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The presence of a retrograde amnesia, when caused by medications given prior to a medical procedure, can pose the medicolegal question of informed consent. This study investigated the retrograde amnesic effects of intravenous diazepam administered prior to gastrointestinal endoscopy. No significant retrograde amnesia was found in case subjects when compared with controls.
The four papers in this issue of Hippocampus dealing with retrograde amnesia, together with relevant animal studies in the literature, are reviewed from the perspective of the anatomical location of the lesion and extent of damage to the brain. In order to evaluate the underlying damage in these and related prospective experimental studies, it is necessary to consider both the lesion techniques that were used as well as the care with which the resulting damage was determined. Both temporally graded and flat, ungraded retrograde amnesia have been reported, as well a lack of effects, following damage to structures in the medial temporal area. Most research has centered around damage to the hippocampus, but differences in selectivity of the lesions and behavioral testing procedures preclude any definite conclusions regarding the precise nature of the involvement of this structure. With a greater appreciation for the importance of the locus and extent of the damage, together with the kind of information being processed, it should be possible to obtain a better understanding of the neural substrates underlying retrograde amnesia.
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We describe a patient who, in the absence of anterograde amnesia, experienced sudden onset of profound retrograde amnesia for the last forty years of his life. The amnesia encompassed all knowledge, including motor skills, acquired during these forty years. There has been no recovery in over eighteen months. His symptoms seem most consistent with a vascular etiology. Current understanding of memory disorders fails to explain these symptoms. It may be that his case represents a previously undescribed disorder.
We describe a patient who presented with isolated retrograde amnesia of 2-year duration after recovery from viral encephalitis. The patient was a 29-year-old right-handed male dentist and was admitted to our hospital with a complaint of generalized convulsion. Cerebrospinal fluid (CSF) showed mononuclear pleocytosis. Neuroradiological examinations (X-ray CT, MRI and 123I-IMP SPECT) revealed no significant abnormality. Immunological method showed no specific increase of viral antibody titers. However, with a tentative diagnosis of viral encephalitis, administration of acyclovir was started. After 3 weeks he became comprehensive, and several kinds of neuropsychological tests were performed. His intelligence and immediate memory were normal, and his procedural memory of dentist was intact. On the other hand, he could not recall any information about events, both personal and public, occurred within 2 years before the onset of present illness. His autobiographical memory disorder was also demonstrated using a series of weekly comic. In isolated retrograde amnesia following viral encephalitis like this case, memory of relatively short time duration, acquired prior to the onset of present illness, tend to be disturbed.
Two once-daily electroconvulsive shocks (ECS) produced retrograde amnesia in rats trained on a Hebb-Williams maze; Verapamil (12.5 mg/kg, i.p.) or felodipine (10 mg/kg, p.o.) administered half an hour before each ECS attenuated this ECS-induced amnesia. Hence, these drugs may hold promise for the containment of amnesia induced by electroconvulsive therapy (ECT). Speculatively, one or more of several mechanisms may be involved: cerebral vasodilatation, enhancement of cholinergic tone, and inhibition of calcium-mediated impairment of neuronal function. These drugs may also act by attenuating the systolic surge in blood pressure during ECT, thereby decreasing edema due to cerebral hyperperfusion, as well as decreasing the possible transfer of potentially neurotoxic macromolecules through a putative breach in the blood-brain barrier.
The relationships between cooling-induced retrograde amnesia and associations in Pavlovian conditioning in the terrestrial mollusk Limax flavus were studied. In the first experiment, the slugs were conditioned to avoid carrot odor and the experimental conditions required for amnesia induction were studied. Memory reactivation before cooling was found to be necessary for amnesia induction and the induced amnesia was selective for the reactivated memory. In the subsequent experiments, slugs were conditioned to avoid both carrot and cucumber odors using one of three Pavlovian conditioning paradigms, namely two-independent first-order conditioning, phase-2-sequential second-order conditioning and phase-2-simultaneous second-order conditioning, after which amnesia was induced by cooling immediately after presentation of one of the conditioning odors. The amnesia pattern induced differed depending upon the conditioning procedure used, which indicated that amnesia induction was related closely to stimulus associations in slugs. The possible role of cooling-induced retrograde amnesia as a tool for studying memory associations is also discussed.
A nonbarbiturate anesthetic consisting of ketamine HCl (Ketaset) and xlyazine (Rompun) was administered to assess the effects of anesthesia on hypothermia-induced retrograde amnesia in Long Evans hooded and Sprague-Dawley albino rats. Results from Experiment 1a indicate that this anesthetic does not attenuate retrograde amnesia, and the findings from Experiment 1b suggest that awakening from Ketaset/Rompun anesthesia at normal body temperature (following administration of deep body cooling) does not attenuate the resulting hypothermia-induced retrograde amnesia. Experiment 2 demonstrated that various delays between training and hypothermia resulted in a temporal gradient that was the same for animals cooled while either conscious or under anesthesia. The results of Experiment 3 showed that rats made amnesic while under anesthesia did not recover the target memory if given a recooling treatment, but rats that were made amnesic while conscious did recover the memory with the same reminder treatment. These findings indicate that the conscious processing of stimuli associated with hypothermia treatment is not necessary in inducing hypothermia-induced retrograde amnesia, but that conscious processing is an important factor if the amnesia is to be recovered with a recooling treatment.
This experiment tested the general validity of recent findings that retrograde amnesia can be produced by electroconvulsive shock only if the shock is administered within 10 to 30 seconds after the learning trial. Precautions were taken to avoid confusion of other shock effects with retrograde amnesia. A temporal gradient of elec- troconvulsive shock-produced retrograde amnesia, extending up to at least 1 hour, for a well-discriminated stimulus, was demonstrated in mice in a one-trial learning passive avoidance situation.
I firstly consider general issues relating to our attempts to understand retrograde amnesia. Three main hypotheses are reviewed that have been proposed to account for retrograde amnesia. A theory is outlined to explain the dense autobiographical amnesia that is a focal phenomenon in some cases of severe head injury. This theory postulates that autobiographical retrieval requires the activation of a distributed network of cognitive operations, and that autobiographical amnesia results from the occurrence of multiple areas of pathology, distributed over both space and time.
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Models of the neurobiology of memory have been based on the idea that information is stored as distributed patterns of altered synaptic weights in neuronal networks. Accordingly, studies have shown that post-training treatments that alter synaptic weights, such as the induction of long-term potentiation (LTP), can interfere with retrieval. In these studies, LTP induction has been relegated to the status of a methodological procedure that serves the sole purpose of disturbing synaptic activity in order to impair memory. This perspective has been expressed, for example, by Martin and Morris (2002: Hippocampus 12:609-636), who noted that post-training LTP impairs memory by adding "behaviorally meaningless" noise to hippocampal neural networks. However, if LTP truly is a memory storage mechanism, its induction should represent more than just a means with which to disrupt memory. Since LTP induction produces retrograde amnesia, the formation of a new memory should also produce retrograde amnesia. In the present report, we suggest that one type of learning experience, the storage of fear-related (i.e., stressful) memories, is consistent with this prediction. Studies have shown that stress produces potent effects on hippocampal physiology, generates long-lasting memories, and induces retrograde amnesia, all through mechanisms in common with LTP. Based on these findings, we have developed the hypothesis that a stressful experience generates an endogenous form of hippocampal LTP that substitutes a new memory representation for preexisting representations. In summary, our hypothesis implicates the induction of endogenous synaptic plasticity by stress in the formation of emotional memories and in retrograde amnesia.
The memory impairment of a patient suffering from functional retrograde amnesia was assessed both during the amnesic episode and after its termination. The patient's performance on a task tapping semantic memory was nearly identical on the two test occasions, but his performance on a task tapping episodic memory substantially changed across test sessions. Cueing procedures revealed that in spite of the patient's restricted access to episodic memory during the amnesic period, a relatively intact "island" of episodic memories could be uncovered. The distinction between episodic and semantic memory, as well as the relation between organic and functional retrograde amnesia, are discussed in light of the case study.
Results from recent studies of retrograde amnesia following damage to the hippocampal complex of human and non-human subjects have shown that retrograde amnesia is extensive and can encompass much of a subject's lifetime; the degree of loss may depend upon the type of memory assessed. These and other findings suggest that the hippocampal formation and related structures are involved in certain forms of memory (e.g. autobiographical episodic and spatial memory) for as long as they exist and contribute to the transformation and stabilization of other forms of memory stored elsewhere in the brain.
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