Retrograde amnesia
In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred.
[1] RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset.
[4] 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).
[4] This type of RA is commonly triggered in individuals with Korsakoff syndrome due to a combination of long-term alcohol use and Wernicke encephalopathy.
[12] 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.
[13] 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.
[17] Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of RA.
Normally, there is a very gradual recovery, however, a dense period of amnesia immediately preceding the trauma usually persists.
[25] Korsakoff's syndrome patients develop retrograde amnesia due to a thiamine deficiency (lack of vitamin B1).
[25] These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for typical development and maintenance.
[26] 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.
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.
Unfortunately, due to a lack of overall known neurological knowledge, Molaison's surgeons removed his bilateral medial temporal lobe, causing profound AA and RA.
[28] The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system.
[5] As a result, some clinicians diagnose RA by testing patients about factual knowledge, such as current public events.
[5] 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.
[5] For each period of that individual's life, researchers ask questions that require the patient to use either their autobiographical or semantic memory.
[13] For example, older memories are consolidated over time and in various structures of the brain, including Wernicke's area and the neocortex, making retrieval through alternate pathways possible.
[46] A few case examples are: Although it may seem that people living with brain damage have great difficulty continuing the usual day-to-day aspects, they still can accomplish many feats.
[45] In addition, patient HC graduated high school and continued into post-secondary studies,[46] an obvious accomplishment despite her condition.
