Elsevier

The Lancet

Volume 380, Issue 9851, 20–26 October 2012, Pages 1429-1440
The Lancet

Review
Amnesic disorders

https://doi.org/10.1016/S0140-6736(11)61304-4Get rights and content

Summary

Memory disturbances frequently occur after brain damage, but can be associated with psychiatric illnesses as well. Amnesia—the most severe form of memory impairment—has several variants, including anterograde and retrograde amnesia, material-specific and modality-specific amnesia, and transient global amnesia. We searched databases to obtain an overview of amnesia research from the past 5 years. Research into amnesia has increased exponentially, probably because of the availability of modern brain-imaging techniques. In line with the view that memory is not a unity but is organised into several systems, amnesia is described as a multifaceted disease with a frequently poor prognosis.

Introduction

The term amnesia is mainly used in two ways. First, it is generally used to describe any severe memory impairment or deficit, irrespective of the cause. Second, it is used in line with the traditional view that amnesia is a memory impairment that occurs in the absence of other substantial cognitive impairments, and is restricted to specific disorders. These disorders—referred to as either amnesic or amnestic disorders according to different international classifications—have as a core feature a memory impairment that is not due to dementia or delirium and represents a decline from a previously attained functional level. This decline in function differentiates them from infantile amnesia or neurodevelopmental disorders.

In this Review, we outline the classification of memory systems and summarise relevant aspects of what causes amnesic disorders, their neurobiology, epidemiology, diagnosis, and management. We discuss neuroimaging and genetic studies and emphasise the need for methodological rigour with respect to memory-testing paradigms.

Section snippets

Memory systems and memory processes

Although the term amnesia was used rather loosely until the 1980s1—often to describe total memory loss—we now know that memory impairment in amnesic disorders is likely to be restricted to specific kinds of memory. This view is supported by the existence of several distinct memory systems, each with different neuroanatomical substrates. In addition to the division into short-term and long-term memory, the work of Tulving,2, 3, 4 especially, led to a content-based classification of long-term

Neuroanatomy and neurobiology of memory

The debate about whether the brain contains functionally specialised regions or acts Gestalt-like1 (as a whole) took on a new dimension with the advent of functional imaging, which sometimes points towards a high degree of cortical specialisation.8 Amnesias arise after damage to bottleneck structures through which information has to pass before it is stored long-term,9 but can also take place after widespread cortical damage (panel 2; see appendix for a schematic of the two main circuits

International classifications of amnesic disorders

The International Statistical Classification of Diseases and Related Health Problems, tenth revision (ICD-10)18 and the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV-TR)19 classify amnesic disorders on the basis of their strong aetiological link to general medical disorders, the direct effects of psychoactive substances in the patient's body persisting beyond the intoxication or withdrawal period, or psychological factors. Although the terms

Brain damage of the limbic system and amnesia

Data for amnesia come from case reports and group studies. These group studies frequently combine patients whose amnesia has different causes, but who presumably have the same main locus of brain damage. Three main forms of amnesia have been classically described on the basis of the locus of brain damage: hippocampal or medial temporal lobe (MTL) amnesia, diencephalic amnesia, and basal forebrain amnesia. Despite some differences (table 1), they share many features. Various portions of the

White-matter damage and amnesia as a disconnection syndrome

The occurrence of amnesia after fibre tract damage was first reported some time ago.1 Several fibre bundles are of special interest in memory processing because they interconnect relevant bottleneck structures9, 59, 60 (see appendix). The fornix connects all three major regions that are important for memory consolidation and transfer into long-term memory (MTL, diencephalon, and basal forebrain). In a study of 38 patients who had undergone colloid cyst removal, significant negative correlations

Amnesias with mixed psychological and physiological causes

Transient global amnesia happens suddenly, usually in adults older than 60 years, and is triggered by physiological or psychological factors.68 Its course is benign because it (typically) disappears within a day. Slight memory deficits might, however, persist for months, especially if patients continue to have anxiety or depression.69 Transient global amnesia affects mostly anterograde memories, but can partly affect retrograde memories as well.70 The cause of transient global amnesia is still

Epidemiology and genetics

Epidemiological data are available for only specific amnesic disorders. The incidence of transient global amnesia is 3–8 per 100 000 people per year.70 Head trauma is the most probable cause of amnesic disorders that are due to a general medical disorder. Although decreases in the incidence of thiamine-related disorders were reported in several countries after fortification of bread with thiamine, an increase in the incidence of Korsakoff's syndrome was described in some European countries.49

Assessment of amnesic disorders

Assessment of amnesic disorders includes anamnesis and medical, laboratory, and occupational-therapy evaluations (see appendix for a flow diagram on assessment strategies). Neuropsychological testing is invaluable to objectively establish the nature and severity of the memory impairment, to quantify longitudinal changes, and to distinguish between amnesias of different causes and feigned amnesia. Cognitive disturbances due to infarct or closed head injury can change over time. Furthermore,

Prognosis and treatment of amnesic disorders

A few amnesic disorders (such as transient global amnesia) have good prognosis, others partly improve, and for some disorders—especially those with complete bilateral damage to MTL, diencephalon, or basal forebrain—prognosis remains poor. Traditionally, most cases of dissociative amnesia were reported to resolve spontaneously; however, reports have since suggested that chronic forms exist.10, 13

Parenteral thiamine given routinely to patients at risk decreases their likelihood of developing

Future directions

Amnesia in the strict sense—ie, a total and exclusive loss of the ability to store new information consciously and long term, or to retrieve long-term stored information consciously—is rarely found. In fact, proposals were made by the DSM-V neurocognitive disorders work group to replace the DSM-IV-TR category of delirium, dementia, amnestic and other geriatric cognitive disorders with a new category called neurocognitive disorders. Longitudinal studies of (dissociative) amnesia might be needed

Search strategy and selection criteria

This Review is based on material identified through searches of PubMed, Medline, and Scopus for original research or review articles from 2005 to early 2011 written in English, German, and French, with a combination of the words “amnesia”, “memory”, “memory impairments”, “memory disturbances”, “genetics”, and “treatment”. We based selection of material on its quality, originality, and relevance to the subject. We also cited a few book chapters and older seminal articles on the topic.

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      Citation Excerpt :

      As the patient probably incorporates them as having been acquired with particular personal effort (that is, in a more stressful milieu), and is under psychic pressure of being able to retrieve them in the future in order to fulfill professional demands, this repertoire is blocked or encapsulated as well under conditions of dissociative (psychogenic) amnesia. Consequently, it not only makes sense to follow Tulving's division of memory into episodic or episodic-autobiographical memory on the hand, and semantic memory into the other (cf. Fig. 1 in Markowitsch and Staniloiu, 2012a, or Fig. 2 in Staniloiu and Markowitsch, 2014) – instead of subsuming both under the term ‘declarative memory’ (cf. Tulving and Markowitsch, 1998) – but also to specify semantic memory further (Fig. 4), at least when it comes to patients with dissociative or functional amnesia. As Fig. 4 shows, episodic-autobiographical memory largely feeds episodes or events directly into autobiographical memory.

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