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Transient global amnesia: disease or syndrome?

Transient global amnesia (TGA) has been defined as the presence of an impairment of short-term memory, retrograde amnesia and repetitive queries, without any other neurological signs or symptoms. The precise pathophysiology of TGA is unclear, although thromboembolic, epileptic, migrainous and metabolic mechanisms have been suggested. We have studied the clinical, biohumoral, electroencephalographic and neuro-imaging data relating to 25 patients with TGA, and found a prevalence of hypertension and hypercholesterolemia. We also found a higher incidence of electrical changes in the patients whose TGA was of shorter duration, whereas brain CT scans revealed ischemic lesions more frequently in the patients with TGA of longer duration. Our findings seem to confirm the hypothesis that TGA is a heterogeneous clinical syndrome consisting of pure and ischemic forms.

Adult↗

Retrograde amnesia produced by intrastriatal atropine and its reversal by choline.

A number of studies have shown that cholinergic blockade of the striatum produces amnesia. In the present experiment it was predicted that by increasing the synthesis of striatal acetylcholine such amnesic state would be prevented. Atropine was injected into the striatum of rats before training of passive avoidance; some of these rats were also injected, intrastriatally, with choline before testing the retention of the task. Atropine alone produced amnesia while the combination of treatments reversed this effect.

Acetylcholine↗

Functional retrograde amnesia: a quantitative case study.

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.

Adult↗

Preserved memory in retrograde amnesia: sparing of a recently acquired skill.

Recent work with amnesic patients has revealed a preserved capacity for acquiring and retaining new skills despite otherwise profound anterograde impairment. In addition to their anterograde impairment, amnesic patients also have retrograde memory loss for some information acquired prior to the amnesic event. The present experiment addresses for the first time the question of whether preservation of memory for skills is also a feature memory impairment. To determine the susceptibility of a recently learned skill to retrograde amnesia, we taught patients to read mirror-reversed words before and during the early part of a prescribed course of electroconvulsive therapy (ECT) and then tested retention of the skill after the course of treatment had been completed. Patients prescribed bilateral or right unilateral ECT and depressed patients not receiving ECT acquired the mirror-reading skill at the same rate and then retained it at the same level. For the patients prescribed ECT, intact learning and retention of the skill occurred despite retrograde amnesia for the previous testing sessions and for the words that they had read previously.

Adult↗

Effect of lysine vasopressin on pentylenetetrazol-induced retrograde amnesia in rats.

Lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial facilitated passive avoidance retention. Amnesia was produced when a single 50 mg/kg (IP) injection of pentylenetetrazol was given immediately following the passive avoidance acquisition trial. A single injection of lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial antagonized the amnesia.

Amnesia↗

Retrograde amnesia in chicks and mice induced by 3,4-dehydro-DL-proline, a proline analog.

L-proline induces retroactive amnesia without causing brain seizures or isoelectric activity. 3,4-dehydro-DL-proline, a proline analog containing a double-bond in the 5-membered ring, has similar effects at a smaller dose. Three experiments describe the amnestic qualities of 3,4-dehydro-DL-proline in a chick memory paradigm, the retrograde quality of this amnesia, and its existence in a mammalian (mouse) preparation. Finally, EEG records show that chicks injected with amnestic doses of 3,4-dehydro-DL-proline do not exhibit seizure spiking or abnormal electrical activity.

Amnesia↗

Intracerebroventricular somatostatin attenuates electroconvulsive shock-induced amnesia in rats.

In the present study the effect of intracerebroventricularly (ICV) administered somatostatin on electroconvulsive shock-(ECS) induced retrograde amnesia was investigated in rats. The ECS significantly decreased foot shock-induced avoidance latency. Somatostatin in a dose of 1 microgram/4 microliter (ICV) had no action on the ECS-induced retrograde amnesia, while in a dose of 4 micrograms/4 microliters it significantly increased the avoidance latency if the treatment was performed immediately, 4 hr, 20 hr or 23 hr after the ECS. The results suggest that ICV administered somatostatin has an antiamnesic effect.

Amnesia↗

Somatostatin and (D-Trp8, D-Cys14)-somatostatin delay extinction and reverse electroconvulsive shock induced amnesia in rats.

In the present study the effects of somatostatin and its analogs on active avoidance behavior, electroconvulsive shock (ECS)-induced retrograde amnesia, and spatial-discrimination learning were compared in rats. (D-Trp8, D-Cys14)-somatostatin (as did the somatostatin molecule itself) delayed the extinction of active avoidance behavior, antagonized ECS-induced amnesia, and did not modify spatial-discrimination learning. Des-Asn5-(D-Trp8, D-Ser13) somatostatin and des-AA1,2,4,5,12,13,-(D-Trp8) somatostatin did not influence these behaviors. The data suggest that certain parts of the somatostatin molecule are important for its behavioral actions.

Amnesia↗

Is organic amnesia caused by a selective deficit in remembering contextual information?

An influential view of amnesia is that the recognition and recall failure is a consequence of a selective loss of memory for contextual, rather than target, information. The various forms of this viewpoint are outlined and one is considered in more detail. This hypothesis claims that amnesics suffer from a selective inability to remember background context i.e. spatiotemporal or extrinsic context. The evidence cited in support of this hypothesis is then critically reviewed and assessed in relation to two methodological problems. The first problem shows that when weak amnesic memory is compared with good normal memory qualitative differences in contextual memory may arise artefactually. The second problem is that contextual memory deficits, found in amnesics, may be incidental consequences of frontal cortex damage rather than essential to the core memory deficit. In the light of these problems it is concluded that currently there is no convincing support for the contextual memory deficit hypothesis of amnesia. Finally, guidelines are laid down which should enable the hypothesis to be more appropriately assessed, and an alternative kind of hypothesis is briefly outlined.

Alcoholism↗

Retrograde amnesia effects of intravenous diazepam in endoscopy patients.

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.

Adult↗

Remote memory in a patient with amnesia due to hypoxia.

It has been suggested that amnesic patients suffer a selective loss of episodic memory while semantic memory remains well preserved. To assess the validity of this idea we studied remote memory in an amnesic patient, (M.R.L.), using several different measures that differ in the extent to which they engage episodic or semantic memory. On two different versions of the Albert et al. (1979) remote memory battery M.R.L. displayed severe retrograde amnesia (RA) extending backwards in time for about 15 years with excellent preservation of older memories. With standard recall instructions his overall performance on the Crovitz test of autobiographical memory was impaired and all of M.R.L.'s specific, temporally dated memories were given from the first half of his life. When asked to reconstruct his past residential history in detail, M.R.L. provide specific and generally accurate information for residences occupied from his boyhood until 1970, but thereafter his memory became quite unreliable. On a test of knowledge of terms commonly employed in the surveying profession, in which he worked for the past 20 years, M.R.L.'s performance was also impaired. The consistent pattern of RA displayed by this patient on all of the tests of remote memory indicates that both episodic and semantic memory are impaired in amnesia.

Amnesia↗

Long gradient of retrograde amnesia in mice: continuity with the findings in humans.

Mice were given a single training trial and then received either sham treatment or electroconvulsive shock (ECS; four treatments at hourly intervals) at 1 of 7 times (1-70 days) after training. Retention was always tested 2 weeks after treatment. Control animals exhibited gradual forgetting with increasing retention intervals. Mice given ECS exhibited severe retrograde amnesia, which diminished as the interval between training and ECS increased from 1 to 21 days. ECS given 21-70 days after training had no effect on memory. The finding of long, temporally graded retrograde amnesia in mice establishes continuity between the results for laboratory animals and those for humans and indicates that the neural changes involved in the consolidation of memory can continue for a significant portion of the lifetime of a memory.

Amnesia↗

A SPECT study of the anatomy of transient global amnesia.

This report describes single photon emission tomography (SPECT) evidence of transient, relative hypoperfusion of the right basal ganglia and left temporal lobe in a 60-year-old man studied during the acute phase of classical transient global amnesia (TGA). The findings are interpreted in the light of previous reports indicating that involvement of the right hemisphere or both cerebral hemispheres consistently predicts severe retrograde amnesia, in addition to the typical loss of anterograde memory observed during TGA. These deficits involving the right hemisphere and left temporal lobe may reflect disruption of circuits mediating episodic memory retrieval and memory encoding, respectively.

Amnesia, Retrograde↗

The dissociation of anterograde and retrograde amnesia in a patient with herpes encephalitis.

Establishing the precise relationship between anterograde amnesia (AA) and retrograde amnesia (RA) has implications for psychological and neuroanatomical models of memory. Many patients have been described who demonstrate AA in conjunction with RA or who demonstrate AA with little, or no apparent, RA. Intact anterograde memory in conjunction with deficits on tasks of retrograde memory is rarely encountered. In this paper, we describe a young female patient (LD) whose RA is extremely severe when contrasted with her mild to moderate deficits on tasks of verbal anterograde memory. In addition, on tests of episodic and semantic autobiographical memory, LD appeared more impaired in her recall of specific episodes than of factual information about her past. The importance of this dissociation in RA for the episodic-semantic distinction and the possible role of visual imagery in recalling remote episodic events are discussed.

Adult↗

Transient global amnesia triggered by mild head trauma.

In 9 patients, aged 11 to 28 years, minor head injury triggered an amnesic attack grossly disproportionate to the degree of trauma. During these attacks, patients were unable to form new memories for 2 to 24 hours, had extensive retrograde amnesia, voiced repetitive queries and were disorientated for time, but were otherwise intact neurologically. We suggest that these episodes were attacks of transient global amnesia triggered by the mild blows to the head. We also suggest that they constitute a previously unrecognized variety of traumatic migraine.

Adolescent↗

Transient global amnesia.

Transient global amnesia is a clinical syndrome characterized by sudden onset of short-term memory loss followed by retrograde amnesia in an otherwise healthy subject. During the attack, the patient remains alert and retains much of his personal identity. The patient usually becomes upset and concerned about his memory loss. This condition may be diagnosed incorrectly as hysteria, psychosis, or temporal lobe seizure, despite its unique clinical features.

Adult↗

The amnesia gradient: inadequate as evidence for a memory consolidation process.

Rats were conditioned to fear a tone paired with shock to the feet. Retention tests 4 days later showed that consolidation had occurred. Other animals were not tested for retention at 4 days, but the tone was presented in order to reactivate their memories of the conditioning. An amnesia gradient was generated by low-intensity electrical stimulation of the amygdaloid complex at different intervals after the tone, but stimulation was without effect either when given to rats not previously conditioned or when given to conditioned rats without preceding memory reactivation. Thus, stimulation of the amygdaloid complex can can affect memory retrieval. Moreover, the data call into question the assumption that an amnesia gradient indicates that the memory consolidation process has been modified.

Amnesia↗

Transient global amnesia in four brothers.

The case histories are described of four brothers who suffered attacks of transient global amnesia. The coincidence of this disorder in four siblings suggests that the causative factors in transient global amnesia may have a familial basis and that its incidence is more common than generally realised.

Aged↗