OBJECTIVES:

To review the clinical aspects, new imaging findings and recent clinicoepidemiological data with regard to the phenotype, functional anatomy and putative cellular mechanisms of transient global amnesia (TGA). Despite several new hypotheses concerning the pathogenesis of TGA, there is still not consensus about its cause. Herein, the evidence in support of and against the main pathogenic hypotheses are critically evaluated.

METHODS:

Relevant literature published since the first reports of TGA published in 1956 is reviewed, with the aim of accurately describing the demographic and clinical features of TGA. A systematic review of the literature on the relationships between focal ischaemia, migraine, epileptic phenomena, venous flow abnormalities and TGA was performed by searching the literature for all relevant studies. References were identified through searches with the search terms 'amnesia', 'transient global amnesia', 'TGA', 'hippocampus' and 'CAI'. Only papers published in English were included.

RESULTS:

Classical proposals about its possible aetiology (epilepsy, vascular disease and migraine) and other new theories (Leao 's spreading depression or influence of stress) have been assessed. While there is data in favour and against hypotheses of the aetiology of TGA, there is no current consensus which satisfactorily explains the nature of this type of amnesia. A number of recent neuroimagmg studies suggests involvement of the mesial temporal area (amygdala and hippocampus) and/or thalamus leading to transient disruption of blood flow, and appearing as focal magnetic resonance (MR) hypenntensities showing restricted diffusion on diffusion-weighted MR imaging (DW-MRI).

CONCLUSIONS:

TGA is defined as a selective deficit of memory that appears suddenly and lasts less than 24 hours. The present state of knowledge about memory deficits associated with TGA is still limited, and there are still several aspects that require clarification, particularly regarding recovery. Recent neuroimaging findings suggest that transient perturbation of hippocampal function is correlated with TGA, as focal lesions can be reliably detected in the CAI field of the cornu ammonis with DW-MRI. Tuture research should focus on elucidating the pathophysiological correlates of the acute phase, particularly on deciphering which trigger induces the pathophysiological cascade that affects CA I neurons. (PsycINFO Database Record (c) 2016 APA, all rights reserved)

Professor Ritchie Russell`s monograph maintains the high standard and high degree of interest established by the other contributors to this series. His early work, founded on detailed studies of head-injured patients was published in early 1930s. Since then has gone on to develop his concepts of memory, learning, and amnesia in the ligth of experience and expanding biological knowledge. Some of the earlier papers are no longer easily avaible; annotated extracts from these, toghether with more recent contributions, are presented in this volume.

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Patients, when admitted to an intensive care unit (ICU), have one thing in common: their illness is life-threatening. Patients may remain on ICU in a critical condition, needing support with their breathing, circulation, and/or kidneys for varying lengths of time, from days to weeks. During that time the patients will receive sedative and analgesic drugs to ensure compliance with artificial ventilation. Patients recovering from critical illness frequently have little or no recall of their period in ICU, or remember nightmare, hallucinations, or paranoid delusions. The nature, extent and reason for these difficulties, have been under-reported and consequently our purpose was to conduct a review of memory problems experienced by ICU patients. A systematic literature review of computer databases (Medline, PsycLit, and CINAHL) identified 25 relevant papers. In addition, other relevant articles were obtained, citation lists and associated articles retrieved. Due to lack of research on processes underlying memory problems in ICU patients all articles that introduced an insight into possible mechanisms were included in the review. There seem to be two possible processes contributing to memory problems in ICU patients. First the illness and treatment may have a general dampening effect on memory. Delirium and sleep disturbance are both common in ICU patients. Delirium can result in a profound amnesia for the period of confusion. Sleep deprivation exacerbates the confusional state. Slow wave sleep is important for the consolidation of episodic memories. Treatment administered to patients in ICU can have effects on memory. Opiates, benzodiazepines, sedative drugs such as propofol, adrenaline, and corticosteroids can all influence memory. In addition, the withdrawal of drugs, such as benzodiazepines, can cause profound withdrawal reactions, which may contribute to delirium. Second, we hypothesise that there is a process that affects memory negatively for external events but enhances memory for internal events. The physical constraints and social isolation experienced by ICU patients and the life-threatening nature of the illness may increase the experience of hypnagogic hallucinations. Attentional shift during hypnagogic images from external stimuli to internally generated images would explain why ICU patients have such poor recall of external ICU events, but can clearly remember hallucinations and nightmares. Patients describe these memories as being very vivid and this is explored in terms of flashbulb memory formation. The absence of memories for real events on ICU can result in ICU patients remembering paranoid delusions of staff trying to kill them, with little information to reject these vivid memories as unreal. This has implications for patients' future psychological health.

A questionnaire is described and data are analyzed from 1000 young adults who retrospectively reported on features of memory lapses associated with head injury with loss of consciousness as it may have occurred in their lifetimes. It was found that 24% of the males and 16% of the females claimed a former head injury with loss of consciousness. Lengths of retrograde amnesia, post-traumatic amnesia, and the length of time that had passed since the head injury are shown to be related to each other.

The cognitive symptoms that characterise the Wernicke-Korsakoff's syndrome include anterograde amnesia, confabulation, temporal–spatial disorientation, severe apathy, poor awareness of one's own mental state and changes in executive functions. Such deficits may persist even after the clinical profile stabilises. There are no studies that report an intervention after the acute phase, possibly due to the complexity of these cases. This study provides a descriptive analysis of neuropsychological rehabilitation concomitant to the neurological and psychiatric treatment of a woman who presented the symptoms described by Korsakoff. The intervention focused on reducing the impact caused by the cognitive and behavioural sequelae in the patient's daily life. It described a 25-week neuropsychological program, providing education and compensatory strategies for the patient, and also orientation and support from 2 professional caregivers and family members. Quantitative and qualitative measures were used to evaluate the effect of the intervention on memory efficacy, emotional state and social participation. Both caregivers reported a decrease in the frequency of memory lapses after treatment. Positive changes were also seen in self-care, activities at home, decision-making and participation in social activities. It is concluded that this case achieved results through the collaboration between members of an interdisciplinary team and caregivers providing daily support.

To assess the duration of post-traumatic amnesia (PTA) in children, a new procedure is described, derived from a method described previously for adults. The procedure was tested on 70 healthy children between 3.5 and 10 years of age, then applied in a longitudinal prospective study of 54 children with brain damage resulting from closed head-injury. The procedure consistently measured PTA in children of various ages. The duration of PTA was found to be as good a prognostic indicator for the occurrence of long-term residual sequelae as is duration of coma.

ABSTRACT :

A large sample of chronic postconcussive patients with and without overt malingering signs was compared with objectively brain-injured patients on common episodic memory and malingered amnesia measures. Probable malingerers and traumatically brain-injured subjects were not differentiated on popular episodic recall tests. In contrast, probable malingerers performed poorly on the Rey 15-Item, Rey Word Recognition List, Reliable Digit Span, Portland Digit Recognition Test, and Rey Auditory Verbal Learning Test recognition trial. These findings validated both commonly cited malingering measures and newly introduced methods of classifying malingering in real-world clinical samples

Our earlier retrospective study presented a formula relating lengths of retrograde amnesia to length of post-traumatic amnesia (PTA) and length of time since injury (Crovitz, Horn and Daniel, 1983). The earlier study derived the formula from 27 cases with retrograde amnesia. The present study adds another 75 cases, and we discuss similarities and differences between the two samples.

Introducción: La encefalitis viral posvacunal es un cuadro poco frecuente y con escaso estudios acerca de sus efectos. Objetivo: Presentar el caso de una paciente de 59 años de edad que desarrolló un cuadro de encefalitis viral posterior al uso de una vacuna con virus vivos atenuados para fiebre amarilla. Diseño: Reporte de caso. Resultados: La encefalitis mencionada provocó un daño hipocampal bilateral, con un subsiguiente deterioro de la memoria declarativa anterógrada. Se presentan y discuten las imágenes y evaluaciones neuropsicológicas del caso. Se comparan las imágenes, la clínica y las evaluaciones neuropsicológicas de este caso con otros caso semejantes reportados en la literatura médica mundial. Se realiza una correlación anatomo-clínica. Conclusión: Las estructuras mediales de los lóbulos temporales son la base anatómica de la memoria declarativa; su lesión provoca un deterioro grave de la memoria, generalmente con características poco o nada reversibles...