<unk>  commonly results from damage to regions of the brain that are associated with episodic and declarative memory, including autobiographical information. In extreme cases, individuals may completely forget who they are. Generally, this is a more severe type of<unk>  known as global, or generalized<unk> . However, memory loss can also be selective or categorical, manifested by a person's inability to remember events related to a specific incident or topic. Patients also differ in durations of<unk>  (how long they can't recall information) and durations of what is forgotten (past time frame for which information is unavailable). Temporally graded<unk>  In temporally graded<unk> , victims eventually recover most memories following the onset of<unk> . This suggests that the hippocampal formation/ consolidation, the process of coding new information, is only used in systematic consolidation for temporary storage, and short periods of time. Systemic consolidation then moves the information and long-term consolidation takes place in other brain structures. The fact that damage to the hippocampal formation can eventually overcome<unk>  suggests that other brain structures are able to take over the jobs of the malfunctioning regions.<unk>  can also progress and further deteriorate memory recollection, as in the case of Korsakoff syndrome and Alzheimer's disease, due to the ongoing nature of the damage caused by the illnesses. The degree to which different patients recover from<unk>  differs in time (some take a few days while others a few decades) and content (some will only remember certain specific instances while others more). Focal, isolated, and pure<unk>  Focal isolated, and pure<unk>  are terms used to describe a pure form of<unk> , with an absence of anterograde<unk>  (AA). In addition, Focal<unk>  in particular, has also been used to describe a<unk>  situation in which there is a lack of observable physical deficit as well. This could be described as a psychogenic form of<unk>  with mild anterograde and<unk>  loss. A case study of DH revealed that the patient was unable to provide personal or public information, however there was no parahippocampal or entorhinal damage found. Individuals with focal brain damage have minimal<unk> . Isolated<unk>  is associated with a visible thalamic lesion. Consistent with other forms of<unk> , the isolated form is marked by the inability to recall past information. Pure<unk>  (PRA) refers to the behavioral syndrome that is characterized by the inability to retrieve remote information in the face of a normal ability to learn new information, with no other ecological or psychometric evidence of cognitive impairment. It should not be confused with brief periods of peritraumatic<unk>  that are common in mild concussive head traumas. The findings of pure<unk>  have helped form the dissociation between mechanisms for<unk>  and AA. Several studies have found numerous causes for PRA like vascular diseases, head traumas<unk> nging from mild to severe, encephalitis, as well as purely psychological conditions and totally unidentifiable etiologies. Most people who suffer from PRA can function normally and learn new information A pure form of<unk>  is<unk> re as most cases of<unk>  co-occur with AA. A famous example is that of patient ML. The patient's MRI revealed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a band of fibers previously thought to mediate retrieval of specific events from one's personal past. During consolidation, the hippocampus acts as an intermediate tool that quickly stores new information until it is transferred to the neocortex for the long-term. The temporal lobe, which holds the hippocampus, entorhinal, perirhinal and parahippocampal cortices, has a reciprocal connection with the neocortex. The temporal lobe is temporarily needed when consolidating new information; as the learning becomes stronger, the neocortex becomes more independent of the temporal lobe. Studies on specific cases demonstrate how particular impaired areas of the hippocampus are associated with the severity of<unk> . Damage can be limited to the CA1 field of the hippocampus, causing very limited<unk>  for about one to two years. More extensive damage limited to the hippocampus causes temporally graded<unk>  for 15 to 25 years. Another study suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive<unk> , covering 40 to 50 years. These findings suggest that density of<unk>  becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures. The common studied causes of<unk>  do not always lead to the onset of<unk> . It may even be that in some cases both conscious feigning and unconscious processes are at play. Traumatic brain injury (TBI) or post-traumatic<unk>  Traumatic brain injury (TBI), also known as post-traumatic<unk> , occurs from an external force that causes structural damage to the brain, such as a sharp blow to the head, a diffuse axonal injury, or childhood brain damage (e.g., shaken baby syndrome). In cases of sudden<unk> pid acceleration, the brain continues moving around in the skull, harming brain tissue as it hits internal protrusions. TBI varies according to impact of external forces, location of structural damage, and severity of damage<unk> nging from mild to severe.<unk>  can be one of the many consequences of brain injury but it is important to note that it is not always the outcome of TBI. An example of a subgroup of people who are often exposed to TBI are individuals who are involved in high-contact sports. Research on football players takes a closer look at some of the implications to their high-contact activities. Enduring consistent head injuries can have an effect on the neural consolidation of memory. Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of<unk> . In this specific case there was an onset of isolated<unk>  following a severe head injury. The brain damage did not affect the person's ability to form new memories. Therefore, the idea that specific sections of<unk>  memory are independent of anterograde is supported. Normally, there is a very gradual recovery, however, a dense period of<unk>  immediately preceding the trauma usually persists. Traumatic events<unk>  can occur without any anatomical damage to the brain, lacking an observable neurobiological basis. Primarily referred to as psychogenic<unk>  or psychogenic fugue, it often occurs due to a traumatic situation that individuals wish to consciously or unconsciously avoid through intrapsychic conflicts or unconscious repressions. The onset of psychogenic<unk>  can be either global (i.e., individual forgets all history) or situation specific (i.e., individual is unable to retrieve memories of specific situations). Patients experiencing psychogenic<unk>  have impaired episodic memory, instances of wandering and traveling, and acceptance of a new identity as a result of inaccessible memories pertaining to their previous identity. Recent research has begun to investigate the effects of stress and fear-inducing situations with the onset of<unk> . Long-term potentiation (LTP) is the process by which there is a signal transmission between neurons after the activation of a neuron, which has been known to play a strong role in the hippocampus in learning and memory. Common changes in the hippocampus have been found to be related to stress and induced LTP. The commonalities support the idea that variations of stress can play a role in producing new memories as well as the onset of<unk>  for other memories. The amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking<unk> . Studies of specific cases, such as 'AMN', support evidence of traumatic experiences as a plausible cause of<unk> . AMN escaped a small fire in his house, did not inhale any smoke, and had no brain damage. Nevertheless, he was unable to recall autobiographical knowledge the next day. This case shows that<unk>  can occur in the absence of structural brain damage. After a traumatic head injury, emotional disturbances can occur at three different levels: neurological, reactionary, and long-term disturbances. Neurological disturbances can change emotional and motivational responses. Reactionary disturbances effect emotional and motivational responses as well, but reflect the failure to cope with environmental demands. Someone with this might withdraw from the environment that they are placed in because they no longer know how to handle the cognitive resources. Nutritional deficiency<unk>  has been found among alcohol-dependent patients who suffer from Korsakoff's syndrome. Korsakoff's syndrome patients suffer from<unk>  due to a thiamine deficiency (lack of vitamin B1). Also, chronic alcohol use disorders are associated with a decrease in the volume of the left and right hippocampus. These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for healthy development and maintenance. Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately suffer from<unk> . However, some of the drawbacks of using Korsakoff patients to study<unk>  is the progressive nature of the illness and the unknown time of onset. Infections Infections that pass the blood–brain barrier can cause brain damage (encephalitis), sometimes resulting in the onset of<unk> . In the
Retrograde amnesia
Anterograde amnesia
Psychogenic amnesia
Transient loss of consciousness
Emergence delirium
Semantic amnesia
Confusion
Syndrome