Does anyone ever heard about research/litterature on self-induced false memories?

I have a 15 year old patient who had a concussion 2 years ago. Her parents report that she is unable to recall past events, As an illustration, they said in the past summer she spent a week at the shore with her friends. With coaching she can remember the event but can recall no details of the vacation. They claim she never had this problem before the concussion.

TGA is generally defined as a benign episode. However, (apart from a residual amnesic lacuna for the events which occur during the episode) apparently it does not seem to influence the successive memory performance of a person who has one or more TGA episodes. Nevertheless, some data (for example, our old paper: Transient Global Amnesia: neuropsychological findings after single and multiple attacks, Gallassi et al., Eur Neurol 1993:33:294-298) suggests a residual fragility with some impaired tasks of memory, especially of verbal type, and especially in subjects having more than one episode. However, these neuropsychological findings in the majority of the cases do not seem to influence general cognition and daily activity, although some subjects denounce a few memory difficulties after a TGA. Nevertheless, an emotive reaction could play a role in some cases.

Borroni et al. (Is transient global amnesia a risk factor for amnesic mild cognitive impairment?, J Neurol 2004: 251: 1125-1127) found that TGA “appears to be a relatively benign syndrome although objective memory deficits fulfilling MCI amnesic criteria persist over time as detected by multidimensional neuropsychological tasks performed at long-term follow-up”. Nevertheless, there are conflicting results of the literature on this argument.

Therefore, my question is: the TGA represents a cause of memory impairment per se, although slight, or it is an effect of meiopragic condition of the brain, playing also a role of further worsening? Do you have data or experience regarding this argument?

Buschke, 1984. Cued recall in Amnesia

Grober and Guschke, 1987. Genuine memory deficits in dementia

More specifically, suffering from anterograde amnesia:

1. if only the hippocampus is damaged, can the individual still learn procedural skills? or are procedural skills processed in a different area, independent of the hippocampus?

or

2. if only the hippocampus is damaged, aside from not being able to create new long term declarative memories, is the patient also unable to learn new procedural skills? or are both declarative and procedural knowledge dependent of the hippocampus in order for the learning to be encoded into its specific memory region in the cortex/brain?

The radial arm maze can be used to investigate multiple forms of memory, including episodic. Can we also use the Morris water maze to study episodic memory? If yes, how? If no, why not?

Are there studies that prove that it can be effective in the cure of depression?

If there is Immunological Memory, there is also possibility of;

Immunological Dyslexia.

Immunological Dementia.

Immunological Amnesia.

Is it not ?

And such effects might occur as a result of adaptations in epigenetic system of individuals accompanied by ageing, co-morbidities, polypharmacy etc ?

What is the difference between amnesia and dementia?

There is a consensus among researchers that late life depression and depression in AD comprehend two different pathologies, with some shared symptoms. For example, apathy and amnesia are common features in both diseases, and could be explained by consequences of a mood disorder or a cognitive syndrome. In addition, frontal lobe dysfunction is linked to a variety of geriatric neuropsychiatric syndromes, representing an area of intersection in depression and dementia (Steffens, 2012).

Therefore, identification of depression as marker for increased risk of conversion from depression to dementia among patients with MCI has become the main focus for those caring for individuals with depression or cognitive impairment. We now need further investigation.