Amnesia is categorized as organic when it occurs as a result of damage to brain structures due to processes such as infection, degenerative diseases, or stroke. It is categorized as functional when it occurs as a result of a traumatic psychological experience. Typically, organic amnesia allows for retention of older memories, but gives rise to difficulties in acquiring new memories (Moscovitch 2004). Functional amnesia is often characterized by the loss of personal identity (Kritchevsky 2004; Staniloiu 2012). Amnesia can also be classified into different types depending on which aspect of memory is affected; this is often determined by the areas in the brain that are damaged.
Anterograde amnesia refers to the situation wherein people are unable to recall events or information presented to them just a few minutes previously (Dewar 2010). People with anterograde amnesia may have normal memory for anything that happened prior to the onset of amnesia. However, their ability to recall information presented to them after the onset of amnesia is severely impaired (Paller 2009; McLeod 2011). Short-term memory allows people with anterograde amnesia to temporarily retain information, but distraction causes the new information to be lost (Mayes 2010).
Anterograde amnesia is usually caused by damage to the hippocampus or other regions of the brain that work with the hippocampus in making new memories (Gilboa 2006; Aggleton 2008). Additional causes of anterograde amnesia include damage to the temporal lobe and Alzheimer’s disease (Cavaco 2012). Anterograde amnesia sometimes occurs in people treated with benzodiazepines; it can also occur in association with a form of thiamine deficiency called Korsakoff’s syndrome, which is often a complication of chronic alcoholism (Moscovitch 2004; Uzun 2010; Staniloiu 2012).
One interesting feature of anterograde amnesia is that it can specifically affect recognition but not “familiarity” based recall; as a result, people presented with a new object several times may feel as if they have seen the object before but fail to remember when (Gilboa 2006; Aggleton 2008). People with anterograde amnesia may also be able to learn and retain new habits or acquire new perceptual and motor skills, such as reading text from a reflection in a mirror or swinging a golf club (Cavaco 2012).
Retrograde amnesia is a deficit in recalling information or memories stored before the onset of the amnesia. One characteristic of retrograde amnesia is that information stored close to the time of brain damage is affected more than the remote memories (Paller 2009). However, this is not always true, especially in the case of extensive brain damage. Retrograde amnesia usually occurs along with anterograde amnesia (Squire 1995). Retrograde amnesia has been associated with damage to the hippocampus or related structures (Winocur 2001; Winocur 2013).
One of the more commonly accepted theories about retrograde amnesia is that damage to the hippocampus impairs a process called memory consolidation. During memory consolidation, memories are first stored in the hippocampus, and then gradually transferred to other parts of the brain so the hippocampus is no longer needed to retain and access them. Retrograde amnesia affects memories made close to the time of injury, but usually does not impact older memories, which have already been consolidated (Squire 2007; Winocur 2013). Retrograde amnesia can result from head injury or can occur along with anterograde amnesia as part of Korsakoff’s syndrome (Paller 2009). Retrograde amnesia can also occur after electroconvulsive therapy (Meeter 2011), a type of infection known as encephalitis (Yoneda 1992), and after epileptic seizures (Hornberger 2010). Another form of retrograde amnesia, called functional retrograde amnesia, is characterized by memory deficits that occur in the absence of identifiable brain injury (Fujiwara 2008). In these cases, it is thought that psychological trauma can induce memory loss.