retrograde amnesia retrograde amnesia in neurology, retrograde amnesia (ra) is the inability to access memories or information from before an injury or disease occurred. ra differs from a similar condition called anterograde amnesia (aa), which is the inability to form new memories following injury or disease onset. although an individual can have both ra and aa at the same time, ra can also occur on its own; this 'pure' form of ra can be further divided into three types: focal, isolated, and pure ra. ra negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because ra leaves procedural memory intact. depending on its severity, ra can result in either temporally graded or more permanent memory loss. however, memory loss usually follows ribot's law, which states that individuals are more likely to lose recent memories than older memories. diagnosing ra generally requires using an autobiographical memory interview (ami) and observing brain structure through magnetic resonance imaging (mri), a computed tomography scan (ct), or electroencephalography (eeg). retrograde amnesiaspecialtyneurology types types of ra can be divided into two main categories: temporally graded ra and pure forms of ra. individuals with pure forms of ra like focal, isolated, and pure ra do not have anterograde amnesia (aa). temporally graded ra memory loss in patients with temporally graded ra strongly follows ribot's law, meaning that one will experience more memory loss for events closer to the injury or disease onset. this type of ra is commonly triggered in individuals with korsakoff syndrome due to a combination of long-term alcohol use and wernicke encephalopathy. debate has risen about why this temporal gradient forms in the first place. initial theories proposed that the hippocampus and medial temporal lobe are not nearly as important for long-term memories compared to short-term memories. as memory processing occurs in the brain over time, neocortical regions can directly communicate with each other, so they do not rely as heavily on the hippocampus for long-term memory storage. therefore, if an individual experiences ra that damages the hippocampus, they will lose more short-term memories according to this theory. however, this theory has been challenged by the multiple-trace theory, which claims that the brain develops a hippocampal trace each time a memory is retrieved. since more hippocampal traces are present for older memories, it is easier for older memories to remain intact when ra occurs. focal, isolated, and pure ra an absence of anterograde amnesia (aa) characterizes pure forms of ra, which fall into three main categories: focal, isolated, and pure ra. slight differences in the use of these terms to describe a pure form of ra are summarized below: pure forms of ra focal ra isolated ra pure ra focal ra generally results from neurological problems like epilepsy and is characterized by memory loss prior to – but not after – injury or disease onset. when an individual experiences focal ra, a combination of their episodic and semantic memories may be affected. take a case study of a middle-aged female, for instance, who experienced focal ra after significant head trauma. although she could be re-taught information from her past, these memories were not episodic, but rather, semantic. with focal ra, the details of a patient's life prior to amnesia onset can be reintroduced, but they are unable to recall how they perceived the experience. isolated ra is usually associated with a visible thalamic lesion. similar to other forms of ra, the inability to recall past information characterizes the isolated form. take the case of a middle-aged man identified as jg, whose thalamic lesion expanded as he grew older. this lesion growth induced his isolated ra, resulting in both autobiographical memory loss and the inability to recognize information from popular culture. pure ra (pra) is caused by a range of factors such as vascular diseases, encephalitis, and head injuries. it is often confused with peritraumatic amnesia that commonly follows mild concussions, but the severity and duration of pra differs from that of peritraumatic amnesia. current discussion in neuropsychiatry literature centers on whether pra is possibly psychogenic in nature. causes ra 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 amnesia known as global, or generalized amnesia. 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 ra (how long they can't recall information) and durations of what is forgotten (past time frame for which information is unavailable). 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 ra. damage can be limited to the ca1 field of the hippocampus, causing very limited ra for about one to two years. more extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years. another study suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive ra, covering 40 to 50 years. these findings suggest that density of ra becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures. traumatic brain injury (tbi) traumatic brain injury (tbi), also known as post-traumatic amnesia, 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 rapid 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 ranging from mild to severe. retrograde amnesia 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 ra. in this specific case there was an onset of isolated ra 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 retrograde memory are independent of anterograde is supported. normally, there is a very gradual recovery, however, a dense period of amnesia immediately preceding the trauma usually persists. traumatic events ra can occur without any anatomical damage to the brain, lacking an observable neurobiological basis. primarily referred to as psychogenic amnesia 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 amnesia 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 amnesia 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 ra. 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 ra for other memories. the amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking ra. studies of specific cases, such as 'amn', support evidence of traumatic experiences as a plausible cause of ra. 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 ra 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 ra has been found among alcohol-dependent patients who have korsakoff's syndrome. korsakoff's syndrome patients develop retrograde amnesia 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 typical development and maintenance. therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately develop ra. however, some of the drawbacks of using korsakoff patients to study ra 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 ra. in the case of patient 'ss', the infection led to focal or isolated retrograde amnesia where there was an absence of or limited aa. brain scans show abnormalities in the bilateral medial temporal lobes, including two thirds of the hippocampal formation and the posterior part of the amygdala. surgery henry molaison had epilepsy that progressed and worsened by his late twenties. the severity of his condition caused him to undergo surgery in an effort to prevent his seizures. unfortunately, due to a lack of overall known neurological knowledge, molaison's surgeons removed his bilateral medial temporal lobe, causing profound aa and ra. the removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system. hm was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory. patients who have ra due to surgery are "p.b." and "f.c." who had unilateral removal of the medial areas in the left temporal lobe. controlled induction clinically induced ra has been achieved using different forms of electrical induction. electroconvulsive therapy (ect), used as a depression therapy, can cause impairments in memory. tests show that information from days and weeks before the ect can be permanently lost. the results of this study also show that severity of ra is more extreme in cases of bilateral ect rather than unilateral ect. impairments can also be more intense if ect is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation). electroconvulsive shock (ecs): the research in this field has been advanced by using animals as subjects. this is done to further understand ra. diagnosis since ra affects people's memories to varying degrees, testing is required to fully diagnose ra; these tests, however, are inherently limited if a patient's previous neuropathological medical history is unknown. as a result, some clinicians diagnose ra by testing patients about factual knowledge, such as current public events. this testing is limited, however, because people's knowledge about current events differs. furthermore, these tests must be adjusted to account for the time period that a patient is alive, which affects the amount of detail included in the questions. since some information obtained