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PubMed2002

Two cases of functional focal retrograde amnesia with impairment of object use.

We report on two patients, TH and KN, with focal retrograde amnesia (FRA). Their memory loss regarding life events extended to their whole lives, whereas they could acquire and retain new information. They also showed prominent deficits in production and comprehension of common words. In addition, at least in the testing situation, they were impaired in their recognition and use of familiar objects. Although both cases of FRA followed an episode that can cause brain pathology, MRI revealed no structural abnormality in either patient. Stressful situations preceding the onset were evident in KN, but not in TH. We discuss their impairments of object knowledge from a neuropsychological perspective, and we interpret the etiology of their condition as a functional rather than a psychogenic amnesia.

Adult↗
PubMed1997

Preservation of famous person knowledge in a patient with severe post anoxic amnesia.

A 58 year old patient (ES) suffered severe anterograde and retrograde amnesia following prolonged cardiac arrest with presumed hypoxic brain damage. Personally relevant autobiographical memory was severely impaired as was knowledge of public events. In contrast, knowledge of famous people was very well preserved. This findings has implications for the organisation of remote memory. Knowledge of people is clearly represented independently from autobiographical memory. We argue that this pattern of profound autobiographical amnesia may result from either multifocal neocortical damage (as in this case) or a failure of the "thematic framework" system involved in the active reconstruction of autobiographical memory, as hypothesised in another patient with thalamic infarction who showed a similar pattern of results (Hodges and McCarthy, 1993).

Amnesia↗
PubMed1999

Retrograde amnesia for world knowledge and preserved memory for autobiographic events. A case report.

A patient (PC) with severe and chronic retrograde amnesia for world knowledge (tested with famous events and famous faces), but unimpaired autobiographical memory is described. The 64-year-old man had traumatic brain injury four years prior to the present evaluation. Current brain imaging showed principally damage involving the infero-lateral prefrontal and the lateral temporal regions of the left-hemisphere. PC was of average intelligence, had no depression and only minor language problems, but manifested some additional anterograde memory deficits and performed subaverage in various frontal lobe-sensitive tests. Patient PC represents one of the very few cases with a preserved retrograde episodic and an impaired retrograde knowledge system, showing a dissociation between preserved retrieval of autobiographical events and amnesia for nonpersonal famous events. It is hypothesized that the sparing of autobiographical memories can be linked to the integrity of the right frontal and temporo-polar cortices.

Amnesia, Retrograde↗
PubMed1994

Post-traumatic retrograde amnesia with selective impairment of autobiographical memory.

A selective, temporally limited retrograde amnesia, confined to autobiographical memory, was the only sequela of a "minor" head trauma in two young men. The retrograde memory gap covered about one year of life before the trauma and persisted for several months, without any anterograde deficit or other cognitive disturbances. This unusual pattern of retrograde amnesia deserves close consideration and points to the dissociation of memory subsystems and mechanisms.

Adult↗
PubMed1979

Normal and abnormal forgetting in organic amnesia: effect of locus of lesion.

Speed of forgetting by the patient H.M. was examined in two experiments using picture recognition tests. In both experiments stimulus duration was manipulated to equalize initial performance by H.M. and others, and speed of forgetting was investigated over a period of one week. In the first experiment, where initial performance was high, H,M. appeared to forget faster than normal controls. In the second experiment, where initial performance was somewhat lower, H.M. was shown to forget faster than both controls and Korsakoff patients (who forget at a normal rate). These results suggest a functional difference between the amnesia with hippocampal lesions and the amnesia of Korsakoff's disease.

Alcohol Amnestic Disorder↗
PubMed1983

Color "amnesia" without aphasia.

Following an apparent left parietal CVA, a patient developed a severe and nearly complete color amnesia which was not associated with any disturbance in color vision or color perception. Like all previously reported cases with color amnesia, this patient was alexic but, unlike most previously reported cases, he was not aphasic.

Agnosia↗
PubMed1984

Can amnesia be caused by damage of a single brain structure?

The relation of amnesia and damage to some particular brain regions is discussed by reviewing the main findings of selected human case reports. It is argued that frequently a too straightforward and unidimensional interpretation of the relations between brain damage and a behavioral deficit is formulated in such reports. Evidence obtained by modern anatomical techniques as well as the widespread and time-dependent effects of lesions make it necessary to consider a lesion of a particular structure of the brain and correlated mnemonic disturbances as possibly due to an altered equilibrium in an extensive network of the brain. The primary lesion of one or the other specific structure may lead to severe and lasting amnesia or may fail to do so depending on its influence on other brain regions.

Adult↗
PubMed1996

Spared retrograde memory with anterograde amnesia and widespread cognitive deficits.

A case is described of a young male who suffered head injuries in a motor accident and subsequently displayed a severe anterograde amnesia in the presence of a relatively intact retrograde memory. He also demonstrated marked impairment of general intellectual ability, naming, perceptual skills and executive functioning. This case demonstrates a striking dissociation between anterograde and retrograde memory. Moreover the retention of retrograde memory in the face of such severe and global cognitive impairment accentuates the dissociation or isolability of retrograde memory. It is further argued that while frontal impairment occurred in this case it lacks any of the hallmarks of frontal amnesia. The case is further evidence for the fractionation of amnesic syndromes.

Adult↗
PubMed2001

Effects of adenosine receptor agonists and antagonists on pentylenetetrazole-induced amnesia.

The effect of adenosine agents on amnesia induced by pentylenetetrazole was examined in mice. Post-training administration of pentylenetetrazole (50 and 60 mg/kg) disrupted 24-h retention of a single-trial passive avoidance task. The adenosine receptor antagonists, theophylline (2.5-25 mg/kg) and 8-phenyltheophylline (0.5-2 mg/kg), administered 30 min before and just after training at doses which did not affect retention, reduced the amnestic effect of pentylenetetrazole in a dose-dependent manner. Post-training administration of the adenosine A(1) receptor agonists, N(6)-cyclohexyladenosine (CHA, 0.1 and 0.5 mg/kg) and N(6)-phenylisopropyladenosine (R-PIA, 0.03 and 0.1 mg/kg), but not the adenosine A(2) receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA, 0.01 and 0.001 mg/kg), impaired retention. Nonamnestic doses of CHA and R-PIA potentiated the disruption induced by a lower dose of pentylenetetrazole (40 mg/kg). NECA did not induce any response in this respect. It is suggested that an adenosine A(1) receptor mechanism is involved in amnesia induced by pentylenetetrazole.

Adenosine↗
PubMed1996

U-50488H, a selective kappa-opioid receptor agonist, improves carbon monoxide-induced delayed amnesia in mice.

The effects of trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl] cyclohexyl) benzeneacetamide methanesulfonate salt (U-50488H) on carbon monoxide (CO)-induced amnesia in mice were investigated using spontaneous alternation and step-down type passive avoidance tasks. The lower percentage alternation and shorter median step-down latency in the retention test of the CO-exposed group indicated that memory deficiency occurred in mice when behavioral testing commenced 5-7 days after CO exposure. Administration of U-50488H (0.21 and 0.64 mumol/kg s.c.) 25 min before spontaneous alternation performance or the first training session of the passive avoidance task improved the CO-induced impairment of alternation performance and passive avoidance tasks. To determine whether the effect of U-50488H was mediated via kappa-opioid receptors, we attempted to block its action using a selective kappa-opioid receptor antagonist (nor-binaltorphimine). Nor-binaltorphimine (5.44 nmol/mouse i.c.v.) blocked the effect of U-50488H on CO-induced delayed amnesia. Furthermore, a low dose of scopolamine (0.41 mumol/kg s.c.) also blocked the ameliorating effect of U-50488H. U-50488H (0.21-2.15 mumol/kg s.c.) did not facilitate the acquisition of memory in normal mice. These results suggest that U-50488H modulates the kappa-opioid receptor-mediated opioid neuronal system and activates the cholinergic neuronal system, and that it ameliorates the disruptive effect of CO on acquisition and/or consolidation of memory.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1997

In vitro aggregation facilities beta-amyloid peptide-(25-35)-induced amnesia in the rat.

The beta-amyloid peptide-(25-35) fragment, but not beta-amyloid peptide-(1-28), shares with beta-amyloid protein-(1-42) the ability to self-aggregate and to induce neurotoxicity in vitro. This study examined the induction of amnesia in rats given intracerebroventricularly soluble or aggregated beta-amyloid peptide-(25-35) (5-45 nmol), or beta-amyloid peptide-(1-28) (15 nmol). Memory deficit in the water-maze test, examined 14 days after aggregated beta-amyloid peptide-(25-35) injection, was more pronounced than with soluble beta-amyloid peptide-(25-35). beta-Amyloid peptide-(1-28) only affected retention. These results confirm the direct amnesic properties of beta-amyloid peptides in the rat brain and showed that prior peptide aggregation markedly facilitates the appearance of amnesia.

Amnesia↗
PubMed1998

Proton magnetic resonance spectroscopy during transient global amnesia.

There is uncertainty about the etiology of transient global amnesia and none of the pathogenetic hypotheses proposed so far, i.e. transient ischemia, epileptic discharge and spreading depression of cortical electrical activity, is completely satisfactory. Using water suppressed proton magnetic resonance spectroscopy we studied one patient during a typical episode of transient global amnesia and 2 weeks thereafter in order to investigate the metabolic changes in the hippocampal region. In both hippocampi, spectra of N-acetyl-aspartate, creatine-phosphocreatine, compounds containing choline and lactate failed to show changes consistent with cerebral ischemia, both in the acute phase and in the follow-up. Spreading depression in response to emotional stress seems a likely explanation in this patient, who suffered from migraine in the past.

Aged↗
PubMed1986

Transient global amnesia and the amnestic syndrome.

Transient global amnesia is an unusual form of the amnestic syndrome in that it is completely reversible in most patients. The etiology of transient global amnesia is poorly understood, although involvement of the medial temporal lobe is most likely. The literature suggests that once an underlying structural lesion has been ruled out, cases can be divided into three groups: patients with a past history of migraine headaches, those who have no obvious underlying precipitating factors, and those with associated neurologic deficits during a spell and risk factors for cerebrovascular disease. Patients in the first group tend to have attacks at an earlier age and to have an increased recurrence rate but, like those in the second group, have a good prognosis. Patients in the third group often have onset later in life, and as many as 10% may have a stroke or dementia. Whether or not this is a higher incidence than should be expected in persons of this age group has not been determined. Although sophisticated testing may show persistence of the memory defect, most patients eventually recover completely.

Adolescent↗
PubMed2002

Temporal order memory in patients with Korsakoff's syndrome and medial temporal amnesia.

Two groups of patients with global amnesia resulting either from Korsakoff's syndrome (KS) or from medial temporal lobe (MTL) damage were compared with groups of matched healthy control subjects on a list discrimination paradigm. Item recognition memory was matched across the amnesic and control groups in order to determine whether KS, but not MTL amnesics are disproportionately impaired on list discrimination as predicted by Parkin's [Functional significance of etiological factors in human amnesia. In: Squire LR, Butters N, editors. Neuropsychology of memory, 2nd ed. New York: The Guilford Press, 1992] hypothesis. However, both patient groups were impaired disproportionately on the temporal order memory task, which is inconsistent with Parkin's hypothesis. It remains possible that the KS patients are more disproportionately impaired than those with MTL damage because both patient groups performed at floor on the list discrimination task. The results are consistent with theories that postulate a critical role for the hippocampus in the kind of associative memory which underlies memory for temporal order, but not in recognition of single items or arbitrary associations between items of similar kinds.

Adolescent↗
PubMed2002

The effect of retrieval instructions on false recognition: exploring the nature of the gist memory impairment in amnesia.

In previous studies, we found that amnesic patients show reduced levels of false recognition in a converging semantic associates paradigm. This finding was interpreted as reflecting an impairment in amnesia in the ability to form, retain and/or retrieve a well-organized representation of the semantic 'gist' of studied items. To further explore the nature of amnesics' impairment in gist memory, the current study compared performance in two retrieval conditions. In a standard retrieval condition, participants were asked to endorse on a recognition test only items that had appeared on the study list. In a meaning retrieval condition, participants were asked to endorse any item that shared the meaning of studied items. Meaning retrieval instructions failed to eliminate the reduction in false recognition in amnesia. These results suggest that amnesics' impairment in gist memory is not attributable to a failure to access well-formed gist representations when given item-specific retrieval cues. Rather, it suggests that amnesic patients are impaired in their ability to encode, store, or maintain strong gist information.

Adult↗
PubMed1999

Ketaset-Rompun extends the temporal gradient for hypothermia-induced retrograde amnesia.

In studies of experimentally induced retrograde amnesia (RA), as the interval between training and the amnestic treatment is lengthened, amnesia decreases (4). This temporal gradient for RA has been reported with a wide variety of amnestic agents, including RA produced by thermoregulatory disturbances (8). This temporal gradient for RA is not unlike certain characteristics of classical conditioning, where weaker conditioned responding occurs when the interval between the conditioned stimulus (CS) and unconditioned stimulus (US) is lengthened. Furthermore, there is evidence that administration of anesthetics can lengthen the "effective conditioning" interval between the CS and US, as demonstrated in a conditioned taste-aversion (CTA) procedure (10). In that study, little conditioning was observed when a 3-h delay (or more) was incorporated between presentations of the CS (flavor) and the US (toxin). However, if subjects were anesthetized immediately after the CS was delivered and remained anesthetized during the CS-US interval, strong conditioning was observed with CS-US intervals of up to 9 h. The aim of the present experiment was to determine if the temporal gradient for hypothermia-induced RA could also be lengthened. That is, we tested whether the interval between training and hypothermia treatment could be lengthened by anesthetizing subjects with Ketaset-Rompun. The results indicate that the training-to-amnestic agent interval could be lengthened within moderate limits. The implications for hypothermia-induced RA is further discussed.

Adrenergic alpha-Agonists↗
PubMed1999

The neurology of traumatic "dissociative" amnesia: commentary and literature review.

BACKGROUND: The relationship between traumatic emotional stress, hippocampal injury, memory loss, and traumatic ("dissociative") amnesia was examined. METHOD: A survey of the research on emotional trauma, learning, memory loss, glucocosteroid stress hormones, and the hippocampus was conducted, and animal and human studies were reviewed. RESULTS: It is well documented and has been experimentally demonstrated in animals and humans that prolonged and high levels of stress, fear, and arousal commonly induce learning deficits and memory loss ranging from the minimal to the profound. As stress and arousal levels dramatically increase, learning and memory deteriorate in accordance with the classic inverse U-shaped curve. These memory deficits are due to disturbances in hippocampal activation and arousal, and the corticosteroid secretion which can suppress neural activity associated with learning and memory and induce hippocampal atrophy. Risk and predisposing factors include a history of previous emotional trauma or neurological injury involving the temporal lobe and hippocampus, the repetitive and prolonged nature of the trauma, and age and individual differences in baseline arousal and level of cortisol. CONCLUSIONS: Although some victims may be unable to forget, amnesia or partial memory loss is not uncommon following severe stress and emotional trauma. Even well publicized national traumas may induce significant forgetting. Memory loss is a consequence of glucocosteroids and stress-induced disturbances involving the hippocampus, a structure which normally plays an important role in the storage of various events in long-term memory.

Amnesia↗
PubMed1994

Inhibitors of phospholipase A2 produce amnesia for a passive avoidance task in the chick.

The effects of blocking phospholipase A2 (PLA2), a key enzyme in arachidonic acid (ArA) release, on memory retention have been studied in a one-trial passive avoidance task in the day-old chick. Bilateral intracerebral injections of the PLA2 and lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) (15 microliters of 4 mM NDGA/hemisphere, calculated to give an equivalent intracerebral concentration of 120 microM) or the PLA2 inhibitor aristolochic acid (AST) (5 microliters of a 4 mM AST/hemisphere, calculated to give an equivalent intracerebral concentration of approximately 40 microM) were made into the intermediate medial hyperstriatum ventrale (IMHV), an area that is of crucial importance for memory formation in the chick in this task. Pretraining injections of either inhibitor resulted in the chicks showing lasting amnesia for the avoidance response. The onset of amnesia with both inhibitors NDGA and AST was at 1.25 h post-training. Injection of drugs post-training had no effect on retention. Time and dose dependencies of both drugs were evaluated. Additional tests showed that the amnestic effect is not due to state-dependent learning nor to interference of the drugs with general motor ability or motivation. The results support the theory that arachidonic acid release is a necessary step in the early, although not immediate, events mediating the synaptic plasticity associated with memory formation. This is compatible with the hypothesis that ArA may serve as a late retrograde messenger between post- and presynaptic sites of plasticity, although it is not proof of such a role.

Amnesia↗