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The permanence of retrograde amnesia produced for a single training trial by a single electroconvulsive shock was studied. No recovery from amnesia was found with either single or repeated retention tests. Amnesic effects were found to be permanent with retention intervals as long as 1 month.
Retrograde amnesia for a passive avoidance response was produced in rats by electroconvulsive shock and in mice by cycloheximide, an inhibitor of protein synthesis. One day after training the memory could be restored if a "reminder" of the original foot shock was given after the retention test on which the amnesia was demonstrated. Memory did not return if the reminder was given without the prior retention test or if the reminder and the test were separated by 23 hours.
Mice that were deprived of rapid eye movement sleep for 2 days immediately after one-trial training in an inhibitory avoidance task and were given an electroconvulsive shock after deprivation displayed retrograde amnesia on a retention test given 24 hours later. Electroconvulsive shock produced no amnesia in comparable groups of animals that were not deprived of rapid eye movement sleep.
Electrical stimulation was delivered bilaterally to either the anterior or posterior cortex in rats from 0.1 second to 4 hours after a single training trial on an inhibitory avoidance task. As indicated by a retention test given 24 hours later, the length of the retrograde amnesia gradients ranged from 5 seconds to 240 minutes, depending on the brain region stimulated and the intensity of the stimulating current. The stimulation intensity that was threshold for amnesia varied directly with the length of the interval between training and treatment.
Amnesic patients acquired a mirror-reading skill at a rate equivalent to that of matched control subjects and retained it for at least 3 months. The results indicate that the class of preserved learning skills in amnesia is broader than previously reported. Amnesia seems to spare information that is based on rules or procedures, as contrasted with information that is data-based or declarative--"knowing how rather than "knowing that." The results support the hypothesis that such a distinction is honored by the nervous system.
The ability to learn to criterion a visually-guided stylus maze was found impaired in patients with right posterior cerebral damage, not only in comparison with controls but also with other hemisphere-damaged groups. The contribution of the corresponding left sided area to this task is dubious, and certainly not substantial. This finding points to the independent organisation of long-term spatial memory in the right posterior cerebral cortex, an inference that was further supported by the study of two cases. The first was a female patient with right temporo-parietal softening (as suggested by clinical, EEG, and brain scan data) who showed topographical amnesia and inability to learn the visual maze over 275 trials. On an extensive battery of tests she was found free from disorders of space perception, and from verbal and visual memory impairment. The second was a patient presenting with severe global amnesia who, nevertheless, had no difficulty in route finding, and reached the criterion on the maze in 31 trials.
Five personal observations of an acute amnestic episode in younger individuals after intake of clioquinol are described together with three observations from the medical literature. In five of these cases the episode began after an unusually large dose, in three after a therapeutic one with a latency of about 24 hours. The clinical aspect closely resembled classical transient global amnesia but the episode after clioquinol lasted longer (24 hours to three days) and a more or less extensive retrograde amnesia persisted permanently. In one patient after three tablets of Mexase a clioquinol concentration of 12 microgram/ml in plasma was found 24 hours after the specified dose, which is an unexpectedly high concentration compared to those reported as late as 24 hours after a single equal dose of Mexase or any other clioquinol-containing preparation. Another patient had a brief relapse two years after the first episode, after a single therapeutic dose of another clioquinol preparation.
A simple quantitative test is described for measuring the duration of post-traumatic amnesia. It was used in a study of 336 patients with closed head injury; and the results matched closely the independent estimates of experienced neurosurgeons. A systematic procedure of this kind is clinically useful in its sensitivity to fluctuations or deterioration in the patient's mental state. It could also be used with advantage in multi-centre research by providing a standard criterion for the assessment of post-traumatic amnesia.
Tumours of the septum pellucidum (SP) are rare and seldom associated with memory impairment either before or after operation. A patient is described who developed amnesia after transcallosal excision of a tumour of the SP. Radiology did not show any major lesion of the brain areas traditionally associated with amnesia. Because septal nuclei could have been damaged during surgery their possible role in memory functions is discussed.
While absence attacks and complex partial seizures have been well documented in patients with epilepsy, the delineation of pure episodes of memory loss without additional clinical manifestations remains poorly characterised. The recently described condition of transient epileptic amnesia (TEA) is critically examined, and four new cases are described, in each of which there were episodes of pure memory loss which subsequently proved to be epileptic in origin. The anatomical and pathophysiological basis of TEA is presumed to be similar to transient global amnesia (TGA), that is, it is likely to be primarily hippocampal in origin, but with more variable involvement of limbic and adjacent temporal lobe neocortical structures.
A patient had neuropsychological testing during, and at two days and seven weeks after a transient global amnesia (TGA) attack. During the attack she exhibited a characteristically profound anterograde amnesia but a limited remote memory loss; the most striking impairment was a deficit in personal episodic memory revealed by her performance on the Autobiographical Memory Interview. Personal and general semantic information was less impaired although there were indications of a temporal gradient in the impairment. When tested after the attack, she demonstrated normal anterograde and retrograde memory. A SPECT scan performed during TGA showed a focal reduction in cerebral perfusion in the postero-medial temporal lobes bilaterally which had resolved after seven weeks.
An industrial manager had severe retrograde and variable but usually mild anterograde amnesia four years after a head injury. MRI showed damage of both temporal poles and the lateral portion of the right prefrontal cortex. The prefrontal and temporal cortical damage on the right side extended deeply into the white matter while the temporal cortical damage on the left side was much smaller. There was an additional left temporo-parietal lesion. The patient was of average intelligence. His attention, short term memory and learning ability were average or somewhat below average. His old memories were severely affected for the personal-episodic domain and less so for semantic remote memory abilities. Therefore an anatomical dissociation between anterograde and retrograde amnesia is possible at the anterior temporal regions, possibly interacting with the prefrontal cortex; these regions seem necessary for the retrieval of old episodic memories.
A 54-year-old patient who had an isolated small polar thalamic infarct and acute global amnesia with slight frontal type dysfunction but without other neurological dysfunction was studied. Memory improved partially within 8 months. At all stages the impairment was more severe for verbal than non-verbal memory. Autobiographic recollections and newly acquired information tended to be disorganised with respect to temporal order. Procedural memory was unaffected. Both emotional involvement and pleasure in reading were lost. On MRI, the infarct was limited to the left anterior thalamic nuclei and the adjacent mamillothalamic tract. The regional cerebral metabolic rate of glucose (measured with PET) was decreased on the left in the thalamus, amygdala, and posterior cingulate cortex 2 weeks after the infarct, and in the thalamus and posterior cingulate cortex 9 months later. These findings stress the specific role of the left anterior thalamic region in memory and confirm that longlasting amnesia from a thalamic lesion can occur without significant structural damage to the dorsomedial nucleus. Furthermore, they suggest that the anterior thalamic nuclei and possibly their connections with the posterior cingulate cortex play a role in emotional involvement linked to ipsilateral hemispheric functions.
Ten healthy middle aged or elderly women experienced isolated episodes of topographical amnesia without an obvious aetiology. It is likely a benign cognitive disorder, similar to transient global amnesia.
A case of paraneoplastic limbic encephalitis presenting with topographical disorientation is reported. A 70 year old woman became unable to identify familiar buildings and landscapes and could not recall the way to destinations she had known very well for years. She also showed attentional disturbance and severe anterograde amnesia. Her retrograde amnesia extended for one year at most. No other neuropsychological deficits were noted. Thus her topographical disorientation was of the primary form. Specific tests related to topographical disorientation showed that her two main symptoms seem to fall into the categories of landscape agnosia and heading disorientation. T2 weighted magnetic resonance imaging revealed high intensity signals in the anteromedial temporal lobes bilaterally, in the right posterior parahippocampal gyrus, in the right retrosplenial region, and in the right inferior precuneus. Anti-Hu antibody was found in the serum. This case shows that topographical disorientation can be a primary symptom of limbic encephalitis.
A patient developed spontaneous, acute, dominant frontal lobe haemorrhage neighbouring on a zone of pre-existing post-traumatic encephalomalacia manifesting clinically as transient global amnesia. Amnesia can be secondary to disease of the frontal lobe, affecting pathways interconnecting the basal forebrain and hippocampus of the temporal lobe.
Transient global amnesia has been associated with cerebral angiography performed with use of ionic agents. Nonionic contrast agents are associated with fewer complications, but complications do occur. The authors describe two patients who developed transient global amnesia after they underwent cerebral angiography with iopamidol. The precise pathophysiologic mechanism remains unclear, but the syndrome is by definition self-limited.
We examined the effect of the acetylcholinesterase (AChE) inhibitor, donepezil hydrocloride (DONP), on group II metabotropic glutamate (mGlu) receptor agonist- or antagonist-induced amnesia in the step-through passive avoidance task in male mice. DCG-IV, a group II mGlu receptor agonist, at dose of 50 ng and LY341495, a group II mGlu receptor antagonist, at dose of 300 ng, significantly attenuated the latency on the step-through task. The subcutaneous injection of DONP at dose of 1 mg/kg 1 hour before passive avoidance performance ameliorated the amnesia induced by DCG-IV and LY341495, whereas donepezil alone did not affect task latency. The results suggest that activation of group II mGlu receptors and disinhibition of the cAMP/PKA signaling pathway (caused by group II mGlu receptor antagonist) have a negative action on step-through passive avoidance memory performance, and that group II mGlu receptors and ACh interact to modulate learning and memory function.