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PubMed1999

Trauma-induced dissociative amnesia in World War I combat soldiers.

OBJECTIVE: This study relates trauma-induced dissociative amnesia reported in World War I (WW I) studies of war trauma to contemporary findings of dissociative amnesia in victims of childhood sexual abuse. METHOD: Key diagnostic studies of post-traumatic amnesia in WW I combatants are surveyed. These cover phenomenology and the psychological dynamics of dissociation vis-à-vis repression. RESULTS: Descriptive evidence is cited for war trauma-induced dissociative amnesia. CONCLUSION: Posttraumatic amnesia extends beyond the experience of sexual and combat trauma and is a protean symptom, which reflects responses to the gamut of traumatic events.

Adult↗
PubMed1991

[The concept of amnesia and quantitative assessment of amnesic disorders].

This article presents first a short historical overview of the different viewpoints concerning psychiatric approaches to define the concept "amnesia" (Ribot, Korsakow, K. Schneider, Bleuler, Bonhoeffer et al.). A generally accepted result is the differentiation between retrograde and anterograde amnesia. Research work of the last two decades has focussed on the experimental investigation of anterograde amnesia, the so-called amnesic syndrome. In this context four main factors responsible for memory performance are distinguished: encoding, retrieval, forgetting and interference. One of the main results of neuropsychological research in amnesia consists in having discovered a set of symptoms or features common to most if not all forms of amnesia. These features appear regardless of etiology and locus of lesion. This set or features is described in detail in the paper. On the basis of these amnesic features a clinical test was developed, the Berliner Amnesie Test (BAT). This standardized test can be used for the assessment from mild up to severe memory disorders.

Alzheimer Disease↗
PubMed1991

A developmental account of early childhood amnesia.

This study was an attempt to demonstrate the utility of a developmental approach to the study of early childhood amnesia. Working from a model of early childhood memory development proposed by Nelson and Ross (1980), I hypothesized that children would show early childhood amnesia and that this could be tested by comparing obtained estimates of memory strength to values predicted by a standard retention function. The data confirm this hypothesis for 6- and 10-year-old children, and suggest that the early childhood amnesia period extends from birth to a point between the third and fourth birthdays. The data also support a prediction, derived from the aforementioned model, that children would report a disproportionate number of general memories from the amnesia period. Thus, the developmental model provides a useful vehicle for examining early childhood amnesia and helps to frame further questions such as why some specific memories from this period are retained even though most are lost.

Amnesia↗
PubMed1995

Dense amnesia in a professional musician following herpes simplex virus encephalitis.

We describe the memory functioning of C, a professional musician who became amnesic following herpes simplex encephalitis in 1985. Although transient amnesia in a professional musician has previously been described, this is the first reported case of chronic amnesia in a highly talented professional musician. C is unusual in three respects. First, his amnesia is particularly severe. Second, his amnesia includes semantic as well as episodic memory deficits. Third, he believes he has just woken up and his preoccupation with this state of 'just wakening' has persisted for over 9 years. This appears to be the result of a delusion rather than the consequence of his amnesia.

Amnesia↗
PubMed2005

Functional focal retrograde amnesia: lost access to abstract autobiographical knowledge?

We describe three patients exhibiting an acute reversible amnesia characterised by an impaired recollection of past events with preserved anterograde memory, thus consistent with a focal retrograde amnesia (FRA). This occurred after variable events: state of fugue, road accident, post-traumatic headache. Retrograde amnesia affected autobiographical memory so severely as to cover all of the patients' lives and to erase knowledge of their own identity. The retrieval of public events was variably affected, ranging from normality to severe impairment. No lesions were found on neuroimaging, and neurophysiological findings were unimpressive. FRA subsided in a few days, leaving a gap for the onset. The hypothesis of a psychogenic amnesia is considered, but overcoming the organic/psychogenic dichotomy the episodes appear as examples of "functional" memory inhibition, potentially triggered by different conditions, including events classifiable as psychic trauma. The clinical and neuropsychological traits of functional FRA are discussed. According to a current theory of autobiographical memory, the memory profile may be explained by a lost access to abstract autobiographical knowledge. Given some analogies with the more common transient global amnesia, a mechanism of spreading depression may also be hypothesised for functional FRA.

Adult↗
PubMed1990

Effect of flumazenil on midazolam-induced amnesia.

We have studied the effect of i.v. flumazenil 0.01 mg kg-1 on the amnesia and sedation caused by midazolam 2 mg and 5 mg i.v. in volunteers in order to determine the relationship between the actions of the antagonist on these two effects. Midazolam caused dose-dependent central neural depression as assessed by critical flicker fusion frequency, and dose-dependent amnesia for word cards. In subjects given flumazenil 5 min after administration of midazolam, fusion frequency readings and memory were restored to levels comparable to those before midazolam administration. These two effects of flumazenil were similar in time course and extent, suggesting that they share the same mechanism of action. Flumazenil given alone had no effect on memory. The study has demonstrated anterograde amnesia following benzodiazepine administration and antagonism by flumazenil. There was neither retrograde amnesia nor retrograde antagonism of amnesia.

Adult↗
PubMed2004

Double-blind randomized controlled trial to determine extent of amnesia with midazolam given immediately before general anaesthesia.

BACKGROUND: Anterograde, but not retrograde, amnesia has been demonstrated following midazolam administration. However, there have been no studies investigating whether or not immediate retrograde amnesia can be produced with midazolam. METHODS: After ethics committee approval and consent, 40 adult patients undergoing surgery and general anaesthesia were randomly allocated to one of four groups: midazolam 2 mg, midazolam 5 mg, midazolam 10 mg or control (normal saline). Measurements were made from 12 min prior to induction of anaesthesia, and the study drug was administered 8 min prior to induction of anaesthesia. Midazolam effects were measured using visual recognition of posters, recall of specific events, bispectral index (BIS) and sedation visual analogue score. RESULTS: Recognition and recall rates were similar between groups up until the time of study drug administration, with no evidence of retrograde amnesia (all P>0.3). There was a dose-dependent deterioration in visual recall (P=0.002), event recollection (P<0.001), BIS (P<0.001) and sedation score (P<0.001) following i.v. midazolam when compared with control. CONCLUSIONS: We found no evidence that i.v. midazolam 2-10 mg produces immediate retrograde amnesia. Midazolam causes anterograde amnesia in a dose-responsive manner.

Adult↗
PubMed1990

Diencephalic amnesia.

The anatomical basis and cognitive profile of diencephalic amnesia remain unclear. We report a two-part study. First, we studied 4 patients with bilateral medial thalamic infarctions using magnetic resonance imaging and comprehensive neuropsychological testing. All patients were followed for more than 1 year. Using a stereotactic method, we plotted the lesions in an atlas delineating the probable structure involved. Secondly, in 2 monkeys, using autoradiography, we traced the pathway from the amygdala to the dorsomedial nucleus, paying particular attention to the intrathalamic course of the amygdalothalamic projections. Our findings were (1) patients develop amnesia when infarctions are located anteriorly; (2) in patients with amnesia, the lesions can be small and strategically located, probably interfering with both hippocampal-related neural structures such as the mamillothalamic tract, and amygdala-related neural structures such as the ventroamygdalofugal pathway; and (3) a specific component of the latter is situated lateral but immediately adjacent to the mamillothalamic tract in the monkey, enabling both structures to be damaged bilaterally by small mirror image lesions. The amnesia is characterized by deficits in anterograde verbal and visual learning and in retrograde amnesia, but motor learning is preserved. We raise the possibility that bilateral diencephalic lesions may interfere particularly with temporal aspects of memory.

Adult↗
PubMed2001

Profound amnesia and confabulation following traumatic brain injury.

Amnesia and confabulation may persist following acute aneurysmal hemorrhage of the anterior communicating artery, chronic alcoholic Korsakoff's syndrome, and late-stage dementia of the Alzheimer type. However, there is a paucity of information regarding the persistence of these symptoms following traumatic brain injury. We present the case of JL, a 43-year-old male with persistent and severe anterograde amnesia for verbal and visual information with co-occurring provoked confabulation which persists well into the chronic phase of recovery after a severe traumatic brain injury. Neuropsychological testing at 7 weeks post-injury demonstrated severe anterograde amnesia with co-occurring confabulation. Follow-up testing at 9.5 months post-injury showed persistent and severe anterograde amnesia and provoked confabulation despite superior non-verbal intelligence and above average attentional and perceptual abilities. Late computed tomography showed chronic hypodense regions in the temporal lobes, bilaterally (L > R), and in the region of the left ventrolateral frontal lobe. This case demonstrates that anterograde amnesia and provoked confabulation may persist long after the acute phase of recovery after traumatic brain injury, and also supports previous research which asserts that medial temporal lobe damage must be accompanied by ventral frontal lobe pathology to produce the amnestic-confabulatory syndrome.

Adult↗
PubMed1998

Nefiracetam prevents propofol-induced anterograde and retrograde amnesia in the rodent without compromising quality of anesthesia.

BACKGROUND: Propofol is a short-acting intravenous anesthetic agent. However, cognitive function remains depressed for several hours thereafter. We have evaluated the ability of nefiracetam, a novel cognition-enhancing agent, to alleviate propofol-induced amnesia in a rodent model of learning. METHODS: Rats were trained in a one-trial, step-through, light-dark passive avoidance paradigm. Propofol (10 and 75 mg/kg) was administered by the intraperitoneal route at 15 min before training and separately at increasing times in the immediate 0-6 h post-training period (100 and 150 mg/kg). Nefiracetam, 9 mg/kg, was administered by the intraperitoneal route 1 h before training. Animals were tested for recall at the 12 h post-training time, and after their killing, immunocytochemistry was used to determine the increase in hippocampal neuronal polysialylation, an event associated with memory consolidation. Induction and duration of anesthesia induced by propofol was determined using tail pinch and pedal withdrawal reflexes. RESULTS: Propofol-induced anterograde amnesia occurred in a dose-dependent manner. Induction of retrograde amnesia required a higher dose of propofol, which anesthetized the animals and was effective only in the immediate 3-h post-training period. In the absence of any evident effect on the onset or duration of anesthesia, nefiracetam prevented both forms of propofol-induced amnesia and preserved the learning-associated changes of neuronal polysialylation state. CONCLUSIONS: The ability of nefiracetam to prevent propofol-induced anterograde and retrograde amnesia is proposed to be indirect and to result from modulation of gene transcription in a manner that initiates a cascade of events involving protein synthesis leading to synaptic growth associated with the formation of the long-term memory trace.

Amnesia↗
PubMedDate not supplied

Transient epileptic amnesia in dementia: a treatable unrecognized cause of episodic amnestic wandering.

The authors present two patients with dementia who displayed recurrent transient episodes of amnestic wandering and disorientation characterized by getting lost in familiar environments. At other times these patients did not wander or become disoriented. The inability to recall any information during these episodes, and the marked difference of the episodic amnesia exacerbations from the progressive amnesia characteristic of Alzheimer disease seen in these patients led to their evaluation. These clinical episodes and the bilateral interictal epileptiform electroencephalographic changes found in both patients led to the diagnosis of transient epileptic amnesia, a syndrome that can be diagnostically elusive. These transient amnestic wandering events subsided after treatment with antiepileptic drugs in both patients. The authors suggest that transient wandering of this type may be caused by ictal events or postictal confusional states. This report emphasizes the importance of recognizing transient epileptic amnesia as an easily treatable cause of episodic behavioral abnormalities responsive to antiepileptic therapy, especially in those patients who have a markedly inconsistent pattern of wandering, disorientation in familiar settings, and amnesia exacerbation manifested by no recall of the emotional stress of getting lost or of any information during these episodes. Recognition of this type of behavioral disruption and its proper treatment can lead to improved quality of life for these patients, maintain these patients in their homes and out of chronic care institutions longer, and facilitate the community's and caretaker's interactive roles with the patient.

Aged↗
PubMed1979

Transient global amnesia: an extensive case report.

A case of transient global amnesia was studied in detail. Of note was a temporally extensive, although quite patchy, retrograde amnesia during the event for information recallable at other times. While a consolidation block can explain the anterograde amnesia in transient global amnesia, the profound retrograde amnesia requires an additional block in the retrieval of old, established memories.

Amnesia↗
PubMed1997

Transient global amnesia: implicit/explicit memory dissociation and PET assessment of brain perfusion and oxygen metabolism in the acute stage.

OBJECTIVES: To assess explicit memory and two components of implicit memory--that is, perceptual-verbal skill learning and lexical-semantic priming effects--as well as resting cerebral blood flow (CBF) and oxygen metabolism (CMRO2) during the acute phase of transient global amnesia. METHODS: In a 59 year old woman, whose amnestic episode fulfilled all current criteria for transient global amnesia, a neuropsychological protocol was administered, including word learning, story recall, categorical fluency, mirror reading, and word stem completion tasks. PET was performed using the (15)O steady state inhalation method, while the patient still exhibited severe anterograde amnesia and was interleaved with the cognitive tests. RESULTS: There was a clear cut dissociation between impaired long term episodic memory and preserved implicit memory for its two components. Categorical fluency was significantly altered, suggesting word retrieval strategy--rather than semantic memory--impairment. The PET study disclosed a reduced CMRO2 with relatively or fully preserved CBF in the left prefrontotemporal cortex and lentiform nucleus, and the reverse pattern over the left occipital cortex. CONCLUSIONS: The PET alterations with patchy CBF-CMRO2 uncoupling would be compatible with a migraine-like phenomenon and indicate that the isolated assessment of perfusion in transient global amnesia may be misleading. The pattern of metabolic depression, with sparing of the hippocampal area, is one among the distinct patterns of brain dysfunction that underlie the (apparently) uniform clinical presentation of transient global amnesia. The finding of a left prefrontal hypometabolism in the face of impaired episodic memory and altered verbal fluency would fit present day concepts from PET activation studies about the role of this area in episodic and semantic memory encoding/retrieval. Likewise, the changes affecting the lenticular nucleus but sparing the caudate would be consistent with the normal performance in perceptual-verbal skill learning. Finally, unaltered lexical-semantic priming effects, despite left temporal cortex hypometabolism, suggest that these processes are subserved by a more distributed neocortical network.

Acute Disease↗
PubMed1997

Changes in cerebral blood flow and vasoreactivity in response to acetazolamide in patients with transient global amnesia.

OBJECTIVE: Previous reports about changes in cerebral blood flow (CBF) in transient global amnesia disclosed decreased flow in some parts of the brain. However, CBF analyses in most reports were qualitative but not quantitative. The purpose of this study was to determine changes in CBF in transient global amnesia. METHODS: The CBF was measured and the vasoreactive response to acetazolamide was evaluated in six patients with transient global amnesia using technetium-99m hexamethylpropylene amine oxime single-photon emission computed tomography (SPECT). The CBF was measured during an attack in two patients and soon after an attack in the other four. About one month later, CBF was re-evaluated in each patient. RESULTS: Two patients examined during an attack and one patient examined five hours after an attack had increased blood flow in the occipital cortex and cerebellum. Three patients examined at six to 10 hours after an attack had decreased blood flow in the thalamus, cerebellum, or putamen. These abnormalities of blood flow almost disappeared in all patients one month after onset. The vasodilatory response to acetazolamide, which was evaluated initially using SPECT, was poor in areas of increased blood flow. By the second evaluation of CBF with acetazolamide, the vasodilatory response had returned to normal. CONCLUSIONS: In a patient with transient global amnesia, CBF increased in the vertebrobasilar territory during the attack and decreased afterwards. The vasodilatory response to acetazolamide may be impaired in the parts of the brain with increased blood flow. It is suggested that transient global amnesia is distinct from migraine but may share the same underlying mechanism.

Acetazolamide↗
PubMed1998

Possible mechanism of alprazolam-induced amnesia in mice.

Alprazolam produced anterograde as well as retrograde amnesia in mice assessed using elevated plus-maze. Flumazenil (10 mg/kg i.p.) attenuated anterograde and retrograde amnesia produced by alprazolam. It is proposed that anterograde amnesia produced by alprazolam may be mediated through the activation of benzodiazepine receptors. Retrograde amnesia of alprazolam may be mediated through the blockade of PAF receptors. Moreover, flumazenil facilitates learning and memory perhaps by modulating the release of PAF and consequently attenuated alprazolam and BN-50730-(PAF receptor antagonist)-induced retrograde amnesia.

Alprazolam↗
PubMed1999

Memories of childhood abuse: dissociation, amnesia, and corroboration.

OBJECTIVE: This study investigated the relationship between self-reported childhood abuse and dissociative symptoms and amnesia. The presence or absence of corroboration of recovered memories of childhood abuse was also studied. METHOD: Participants were 90 female patients admitted to a unit specializing in the treatment of trauma-related disorders. Participants completed instruments that measured dissociative symptoms and elicited details concerning childhood physical abuse, sexual abuse, and witnessing abuse. Participants also underwent a structured interview that asked about amnesia for traumatic experiences, the circumstances of recovered memory, the role of suggestion in recovered memories, and independent corroboration of the memories. RESULTS: Participants reporting any type of childhood abuse demonstrated elevated levels of dissociative symptoms that were significantly higher than those in subjects not reporting abuse. Higher dissociative symptoms were correlated with early age at onset of physical and sexual abuse and more frequent sexual abuse. A substantial proportion of participants with all types of abuse reported partial or complete amnesia for abuse memories. For physical and sexual abuse, early age at onset was correlated with greater levels of amnesia. Participants who reported recovering memories of abuse generally recalled these experiences while at home, alone, or with family or friends. Although some participants were in treatment at the time, very few were in therapy sessions during their first memory recovery. Suggestion was generally denied as a factor in memory recovery. A majority of participants were able to find strong corroboration of their recovered memories. CONCLUSIONS: Childhood abuse, particularly chronic abuse beginning at early ages, is related to the development of high levels of dissociative symptoms including amnesia for abuse memories. This study strongly suggests that psychotherapy usually is not associated with memory recovery and that independent corroboration of recovered memories of abuse is often present.

Adolescent↗
PubMed2000

Electroencephalographic indices related to hypnosis and amnesia during propofol anaesthesia for cardioversion.

Most previous studies which have assessed the depth of anaesthesia using the Bispectral Index (BIS) have used multi-agent anaesthetics with relatively slow induction and recovery times. Elevation of electroencephalographic (EEG) Beta/Alpha Ratio has been linked to onset of midazolam amnesia. Propofol anaesthesia for cardioversion in 19 patients enabled us to profile the changes in BIS and Beta/Alpha Ratio during a short, single-agent anaesthetic with a relatively rapid induction and recovery period. BIS values did not alter significantly through onset of amnesia and hypnosis as compared with awake values. Cardioversion occurred over a wide range of BIS values (38 to 94), with recovery at a median BIS value of 79. We observed the BIS to lag about 60 s behind the clinical situation (termed BIS60). The BIS60 more closely tracked the clinical level of consciousness, showing statistically significant differences from the uncorrected BIS. (amnesia (median BIS60 = 82, P = 0.02), hypnosis (median BIS60 = 67, P = 0.01), eye opening (median BIS60 = 90, P = 0.001)). An early EEG Beta/Alpha Ratio peak occurred at a mean of 4.6 s (SD = 16.6) after clinical amnesia onset and a late peak at a mean 58 s (SD = 144) after eye opening. There was no significant EEG response to cardioversion. We conclude that: (1) in rapidly changing conditions, the value of the BIS most accurately reflects the level of consciousness of the patient about 60 s in the past, and (2) the onset and offset of propofol-induced amnesia commonly corresponds to a peak in Beta/Alpha Ratio of the EEG.

Adult↗
PubMed1995

Probable propafenone-induced transient global amnesia.

OBJECTIVE: To describe a probable case of transient global amnesia caused by propafenone. This adverse effect has not been previously described for this agent. CASE SUMMARY: A 61-year old man with a history of sick sinus syndrome with persistent atrial fibrillation and infrequent premature ventricular contractions was admitted to the hospital for symptoms of amnesia and disorientation to time, place, and date. He began taking propafenone only 6 days prior to admission because of uncontrolled atrial fibrillation and symptoms of fatigue. His atrial fibrillation subsequently had converted to normal sinus rhythm while he received propafenone without adverse effects prior to this episode. His symptoms of amnesia resolved approximately 6-7 hours after discontinuing the propafenone therapy. DISCUSSION: Propafenone is a class 1C antiarrhythmic agent that blocks fast sodium channels in heart muscle and Purkinje fibers similar to the action of encainide and flecainide. It also produces weak beta- and calcium-channel blockade. It has a significant adverse effect profile, with 30-45% of patients reporting cardiac adverse effects and 15-20% experiencing noncardiac events. Central nervous system effects that parallel amnesia have been reported in 10-15% of the patients, including dizziness, ataxia, drowsiness, fatigue, confusion, and paranoia. Propafenone's distribution, clearance, and structural similarity to propranolol contribute to its central nervous system effects. CONCLUSIONS: The rapid resolution of this patient's symptoms after discontinuing propafenone therapy and the absence of recurrence lend credence to the probability of this effect. Comparable adverse effects, such as disorientation and temporary amnesia, have been reported in patients in the analogous agent, propranolol. Consequently, this is a likely, although rare, possible adverse effect with propafenone for which patients should be monitored.

Amnesia↗