Amnesia in a patient with bilateral lesions to the thalamus

A case of anterograde amnesia is described in a 38-yr-old man with bilateral thalamic lesions. The patient appeared to have suffered no general intellectual loss and performed normally on standard memory tasks involving immediate recall of new material. There was, however, consistent impairment in recalling material, verbal and non-verbal, over delays as brief as a few seconds. Impairment was especially marked on tests involving free recall and partial cueing procedures; recognition memory was also impaired. Premorbid memory tested normally and susceptibility to interference was less than in other organic amnesics. Various interpretations of the patient's amnesia were considered but a deficit at the initial stages of information processing appeared to be indicated.     

Amnesia can facilitate memory performance: evidence from a patient with dissociated retrograde amnesia

A case is reported of a patient who experienced numerous episodes of transient global amnesia (TGA) during which anterograde amnesia was less prominent than usual, and who developed a permanent selective retrograde amnesia. On formal testing, he performed well on traditional verbal memory tests, but showed marked retrograde amnesia for verbal material, including items on a famous voices recognition test. He was administered a paired-associate learning test where the names of famous personalities for which he was amnesic were associated with incongruous activities (e.g. John Newcombe-singing). Our patient performed better on this task than a group of five matched control subjects. Our observations indicate that in the organization of human memory retrograde amnesia may be fractionated from anterograde amnesia and that in certain situations specific types of amnesia can produce a facilitation effect compared to the performance of control subjects.     

Crime in Huntington's disease

OBJECTIVES—To clarify the clinical and neuropsychological aspects of transient epileptic amnesia (TEA) based on 10 personally studied cases as well as review of 21 previously published cases; and to propose tentative diagnostic criteria for the diagnosis of TEA.
METHODS—All 10 patients and informants underwent a standardised clinical interview. The radiological and neurophysiological (EEG) data were also reviewed in all cases. The diagnosis of transient epileptic amnesia was made on the basis of the following criteria: (1) there was a history of recurrent witnessed episodes of transient amnesia; (2) cognitive functions other than memory were judged to be intact during typical episodes by a reliable witness; (3) there was evidence for a diagnosis of epilepsy. This evidence was provided by either (a) wake or sleep EEG, or (b) the co-occurrence of other seizure types (if their roughly concurrent onset or close association with episodes of transient amnesia suggested a connection), or (c) a clear cut response to anticonvulsant therapy, or by a combination of these three factors. In addition all patients were administered a comprehensive neuropsychological test battery designed to assess verbal and non-verbal anterograde memory and retrograde memory for famous personalities and personal events. Their results were compared with those of 25 age and IQ matched normal controls.
RESULTS—TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to "remember not being able to remember". The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. The epochs affected may predate the onset of epilepsy by many years.
CONCLUSIONS—TEA is an identifiable syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. Future studies should consider the question of whether TEA reflects ictal activity or a postictal state, and the mechanism of the persistent autobiographical amnesia. It is hypothesised that the latter may result in part from impairment of very long term memory consolidation as a result of epileptic activity in mesial temporal structures.

     

The performance of postencephalitic amnesic subjects on two behavioural tests of memory: concurrent discrimination learning and delayed matching-to-sample.

The performance of a group of three postencephalitic subjects with anterograde amnesia was examined on a series of concurrent visual discrimination problems and on a test of visual recognition, delayed matching-to-sample. These tests were chosen as they have been used to assess experimental models of anterograde amnesia in nonhuman primates. In comparison with a group of normal subjects the postencephalitic group were impaired on the more difficult concurrent discrimination problems. They also performed poorly on the matching-to-sample task when given lists of items to remember or given increased retention intervals. The pattern of performance of the postencephalitic group matched closely that of a group of Korsakoff subjects, indicating that these behavioural tests are equally sensitive to different types of anterograde amnesia.     

Experimental animal model of transient global amnesia: Role of the hippocampus

Different groups of rats were given a hippocampal seizure after-discharge 1 or 7 days after acquiring a passive avoidance, active avoidance, or bar-pressing habit. At various delays after the cessation of the seizure after-discharge, the animals were tested for retention of the previously acquired habit. The results indicate that 1 day, but not 7 days after learning, hippocampal seizures are capable of producing a temporary retrograde amnesia for well-learned responses and an anterograde amnesia for experiences that occur during the retrograde amnesia period. These data suggest that hippocampal seizures can serve as an experimental prototype of “transient global amnesia” and that the hippocampus is critically involved in retrieval of information from long term memory.     

Hippocampal contributions to recollection in retrograde and anterograde amnesia

Lesions restricted to the hippocampal formation and/or extended hippocampal system (hippocampal formation, fornix, mammillary bodies, and anterior thalamic nuclei) can disrupt conscious recollection in anterograde amnesia, while leaving familiarity-based memory relatively intact. Familiarity may be supported by extra-hippocampal medial temporal lobe (MTL) structures. Within-task dissociations in recognition memory best exemplify this distinction in anterograde amnesia. The authors report for the first time comparable dissociations within recognition memory in retrograde amnesia. An amnesic patient (A.D.) with bilateral fornix and septal nuclei lesions failed to recognize details pertaining to personal past events only when recollection was required, during recognition of episodic details. His intact recognition of generic and semantic details pertaining to the same events was ascribed to intact familiarity processes. Recollective processes in the controls were reflected by asymmetrical Receiver's Operating Characteristic curves, whereas the patient's Receiver's Operating Characteristic was symmetrical, suggesting that his inferior recognition performance on episodic details was reliant on familiarity processes. Anterograde and retrograde memories were equally affected, with no temporal gradient for retrograde memories. By comparison, another amnesic person (K.C.) with extensive MTL damage (involving extra-hippocampal MTL structures in addition to hippocampal and fornix lesions) had very poor recognition and no recollection of either episodic or generic/semantic details. These data suggest that the extended hippocampal system is required to support recollection for both anterograde and retrograde memories, regardless of their age.     

Hippocampal Amnesia

This article reviews 147 cases of amnesia following damage including the hippocampus or fornix as reported in 179 publications. The aetiology, mnestic abilities and reference(s) are tabulated for each case. Consistent findings across cases include the association of bilateral hippocampal damage with a deficit in anterograde episodic memory combined with spared procedural and working memory. The limited nature of retrograde amnesia following lesions to the fornix is also noted. Less consistent and thus more controversial findings, include effects of lesion size or laterality, deficits in semantic memory or familiarity-based recognition and the extent of retrograde amnesia. The evidence concerning these issues is reviewed across cases.     

The intracarotid amobarbital procedure as a predictor of memory failure following unilateral temporal lobectomy

We investigated the efficacy of the intracarotid amobarbital procedure to accurately predict post-temporal lobectomy anterograde amnesia. We presented items at 2 separate times during amobarbital assessment; both early and late item recall were decreased during the injection contralateral to seizure onset indicating sensitivity to bilateral temporal lobe dysfunction. Ten patients for whom follow-up neuropsychological assessment was available failed either the early or late item recognition portions of their amobarbital evaluation ipsilateral to seizure onset, but had hippocampus included in the temporal lobectomy by virtue of satisfactory performance on other tests of hippocampal function. None of these 10 patients displayed postoperative anterograde amnesia, although there was a reduction in material-specific memory in some patients. These results indicate that relying solely on amobarbital memory testing to assess the functional ability of the contralateral temporal lobe to sustain global memory prior to temporal lobectomy may needlessly exclude patients from a viable therapeutic option.     

The pattern of memory loss resulting from intravenously administered diazepam.

A word recognition task was designed to determine the stage in memory affected by a single 10-mg intravenous injection of diazepam and the duration of the effect. Injection in three experimental subjects produced an anterograde amnesia for the 14 to 24-minute period immediately after injection. Memory loss resulted from impaired storage, the stage during which information is entered into memory. Retention and retrieval stages of memory were unaffected. This temporary amnesia may result from increased inhibition in the hippocampal system produced by diazepam, which shares many properties with the inhibitory neurotransmitter gamma-aminobutyric acid.     

Basal forebrain amnesia: does the nucleus accumbens contribute to human memory?

OBJECTIVE: To analyse amnesia caused by basal forebrain lesions. METHODS: A single case study of a patient with amnesia after bleeding into the anterior portion of the left basal ganglia. Neuropsychological examination included tests of attention, executive function, working memory, recall, and recognition of verbal and non-verbal material, and recall from remote semantic and autobiographical memory. The patient's MRI and those of other published cases of basal forebrain amnesia were reviewed to specify which structures within the basal forebrain are crucial for amnesia. RESULTS: Attention and executive function were largely intact. There was anterograde amnesia for verbal material which affected free recall and recognition. With both modes of testing the patient produced many false positive responses and intrusions when lists of unrelated words had been memorised. However, he confabulated neither on story recall nor in day to day memory, nor in recall from remote memory. The lesion affected mainly the nucleus accumbens, but encroached on the inferior limb of the capsula interna and the most ventral portion of the nucleus caudatus and globus pallidus, and there was evidence of some atrophy of the head of the caudate nucleus. The lesion spared the nucleus basalis Meynert, the diagnonal band, and the septum, which are the sites of cholinergic cell concentrations. CONCLUSIONS: It seems unlikely that false positive responses were caused by insufficient strategic control of memory retrieval. This speaks against a major role of the capsular lesion which might disconnect the prefrontal cortex from the thalamus. It is proposed that the lesion of the nucleus accumbens caused amnesia.     

Dissociable anterograde amnesic effects of retrosplenial cortex and hippocampal lesions on spontaneous object recognition memory in rats

The amnesic effects of excitotoxic lesions of the rat retrosplenial cortex (RS) and hippocampus (HPC) in the spontaneous object recognition (SOR) performance were investigated. The SOR test consisted of the sample‐exposure session(s) and a test session. First, to test retrograde amnesia, rats received four sample‐exposure sessions within a day at 4 weeks and 1 day before the surgery, respectively. In the test sessions conducted 1 week after the surgery, both lesion groups showed a temporally ungraded retrograde amnesia. Second, to test anterograde amnesia, 1‐ and 4‐week retention intervals were inserted between the four sample‐exposure sessions and the test session. The RS‐lesioned rats showed a retention interval‐dependent impairment in the test sessions, while the HPC‐lesioned rats showed an impairment regardless of the retention interval. Finally, to test short‐term recognition memory, 5‐ or 30‐min delay was interposed between the single sample‐exposure session and the test session. Both lesion groups performed normally irrespective of the delay length. These results suggest that both the RS and HPC are important for long‐term object recognition memory, but these areas have different roles in it. © 2012 Wiley Periodicals, Inc.     

Response Bias in Korsakoff's Syndrome

The contribution of response bias to the amnesia of Korsakoff's syndrome was studied. Ten Korsakoff patients and ten alcoholic controls were asked for confidence ratings in a recognition memory task. Parametric signal detection measures (d', Cx) were considered appropriate. Korsakoff subjects displayed a more cautious response bias to patterns than did alcoholics.     

Sustained inhibition of brotizolam induced anterograde amnesia by norharmane and retrograde amnesia by L-glutamic acid in mice

Benzodiazepines such as diazepam, lorazepam, are reported to produce anterograde amnesia but these do not affect the retrieval mechanism. Triazodiazepines such as alprazolam, triazolam and brotizolam produce both anterograde and retrograde amnesia. Because benzodiazepine receptor antagonists are known to reverse anterograde amnesia, we wanted to test if inverse agonist can also improve learning and memory. The present study was designed to investigate the effect of norharmane (benzodiazepine receptor inverse agonist) and L-glutamic acid (glutamate receptor agonist) on brotizolam induced anterograde and retrograde amnesia using Morris water maze task in mice. Norharmane reversed anterograde amnesia induced by brotizolam and did not reverse retrograde amnesia induced by it. L-Glutamic acid attenuated retrograde amnesia but did not affect anterograde amnesia induced by brotizolam. These results provide an opportunity to understand the mechanisms of anterograde and retrograde amnesia which may occur with interaction of presynaptic molecules or LTP modulation.     

Clinically relevant anterograde amnesia and its relationship with blood levels of benzodiazepines in suicide attempters who took an overdose

The relationship between anterograde amnesia, sedation and plasma levels of benzodiazepines was studied prospectively in a group of 24 patients who took an overdose of benzodiazepines. Patients were tested on two sequential days after having taken an overdose. Anterograde amnesia was tested by using a verbal recall test and a photo recognition test. Sedation was scored on a visual analogue scale (VAS) by the patient and the interviewer. The concentration of benzodiazepines in plasma was measured by using a radioreceptor assay that adds benzodiazepines and their active metabolites. The cumulative amount of benzodiazepines was expressed as diazepam equivalents (DZE). Diazepam equivalents determined by this radioreceptor assay were significantly higher on the first day than on the second day. Ratings on the verbal recall test were significantly lower on the first day than on the second day. There was a significant relation between decrease of diazepam equivalents and increase of verbal recall: more than 30% of increase of verbal recall was explained by decrease of diazepam equivalents. There was not a strong relation between decrease of diazepam equivalents and reduction of level of sedation as scored by the patients. There was almost no relation between decrease of diazepam equivalents and reduction of level of sedation as scored by the interviewer. No relation was found between verbal recall, sedation and diazepam equivalents. There was no relation between diazepam equivalents and photo recognition. It was concluded that anterograde amnesia was strongly associated with benzodiazepines in patients who take benzodiazepines in an overdose. Sedation does not predict the degree of anterograde amnesia.     

Massive and persistent anterograde amnesia in the absence of detectable brain damage: Anterograde psychogenic amnesia or gross reduction in sustained effort?

Abstract

The case of a young patient with severe and persistent anterograde amnesia of no known cause is reported. Anterograde amnesia arose within a 1-month period and has persisted for more than 1 year. Although a wide variety of neurological and neuroradiological assessments were completed (EEG, evoked potential recordings, Doppler sonography, MRI, PET), no evidence of brain damage was detected. Neuro-psychologically, the patient was of high intelligence, had average to above-average short-term memory, and normal retrograde memory abilities, but severe and persistent anterograde amnesia in both verbal and nonverbal domains. Furthermore, he demonstrated grossly reduced long-term concentration. It is likely that a complex chain of interacting variables can produce a syndrome that appears phenomenologically as anterograde amnesia without organically measurable correlates.     

Primary loss of consciousness and amnesia in subarachnoid hemorrhage--a quantitative study

Subarachnoid hemorrhages (SAH) being sudden events affecting the brain in a rather wide-spread fashion are apt to induce loss of consciousness (LOC) and amnesia. The aim of the present study was to collect data on their frequency and extent. To this end we examined 48 patients at a mean of one year post-onset. Two thirds of them reported anterograde and an additional 17% retrograde amnesia; in 40% LOC (median 6 minutes) was observed. The durations were extremely skewed towards shorter times with a median of 2.7 days for anterograde and 1.3 days for retrograde amnesia who--with a single exception--were markedly shorter than anterograde amnesia. Summing up, a significant proportion of all SAH suffered LOC and amnesia occurred in the majority of cases. SAH therefore are events which with respect to LOC and amnesia bear some resemblance with closed head injuries. Exact observation and history taking may disclose important data on their severity and possible sequelae.     

Psychological therapy for psychogenic amnesia: Successful treatment in a single case study

Psychogenic amnesia is widely understood to be a memory impairment of psychological origin that occurs as a response to severe stress. However, there is a paucity of evidence regarding the effectiveness of psychological therapy approaches in the treatment of this disorder. The current article describes a single case, “Ben”, who was treated with formulation-driven psychological therapy using techniques drawn from cognitive behavioural therapy (CBT) and acceptance and commitment therapy (ACT) for psychogenic amnesia. Before treatment, Ben exhibited isolated retrograde and anterograde memory impairments. He received 12 therapy sessions that targeted experiential avoidance followed by two review sessions, six weeks and five months later. Ben's retrograde and anterograde memory impairments improved following therapy to return to within the “average” to “superior” ranges, which were maintained at follow-up. Further experimental single case study designs and larger group studies are required to advance the understanding of the effectiveness and efficacy of psychological therapy for psychogenic amnesia.     

Focal retrograde amnesia associated with vascular headache

We report the case of a 42-year-old man with repeated attacks of headache associated with retrograde amnesia. Neuropsychological tests before and after the major episode of amnesia showed mild neuropsychological deficits but with spared anterograde memory and learning functions. The amnesia was dense for a period of 15–20 years and included people and events (public and private). There was also a suggestion of amnesia for learned skills. Neurologically he had mild clinical signs and focal EEG-abnormalities in the left fronto-temporal region, but CT, MRI, and SPECT showed no abnormality. Five years after the onset of amnesia there was no recovery of the retrograde memory deficit, but a PET (glucose) scan was normal and neuropsychological testing showed no deficits. An association with migraine has been reported for some non-classical amnesias, but this is the first case of selective retrograde amnesia in a patient with headache as a primary neurological diagnosis.     

A comparison between transient amnesias induced by two drugs (diazepam or lorazepam) and amnesia of organic origin

The transient amnesias produced by drugs may have much in common with the more permanent amnesias associated with organic brain damage. This possibility was investigated using two benzodiazepines, diazepam and lorazepam, with medical student volunteers. In Experiment 1, 27 subjects received a 2ml intravenous injection of either diazepam (7.5 mg) or of lorazepam (3.0 mg) or of normal saline. In Experiment 2, a further 13 subjects were given lorazepam (2.5 mg) or saline. A double blind procedure was used. Neither drug had an appreciable effect on span-type short-term memory (except with 2-channel presentation). Both drugs produced severe anterograde amnesia in other forms of memory test: the amnesic effect of lorazepam lasted for several hours. This amnesia was not attributable to failures of perception. Lorazepam appeared to affect recognition even more than recall. In a test with lorazepam no evidence was obtained that the drug increases susceptibility to proactive interference. With both drugs, recall and recognition were unimpaired of material presented about 10 min before the injection; this shows that the drugs did not affect retrieval mechanisms.     

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).