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We report an unusual case of sudden isolated transient amnesia triggered by acute marijuana use. The memory disorder, apart from the long duration, had the characteristics of a transient global amnesia-like episode. Acute marijuana intoxication can affect memory more globally and severely than previously reported.
The putative generators of the event-related P3 component are still a matter of debate. There is reasonable evidence that the mesial temporal lobe structures are crucial in the generation of event-related potentials. Transient global amnesia (TGA) is characterized by anterograde and retrograde amnesia without neurological deficits in which a temporal hypoperfusion is the most likely pathomechanism. The aim of this study is to evaluate a possible delay in the P3 latency in a cohort of patients with TGA (n = 18). We used classic oddball paradigms with visual and auditory stimuli. The P3 latencies were compared to 18 age-matched patients with transient ischaemic attacks (TIAs) in the carotid artery territory and 23 age-matched controls. The mean age of the patients was 60.1 years (SD 14.1), in the TIA group 64.7 (SD 12.1) and 57.7 (SD 10.1) in the controls; the mean time interval between onset of TGA symptoms and performance of P3 investigations was 4.3 days (range 1-7 days); and the mean latencies measured at the vertex (Cz electrode) were 422.9 ms (SD 44.6) for the TGA patients, 436.4 ms (SD 62.1) for the TIA group, and 409.3 ms (SD 48.5) for the controls in the visual paradigm and 371.7 ms (SD 41.7), 399.7 ms (SD 51.2) and 385.3 ms (SD 46.5) in the auditory paradigm for the TGA, the TIA and the control groups. The P-values were not significant. These results suggest different neuronal networks in the generation of scalp P3 from those responsible for the disturbance of episodic memory in TGA.
Twelve consecutive patients having previously experienced one or more episodes of isolated transient topographical amnesia (TTA) underwent neuropsychological examination 6-12 months after the last episode to detect signs of global cognitive decline and to assess, in particular, cognitive functions deemed critical for topographical orientation. The test scores were compared with those of 12 normal subjects matched for age, sex, educational level and place of residence. Both patients and controls showed normal performances in all tasks. The comparison between the two groups revealed a significantly lower performance of the patient group in a task of geographical orientation, namely 'Map of Italy'. We conclude that isolated episodes of TTA in the elderly per se do not represent a sign of mental deterioration, but can be associated with frailty on survey components of spatial orientation. It remains to be explained whether this feature is a pre-existing condition favouring the occurrence of the episodes of topographical amnesia or represents a sequela.
Two groups of adolescents, one born preterm and one with a diagnosis of developmental amnesia, were compared with age-matched normal controls on measures of hippocampal volume and memory function. Relative to control values, the preterm group values showed a mean bilateral reduction in hippocampal volume of 8-9% (ranging to 23%), whereas the developmental amnesic group values showed a reduction of 40% (ranging from 27% to 56%). Despite equivalent IQ and immediate memory scores in the two study groups, there were marked differences between them on a wide variety of verbal and visual delayed memory tasks. Consistent with their diagnosis, the developmental amnesic group was impaired relative to both other groups on nearly all delayed memory measures. The preterm group, by contrast, was significantly impaired relative to the controls on only a few memory measures, i.e., route following and prospective memory. We suggest that early hippocampal pathology leads to the disabling memory impairments associated with developmental amnesia when the volume of this structure is reduced below normal by approximately 20-30% on each side. Whether this is a sufficient condition for the disorder or whether abnormality in other brain regions is also necessary remains to be determined.
Because the Galveston Orientation and Amnesia Test (GOAT) requires oral or written response, it risks misclassifying as amnestic aphasic patients who are not, in fact, amnestic. To correct for possible classification errors due to anomia, a modified multiple-choice format of the GOAT (AGOAT) was developed. The average GOAT score of 10 control nonaphasic head-injured patients suggested that an AGOAT score of 90 corresponds to the standard GOAT cutoff of 75 for resolution of posttraumatic amnesia (PTA). Using this criterion, 8 of 15 aphasic head-injured patients who technically were classified as amnestic on the GOAT were classified as nonamnestic on the AGOAT.
Earlier research has supported the use of a P300 (P3)-based procedure to detect simulated amnesia. In the present experiment, an attempt was made to model the behavior and event-related potentials (ERPs) that amnestic patients might demonstrate with relatively easy recognition memory tests, by increasing the difficulty of a match-to-sample recognition memory test taken by 18 memory-unimpaired undergraduates. None of the participants in the modeled amnesic condition were classified as having intact recognition memory as the result of P3-based intra-individual tests (specificity = 100%). The results support the utility of a P3 procedure for the detection of malingering by demonstrating the procedure to be a valid measure of impaired recognition with this model of amnesia.
C.B., a right-handed 33-year-old man, presented with anterograde amnesia after acute heart block. Cognitive abilities were normal except for serious impairment of long-term episodic memory. The access to semantic information was fully preserved. Magnetic resonance showed high signal intensity and marked volume loss in the hippocampus bilaterally; the left and right parahippocampal gyrus, lateral occipito-temporal gyrus, inferior temporal gyrus, and lateral temporal cortex were normal. This case underlines that global amnesia associated with hippocampal damage does not affect semantic memory. Although the hippocampus is important in retrieving context-linked information, its role is not so crucial in retrieving semantic contents. Cortical areas surrounding the hippocampus and lateral temporal areas might guide the recall of semantic information.
A case study is presented of a woman suffering from global amnesia so profound that she had lost all sense of personal identity. Hypnotherapy was used to establish, through imagery, a solid inner core on which to rebuild a sense of self. From the image of a strong column on which rested a book with a golden lock (her history), to reading about other lives, books and stories were utilized to establish a safe external environment in which the reawakening of repressed memories was no longer perceived as dangerous. A discussion of relevant literature on the subjects of global amnesia, loss of personal identity, and post-traumatic stress is offered as a basis for discussing the present case.
Transient global amnesia is a benign condition in which an isolated episode of amnesia occurs and then clears completely. No loss of motor or sensory function occurs and patients are not aphasic during the episodes. Neurologic workup is not likely to reveal any specific cause. It is necessary to eliminate treatable causes of transient ischemic attacks and also to rule out seizure disorders and brain tumors as a cause of this often unrecognized phenomenon. Cerebrovascular disease is often postulated as the underlying mechanism.
This study attempted to establish criteria for distinguishing patients with genuine memory problems from those who are attempting to simulate amnesia. The performance of simulators and genuine amnesics was compared under distraction conditions in which subjects had to count backwards between presentation and recall, and under no-distraction conditions in which the retention interval was unfilled. Genuine amnesics performed significantly worse than controls under distraction conditions, but did not perform significantly worse than controls under no-distraction conditions. However, those attempting to fake amnesia performed significantly worse than controls under no-distraction as well as under distraction conditions. They also exaggerated the memory deficit overall relative to genuine amnesics. It is suggested that these two criteria might be used successfully in clinical settings to assist in the detection of simulators.
This study employed a semantic decision-making task to examine both item priming and skill learning in amnesia, which traditionally have been demonstrated with separate tasks. Fourteen amnesic patients of mixed etiologies and 14 normal control subjects judged whether words represented animate or inanimate objects. One list was presented repeatedly on four continuous blocks of trials, and a new list was presented on the fifth block. For both groups, decision times decreased significantly from Block 1 to Block 5 (indicating skill acquisition) and increased significantly from Block 4 to Block 5 (indicating item-specific learning). The amnesic patients demonstrated a normal rate of skill learning, but a reduced magnitude of item priming. As expected, the amnesics had significantly impaired explicit memory of the implicitly learned items, as measured by recognition accuracy. The results suggest that both implicit and explicit learning of individual items is impaired in amnesia, despite normal semantic skill learning.
BACKGROUND: There is controversy as to whether PTSD can develop following a brain injury with a loss of consciousness. However, no studies have specifically examined the influence of the memories that the individuals may or may not have on the development of symptoms. AIMS: To consider how amnesia for the traumatic event effects the development and profile of traumatic stress symptoms. METHOD: Fifteen hundred case records from an Accident and Emergency Unit were screened to identify 371 individuals with traumatic brain injury who were sent questionnaires by post. The 53 subsequent valid responses yielded three groups: those with no memory (n = 14), untraumatic memories (n = 13) and traumatic memories (n = 26) of the index event. The IES-R was used as a screening measure followed by a structured interview (CAPS-DX) to determine caseness and provide details of symptom profile. RESULTS: Groups with no memories or traumatic memories of the index event reported higher levels of psychological distress than the group with untraumatic memories. Ratings of PTSD symptoms were less severe in the no memory groups compared to those with traumatic memories. CONCLUSIONS: Psychological distress was associated with having traumatic or no memories of an index event. Amnesia for the event did not protect against PTSD; however, it does appear to protect against the severity and presence of specific intrusive symptoms.
This case study describes rehabilitation efforts with a 24-year-old woman who exhibited dense amnesia secondary to status epilepticus following a motor vehicle accident. She was 20 months post-injury upon entry into our day treatment programme. The functional severity of her amnesia was reflected in numerous ways, including no recall of what she wore from day to day and an inability to find the toilet after 2 weeks in the programme. A multidisciplinary comprehensive programme of external cueing was established to exploit her preserved procedural memory. Objective measures of functional compliance were gathered over time and contrasted with both standard neuropsychological test scores and early levels of functioning in rehabilitation. Results demonstrated enhanced functioning via utilization of procedural memory. In addition, the patient actually demonstrated increased independent generalization of strategies and techniques over time. Practical treatment implications are reviewed and discussed.
We modified Bruce, Dolan, and Phillips-Grant's (2000) threshold procedure for determining the wane of childhood amnesia. In two experiments, undergraduates labelled childhood events (e.g., your first permanent tooth came in) as know or recollect memories and estimated their age at the event's occurrence. In both studies the estimated transition from mostly know memories to mostly recollect memories was roughly 4.7 years. This transition estimate was replicated in a sample of adults (ages 24-65 years) with both Bruce et al.'s event-generation task and the Experiment 1a questionnaire. By contrast, in two experiments a transition estimate of roughly 6 years was found for undergraduates' memories of public events (e.g., the Challenger explosion). The wane of childhood amnesia appears to occur around 4.7 years.
This experiment investigated the impact of suggestion focus on posthypnotic amnesia (PHA) for memories of a first romantic relationship. During hypnosis, high and low hypnotisable participants recalled specific memories from this period in response to 10 cue phrases (Elicitation). They then received a PHA suggestion that targeted either the entire period or specific memories from that period. Participants' explicit memory was indexed by cued recall after PHA was administered (memories recalled to "old" and "new" cues; Recall 1) and after it was cancelled (Recall 2). A social judgement task indexed dissociations between implicit and explicit memory. PHA had the greatest impact on highs', but not lows', memory performance (in terms of memories recalled to old cues, recall latency, and qualitative memory ratings) when the suggestion targeted the entire period rather than specific events. We discuss these findings in terms of the parameters of PHA's influence on memory, its value for exploring the nature and structure of autobiographical memory, and its utility as a laboratory analogue of functional amnesia.
Patients with mild to moderate Alzheimer's disease and normal controls were tested on two retrograde memory tests, one based on public events, and the other querying autobiographical memory. On both tests, patients showed strong decrements as compared to normal controls, pointing to retrograde amnesia. Evidence for a gradient in retrograde amnesia was conflicted, with analyses of variance revealing no gradient beyond the most recent period, and more sensitive analyses pointing to shallow Ribot gradients on both tests. A literature review shows that this is the case in most published studies. In autobiographical remote memory patients generated many incorrect answers, a tendency correlated with the number of false alarms on an anterograde memory test administered several months earlier. This suggests a stable, possibly executive, factor underlying memory errors.
Sixteen patients, who had suffered only one episode of transient global amnesia and showed no clinically evident abnormalities in their follow-up, were examined with psychometric and memory tests. Deficits in verbal long-term memory and in verbal IQ were found. These observations seem to demonstrate that in transient global amnesia patients regarded as being 'normal' in their follow-up there is no complete recovery and the sequelae seem to conform to a definite pattern. Problems of nosology and localization are discussed.
A 39-year-old man developed retrograde and anterograde amnesia following haemorrhage from an arteriovenous malformation situated near the splenium of the corpus callosum. MRI studies demonstrated damage to the splenium, and to a region containing the retrosplenial cortex and the cingulate bundle. The fornix was anterior and inferior to the site of maximal damage, but may have been involved; the stria terminalis was probably spared. Structures known to be important in memory but spared by the lesion included the hippocampus, thalamus, and basal forebrain. The retrosplenial cortex receives input from the subiculum and projects to the anterior thalamus, thus providing an alternative route between hippocampus and thalamus. Perhaps more importantly, medial temporal structures involved in memory receive anterior thalamic input directly via the cingulate bundle and indirectly through a relay in the retrosplenial cortex. We suggest that this thalamocortical portion of Papez' circuit may be important in memory, and that lesions of the cingulum and retrosplenial cortex may cause amnesia by disrupting this pathway.