assistance in remembering certain things, should you forget. They can keep reminders or save you the trouble of referring to your notes, by reminding you on the same day about what you need to get done or do, while you jot it down somewhere before you forget. Hiring an assistant or secretary would be ideal, since they can keep track of everything you need to do without you worrying about events / deadlines / dates. Medication There are no medications that deal with severe cases of anterograde, but a diet that is rich with brain food, like almonds, sage, cumin, apples and so on, can help boost one's memory. Cutting out alcohol consumption completely would help patients drastically. Researchers are still finding ways on how to work with the brain when it comes to amnesiacs. Therapy Amnesiacs can seek help from occupational therapists, who can aid you in retaining new information by connecting it to the old, in order to remember and associate it with current happenings. Memory training, which is a form of memory improvement, is a great way to help patients learn how to train their minds to remember information that is currently being received. Anterograde amnesia is not something that is easy to live with every single day, but with help and support from family and friends, it can easy to deal with in the long run. Patients should make use of the treatment methods mentioned, and should they find medication that can be of any help, then it would serve them well. Read more at Buzzle: http://www.buzzle.com/articles/anterograde-amnesia.html

Midazolam

(Versed)
View Studies

2. 3. 4. 5.

Diazepam (Dialar)
View Studies

Aspirin (Solprin)
View Studies

Flumazenil (Romazicon)
View Studies

Atropine (Isopto Atropin

ndividuals with Retrograde amnesia (RA) are unable to recount incidents or experiences, preceding a specific event in time. Get detailed information about this memory disorder, including its causes, symptoms, diagnosis, and treatment approaches.

Retrograde amnesia Definition

This disorder exhibits a marked impairment of autobiographical memory a memory system consisting of episodes recollected from the life of an individual based on personal experiences and descriptive knowledge. The ailment is completely in contrast to anterograde amnesia, which refers to a deficit in consolidating new information subsequent to a traumatic event.

Retrograde amnesia Types

Severe cases of RA, causes individuals to undergo permanent memory loss and forget their own identity. However, such an extreme form of amnesia is rarely seen and most patients suffer from any one of the following:

Temporally graded retrograde amnesia

Systemic consolidation, which describes the processes involved in the retrieval of memory, becomes impaired for a temporary period of time. Traces of anterograde amnesia could be found in this type.

Pure retrograde amnesia

The type is marked by the absence of anterograde amnesia.

Focal retrograde amnesia

Physical abnormalities are usually not observed in this form of RA. This condition is more of a psychological type of memory loss with few traits of anterograde amnesia.

Isolated retrograde amnesia

This is an intense form of RA and affected patients normally have extreme difficulty recalling past information.

Retrograde amnesia Symptoms

Although patients are not able to remember specific events or situations of the past, most of them retain long-term declarative memory- the memory of meanings, understandings and other factual information. However, individuals

who inflict serious injuries on the brain can exhibit problems like: Improper organization and categorization of verbal material Incorrect way of language formation Long-term memory loss Difficulty recollecting non-verbal information Unplanned travel or wandering from home, or workplace

Retrograde amnesia Causes

RA is a complex disorder and clinical psychoanalysts have not been able to ascertain the cause of the amnesiatic condition. As aforementioned, the loss of episodic and declarative memory could be attributed to damage to certain components of the brain such as:

Hippocampus

It is the major portion of the brain responsible for storing and encoding both short-term and long-term information.

Diencephalon
This is the posterior section of the forebrain that relays sensory information between the cerebral hemispheres and controls functions of the peripheral nervous system.

Temporal lobes
These form a part of the cerebral cortex and are mainly involved in speech, language, memory, hearing, and high level visual processing. The potential factors that could probably affect the vital areas of the brain include:

Traumatic injuries
Structural damage to the brain is predominantly caused by a hard blow to the head, or even due to a congenital brain anomaly. The brain may also get traumatically afflicted due to diffuse axonal injury- tearing of its nerve fibers and subsequent formation of extensive lesions. The severity of the damage is highly dependent on the impact of external forces and location of injury. Repetitive head injuries may also prove lethal to individuals who are into regular contact sports.

Psychologically disturbing events

As discussed earlier, focal retrograde amnesia does not have a neurological basis and is generally an outcome of a traumatic incident. In fact, recent studies have proved that regular episodes of mental stress and emotional fear can trigger the onset of RA.

Korsakoff syndrome
Chronic alcohol abuse as well as severe malnutrition can cause depletion of thiamine in the brain. The water-soluble vitamin is needed daily to facilitate the orderly functioning of the brain. Replacement of nutritional food with hard alcohol can gradually erode the brain and lead to amnesia.

Infectious conditions
Bacteria and viruses are the most common offenders of infecting the brain, spinal cord, and its surrounding structures. The infectious agents invade various regions of the brain and cause inflammation. A wide variety of

disorders can occur depending on the location of infection. Some of the common ones include: Meningitis Myelitis Encephalitis Abscess

Surgery
Sometimes, a surgery of the brain can pose huge risks and may even be responsible for inactivating few essential parts of the organ. In an attempt to cure an existing brain disorder, surgeons often remove the hippocampus and temporal lobes that leads to loss of both episodic and declarative memory.

Psychiatric treatment
Psychological disorders normally warrant therapeutic methods that would aid in the treatment. However, the techniques have adverse effects on the brain and may clinically induce RA in the patients. Electroconvulsive therapy

(ECT) is one such procedure, in which an electric current is passed through the brain to produce controlled convulsions. Individuals with significant depression and who are not responding to antidepressants undergo ECT. Despite the benefits, short-term memory loss is the most common side effect of the method.

Retrograde amnesia Diagnosis

The assessment of episodic and declarative memory is usually done by testing the factual knowledge of the patients. Autobiographical memory interview is a useful research tool for investigating RA. The test evaluates a patients recall of specific incidents that has occurred earlier. It assays the three broad time bands, which are the childhood, early adult life and recent facts. In this way, the test allows measurement of the pattern of autobiographical memory deficit as well as detection of any signs of anterograde amnesia. Neuroimaging studies, comprising of computed tomography and magnetic resonance imaging can produce high quality images of the brain structures for quick viewing of any traumatic injury. Electroencephalography enables health specialists to record the electrical activity along the scalp and infer the test. Abrupt decrease in brain activity is usually associated with large slow EEG waves, a possible indicator of a structural damage.

Retrograde amnesia Treatment

Treatment for RA will be individualized for each patient depending upon the specific underlying cause and the individuals situation. Diuretics, anti-seizure drugs and surgical resection are the options available for minimizing additional damage to the brain tissues in patients with traumatic injuries. In emergency cases, adequate oxygen and blood supply is a must to restore breathing and circulation. Antibiotics, steroids and anticonvulsants can control the spread of bacterial infection in the brain. Special antiviral drugs are used to treat brain infections caused by herpes strains. Alcoholic patients must be counseled and educated about the negative effects of heavy drinking. Replacement or supplementation of thiamine by intravenous or intramuscular injection, together with proper nutrition and hydration can hasten recovery. Psychotherapeutic techniques such as hypnotherapy conducted by experienced practitioners can be beneficial for individuals who are suffering from RA due to an emotionally traumatic event. Spontaneous recovery utilizes a method called classical conditioning, a form of learning in which a biologically significant stimulus elicits a response from the patient. The appearance and sudden extinction of the response may accelerate the activity of the brain and helps restore the autobiographical information. Retrograde amnesia still requires a standardized test as many criminals claim to have the disorder in order to escape from a harsh punishment. If you or any of your family members is experiencing difficulty in recalling incidents prior to a sudden or progressive onset of brain damage, seek immediate aid from a mental health counselor. Regular counseling sessions with your doctor can help you bring back memories of the past and regain a normal life.

Glossary
Anterograde Amnesia

Anterograde amnesia is a selective memory deficit, resulting from brain injury, in which the individual is severely impaired in learning new information. Memories for events that occurred before the injury may be largely spared, but events that occurred since the injury may be lost. In practice, this means that an individual with amnesia may have good memory for childhood and for the years before the injury, but may remember little or nothing from the years since. Short-term memory is generally spared, which means that the individual may be able to carry on a conversation; but as soon as he is distracted, the memory of the conversation fades. It is now becoming apparent that while anterograde amnesia devastates memory for facts or events, it may spare memory for skills or habits. Thus, an individual with amnesia can be taught a new skill, such as how to play a game or how to write backwards. The next day, the amnesic individual will claim to have no memory of the prior session, but when asked to try executing the skill, can often perform quite well - indicating that some memories have been formed. It is an important area of current research to document exactly which kinds of memory can be formed in amnesia, and how this may be used to help rehabilitate amnesic individuals. Anterograde amnesia can occur following damage to at least three distinct brain areas. The first, and most well-studied, is the hippocampus and associated areas in the medial temporal lobes of the brain. The hippocampus seems to act as a "gateway" through which new fact information must pass before being permanently stored in memory. If it is damaged, no new information can enter memory although older information which has already passed through the gateway may be safe. Damage to the hippocampus (and medial temporal lobes) can occur following stroke or aneurysm to one of the arteries which supplies blood to these areas, as well as following epilepsy, encephalitis, hypoxia, carbon monoxide poisoning, near-drowning or near-suffocation, and the earliest stages ofAlzheimer's disease. Some damage to the hippocampus also occurs in the course of normal aging. Anterograde amnesia can also occur following damage to the basal forebrain, a group of structures which produce acetylcholine, a chemical which helps cells in the brain store new information during learning. The basal forebrain can be damaged by aneurysm of the anterior communicating artery, which supplies blood to the basal forebrain. Finally, anterograde amnesia can sometimes occur following damage to the diencephalon - a set of structures deep in the brain including the medial thalamic nuclei. Currently, there is no good understanding of why damage to these brain areas should sometimes result in a selective memory deficit such as amnesia. Korsakoff's disease is a syndrome which can damage the diencephalon and cause anterograde amnesia.

ANTEROGRADE AMNESIA
??? Did You Know ???
The most famous case of anterograde amnesia is that of the patient known as "H.M.", whose hippocampus was removed in brain surgery. He started as a patient ofScoville and Milner in 1957 and was still being studied up until his death in 2008. Another remarkable case is that of "E.P.", a severely amnesic patient who was however able to learn simple 3-word sentences.

Anterograde amnesia is the loss of the ability to create new memories, leading to a partial or complete inability to recall the recent past, even though long-term memories from before the event which caused the amnesia remain intact. Sufferers may therefore repeat comments or questions several times, for example, or fail to recognize people they met just minutes before.

The British musician Clive Wearing suffers from an acute and long-lasting case of both anterograde amnesia andretrograde amnesia.

Anterograde amnesia may be drug-induced (several benzodiazepines are known to have powerful amnesic effects, and alcohol intoxication also has a similar effect) or it follows a traumatic brain injury or surgery in which there is damage to the hippocampus or medial temporal lobe of thebrain, or an acute event such as a concussion, a heart attack, oxygen deprivation or an epileptic attack. Less commonly, it can also be caused by shock or an emotional disorder. Research shows that anterograde amnesia results from a failure of memory encoding and storage. New information is processed normally, but almost immediately forgotten, never making it into the regions of the brain where long-term memories are stored. More specifically, in normal use,neurons in the mammillary bodies of the hypothalamus make connections with the thalamus, which in turn makes connections with the cortex of the brain, where long-term memories are stored. Anterograde amnesia can therefore result from damage to the hypothalamus andthalamus and the surrounding cortical structures, so that encoded memories are never stored since connections between hippocampus and cortex are disrupted. Usually, sufferers from anterograde amnesia lose declarative memory (the recollection of facts), but they retain non-declarative, or procedural, memory (the learning of skills and habits). For instance, they may be able to remember or learn how to do things, such as talking on the phone or riding a bicycle, but they may not remember what they had eaten for lunch earlier that day. This is because procedural memory does not rely on the hippocampus and medial temporal lobe memory system in the same way as declarative memory. There have, however, been cases where anterograde amnesia patients lose only the episodic part of their declarative memory (that part which relates to autobiographical information with a temporal and/or spatial context), and not the semantic part (factual information, such as language, history, geography, etc, with autobiographical association). When there is damage to just one side of the medial temporal lobe, the neuroplasticity of the brain (its ability to re-map its neural connections when necessary) can often allow the opportunity for normal, or near-normal, functioning for memories with time.

RETROGRADE AMNESIA
Retrograde amnesia is a form of amnesia where someone is unable to recall events that occurred before the development of the amnesia, even though they may be able to encode and memorize new things that occur after the onset. Retrograde amnesia usually follows damage to areas of the brain other than the hippocampus(the part of the brain involved in encoding new memories), because already exisiting long-term memories are stored in the neurons and synapses of various different brain regions. For example, damage to Brocas or Wernickes areas of the brain, which are specifically linked to speech production and language information, would probably cause language-related memory loss. It usually results from damage to the brain regions most closely associated with declarative (and particularly episodic) memory, such as the temporal lobe and prefrontal cortex. The damage may result from a cranial trauma (a blow to the head), a cerebrovascular accident or stroke (a burst artery in the brain), a tumour (if it presses against part of the brain), hypoxia (lack of oxygen in the brain), certain kinds of encephalitis, chronic alcoholism, etc. Typically, episodic memory is more severely affected than semantic memory, so that the patient may remember words and general knowledge (such as who their countrys leader is, how everyday objects work, colours, etc) but not specific events in their lives. Procedural memories (memory of skills, habits and how to perform everyday fucntions) are typically not affected at all.

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A man, in his late twenties and with a Yorkshire English accent but no other identification, awoke with severe retrograde amnesia in a Toronto hospital in 1999. He has been known ever since as "Philip Staufen"- actually the name of a medieval German king, but it was the first name the man came up with when he woke up. The famous anterograde amnesia case known as "H.M."also suffered moderate retrograde amnesia, and could not remember most events in the year or two before surgery, nor some events up to 11 years before. The British musician Clive Wearing suffers from an acute and long-lasting case of bothanterograde amnesia and retrograde amnesia.

Retrograde amnesia is often temporally graded, meaning that remote memories are more easily accessible than events occurring just prior to the trauma (sometimes known as Ribot's Law after the 19th Century psychologist Thodule-Armand Ribot), and the events nearest in time to the event that caused the memory loss may never be recovered. This is because the neural pathways of newer memories are not as strong as older ones that have been strengthened by years ofretrieval and re-consolidation. While there is no actual cure for retrograde amnesia, jogging the victims memory by exposing them to significant articles from their past will often speed the rate ofrecall.