Focal retrograde amnesia: voxel-based morphometry findings in a case without MRI lesions

Focal retrograde amnesia (FRA) is a rare neurocognitive disorder presenting with an isolated loss of retrograde memory. In the absence of detectable brain lesions, a differentiation of FRA from psychogenic causes is difficult. Here we report a case study of persisting FRA after an epileptic seizure. A thorough neuropsychological assessment confirmed severe retrograde memory deficits while anterograde memory abilities were completely normal. Neurological and psychiatric examination were unremarkable and high-resolution MRI showed no neuroradiologically apparent lesion. However, voxel-based morphometry (VBM)-comparing the MRI to an education-, age-and sex-matched control group (n = 20) disclosed distinct gray matter decreases in left temporopolar cortex and a region between right posterior parahippocampal and lingual cortex. Although the results of VBM-based comparisons between a single case and a healthy control group are generally susceptible to differences unrelated to the specific symptoms of the case, we believe that our data suggest a causal role of the cortical areas detected since the retrograde memory deficit is the preeminent neuropsychological difference between patient and controls. This was paralleled by grey matter differences in central nodes of the retrograde memory network. We therefore suggest that these subtle alterations represent structural correlates of the focal retrograde amnesia in our patient. Beyond the implications for the diagnosis and etiology of FRA, our results advocate the use of VBM in conditions that do not show abnormalities in clinical radiological assessment, but show distinct neuropsychological deficits.     

The loss of episodic memories in retrograde amnesia: single-case and group studies

Retrograde amnesia in neurological disorders is a perplexing and fascinating research topic. The severity of retrograde amnesia is not well correlated with that of anterograde amnesia, and there can be disproportionate impairments of either. Within retrograde amnesia, there are various dissociations which have been claimed-for example, between the more autobiographical (episodic) and more semantic components of memory. However, the associations of different types of retrograde amnesia are also important, and clarification of these issues is confounded by the fact that retrograde amnesia seems to be particularly vulnerable to psychogenic factors. Large frontal and temporal lobe lesions have been postulated as critical in producing retrograde amnesia. Theories of retrograde amnesia have encompassed storage versus access disruption, physiological processes of 'consolidation', the progressive transformation of episodic memories into a more 'semantic' form, and multiple-trace theory. Single-case investigations, group studies and various forms of neuroimaging can all contribute to the resolution of these controversies.     

Hypnosis,memory and amnesia.

Hypnotized subjects respond to suggestions from the hypnotist for imaginative experiences involving alterations in perception and memory. Individual differences in hypnotizability are only weakly related to other forms of suggestibility. Neuropsychological speculations about hypnosis focus on the right hemisphere and/or the frontal lobes. Posthypnotic amnesia refers to subjects'' difficulty in remembering, after hypnosis, the events and experiences that transpired while they were hypnotized. Posthypnotic amnesia is not an instance of state-dependent memory, but it does seem to involve a disruption of retrieval processes similar to the functional amnesias observed in clinical dissociative disorders. Implicit memory, however, is largely spared, and may underlie subjects'' ability to recognize events that they cannot recall. Hypnotic hypermnesia refers to improved memory for past events. However, such improvements are illusory: hypermnesia suggestions increase false recollection, as well as subjects'' confidence in both true and false memories. Hypnotic age regression can be subjectively compelling, but does not involve the ablation of adult memory, or the reinstatement of childlike modes of mental functioning, or the revivification of memory. The clinical and forensic use of hypermnesia and age regression to enhance memory in patients, victims and witnesses (e.g. recovered memory therapy for child sexual abuse) should be discouraged.     

Effect of bacosides, alcoholic extract of Bacopa monniera Linn. (brahmi), on experimental amnesia in mice

To investigate the effect of bacosides (alcoholic extract of brahmi) on scopolamine (3 mg kg(-1), ip), sodium nitrite (75 mg kg(-1), ip) and BN52021 (15 mg kg(-1), ip) induced experimental amnesia in mice, using Morris water maze test, all the agents were administered 30 min before the acquisition trials on each day and repeated for 4 consecutive days, and on 5th day during the retrieval trials. Bacosides on anterograde administration (before training) in mice, significantly decreased the escape latency time (ELT) during the acquisition trials for 4 consecutive days and increased the time spent (TS) in target quadrant during the retrieval trials on 5th day, and on retrograde administration (after training) bacosides were found not to affect TS significantly. Bacosides also significantly decreased the ELT and increased the TS in mice treated anterogradely with scopolamine and sodium nitrite. Bacosides did not exhibit any significant effect on TS of mice treated retrogradely with sodium nitrite. On the other hand, bacosides significantly increased the TS of mice treated retrogradely with BN52021. On the basis of the present results it can be concluded that bacosides facilitate anterograde memory and attenuate anterograde experimental amnesia induced by scopolamine and sodium nitrite possibly by improving acetylcholine level and hypoxic conditions, respectively. Beside this bacosides also reversed BN52021 induced retrograde amnesia, probably due to increase in platelet activating factor (PAF) synthesis by enhancing cerebral glutamate level.     

Transient global amnesia after ablation of the left lateral accessory pathway

Transient global amnesia (TGA) could be encountered in many situations even during invasive procedures. In ablation therapy for arrhythmia, there was only one reported case in the ablation of premature ventricular beats. We report a 31-year-old man having paroxysmal supraventricular tachycardia who underwent TGA at the end of ablation and recovered quickly after 8-9 hours later. Long-term follow-up showed no neurologic deficits for 8 months.     

Looking beyond the hippocampus: old and new neurological targets for understanding memory disorders

Although anterograde amnesia can occur after damage in various brain sites, hippocampal dysfunction is usually seen as the ultimate cause of the failure to learn new episodic information. This assumption is supported by anatomical evidence showing direct hippocampal connections with all other sites implicated in causing anterograde amnesia. Likewise, behavioural and clinical evidence would seem to strengthen the established notion of an episodic memory system emanating from the hippocampus. There is, however, growing evidence that key, interconnected sites may also regulate the hippocampus, reflecting a more balanced, integrated network that enables learning. Recent behavioural evidence strongly suggests that medial diencephalic structures have some mnemonic functions independent of the hippocampus, which can then act upon the hippocampus. Anatomical findings now reveal that nucleus reuniens and the retrosplenial cortex provide parallel, disynaptic routes for prefrontal control of hippocampal activity. There is also growing clinical evidence that retrosplenial cortex dysfunctions contribute to both anterograde amnesia and the earliest stages of Alzheimer''s disease, revealing the potential significance of this area for clinical studies. This array of findings underlines the importance of redressing the balance and the value of looking beyond the hippocampus when seeking to explain failures in learning new episodic information.     

Transient global amnesia after mild head injury in childhood

In seven entirely healthy children in the age group of 6.5 to 14.5 years, mild head injury produced transient global amnesia (TGA) of median duration of 4.5 hours. None of the patients had convincing signs of brain concussion or clinical focal symptomatology. In four cases CT examination of the brain showed normal findings. Four children had a transient abnormal EEG (intermittent delta rhythms, slowed background activity inconstant local finding (of slow waves). During the period monitored (2-34 months) there was no recurrent attack and the children have had no difficulties. Pathologically, the authors assume ischemia of temporobasal structures induced by mild trauma with a relationship to migraine diathesis and rank the child group among so called benign posttraumatic encephalopathy with a noncomplicated course and good outcome.     

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 $\text{1}\text{μg}\text{4}\text{μl}$ (ICV) had no action on the ECS-induced retrograde amnesia, while in a dose of $\text{4}\text{μg}\text{4}\text{μl}$ 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.     

Studies in traumatic amnesia

Retrograde amnesia is for a period of time, usually for a fraction of a minute in simple concussion, and not loss of memory for an event. The length of time for which there is no recollection is not directly related to the duration of coma but can be for days or even weeks. It is characterized by inability of restoration of memory for the period in question. Any retrograde amnesia of more than a day's duration results from trauma only if the trauma is severe enough to cause prolonged coma, usually weeks. It should be under suspicion of being due pathologically to more than concussion. Careful attention should be given to the possibility of hysteria or malingering as a factor.     

Make love to forget: two cases of transient global amnesia triggered by sexual intercourse

Transient global amnesia (TGA) is characterized by a sudden onset and by a typical resolution within several hours. Several precipitating events have been proposed: physical exertion, emotional experiences, etc. The aim of this paper was to present two cases of TGA triggered by sexual intercourse and to suggest a possible mechanism for the development of TGA. In both patients, clinical examination revealed elevated blood pressure. Laboratory examinations and brain CTs were normal. EEG demonstrated diffuse dysrhythmia and slow spike-waves, respectively. SPECT revealed hypoperfusion in the left frontal and right medial temporal regions. Various explanations of the mechanism of TGA are discussed. Based on the observed hypoperfusion in the medial temporal regions, a new hypothesis is advanced, suggesting the possibility that TGA occurs due to a pathologically changed or less adaptable anterior chorioid artery, initially constricted by hypotension following a blood shift from the center towards periphery.     

Mycalolide B dissociates dynactin and abolishes retrograde axonal transport of dense-core vesicles

Axonal transport is critical for maintaining synaptic transmission. Of interest, anterograde and retrograde axonal transport appear to be interdependent, as perturbing one directional motor often impairs movement in the opposite direction. Here live imaging of Drosophila and hippocampal neuron dense-core vesicles (DCVs) containing a neuropeptide or brain-derived neurotrophic factor shows that the F-actin depolymerizing macrolide toxin mycalolide B (MB) rapidly and selectively abolishes retrograde, but not anterograde, transport in the axon and the nerve terminal. Latrunculin A does not mimic MB, demonstrating that F-actin depolymerization is not responsible for unidirectional transport inhibition. Given that dynactin initiates retrograde transport and that amino acid sequences implicated in macrolide toxin binding are found in the dynactin component actin-related protein 1, we examined dynactin integrity. Remarkably, cell extract and purified protein experiments show that MB induces disassembly of the dynactin complex. Thus imaging selective retrograde transport inhibition led to the discovery of a small-molecule dynactin disruptor. The rapid unidirectional inhibition by MB suggests that dynactin is absolutely required for retrograde DCV transport but does not directly facilitate ongoing anterograde DCV transport in the axon or nerve terminal. More generally, MB''s effects bolster the conclusion that anterograde and retrograde axonal transport are not necessarily interdependent.     

Pre-electroconvulsive shock administration of calcium channel blockers reduces retrograde amnesia induced by ECS

Effect of pre-electroconvulsive shock (ECS) administration of calcium channel blockers (CCBs) like verapamil, diltiazem, nifedipine, nimodipine, flunarizine and cinnarizine on retrograde amnesia induced by ECS was examined using passive avoidance paradigm in rats. The groups (Gr 1-7) of adult, male Wistar rats received true ECS with CCBs (5mg/kg; i.p) or vehicle (10 ml/kg; ip) and other groups (Gr 8-14) received sham ECS with CCBs (5mg/kg; i.p) or vehicle (10 ml/kg; i.p). The anti-amnestic activity of CCBs were evaluated using the passive avoidance paradigm in rats. Results showed that, the baseline latencies for all the groups did not differ significantly. Rats receiving true ECS produced significantly lower latencies. There was increase in the post ECS step through latencies of the rats administered CCBs before ECS. Therefore, pre-ECS administration of calcium channel blockers might reduce retrograde amnesia produced by ECS without altering seizure duration.     

Memory decay and susceptibility to amnesia dissociate punishment- from relief-learning

Painful events shape future behaviour in two ways: stimuli associated with pain onset subsequently support learned avoidance (i.e. punishment-learning) because they signal future, upcoming pain. Stimuli associated with pain offset in turn signal relief and later on support learned approach (i.e. relief-learning). The relative strengths of such punishment- and relief-learning can be crucial for the adaptive organization of behaviour in the aftermath of painful events. Using Drosophila, we compare punishment- and relief-memories in terms of their temporal decay and sensitivity to retrograde amnesia. During the first 75 min following training, relief-memory is stable, whereas punishment-memory decays to half of the initial score. By 24 h after training, however, relief-memory is lost, whereas a third of punishment-memory scores still remain. In accordance with such rapid temporal decay from 75 min on, retrograde amnesia erases relief-memory but leaves a half of punishment-memory scores intact. These findings suggest differential mechanistic bases for punishment- and relief-memory, thus offering possibilities for separately interfering with either of them.     

Long lasting recurrent familiar transient global amnesia after betablocker treatment withdrawal: case report

The etiology of Transient Global Amnesia (TGA) is not yet clear. A small part of TGA has a familiar occurrence. We report a case of recurrent, long-lasting familiar amnesia occurring after betablocker treatment withdrawal in a migrainous patient. We suggest that familiar TGA could be caused by the mechanism of vasospasm rather than venous congestion and that the abnormal cerebral vasomotor control could be the hereditary substrate in this condition.     

Electroconvulsive shock and brain muscarinic receptors: relationship to anterograde amnesia

Rats were administered one electroconvulsive shock daily for 7 days (ECS X 7) and were killed 24 hours after the last treatment. Muscarinic cholinergic receptor number, as determined by [3H] quinuclidinyl benzilate [( 3H]QNB) binding, was significantly reduced in the cerebral cortex. A parallel group of rats was trained on a passive avoidance task 24 hours following the last ECS and tested for retention of the original avoidance response 24 hours later; these animals exhibited a profound amnesia. Animals tested 1 hour following training were not amnestic, indicating that learning was unimpaired. Animals trained 7 days following ECS X 7 were not amnestic and [3H] QNB binding changes were not demonstrable at this time. A single ECS which does not significantly affect cortical [3H] QNB binding, did not induce amnesia in rats trained 24 hours after the treatment and tested 24 hours later. The parallel, cumulative nature of ECS-induced muscarinic receptor down-regulation and ECS-induced anterograde amnesia suggests a possible causative relationship.     

Intact memory for irrelevant information impairs perception in amnesia

Memory and perception have long been considered separate cognitive processes, and amnesia resulting from medial temporal lobe (MTL) damage is thought to reflect damage to a dedicated memory system. Recent work has questioned these views, suggesting that amnesia can result from impoverished perceptual representations in the MTL, causing an increased susceptibility to interference. Using a perceptual matching task for which fMRI implicated a specific MTL structure, the perirhinal cortex, we show that amnesics with MTL damage including the perirhinal cortex, but not those with damage limited to the hippocampus, were vulnerable to object-based perceptual interference. Importantly, when we controlled such interference, their performance recovered to normal levels. These findings challenge prevailing conceptions of amnesia, suggesting that effects of damage to specific MTL regions are better understood not in terms of damage to a dedicated declarative memory system, but in terms of impoverished representations of the stimuli those regions maintain.     

A Highlights from MBoC Selection: Synaptic neuropeptide release by dynamin-dependent partial release from circulating vesicles

Neurons release neuropeptides, enzymes, and neurotrophins by exocytosis of dense-core vesicles (DCVs). Peptide release from individual DCVs has been imaged in vitro with endocrine cells and at the neuron soma, growth cones, neurites, axons, and dendrites but not at nerve terminals, where peptidergic neurotransmission occurs. Single presynaptic DCVs have, however, been tracked in native terminals with simultaneous photobleaching and imaging (SPAIM) to show that DCVs undergo anterograde and retrograde capture as they circulate through en passant boutons. Here dynamin (encoded by the shibire gene) is shown to enhance activity-evoked peptide release at the Drosophila neuromuscular junction. SPAIM demonstrates that activity depletes only a portion of a single presynaptic DCV''s content. Activity initiates exocytosis within seconds, but subsequent release occurs slowly. Synaptic neuropeptide release is further sustained by DCVs undergoing multiple rounds of exocytosis. Synaptic neuropeptide release is surprisingly similar regardless of anterograde or retrograde DCV transport into boutons, bouton location, and time of arrival in the terminal. Thus vesicle circulation and bidirectional capture supply synapses with functionally competent DCVs. These results show that activity-evoked synaptic neuropeptide release is independent of a DCV''s past traffic and occurs by slow, dynamin-dependent partial emptying of DCVs, suggestive of kiss-and-run exocytosis.     

Value of Dynamic Susceptibility Contrast Perfusion MRI in the Acute Phase of Transient Global Amnesia

Purpose

Transient global amnesia (TGA) is a transitory, short-lasting neurological disorder characterized by a sudden onset of antero- and retrograde amnesia. Perfusion abnormalities in TGA have been evaluated mainly by use of positron emission tomography (PET) or single-photon emission computed tomography (SPECT). In the present study we explore the value of dynamic susceptibility contrast perfusion-weighted MRI (PWI) in TGA in the acute phase.

Methods

From a MRI report database we identified TGA patients who underwent MRI including PWI in the acute phase and compared these to control subjects. Quantitative perfusion maps (cerebral blood flow (CBF) and volume (CBV)) were generated and analyzed by use of Signal Processing In NMR-Software (SPIN). CBF and CBV values in subcortical brain regions were assessed by use of VOI created in FIRST, a model-based segmentation tool in the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB) Software Library (FSL).

Results

Five TGA patients were included (2 men, 3 women). On PWI, no relevant perfusion alterations were found by visual inspection in TGA patients. Group comparisons for possible differences between TGA patients and control subjects showed significant lower rCBF values bilaterally in the hippocampus, in the left thalamus and globus pallidus as well as bilaterally in the putamen and the left caudate nucleus. Correspondingly, significant lower rCBV values were observed bilaterally in the hippocampus and the putamen as well as in the left caudate nucleus. Group comparisons for possible side differences in rCBF and rCBV values in TGA patients revealed a significant lower rCBV value in the left caudate nucleus.

Conclusions

Mere visual inspection of PWI is not sufficient for the assessment of perfusion changes in TGA in the acute phase. Group comparisons with healthy control subjects might be useful to detect subtle perfusion changes on PWI in TGA patients. However, this should be confirmed in larger data sets and serial PWI examinations.     

顺行髓内钉、逆行髓内钉及锁定加压钢板内固定治疗股骨远端骨折的对比研究

摘要目的：探讨顺行髓内钉、逆行髓内钉及锁定加压钢板内固定3种方法治疗股骨远端骨折患者的疗效。方法：对2011年1月至2012年12月间我院收治的101例股骨远端骨折进行临床随机分组手术,分别在手术中使用顺行髓内钉、逆行髓内钉以及锁定加压钢板内固定。对三组患者手术时间、术中出血量以及切口长度等一般情况进行比较分析,同时采用Harris评分系统对三组患者术后恢复情况进行分析比较。结果：经过手术治疗后,逆行髓内钉组Harris评分显著高于其他两组（P〈0．05）。另外,逆行髓内钉组手术过程短、出血量少、手术切口小,上述指标与其他两组比较均有统计学意义（P〈0．05）。结论：股骨远端骨折行逆行髓内钉治疗的疗效优于顺行髓内钉以及锁定加压钢板内固定,具有手术时间短、术中出血少、切口小等优点,能够有效提高术后膝关节功能的恢复,值得临床推广使用。     

Neuron death in the developing avian isthmo–optic nucleus,and its relation to the establishment of functional circuitry

The present review covers all the published data on neuron death in the developing avian isthmo–optic nucleus (ION), which provides a particularly convenient situation for studying the causes and consequences of neuron death in the development of the vertebrate central nervous system. The main conclusions are as follows: The naturally occurring neuron death in the ION is related both temporally and causally to the ION's formation of afferent and efferent connections. The ION neurons need to obtain both anterograde and retrograde survival signals in order to survive during a critical period in embryogenesis. They may compete, at least for the retrograde signals, but the nature of the competition is still unclear. The retrograde signals are modified by action potentials. Neurons dying from a lack of anterograde survival signals can be distinguished morphologically from ones dying from a lack of retrograde signals. The neuron death refines circuitry by selectively eliminating neurons with “aberrant” axons projecting to the “wrong” (i.e., ipsilateral) retina or to the “wrong” (topographically inappropriate) part of the contralateral retina. © 1992 John Wiley & Sons, Inc.