Anterograde amnesia or anterograde amnesia is the loss of the ability to create memories after the event that caused the amnesia, resulting in a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact, but he is unable to create new long-term memories. This is the opposite of what happens to a patient with retrograde amnesia; memories that arose before the event are lost while new memories can still be created. Both can occur together in the same patient. Anterograde amnesia remains a largely mysterious disease; because the exact mechanism of memory storage is not yet well understood, although it is known that the areas involved in memory storage are specific locations in the temporal lobe, especially in the hippocampus near the subcortical areas of the brain. People with anterograde amnesia syndrome suffer from varying degrees of forgetfulness. In some advanced and severe cases, the patient may experience retrograde amnesia along with anterograde amnesia; This is sometimes called global amnesia. In drug-induced amnesia, the condition is usually brief and the patient recovers. In other cases that have been studied extensively since the early 1970s, patients are often left with permanent damage. Although some recovery is possible, depending on the nature of the pathophysiology. There is usually a residual capacity for learning, although it may be very rudimentary. In total anterograde amnesia, patients can recall memories of events before the injury, but cannot recall their current day-to-day memories or new facts that have come to them after the injury. In most cases of anterograde amnesia, patients lose declarative memory, or the memory of facts, but they do remember routine memories that we usually do every day without being aware of it, such as how to ride a bike, tie a shoelace, answer the phone, etc. These are procedural memory memories, but they may not be able to remember, for example, what they ate for lunch today. In extensive studies of a patient with anterograde amnesia, Henry Molaison, it was shown that although his amnesia prevented him from learning new declarative memories, his procedural memory was still capable of On the job, even though his ability had been greatly reduced. He was given a maze to solve, as was given to a number of other patients with progressive amnesia, and they were given the same maze to solve every day, and although they could not remember the maze that was given to them the day before their memory loss; However, their unconscious memory was working and their time to solve the maze gradually decreased. From these results, the scientists hypothesized that despite the absence of declarative memory, procedural memory was still able to work. This supports the idea that declarative and procedural memory are located in different areas of the brain. In addition, patients suffer from a deficit in the ability to remember the temporal context in which objects were presented. Some authors claim that the deficit in temporal contextual memory is more important than the deficit in semantic learning ability. This disorder is usually acquired in one of four ways: One cause is benzodiazepine drugs such as midazolam, flunitrazepam, lorazepam, temazepam, nitrazepam, and triazolam; clonazepam, alprazolam, diazepam, and nimatazepam. All of which are known to have a strong effect on memory loss. This has also been reported in non-benzodiazepine tranquilizers or "Z drugs" that act on the same group of receptors, such as Zolpidem, eszopiclone, zopiclone. The second cause is a traumatic brain injury, which usually damages the hippocampus or surrounding cortex. It can also be caused by a traumatic event or emotional disturbance. A rare cause of progressive amnesia is encephalitis. There are types of encephalitis, such as herpes simplex encephalitis, which if left untreated can lead to neurological damage. The cause of herpes simplex encephalitis is unknown; The virus shows a predilection for certain parts of the brain. Initially, it is found in the limbic cortex and then may spread to the frontal and temporal lobes. Damage to certain areas leads to a reduction or elimination of the ability to encode new explicit memories, resulting in progressive amnesia. Patients with anterograde amnesia have impairment or damage to episodic or semantic memory or both types of explicit memory, due to events that occurred after the trauma that caused the amnesia. This suggests that memory consolidation for different types of memory occurs in different areas of the brain. However, current knowledge of human memory is still insufficient to map the brain and discover which parts or lobes are responsible for semantic or episodic knowledge within human memory. Anterograde amnesia may be caused by a disease that affects the memory centers in the medial temporal lobe and that disease removes some of the memory circuits or centers. These cases include some patients with epileptic seizures of medial temporal lobe origin, which may remove a center in one or both halves of the head, in addition to patients with tumors who have undergone surgery, as they often may Significant damage to these centers occurs due to the destruction of some parts of the system such as the hippocampus and the surrounding cortex, which leads to anterograde amnesia. Therefore, people who suffer from strokes may have a high chance of developing cognitive deficits that lead to anterograde amnesia, as strokes may involve the temporal lobe and the temporal cortex, and since the temporal cortex is where the hippocampus is located, their chance of injury is high. Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon known as alcohol-induced blackout or loss of consciousness. Studies indicate that rapid increases in blood alcohol concentration over a short period of time severely impair or in some cases prevent the brain's ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and retrieval at a later time. These rapid increases result from drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as diluting alcohol with food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of alcohol consumption, not just the total amount of alcohol consumed in an episode. Drinking. In a scientific experiment, it was found that people may not suffer from memory loss when drinking slowly, even though they were very drunk by the end of the experiment. But when alcohol is consumed at a rapid rate, the point at which the process of creating long-term memories in healthy people is supposed to begin is disrupted. It is difficult to determine the exact time at which this blackout period is reached, because most people fall asleep before it is finished. Upon returning to a sober state, usually after waking up, the ability to create long-term memories is fully restored. Chronic alcoholism often leads to a deficiency of thiamine in the brain, causing Korsakoff syndrome, a neurological disorder that is usually preceded by a severe neurological condition known as Wernicke's encephalopathy. The memory impairment caused by Korsakoff syndrome mostly affects declarative memory, leaving non-declarative memory relatively normal. This distinguishes the anterograde amnesia resulting from Korsakoff syndrome from other conditions such as alcohol-related dementia. Scientific experiments are still ongoing to determine how different types of memory are affected, and how disorders affect them. The pathophysiology of anterograde amnesia syndrome varies depending on the amount of damage and the areas The brain regions most commonly associated with anterograde amnesia are the medial temporal lobe, the forebrain, and the fornix. The exact process that explains how we remember—in detail—remains a mystery. Psychologists and neuroscientists still do not fully agree on whether forgetting is caused by misencoding, hasty forgetting, or a retrieval defect, although a great deal of information so far points to the encoding hypothesis. In addition, neuroscientists also disagree about the length of time involved in memory consolidation and the transformation of new memories into long-term memories. Although most researchers have found that the consolidation process takes several hours, during which the memories move from a fragile state to a more permanent state, others, including Brown, have hypothesized that memory consolidation can take months or even years in a prolonged process of consolidation and reinforcement. Further research into the length of time that memory consolidation takes will shed more light on why anterograde amnesia affects memories acquired after the event that caused the amnesia, but does not affect other memories. The memory system in the anterior lobe contains The medial temporal lobe includes the hippocampus, the perirhinal cortex, the entorhinal cortex, and the parahippocampal cortex. It is known to be important for the storage and processing of declarative memory, allowing for the retrieval of facts. It is also important in communicating with the neocortex to create and maintain long-term memories, although its known functions are independent of long-term memories. On the other hand, non-declarative memory, which allows for the performance of various skills and habits, is not part of the medial temporal lobe memory system. The division of labor between the parts of the memory management system is currently known, although this is still under debate. In a scientific study of monkeys, researchers showed that monkeys with damage to both the hippocampus and adjacent cortical areas had more severe anterograde amnesia than monkeys with damage to the hippocampus alone. However, conflicting data from another preliminary study suggest that the amount of tissue damaged does not necessarily correlate with the severity of amnesia. Furthermore, the results of the studies do not explain the duality found in the medial temporal lobe memory system. The medial temporal lobe between episodic and semantic memory and the relationship between them. An important finding in patients with anterograde amnesia with damage to the medial temporal lobe memory system is the impairment of memory in all sensory modalities - sound, touch, smell, taste and sight. This reflects the fact that the medial temporal lobe memory system is a processor of all sensory modalities, and helps to store this type of thought in memory. In addition, people can often remember how to perform relatively simple tasks, but when the task becomes more difficult, even on the same time scale, the patient tends to forget. This illustrates the difficulty of separating procedural memory tasks from declarative memory; and that some elements of declarative memory may be used in learning procedural tasks. Patients with medial temporal lobe amnesia, who have localized damage to the hippocampus, retain other cognitive abilities, such as the ability to perform intelligent social functions, hold a conversation, make the bed, etc. In addition, patients with anterograde amnesia not associated with retrograde disorders retain memories of the pre-event that caused the disease. For this reason, the medial temporal lobe is not the place to store all memories; Other areas of the brain also store memories. It can be argued that the medial temporal lobe memory system is responsible for learning and remembering new material. In a limited number of cases of patients with anterograde amnesia, they have been observed to suffer from damage to other parts of the brain that led to anterograde amnesia. Easton and Parker noted that damage to either the hippocampus or the surrounding cortex, or both, did not appear to cause severe memory loss. They suggested that damage to the hippocampus and surrounding structures alone did not explain the memory loss they saw in patients, and that increased damage to those areas was not related to the severity of the disease. Furthermore, the available information does not explain the duality that exists in the medial temporal lobe memory system between episodic and semantic memory and the relationship between them. To prove their hypothesis, they used samples from patients with damage to the basal forebrain. They suggested that dysfunction of neurons that originate at the base of the forebrain and travel to the medial temporal lobe are responsible for some of the impairment in anterograde amnesia. Easton and Parker also reported that MRI scans of patients Those with acute anterograde amnesia showed damage extending beyond the cortical areas surrounding the hippocampus, the amygdala, and the surrounding white matter. In another case, the onset of anterograde amnesia was described as the result of cell death in the fornix, a structure that relays information from the hippocampus to limbic and diencephalic structures. The patient in this case did not show any disconnection syndrome, which was unexpected; Because the structures are divided into two hemispheres of the brain, instead, signs of memory loss were present. The final diagnosis of the condition was made by MRI. This particular case of anterograde amnesia is difficult to diagnose as amnesia, and is often misdiagnosed by doctors as a severe psychiatric disorder. When there is damage or impairment to one side of the medial temporal lobe while the other side remains intact, there is a chance of normal or near-normal memory function. Neuroplasticity explains the ability of the cortex to remap itself when necessary. This remodeling process can occur in a case like the one above, and over time, the patient can recover relatively well and become more adept at remembering. A case report describes a patient who had both medial temporal lobes removed. Initially, doctors removed part of the right medial temporal lobe, due to seizures arising from that area, and then the left part was removed due to a tumor developing there. This case is unique; Because it is the only one in which both sides of the medial temporal lobe were removed at different times. The researchers noted that the patient was able to recover some learning ability when she had only one temporal lobe, but they noted a significant deterioration in the condition when both sides of the medial temporal lobe were affected. The ability to reorganize brain functions in epilepsy patients has not been widely investigated, but the results of current perceptions show that it is likely to be done. Various methods are used to treat those suffering from progressive memory loss. Often, methods based on compensatory techniques are relied upon, such as stimulators, written notes, diaries or through intensive training programs in which the individual concerned with the treatment is actively involved, along with his support network of family and friends. From this standpoint, environmental adaptation techniques are used, such as: compensatory learning methods for training, organizational strategies, expressive imagery and representation of ideas, and verbal education. In addition, other techniques are also used in rehabilitation, such as: implicit tasks, speech and memory improvement methods. So far, the use of educational methods and compensatory strategies for memory disorders has been proven to be effective in Individuals with mild brain injuries. For individuals with moderate or severe injuries, relatively useful techniques are those that focus on external aids, such as the use of reminders to facilitate the acquisition of certain knowledge or the acquisition of a skill. Reality orientation techniques are also considered, which are techniques that aim to enhance the patient's awareness of the surrounding environment, using stimulation and repetition of basic perceptual information. These techniques are regularly applied in patients suffering primarily from dementia and head injury patients. As explained above, patients with anterograde amnesia suffer from significant forgetfulness. Declarative memory can be divided into episodic and semantic memory. Episodic memory is the recollection of information in a person's autobiography with a temporal and spatial context, while semantic memory involves the recall of information and facts without such a connection, such as facts in linguistics, history, geography, etc. For example, semantic memory contains information about what cats are, while episodic memory may contain a specific memory about playing with a particular cat. In a case study of a girl with anterograde amnesia since childhood, it was found that the patient retained the memory Semantic while she suffered from severe impairment of episodic memory. One patient, known as “Jane,” was in a motorcycle accident, which caused significant damage to important parts of the frontal and temporal lobes, including the left hippocampus. As a result, he cannot recall specific episodic memories from his life, such as a train derailment near his home. 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 schoolmates. In stark contrast to previous cases, a woman who lost the frontal part of her temporal lobe due to encephalitis lost her semantic memory; she lost her memory for many simple words, historical events, and other intuitive information that are classified as memories stored in semantic memory. However, her episodic memory was intact; She could recall events from her personal life in great detail, such as her wedding and her father’s death. Vicari said it remains unclear whether the neural circuits involved in semantic and episodic memory overlap partially or completely. The two systems are assumed to be independent, and episodic memory has been postulated to be much more severely impaired in anterograde amnesia than semantic memory. However, it is not always possible to clearly distinguish episodic from semantic memory. For this reason, the topic remains controversial. The right hippocampus is essential for retrieving familiar spatial memories, while the left hippocampus is essential for retrieving familiar verbal memories. Some researchers suggest that the hippocampus is important for memory retrieval, while adjacent cortical areas may be important in supporting the creation of familiar memories. Memory decisions regarding familiar memories are made on the basis of matching existing memories to those that existed at some point prior to the injury. According to Gilbeau et al., patients with localized hippocampal damage can score well on a test of familiar memories. Bourret et al. studied a case of a patient whose Damage to the fornix of the brain rendered the hippocampus useless, but the cortical areas adjacent to it were spared—a fairly rare injury. When the patient was given a test with something familiar to him in his life, the patient was able to score relatively well. Overall, the patient had a severe impairment in episodic memory, but he had some ability to learn some semantic knowledge. Other studies suggest that animals with similar injuries can recognize familiar objects, but when presented in an unexpected context, they do not score well on recognition tests. People with anterograde amnesia have trouble remembering new information or recalling new autobiographical events, but the information is less consistent and definitive about the latter. Medveds and Hirst noted the presence of islands of memory with detailed memories described by some patients. The island memories were a mixture of semantic and episodic memories. The researchers recorded long narratives given by the patients with a fair amount of detail that resembled the memories the patients had had before the trauma. The appearance of islands of memory may be related to the functioning of the cortical areas adjacent to the hippocampus and the cerebral cortex. Modern. In addition, researchers suspect that the amygdala played a role in constructing these narratives.