Refers to the inability to create new memories due to brain damage, while long-term memories from before the event remain intact.
The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma, surgery, Wernicke-Korsakoff Syndrome, cerebrovascular events, anoxia or other trauma.
The two brain regions related with this condition are medial temporal lobe and medial diencephalon.
Anterograde amnesia can't be treated with pharmacological methods due to neuronal loss.
However, treatment exists in educating patients to define their daily routines and after several steps they begin to benefit from their procedural memory.
Likewise, social and emotional support is critical to improving quality of life for anterograde amnesia sufferers.
Refers to inability to recall memories before onset of amnesia. One may be able to encode new memories after the incident.
Retrograde is usually caused by head trauma or brain damage to parts of the brain besides the hippocampus.
The hippocampus is responsible for encoding new memory.
Episodic memory is more likely to be affected than semantic memory.
The damage is usually caused by head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism.
People suffering from retrograde amnesia are more likely to remember general knowledge rather than specifics. Recent memories are less likely to be recovered, but older memories will be easier to recall due to strengthening over time.
Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss.
Another type of consolidation (process by which memories become stable in the brain) occurs over much longer periods of time/days, weeks, months and years and likely involves transfer of information from the hippocampus to more permanent storage site in the cortex.
The operation of this longer-term consolidation process is seen in the retrograde amnesia of patients with hippocampal damage who can recall memories from childhood relatively normally, but are impaired when recalling experiences that occurred just a few years prior to the time they became amnesic. (Kirwan et al.,2008)
is generally due to a head injury (example: a fall, a knock on the head).
Traumatic amnesia is often transient, but may be permanent or either anterograde, retrograde, or mixed type.
The extent of the period covered by the amnesia is related to the degree of injury and may give an indication of the prognosis for recovery of other functions.
Mild trauma, such as a car accident that results in no more than mild whiplash, might cause the occupant of a car to have no memory of the moments just before the accident due to a brief interruption in the short/long-term memory transfer mechanism.
The sufferer may also lose knowledge of who people are. Having longer periods of amnesia or consciousness after an injury may be an indication that recovery from remaining concussion symptoms will take much longer
Results from a psychological cause as opposed to direct damage to the brain caused by head injury, physical trauma or disease, which is known as organic amnesia.
Dissociative amnesia can include:
Repressed memory refers to the inability to recall information, usually about stressful or traumatic events in persons' lives, such as a violent attack or disaster. The memory is stored in long-term memory, but access to it is impaired because of psychological defense mechanisms. Persons retain the capacity to learn new information and there may be some later partial or complete recovery of memory. Formerly known as "Psychogenic Amnesia".
Dissociative fugue (formerly psychogenic fugue) is also known as fugue state. It is caused by psychological trauma and is usually temporary, unresolved and therefore may return. An individual with dissociative fugue disorder is unaware or confused about his or her identity and will travel in journeys away from familiar surroundings to discover or create new identities.
The Merck Manual defines it as " one or more episodes of amnesia in which patients cannot recall some or all of their past and either lose their identity or form a new identity. The episodes, called fugues, result from trauma or stress.
Dissociative fugue often manifests as sudden, unexpected, purposeful travel away from home."While popular in fiction, it is extremely rare.
Posthypnotic amnesia occurs when events during hypnosis are forgotten, or where past memories are unable to be recalled. The failure to remember those events is induced by suggestions made during the hypnosis.
Lacunar amnesia is the loss of memory about one specific event.
Childhood amnesia (also known as infantile amnesia) is the common inability to remember events from one's own childhood. Sigmund Freud notoriously attributed this to sexual repression, while modern scientific approaches generally attribute it to aspects of brain development or developmental psychology, including language development, which may be why people don't easily remember pre-language events.
Researchers have found that implicit memories cannot be recalled or described. Remembering how to play the piano is a common example of implicit memory, as is walking, speaking and other everyday activities that would be difficult to focus on if they had to be relearned every time one got up in the morning.
Explicit memories, on the other hand, can be recalled and described in words. Remembering the first day that you met your piano teacher is an example of explicit memories.
Transient global amnesia is a well-described medical and clinical phenomenon. This form of amnesia is distinct in that abnormalities in the hippocampus can sometimes be visualized using a special form of magnetic resonance imaging of the brain known as diffusion-weighted imaging (DWI).
Symptoms typically last for less than a day and there is often no clear precipitating factor or any other neurological deficits. The cause of this syndrome is not clear. The hypothesis of the syndrome includes transient reduced blood flow, possible seizure or an atypical type of migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.
Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge.
Source amnesia is both part of ordinary forgetting and can be a memory disorder caused by different factors.
People suffering from source amnesia can also get confused about the content of what is remembered.
This confusion has been loosely termed memory distrust syndrome. Individuals who suffer from this syndrome distrust their memory and may be motivated to rely on external (non-self) sources.
Korsakoff's syndrome can result from long-term alcoholism or malnutrition.
It is caused by brain damage due to a vitamin B1 deficiency and will be progressive if alcohol intake and nutrition pattern are not modified.
Other neurological problems are likely to be present in combination with this type of Amnesia. Korsakoff's syndrome is also known to be connected with confabulation. It should be noted that the person's short-term memory may appear to be normal, but the person may have a difficult time attempting to recall a past story, or with unrelated words, as well as complicated patterns.
Drug-induced amnesia is intentionally caused by injection of an amnesiac drug to help a patient forget surgery or medical procedures, particularly those not performed under full anesthesia, or likely to be particularly traumatic.
Such drugs are also referred to as "premedicants." Most commonly a 2'-halogenated benzodiazepine such as midazolam or flunitrazepam is the drug of choice, although other strongly amnestic drugs such as propofol or scopolamine may also be used for this application.
Memories of the short time-frame in which the procedure was performed are permanently lost or at least substantially reduced, but once the drug wears off, memory is no longer affected.
Prosopamnesia is the inability to recognize or remember faces, even in the presence of intact facial recognition capabilities. Both acquired and inborn cases have been documented.
Situation-Specific amnesia can arise in a variety of circumstances (e.g., committing an offence, child sexual abuse) resulting in PTSD. It has been claimed that it involves a narrowing of consciousness with attention focused on central perceptual details and/or that the emotional or traumatic events are processed differently from ordinary memories.
Transient epileptic amnesia is a rare and unrecognized form of temporal lobe epilepsy, which is typically an episodic isolated memory loss. It has been recognized as a treatment-responsive syndrome congenial to anti-epileptic drugs.
Acquisition Of New Memories
Patients with amnesia can learn new information, particularly non-declarative knowledge. However, some patients with dense anterograde amnesia do not remember the episodes during which they learned or observed the information previously.
Acquisition of new declarative information
Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge.
H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years.
The reason patients couldn't form new episodic memories is likely because the CA1 region of the hippocampus was lesioned, and thus the hippocampus couldn't make connections to the cortex.
After an ischemic episode following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.
Acquisition of new non-declarative information
Some retrograde and anterograde amnesics are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do.
Therefore, procedural learning can proceed independently of the brain system required for declarative memory.
According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of declarative memories.
This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoff’s syndrome.
Another example demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming.
Those patients did well in the word fragment completion test.