Anterograde amnesia with fornix damage following removal of IIIrd ventricle colloid cyst.

Two patients developed anterograde amnesia following the apparently uncomplicated transcallosal-transventricular removal of a colloid cyst. Damage to the fornical columns was demonstrated on CT and MRI scans, whilst other memory related structures were entirely normal. Longitudinal neuropsychological evaluation, over 12-24 months, has revealed a very similar pattern of deficit in the two cases: verbal memory has remained persistently impaired whilst nonverbal anterograde memory has improved to some degree. Formal tests of remote public (famous faces and events) and personal autobiographical memory have supported the clinical impression that neither patient has a temporally extensive retrograde amnesia. These findings address the role of the fornix, and the dissociation of memory processes in humans.     

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.     

Focal retrograde amnesia: a long term clinical and neuropsychological follow-up

A patient (E.D.) who had displayed a selective retrograde amnesia in association with transient amnesic episodes (Kapur et al., 1986) was reexamined five years after initial assessment. At the clinical level, his transient amnesic attacks continued, but some of these had clear epileptic features. In addition, EEG investigation indicated temporal lobe abnormality, more prominent in the left temporal region, and supported a clinical diagnosis of temporal lobe epilepsy. Both CT scanning and magnetic resonance imaging were unable to detect the presence of any structural lesion. At the neuropsychological level, there was no evidence of dementia in the form of generalized cognitive dysfunction nor significant deterioration in cognitive functioning since the earlier assessment. Our patient continued to show marked memory loss for public events over the past 20-30 years, in the context of normal or near normal performance on most tests of anterograde memory functioning. While memory for famous scenes and famous faces was markedly impaired, our patient's memory for famous cars was within normal limits and his memory for autobiographical events showed only patchy impairment. Although E.D. performed at an average or above average level on most standard tests of anterograde memory functioning, our patient did show evidence of significant memory loss for public events which had occurred over the past ten years (i.e. since the onset of his illness). The possibility is raised that E.D.'s memory disorder may represent a form of disconnection syndrome.     

The amnesia of transient global amnesia

abstract

A patient was tested during and following an episode of transient global amnesia. During the episode, the patient displayed a profound anterograde amnesia which spared short-term memory. There was also a retrograde amnesia which was transient and which involved recent material but not memory for events and persons that became famous between 1930 and 1975. The results are discussed in the context of current memory models and some speculative interpretations of the amnesia are offered.     

Cognition in a patient with very mild right-sided hemiparkinsonism

Non-demented patients with Parkinson's disease (PD), especially if they are high functioning and early in the course of their disease, usually exhibit mild deficits in anterograde recall memory for verbal and non-verbal material, visuospatial reasoning, visuomotor construction, temporal ordering and sequencing. Impairments in problem solving and verbal fluency tests may also occur. PD patients with predominantly right-sided symptoms usually exhibit more severe difficulties with verbal than with non-verbal tasks. We report a case of a highly educated right-handed man with very mild right-sided hemiparkinsonism who never received anti-Parkinsonian or other psychoactive medication. Our patient showed anterograde and retrograde amnesia for faces and spatial locations and difficulties on complex visuospatial tasks that required manual responses, but normal to above average performance on all other cognitive tests. The specific pattern of cognitive loss early in PD may depend on which spatial, facial or verbal pre-frontal striatal circuits are deprived of their dopaminergic inputs.     

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.     

Cognition in a Patient with Very Mild Right-sided Hemiparkinsonism

Non-demented patients with Parkinson’s disease (PD), especially if they are high functioning and early in the course of their disease, usually exhibit mild deficits in anterograde recall memory for verbal and non-verbal material, visuospatial reasoning, visuomotor construction, temporal ordering and sequencing. Impairments in problem solving and verbal fluency tests may also occur. PD patients with predominantly right-sided symptoms usually exhibit more severe difficulties with verbal than with non-verbal tasks. We report a case of a highly educated right-handed man with very mild right-sided hemiparkinsonism who never received anti-Parkinsonian or other psychoactive medication. Our patient showed anterograde and retrograde amnesia for faces and spatial locations and difficulties on complex visuospatial tasks that required manual responses, but normal to above average performance on all other cognitive tests. The specific pattern of cognitive loss early in PD may depend on which spatial, facial or verbal pre-frontal striatal circuits are deprived of their dopaminergic inputs.     

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.     

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.     

Postencephalitic focal retrograde amnesia after bilateral anterior temporal lobe damage.

BACKGROUND: Marked retrograde amnesia with no or almost no anterograde amnesia is rare. Recently, a combination of ventrolateral prefrontal and temporopolar cortical lesions has been suggested as the cause of such isolated or focal retrograde amnesia. It is also assumed that when the right-sided cortical structures are damaged, autobiographical episodic memories are affected. OBJECTIVE: To search for new anatomic substrates for focal retrograde amnesia. METHODS: We performed extensive neuropsychological tests and obtained detailed neuroimages on a 43-year-old woman who showed a severe, persistent retrograde amnesia but only a limited anterograde amnesia after probable herpes simplex encephalitis. RESULTS: Tests of autobiographical memory revealed that she had a memory loss extending back to her childhood for both semantics and incidents; however, the ability to recall specific episodes appeared much more severely impaired than the ability to recall factual information about her past. The patient also showed profound impairments in recalling public memories; however, her scores improved nearly to a control level on forced-choice recognition memory tasks, although the recall of memories for a decade just before her illness remained mildly impaired. MRI revealed focal pathologies in the temporal poles and the anterior parts of the inferotemporal lobes on both sides, predominantly on the left, with some extension to the anterior parts of the medial temporal lobes. There was additional damage to the left insular cortex and its surrounding structures but no evidence of frontal lobe damage on MRIs or cognitive tests. CONCLUSIONS: A profound retrograde amnesia may be produced by damage to the bilateral temporal poles and anterior inferotemporal lobes in the absence of frontal lobe pathologies, and a dense and persistent episodic old memory loss can arise even with a relatively small lesion in the right anterior temporal lobe if it is combined with extensive damage to the left.     

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).     

Focal retrograde amnesia documented with matching anterograde and retrograde procedures

Focal retrograde amnesia is an unusual and theoretically challenging form of memory disorder. The case of a 65-year-old woman presenting with focal retrograde amnesia is reported. Following a cardiac arrest and subsequent hypoxia she remained in a coma for 24 h with evidence of epileptiform activity during the early recovery period. MR scans, 4 and 7 months post-onset, showed mild bifrontal atrophic changes mainly affecting white matter areas. An [18F]fluorodeoxyglucose resting PET scan 1-year post-onset demonstrated right occipito-temporo-parietal hypometabolism. We were able to document the patient's performance on an extensive range of anterograde and retrograde tests and to monitor her recovery of function by assessing her performance at 4, 12 and 24 months post-onset. Spared anterograde memory was observed on a range of verbal and non-verbal tests, including matched tasks that compared pre-illness and post-illness onset recollections. In contrast, her performance on retrograde memory tests, using detailed autobiographical and public events verbal and photographic tasks, showed a temporally-graded retrograde amnesia, more particularly affecting memory for autobiographical episodes. Possible mechanisms underlying CH's focal retrograde amnesia are discussed in terms of Damasio's time-locked multiregional retroactivation model.     

Cognition and vigilance: differential effects of diazepam and buspirone on memory and psychomotor performance.

Effects of a single dose of the anxiolytic buspirone (15 mg) on memory and psychomotor performance were studied in healthy volunteers and compared to those of the classic benzodiazepine anxiolytic diazepam (15 mg). The study was performed in a double-blind, placebo-controlled way. Three groups of 12 subjects were exposed to an extended test battery before and after intake of drug or placebo. Next to this, an evaluation session took place 1 week later. Immediately after intake, diazepam exerted major effects on memory, impaired psychomotor performance and decreased alertness. In particular, long-term memory had deteriorated, which was interpreted as anterograde amnesia. One week later, more items were recalled from the predrug session compared to the number of items from the postdrug session; this was interpreted as retrograde facilitation. After intake of buspirone, there were no effects of alertness and vigilance, on psychomotor performance and on memory. One week later, a small memory decrement was noticed for verbal material, which was considered as a sign of anterograde amnesia. These results indicate that effects of anxiolytics on memory can be more easily demonstrated 1 week later than immediately after drug intake and, furthermore, that the disruptive effects of diazepam outweight the small effects of buspirone. Finally, it was established that the effects of diazepam on cognition might be mediated by its effects on alertness and vigilance and that cognitive effects are not related to the anxiolytic properties of the drug.     

Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis

We describe a patient who developed a severe but temporally limited retrograde amnesia coupled with a relatively mild anterograde amnesia following herpes simplex encephalitis. The patient showed a profound retrograde amnesia for autobiographical events extending for about 10 years prior to the disease onset. Her knowledge about public events and famous persons was also impaired for this period. An MRI and SPECT demonstrated bilateral medial temporal pathology. This case represents a further instance of a relatively focal retrograde amnesia following brain damage. We review other reported cases with focal retrograde amnesia and consider theoretical and neuroanatomical accounts for the present case. Two factors may account for her amnesic patterns: a partial disruption of the store for premorbid binding codes (i.e., information that multimodal feature representations occurred synchronously); along with a relative preservation of the encoding process required to develop new synchronous codes.     

Mnestic performance profile of a bilateral diencephalic infarct patient with preserved intelligence and severe amnesic disturbances

Abstract

The case of a patient with above-average intelligence and educational background, high motivation, and an approximate IQ-MQ difference of 40 points is documented. The patient has been examined repeatedly for nearly a decade. Extensive neuroradiological material of his focal bilateral brain damage in the dorsal diencephalon is available. A widespread range of cognitive tests was used to investigate his actual performance on all relevant aspects of intelligence, attention, subjective memory, immediate retention, learning, skill and problem solving abilities, concept formation, cognitive flexibility, priming, constructional ability, retrograde memory, and long-term retention. The total of more than 50 tests included German-language forms of the revised Wechsler Memory Scale and of the Rivermead Behavioural Memory Test. The patient's short-term memory and attention were, in spite of his advanced years, average or well above average. He gave a number of examples of still intact skills and implicit memory abilities, though there was no uniformity in his performance on implicit memory tests (e.g., with respect to stored vs. new implicit information). He had no awareness of his severe anterograde and retrograde amnesia, documented over a large range of verbal and figural tests. Taken together, the results from our patient confirm the principal dichotomy between declarative and nondeclarative mnestic functions, but give evidence for some restrictions as well. They furthermore demonstrate that focal diencephalic damage may result in profound anterograde and selective retrograde amnesia, especially with respect to data-based material, and that disconnecting portions of the medial and basolateral limbic circuits has devastating consequences on memory.     

Searching for lost memory: memory loss and recovery mechanisms observed in a patient with pure retrograde amnesia

We describe a patient who developed acute reversible amnesia characterized by impaired recollection of past events with preserved anterograde memory. This occurred after a mild head trauma and in the context of occupational stress. Isolated retrograde amnesia affected autobiographical memory (with lost of identity lasting a few days) and semantic knowledge. Isolated retrograde amnesia subsided for nine months. The patient was no longer able to access to his memories, which did not seem completely lost. Some answers to tests concerning historical events were better than those given at random; his answers to a TV quiz were automatic or he exhibited temporal transfer phenomena (ecmnesia). Gradual, progressive, irregular and spontaneous or "flash" recovery, which was also facilitated by dreams, associations or contextual clues. The persistent and vivid familiarity of the retrieved memories are reported here together with the organization of long-term memory and the clinical and neuropsychological traits of functional isolated retrograde amnesia.     

Transient global amnesia: neuropsychological dysfunction during attack and recovery in two "pure" cases.

Two patients with transient global amnesia are reported. Comprehensive neuropsychological evaluation, during the amnesic episode, as well as follow-up examinations on memory were performed. The course of the amnesia was exemplified by two comparable memory tests in different modalities. Partial retrograde amnesia and complete anterograde amnesia were demonstrated during the transient episode. Objective recovery was found to be slower than subjectively experienced, but test performance was completely normal one month after onset.     

Long-term memory following transient global amnesia: an investigation of episodic and semantic memory

BACKGROUND: Several studies noted persistence of memory impairment following an episode of transient global amnesia (TGA) with standard tests. AIM: To specify long-term memory impairments in a group of patients selected with stringent criteria. METHODS: Both retrograde and anterograde memory were investigated in 32 patients 13-67 months after a TGA episode with original tasks encompassing retrograde semantic memory (academic, public and personal knowledge), retrograde episodic memory (autobiographical events) and anterograde episodic memory. RESULTS: Patients had preserved academic and public knowledge. Pathological scores were obtained in personal verbal fluency for the two most recent periods, and patients produced less autobiographical events than controls. However, when they were provided time to detail, memories were as episodic as in controls regardless of their remoteness. Anterograde episodic tasks revealed a mild but significant impairment of the capacity of re-living the condition of encoding, i.e. the moment at which words were presented. CONCLUSIONS: Patients who have suffered from an episode of TGA manifest deficits of memory focused on the retrieval of both recent semantic information and episodic memories and especially the capacity of re-living. These deficits may not result from a deterioration of memory per se but rather from difficulties in accessing memories.     

The dynamic time course of memory recovery in transient global amnesia

AIMS: To investigate the dynamic time course of transient global amnesia (TGA)--that is, the process of recovery and the interindividual variability--by testing four patients during the day of TGA itself (on three occasions) and at follow up (on two occasions). METHODS: A specially designed protocol focusing on semantic (both conceptual and autobiographical knowledge) and episodic (both anterograde and retrograde components) memory. RESULTS: Every patient showed marked impairment of both anterograde and retrograde episodic memory during the acute phase, with a relative preservation of personal and conceptual semantic knowledge. During the following phase, the authors observed similarities and differences among the patients' patterns of recovery. In general, retrograde amnesia recovered before the anterograde amnesia and anterograde episodic memory was recovered gradually in every case. In contrast, shrinkage of retrograde amnesia was more heterogeneous. In two of the patients, this shrinkage followed a chronological gradient and the most remote events were recovered first. In the two other patients, it depended more on the strength of the trace, and there was no temporal gradient. For the latter, an executive deficit could account for difficulties in accessing both conceptual knowledge and autobiographical memories. CONCLUSIONS: This profile of recovery suggests a "neocortical to medial temporal" process in every case, and the possibility of an additional frontal dysfunction in some cases. Hence, the acute phase seems to be characterised by a common episodic impairment. This variability between subjects appears in the recovery phase with two different patterns of impairment.     

Extensive and temporally ungraded retrograde amnesia in encephalitis associated with antibodies to voltage-gated potassium channels

BACKGROUND: Encephalitis associated with antibodies to voltage-gated potassium channels (VGKC-Ab) is characterized by epilepsy, behavioral changes, and anterograde memory impairment. Magnetic resonance imaging reveals abnormal signal predominantly restricted to the mediotemporal lobes. OBJECTIVE: To determine the temporal extent and potential reversibility of retrograde amnesia in 3 patients with VGKC-Ab-associated encephalitis. DESIGN: Case report. SETTING: Clinical. Patients Three patients diagnosed as having VGKC-Ab-associated encephalitis underwent cognitive testing before and after immunotherapy. MAIN OUTCOME MEASURES: In addition to standard neuropsychological tests, retrograde memory was assessed using 2 novel tests. Memory for past newsworthy events was assessed using a public events test; test material was divided into epochs of 5 years and spanned approximately 25 years. This was complemented by a famous faces test in which patients were required to identify individuals from the recent and remote past. RESULTS: All 3 patients were found to have temporally ungraded retrograde amnesia dating back more than 20 years. Magnetic resonance imaging in all patients revealed high-signal abnormalities predominantly affecting the hippocampi. Subsequent testing performed after immunotherapy revealed subjective improvement but no evidence of a temporal gradient in the recovery of past memories. CONCLUSIONS: Encephalitis associated with VGKC-Ab results in extensive and temporally ungraded retrograde amnesia that is partially reversible with immunotherapy. Magnetic resonance imaging high-signal abnormalities were primarily restricted to the hippocampi. These data are supportive of theories postulating a role for the hippocampus in the storage and retrieval of all past memories, irrespective of age, rather than theories of memory consolidation that propose an involvement of the hippocampus only in the temporary storage of memories.