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The term 'episodic memory' was coined by Endel Tulving, who also created a classification in several memory systems. This classification is presented, and it is described which predecessors existed for the partition of memory into systems. The 'episodic memory system' is discussed as being in general equivalent with the 'episodic-autobiographical memory system'. It is seen as an emotionally colorized system. A special paragraph is devoted to the 'perceptual memory system', as this was not included in Tulving's previous schemes of memory systems. More recent sub-categorizations of the 'episodic memory system' are presented and a perspective on the future of the episodic memory system is developed.

Memory disorders without a direct neural substrate still belong to the riddles in neuroscience. Although they were for a while dissociated from research and clinical arenas, risking becoming forgotten diseases, they sparked novel interests, paralleling the refinements in functional neuroimaging and neuropsychology. Although Endel Tulving has not fully embarked himself on exploring this field, he had published at least one article on functional amnesia (Schacter et al., 1982) and ignited a seminal article on amnesia with mixed etiology (Craver et al., 2014). Most importantly, the research of Endel Tulving has provided the researchers and clinicians in the field of dissociative or functional amnesia with the best framework for superiorly understanding these disorders through the lens of his evolving concept of episodic memory and five long term memory systems classification, which he developed and advanced. Herein we use the classification of long-term memory systems of Endel Tulving as well as his concepts and views on autonoetic consciousness, relationships between memory systems and relationship between episodic memory and emotion to describe six cases of dissociative amnesia that put a challenge for researchers and clinicians due to their atypicality. We then discuss their possible triggering and maintaining mechanisms, pointing to their clinical heterogeneity and multifaceted causally explanatory frameworks.

The memory impairment of neurological and psychiatric patients is seen as occurring mainly in the autobiographical-episodic memory domain and this is considered to depend on limbic structures such as the amygdala or the septal nuclei. Especially the amygdala is a hub for giving an emotional flavor to personal memories. Bastin et al. fail to include the amygdala in their integrative memory model.

Autobiographical amnesia is found in patients with focal or diffuse brain damage ("organic amnesia"), but also without overt brain damage (at least when measured with conventional brain imaging methods). This last condition is usually named dissociative amnesia at present, and was originally described as hysteria. Classically and traditionally, dissociative amnesia is seen as a disorder that causes retrograde amnesia in the autobiographical domain in the aftermath of incidents of major psychological stress or trauma. In the present study one of the probably largest published collections of patients (28) with psychogenically caused autobiographical amnesia, who were assessed with comprehensive neuropsychological tests, will be described and documented in order to identify variables which are central for the occurrence of dissociative amnesia. The presented cases demonstrate that autobiographical amnesia without direct brain damage can have very mixed clinical presentations, causes and consequences. The described cases of psychogenic amnesia are clustered according to a number of manifestations and features, which include a reduced effort to perform cognitively at a normal level, a forensic background, anterograde (instead of retrograde) autobiographical amnesia, the fugue condition, concurrent somatic diseases, and their appearance in childhood and youth. It is concluded that autobiographical amnesia of a psychogenic origin may occur within a variety of symptom pictures. For all patients, it probably serves a protective function by offering them a mechanism to exit a life situation which appears to them unmanageable or adverse.

Lindquist et al. remark that not all fear instances lead to heightened amygdalar activity and, instead, point to roles of the amygdala in detecting “motivationally salient “or “emotionally impactful” stimuli. By reviewing research on the amygdala's functions in episodic-autobiographical memory, we further emphasize the involvement of the amygdala in coding the subjective relevance and extracting the biological and social significance of the stimuli.

Lane et al. view the process of memory reconsolidation as a main ingredient of psychotherapeutic change. They ascertain that in cognitive behavioral therapy (CBT) high priority is given to the “semantic structure.” We argue that memory-related mechanisms of change in CBT are more nuanced than the target article presents. Furthermore, we propose to partially shift the focus from the process of reconsolidation to the retrieval operations.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) – is the most common genetic source of vascular dementia in adults, being caused by a mutation in NOTCH3 gene. Spontaneous de novo mutations may occur, but their frequency is largely unknown. Ischemic strokes and cognitive impairments are the most frequent manifestations, but seizures affect up to 10% of the patients. Herein, we describe a 47-year-old male scholar with a genetically confirmed diagnosis of CADASIL (Arg133Cys mutation in the NOTCH3 gene) and a seemingly negative family history of CADASIL illness, who was investigated with a comprehensive neuropsychological testing battery and neuroimaging methods. The patient demonstrated on one hand severe and accelerated deteriorations in multiple cognitive domains such as concentration, long-term memory (including the episodic-autobiographical memory domain), problem solving, cognitive flexibility and planning, affect recognition, discrimination and matching, and social cognition (theory of mind). Some of these impairments were even captured by abbreviated instruments for investigating suspicion of dementia. On the other hand the patient still possessed high crystallized (verbal) intelligence and a capacity to put forth a façade of well-preserved intellectual functioning. Although no definite conclusions can be drawn from a single case study, our findings point to the presence of additional cognitive changes in CADASIL in middle adulthood, in particular to impairments in the episodic-autobiographical memory domain and social information processing (e.g., social cognition). Whether these identified impairments are related to the patient’s specific phenotype or to an ascertainment bias (e.g., a paucity of studies investigating these cognitive functions) requires elucidation by larger scale research.

It is argued that Llewellyn's hypothesis about the lack of rapid eye movement (REM)-sleep dreaming leading to loss of personal identity and deficits in episodic memory, affectivity, and prospection is insufficiently grounded because it does not integrate data from neurodevelopmental studies and makes reference to an outdated definition of episodic memory.

ObjectivesTraumatic brain injury (TBI) is a main cause of mortality and morbidity. Association studies between hospitalization variables and cognitive impairment after TBI are frequently retrospective, including non-consecutive patients showing variable degrees of TBI severity, and poor management of missing (drop out) cases. Methods We assessed prospectively the demographic and hospitalization variables of 234 consecutive patients with severe TBI (admission Glasgow Coma Scale [GCS] 8) and determined their independent association with cognitive performance in a representative sample (n=46) of surviving patients (n=172) evaluated 3 (1.8) years after hospitalization. Results In all, 85% of patients were male and the mean age was 34 (SD +/- 13) years. The education level was 9 (+/- 4.7) years. As expected, education and age showed a moderately to strong linear relationship with the cognitive performance in 14 of 15 neuropsychological tests (R coefficient=0.6-0.8). The cognitive test scores were not independently associated with gender, admission GCS, associated trauma, and Marshal CT classification. Admission-elevated blood glucose levels and the presence of sub-arachnoid haemorrhage were independently associated with lower scores on Rey Auditory Verbal Learning retention and Logical Memory-I tests, respectively. ConclusionsAfter correction for education and age distribution, the variables that are commonly associated with mortality or Glasgow Outcome Scale including admission pupils' examination, Marshal CT Classification, GCS, and serum glucose showed a limited predictive power for long-term cognitive prognosis. Identification of clinical, radiological, and laboratory variables as well as new biomarkers independently associated with cognitive outcome remains an important challenge for further work involving severe TBI patients.

The human amygdala is strongly embedded in numerous other structures of the limbic system, but is also a hub for a multitude of other brain regions it is connected with. Its major involvement in various kinds of integrative sensory and emotional functions makes it a cornerstone for self-relevant biological and social appraisals of the environment and consequently also for the processing of autobiographical events. Given its contribution to the integration of emotion, perception and cognition (including memory for past autobiographical events) the amygdala also forges the establishment and maintenance of an integrated self. Damage or disturbances of amygdalar connectivity may therefore lead to disconnection syndromes, in which the synchronous processing of affective and cognitive aspects of memory is impaired. We will provide support for this thesis by reviewing data from patients with a rare experiment of nature - Urbach-Wiethe disease - as well as other conditions associated with amygdala abnormalities. With respect to memory processing, we propose that the amygdala's role is to charge cues so that mnemonic events of a specific emotional significance can be successfully searched within the appropriate neural nets and re-activated.

As psychiatric illnesses have correlates in the brain, it is surprising that Cramer et al. make almost no reference to the brain's network character when proposing a network approach to comorbidity of psychiatric diseases. We illustrate how data from combined neuropsychological and functional and structural brain-imaging investigations could inform theoretical models about the role played by overlapping symptoms in the etiology of psychiatric comorbidity and the pathways from one disorder to another.