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PubMedDate not supplied

Implicit memory: what must theories of amnesia explain?

In their target article on explaining functional deficits in amnesia, Mayes and Downes (this issue) discuss the relevance of implicit memory. Our commentary considers a number of implicit memory phenomena that may be especially pertinent to understanding the functional deficits of amnesia. Recent evidence suggests that amnesic patients do not benefit normally from an exact perceptual match of stimuli between study and text. We propose that this impairment may reflect one manifestation of a more general deficit in associative binding of information across different brain subsystems. This idea helps to clarify the distinction between implicit and explicit memory, and suggests that studies of implicit memory can help to elucidate the functional deficits in amnesia.

Amnesia↗
PubMed2006

Acute retrograde amnesia as first presentation in terminal metastatic cancer.

A case is presented of a 2-week onset of acute retrograde amnesia as initial presentation, caused by presumed cancer. While acute retrograde amnesia has been reported in the literature, a report linked to cancer has not previously been published. An 82-year-old Caucasian woman presented to the emergency department, with 3-day history of increasing confusion and mild frontal headaches. Until 2 weeks previously she had been living on her own and coping with her activities of daily life. She believed very firmly that she was living with her husband in the house in which they lived in over 30 years ago. A magnetic resonance imaging scan demonstrated a lesion extending from cortex anteriorly to the right basal ganglia posteriorly. Postgadolinium enhancement was consistent with a diagnosis of a primary or secondary neoplasm. In some patients, cognitive behaviour changes or amnesia is the sole presenting feature of a serious underlying pathology. A lesion in either the temporal or frontal lobe can lead to this presentation. A family conference was convened and there was decision to take a conservative approach and not to investigate further. She was discharged to the care of her daughter and died 3 months later without return of her memory.

Acute Disease↗
PubMed1978

The neuroanatomy of amnesia. A critique of the hippocampal memory hypothesis.

The discovery that medial temporal lobe lesions produce amnesia in humans if the lesion extends sufficiently far posteriorly to include the hippocampus forms the keystone of the hippocampal memory hypothesis. Strong supporting evidence comes from the occurrence of mammillary body disease in Korsakoff's psychosis. Disease of the posterior cerebral artery confirmed the observations on the medial temporal lobectomies by showing that pathology in the ventromedial quadrant of the temporal lobe produces amnesia. The occasional piece of contradictory evidence was sufficiently ambiguous to be dismissed or re-interpreted. Although the contradictory evidence that emerged from animal research created severe difficulties, opinion had crystallized on the matter to the degree that the data were unable to force rejection of the hippocampal memory hypothesis. This necessarily led to the conclusion that the animal model is a poor one: either the human hippocampus is unique with respect to memory or the tests which are used in animals do not tap the same mnemonic processes that are impaired by the human lesions. Both these arguments are nearly impossible to refute. The brain of every species is different and there is no way in which monkeys and humans can be tested under identical conditions. There has never been much enthusiasm for the suggestion that the human hippocampus is so different from other animals that this uniqueness could account for the apparent differences between the behavioural effects of human and animal hippocampal lesions. However, many experimenters have devised clever tests of the possibility that the problem is in the animal behavioural measures. Given sufficient circularity of reasoning, the project must necessarily eventually be successful. The argument is that if the usual tests of learning and memory that are used with animals are not disrupted by hippocampal lesions, then these are not tests of the kinds of learning and memory defects displayed by human amnestics. One has only to search for tasks that are disrupted by hippocampal lesions in animals, and these then must tap the same memory processes that are disrupted by the human lesions. The possibility has rarely been seriously considered that it might be damage to some structure in the ventromedial quadrant of the temporal lobe other than the hippocampus that is responsible for the amnesia. The amygdala and entorhinal area have been ruled out by both the human and animal data. However, the temporal stem is a likely possibility. Its position makes it vulnerable to the surgical approach which was used in human medial temporal lobectomies, and its damage in animals produces deficits in learning and retention. When medial temporal lesions were made in monkeys in the same way that they were made in humans, inadvertent damage to the temporal stem occurred along with the intended amygdaloid and hippocampal injury. Symptoms characteristic of damage to the temporal cortex resulted from these lesions and they were probably caused by the damage to the stem...

Alcohol Amnestic Disorder↗
PubMed1988

Preserved memory abilities in thalamic amnesia.

The pattern of preserved learning abilities is described in a severely amnesic patient after bilateral thalamic infarction. Experimental findings cannot be accounted for both by the view that only episodic memory is impaired in amnesia, while semantic memory is spared, and by the theory that what is spared in amnesia is procedural learning contrasted with impaired declarative memory. In agreement with Warrington and Weiskrantz (1982), diencephalic amnesia is considered to be a disconnection syndrome between the frontal and temporal lobes. The conditions for showing spared and impaired memory in amnesics are specified on the basis of the performance of the patient and of the data available in the literature. This allows us to derive practical suggestions for programmes aimed at remediation of memory defects.

Adult↗
PubMed1992

Amnesia following a discrete basal forebrain lesion.

Destructive lesions of the basal forebrain are associated with memory impairment in both humans and experimental animals. The basal forebrain is thought to contribute to memory function by providing cholinergic innervation to critical memory structures such as the hippocampus and amygdala. In previously reported clinical cases of basal forebrain amnesia, multiple neuroanatomical regions have been damaged, preventing identification of the minimal critical lesion necessary to produce an amnestic syndrome. We describe a patient who developed persistent, global anterograde and retrograde amnesia following resection of a low-grade glioma. Post-surgical magnetic resonance imaging studies revealed a small discrete lesion, centred in the right diagonal band of Broca, that included the preoptic area, the anterior hypothalamus, the lamina terminalis and the paraterminal gyrus. The septal nuclei and the cell bodies of the nucleus basalis of Meynert appeared to have been spared, as were other structures in the medial temporal lobe and diencephalon. Our case provides critical support for the independent contribution of the basal forebrain, in particular the diagonal band nuclei, in memory function. We propose that our patient's amnesia resulted from disconnection of pathways between the diagonal band nuclei and the hippocampal region, depriving the hippocampus of cholinergic innervation.

Amnesia↗
PubMed1998

Episodic memory and the self in a case of isolated retrograde amnesia.

Isolated retrograde amnesia is defined as impaired recollection of experiences pre-dating brain injury with relatively preserved anterograde learning and memory. We present findings from a patient (M.L.) with isolated retrograde amnesia following severe traumatic brain injury (TBI) that address hypotheses of the interrelationships of focal neuropathology, episodic memory and the self. M.L. is densely amnesic for experiences predating his injury, but shows normal anterograde memory performance on a variety of standard tests of recall and recognition. The cognitive processes underlying this performance were examined with the remember/know technique, which permits separation of episodic from non-episodic contributions to memory tests by quantifying subjects' reports of re-experiencing aspects of the encoding episode. The results demonstrated that M.L. does not episodically re-experience post-injury events to the same extent as control subjects, although he can use familiarity or other non-episodic processes to distinguish events he has experienced from those he has not experienced. M.L.'s MRI showed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a frontotemporal band of fibres previously hypothesized to mediate retrieval of specific events from one's personal past. Recent functional neuroimaging evidence of an association between right frontal lobe functioning and episodic retrieval demands suggest that M.L.'s memory deficits are related to this focal injury. This hypothesis was supported by right frontal polar hypoactivation in M.L. in response to episodic retrieval demands when he was examined with a cognitive activation H2(15)O PET paradigm that reliably activated this frontal region in both healthy controls and patients with TBI carefully matched to M.L. (but without isolated retrograde amnesia). He also showed increased left inferomedial temporal activation relative to control subjects, suggesting that his spared anterograde memory is mediated through increased reliance on medial temporal lobe structures. Re-experiencing events as part of one's past is based on autonoetic awareness, i.e. awareness of oneself as a continuous entity across time. This form of awareness also supports the formulation of future goals and the implementation of a behavioural guidance system to achieve them. The findings from this study converge to suggest that M.L. has impaired autonoetic awareness attributable to right ventral frontal lobe injury, including right frontal-temporal disconnection. Reorganized brain systems mediate certain preserved cognitive operations in M.L., but without the normal complement of information concerning the self with respect to both past and future events.

Adult↗
PubMed2005

Pathologically proven frontotemporal dementia presenting with severe amnesia.

Early and severe memory impairment is generally held to be an exclusion criterion for the clinical diagnosis of frontotemporal dementia (FTD). However, clinical experience suggests that some patients with otherwise typical FTD can be amnesic from presentation, or even present solely with amnesia. A review of severe amnesia at presentation in patients with pathologically proven FTD is therefore warranted. The present study examined the records of all patients in the joint Cambridge-Sydney neuropathological series of patients with dementia and a pathological diagnosis of FTD to identify those for whom memory complaints were dominant at presentation. Eight of 71 patients met these criteria. For two patients, memory loss was the only complaint; for one patient, memory loss was accompanied by personality change; for two patients, memory loss was accompanied by prominent dysexecutive symptoms; and for three patients, memory loss was accompanied by apathy but no other behavioural changes. In seven patients local specialist teams initially diagnosed Alzheimer's disease; four patients entered anticholinesterase drug trials. All eight later developed behavioural features: in four, the diagnosis was revised to FTD, while in four the diagnosis of FTD was made only on neuropathological examination after death. In conclusion, severe amnesia at presentation in FTD is commoner than previously thought and the clinical consensus criteria for the diagnosis of FTD may need to be revised. The underlying basis of the memory impairments in patients with FTD may be heterogeneous, with different explanations in different subgroups.

Adult↗
PubMed2000

Midazolam: effects on amnesia and anxiety in children.

BACKGROUND: The minimum time interval between administration of oral midazolam and separation of children from their parents that ensures good anterograde amnesia has not been previously determined. This is of particular importance in a busy operating room setting where schedule delays secondary to midazolam administration may not be tolerated. METHODS: Children (n = 113) undergoing general anesthesia and surgery completed preoperative baseline memory testing using a validated series of picture cards and were randomly assigned to one of three midazolam groups or a control group. Exactly, 5, 10, or 20 min after receiving oral midazolam (0.5 mg/kg) or 15 min after receiving placebo, children were administered a second memory test that used pictures. Anxiety of children was assessed during induction of anesthesia with use of a validated anxiety measurement tool. Postoperatively, recall and recognition for picture cards seen during baseline testing and postintervention testing were assessed. RESULTS: Postoperatively, recall and recognition of pictures presented to patients after drug administration (anterograde amnesia) showed significant group differences (P = 0.0001), with recall impaired in the 10- (P = 0.004) and 20-min groups (P = 0.0001). Similarly, recognition memory was impaired in the 5- (P = 0.0008), 10- (P = 0.0001) and 20-min (P = 0.0001) groups. Significant anxiolytic effects of midazolam were observed as early as 15 +/- 4 min after midazolam administration (P = 0.02). CONCLUSIONS: Midazolam administered orally produces significant anterograde amnesia when given as early as 10 min before a surgical procedure.

Amnesia↗
PubMed1993

High resolution Tc-99m HMPAO SPECT in a patient with transient global amnesia.

This is a report of a patient who underwent high-resolution brain perfusion SPECT studies during and after an episode of transient global amnesia. During the attack, SPECT imaging showed increased perfusion in the left medial temporal region involving the amygdala and hippocampus. After recovery from amnesia, a follow-up SPECT examination showed slightly decreased perfusion in this region. These findings support the hypothesis that transient global amnesia is associated with transient hyperperfusion in the medial temporal brain structures, and confirm the utility of high-resolution SPECT imaging for the evaluation of the fine details of functional brain anatomy.

Adult↗
PubMed2002

Effect of stimulus intensity and number of treatments on ECS-related seizure duration and retrograde amnesia in rats.

BACKGROUND: Animal models are frequently used to generate and test hypotheses about amnesia resulting from electroconvulsive therapy (ECT). Although many predictors of ECT-induced amnesia are known, their relative effects have been inadequately researched in the context of the animal models. OBJECTIVE: We sought to determine the relative retrograde amnestic effects of electroconvulsive shock (ECS) stimulus intensity (dose) and number on strong memories in rats. We also sought to identify dose-dependent ceiling amnestic effects, if any. METHODS: Adult rats (n = 144) were overtrained in a passive avoidance task using a step down apparatus. The rats were then randomized in a factorial design to receive one, two, or three once-daily bilateral ECS at 0-mC (sham ECS), 30-mC, 60-mC, 120-mC, or 180-mC doses. Recall of the pre-ECS training was assessed 1 day after the last ECS. RESULTS: Retrograde amnesia was observed only in rats that received 3 ECS; dose-dependent amnestic effects did not emerge. Higher stimulus intensity was associated with a small (13%) but significant increase in motor seizure duration, but only at the first ECS; stimulus intensity did not influence the attenuation of seizure duration across repeated occasions of ECS. CONCLUSION: With bilateral ECS, the number of ECSs administered is a more important variable than the ECS dose in weakening a strong, recently acquired, noxious memory; this finding may have important clinical implications. Higher stimulus intensity marginally increases motor seizure duration at the first ECS but does not influence the decrease in seizure duration across repeated ECSs.

Amnesia, Retrograde↗
PubMed1989

Transient global amnesia.

Transient global amnesia is a benign, self-limiting disorder primarily involving a disturbance of memory. It occurs in late middle and older aged adults. Patients with this syndrome do not have a history of head trauma, drug or alcohol intoxication, hypoglycemia or psychologic dysfunction. Once the episode has cleared, there are no residual deficits except amnesia for the events which occurred during the episode. This article includes a case presentation in addition to discussion of the clinical features, etiology, treatment and nursing interventions for the patient with a transient global amnesia episode.

Amnesia↗
PubMed1997

Hypnosis, memory and amnesia.

Hypnotized subjects respond to suggestions from the hypnotist for imaginative experiences involving alterations in perception and memory. Individual differences in hypnotizability are only weakly related to other forms of suggestibility. Neuropsychological speculations about hypnosis focus on the right hemisphere and/or the frontal lobes. Posthypnotic amnesia refers to subjects' difficulty in remembering, after hypnosis, the events and experiences that transpired while they were hypnotized. Posthypnotic amnesia is not an instance of state-dependent memory, but it does seem to involve a disruption of retrieval processes similar to the functional amnesias observed in clinical dissociative disorders. Implicit memory, however, is largely spared, and may underlie subjects' ability to recognize events that they cannot recall. Hypnotic hypermnesia refers to improved memory for past events. However, such improvements are illusory: hypermnesia suggestions increase false recollection, as well as subjects' confidence in both true and false memories. Hypnotic age regression can be subjectively compelling, but does not involve the ablation of adult memory, or the reinstatement of childlike modes of mental functioning, or the revivification of memory. The clinical and forensic use of hypermnesia and age regression to enhance memory in patients, victims and witnesses (e.g. recovered memory therapy for child sexual abuse) should be discouraged.

Adult↗
PubMedDate not supplied

The many faces of amnesia.

Results from studies of retrograde amnesia provide much of the evidence for theories of memory consolidation. Retrograde amnesia gradients are often interpreted as revealing the time needed for the formation of long-term memories. The rapid forgetting observed after many amnestic treatments, including protein synthesis inhibitors, and the parallel decay seen in long-term potentiation experiments are presumed to reveal the duration of short-term memory processing. However, there is clear and consistent evidence that the time courses obtained in these amnesia experiments are highly variable within and across experiments and treatments. The evidence is inconsistent with identification of basic temporal properties of memory consolidation. Alternative views include modulation of memory and emphasize the roles that hormones and neurotransmitters have in regulating memory formation. Of related interest, converging lines of evidence suggest that inhibitors of protein synthesis and of other biochemical processes act on modulators of memory formation rather than on mechanisms of memory formation. Based on these findings, memory consolidation and reconsolidation studies might better be identified as memory modulation and "remodulation" studies. Beyond a missing and perhaps unattainable time constant of memory consolidation, some current views of memory consolidation assume that memories, once formed, are generally unmodifiable. It is this perspective that appears to have led to the recent interest in memory reconsolidation. But the view adopted here is that memories are continually malleable, being updated by new experiences and, at the same time, altering the memories of later experiences. Studies of memory remodulation offer promise of understanding the neurobiological bases by which new memories are altered by prior experiences and by which old memories are altered by new experiences.

Amnesia, Retrograde↗
PubMedDate not supplied

Temporally graded retrograde amnesia following separate and combined lesions of the perirhinal cortex and fornix in the rat.

The involvement of the perirhinal cortex and the fornix in retrograde and anterograde amnesia in the rat was investigated in this experiment. Male Sprague-Dawley rats were trained on a series of five visual discrimination problems at distinct time intervals prior to receiving bilateral, electrolytic lesions of the perirhinal cortex or the fornix, combined lesions of both these structures, or sham operations. Following recovery from surgery, rats were retested on the preoperatively learned discrimination problems, as well as learning a new discrimination and discrimination reversal. Results indicated that all animals with lesions exhibited temporally graded retrograde amnesia, whereby memories acquired in the recent past (1-3 weeks) were impaired, and memories acquired in the remote past (6-8 weeks) were spared. There was no difference in the magnitude of retrograde amnesia between the three lesion groups. Animals in the perirhinal, fornix, and combined lesion groups were able to learn a new discrimination problem at a rate comparable to control rats; however, the animals with lesions were impaired at learning the discrimination reversal. The perirhinal, fornix, and combined lesion animals also exhibited a significantly faster forgetting rate over a 2-week retention interval than control rats. These results suggest that medial temporal structures including the perirhinal cortex and the fornix are involved in the consolidation of mnemonic information and that their involvement in this process occurs over a discrete period of time.

Amnesia↗
PubMed2006

The anatomy of amnesia: neurohistological analysis of three new cases.

The most useful information about the anatomy of human memory comes from cases where there has been extensive neuropsychological testing followed by detailed post-mortem neurohistological analysis. To our knowledge, only eight such cases have been reported (four with medial temporal lobe damage and four with diencephalic damage). Here we present neuropsychological and post-mortem neurohistological findings for one patient (NC) with bilateral damage to the medial temporal lobe and two patients (MG, PN) with diencephalic damage due to bilateral thalamic infarction and Korsakoff's syndrome, respectively. All three patients exhibited a similar phenotype of amnesia with markedly impaired declarative memory (anterograde and retrograde) but normal performance on tests of nondeclarative memory (e.g., priming and adaptation-level effects) as well as on tests of other cognitive functions. Patient NC had damage to the hippocampus (dentate gyrus and the CA1 and CA3 fields) and layer III of the entorhinal cortex, but with relative sparing of the CA2 field and the subiculum. Patient MG had damage to the internal medullary lamina and mediodorsal thalamic nuclei. Patient PN had damage to the mammillary nuclei, mammillothalamic tracts, and the anterior thalamic nuclei. These findings illuminate several issues regarding the relation between diencephalic and medial temporal lobe amnesia, the status of recognition memory in amnesia, and the neuroanatomy of memory.

Adult↗
PubMed2001

H.M., word knowledge, and aging: support for a new theory of long-term retrograde amnesia.

This study develops a new theory of long-term retrograde amnesia that encompasses episodic and semantic memory, including word knowledge. Under the theory, retrograde amnesia in both normal individuals and hippocampal amnesics reflects transmission deficits caused by aging, nonrecent use of connections, and infrequent use of connections over the life span. However, transmission deficits cause severe and irreversible retrograde amnesia only in amnesics who (unlike normal persons) cannot readily form new connections to replace nonfunctioning ones. The results of this study are consistent with this theory: For low-frequency but not high-frequency words, a famous "hippocampal amnesic" (H.M.) at age 71 performed worse than memory-normal control participants in a lexical decision experiment and a meaning-definition task (e.g., What does squander mean?). Also as predicted, H.M.'s lexical decision performance declined dramatically between ages 57 and 71 for low-frequency words, but was age-invariant for high-frequency words.

Age Factors↗
PubMed1980

Time-dependency of neurohypophyseal peptide attenuation of puromycin amnesia in mice.

[Ile3, Arg8]vasopressin (arginine-vasotocin), as well as the C-terminal tripeptides of the neurohypophyseal hormones arginine and lysine vasopressin, Pro-Arg-Gly-NH2 and Pro-Lys-Gly-NH2, were protective against puromycin-induced amnesia in mice when administered 24h before training. The N-protected tripeptide derivative, Z-Pro-Lys-Gly-NH2, was effective when given 5 days before training. The effectiveness of all peptides to attenuate puromycin-induced amnesia decreased as the interval between training and peptide treatment increased, indicating that the peptides influence memory processes, rather than general arousal. Z-Pro-Lys-Gly-NH2 was active at 24h after training, when the other peptides were no longer effective. Although it seems clear that neurohypophyseal hormones per se can attenuate puromycin-induced amnesia, these results are in line with the possibility that some portion of hormone action may be mediated via formation of longer-lived hormone fragments in the CNS.

Amnesia↗
PubMed1990

Transient global amnesia: incidence in an urban population.

We prospectively identified patients with transient global amnesia in an urban population of 163,000. In 1982, 16 patients experienced their first transient global amnesia. The annual incidence rate was 10 per 100,000 population, and 32 per 100,000 among those aged 50 years or older. There was a substantial female predominance in the incidence of transient global amnesia.

Aged↗