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Positron emission tomographic study of post-ischaemic-hypoxic amnesia.

BACKGROUND: Despite extensive research, it still remains controversial as to what the precise location of the critical lesions underlying amnesia actually is. The amnesic syndrome is believed to be heterogeneous and due to several distinct functional deficits. PATIENTS AND METHODS: Two patients, a 45-year-old woman and a 56-year-old man, with sudden cardiopulmonary arrest and successful resuscitation, were left with a clear amnesic syndrome as main neurological sequela. During their revalidation period, they underwent a positron emission tomographic (PET) examination, utilizing the (13)NH(3) bolus technique at rest and after intravenous acetazolamide administration. RESULTS: Both PET studies showed more or less similar features with a decrease in regional cerebral blood flow (rCBF) in the frontal, temporal and parietal lobes. In addition, the rCBF was increased in both thalami of the 45-year-old woman and in the striata of the 56-year-old man. Acetazolamide vasoreactivity was most lost in the frontal lobes. CONCLUSIONS: In the present PET study, we demonstrated that destruction of the inhibitory pathways to the thalamus and basal ganglia by ischaemic-hypoxic frontal lesions could be one of the mechanisms leading to amnesia.

Acetazolamide↗

Naringenin from Citrus junos has an inhibitory effect on acetylcholinesterase and a mitigating effect on amnesia.

This study was performed to identify safe and more effective acetylcholinesterase (AChE) inhibitors in the treatment of Alzheimer's disease. The total methanol extract of Citrus junos had a significant inhibitory effect on AChE in vitro. By sequential fractionation of C.junos, the active component was finally identified as naringenin. Naringenin inhibited AChE activity in a dose-dependent manner. In this study, we also evaluated the anti-amnesic activity of naringenin, a major flavanone constituent isolated from C. junos, in vivo using ICR mice with amnesia induced by scopolamine (1 mg/kg body weight). Naringenin, when administered to mice at 4.5 mg/kg body weight, significantly ameliorated scopolamine-induced amnesia as measured in both the passive avoidance and the Y-maze test. These results suggest that naringenin may be a useful chemopreventive agent against Alzheimer's disease.

Acetylcholinesterase↗

The transient global amnesia syndrome. An analysis of 35 cases.

On basis of 35 patients who have suffered from transient global amnesia the pathophysiological mechanisms of this syndrome are discussed. Our impression is that the primary cause of this syndrome is a transient ischemia of the hippocampus, an opinion common with most earlier authors. The possibility of a unilateral hippocampal disturbance resulting in transient global amnesia is discussed. We are inclined to regard the local hippocampal ischemia as arising from insufficiency of the anterior chorioidal artery and thus as a sequel of internal carotid insufficiency, which has earlier been proved to result from various rotatory, flexion, and extension movements of the neck.

Adult↗

Transient global amnesia.

3 cases of transient global amnesia (TGA) are reported. Transient ischaemia is probably the cause of the condition in the majority of cases although other mechanisms, particularly epilepsy, may be responsible in some. TGA may not be reported by the patient and may be misdiagnosed as a psychiatric disturbance. An acute confusional or delirious state can also produce an episode of amnesia with inability to remember events which occurred during the period of cerebral dysfunction. In TGA, however, there is an acute and temporary failure to record events without the evidence of more generalised dysfunction which occurs in delirium. During the 3 episodes reported here the patients were able to carry on with their everyday activities and to complete structured tasks, such as the preparation of a meal. TGA appears, at least in some individuals, to carry the prognosis of transient cerebral ischaemia.

Aged↗

Brain stem dysfunction in transient global amnesia.

A patient with transient global amnesia also had transient bilateral gaze nystagmus which was detected both by conventional bedside examination and upon electronystagmographic recording. The nystagmus was absent one week later indicating recovery of the temporary brain stem deficit. The recording of objective evidence of brain stem dysfunction in the form of gaze nystagmus in a patient who had transient global amnesia, suggests that both were due to a transient ischemic attack involving the cerebral blood supply in the vertebrobasilar distribution.

Aged↗

Transient global amnesia associated with cardiac arrhythmia and digitalis intoxication.

A 54-year-old woman with transient global amnesia (TGA) was found to have digitalis-induced bradyarrhythmia with atrioventricular dissociation. The amnesia cleared only upon resolution of the arrhythmia. Cardiac arrhythmia has been postulated as a cause, but TGA in the setting of cardiac arrhythmia has not been documented previously. Cardiac arrhythmia should be excluded in patients with TGA, and TGA, a syndrome diagnosed on clinical grounds alone, must be recognized as one possible manifestation of treatable, potentially serious cardiac or cerebrovascular disease.

Amnesia↗

Amnesia and the declarative/nondeclarative distinction: a recurrent network model of classification, recognition, and repetition priming.

A key claim of current theoretical analyses of the memory impairments associated with amnesia is that certain distinct forms of learning and memory are spared. Supporting this claim, B. J. Knowlton and L. R. Squire found that amnesic patients and controls were indistinguishable in their ability to learn about and classify strings of letters generated from a finite-state grammar, but that the amnesics were impaired at recognizing the training strings. We show, first, that this pattern of results is predicted by a single-system connectionist model of artificial grammar learning (AGL) in which amnesia is simulated by a reduced learning rate. We then show in two experiments that a counterintuitive assumption of this model, that classification and recognition are functionally identical in AGL, is correct. In three further simulation studies, we demonstrate that the model also reproduces another type of dissociation, namely between recognition memory and repetition priming. We conclude that the performance of amnesic patients in memory tasks is better understood in terms of a nonselective, rather than a selective, memory deficit.

Adult↗

Transverse patterning and human amnesia.

The transverse patterning (TP) task (A+ B-, B+ C-, C+ A-) has played a central role in testing the hypothesis that medial-temporal (and, in particular, hippocampal) brain damage selectively impairs learning on at least some classes of configural (i.e., nonlinear) learning tasks. Results in the animal and human literature generally support that hypothesis. Reed and Squire [Impaired transverse patterning in human amnesia is a special case of impaired memory for two-choice discrimination tasks. Behavioral Neuroscience, 113, 3-9, 1999], however, advanced an alternative account in which impaired TP performance in amnesia reflects a generic scaling artifact arising from the greater difficulty of the TP task compared to the elemental (i.e., linear) control task that is typically used. We begin with a critique of Reed and Squire, countering their conceptual arguments and showing that their results, when analyzed appropriately, support the configural deficit hypothesis. We then report results from eight new amnesic patients and controls on an improved version of the TP task. Despite substantial practice, accuracy of patients with bilateral hippocampal damage due to anoxia reached and maintained an asymptote of only 54% correct, well below the maximum accuracy obtainable (67%) in the absence of configural learning. A patient with selective bilateral damage to the anterior thalamic nuclei exhibited a TP accuracy asymptote that was near 67%, a pattern of two out of three correct consecutive trials, and a pattern of nearly always answering correctly for two of the three TP item pairs. These results are consistent with a set of unique and parameter-free predictions of the configural deficit hypothesis.

Aged↗

Neural mechanisms in dissociative amnesia for childhood abuse: relevance to the current controversy surrounding the "false memory syndrome".

OBJECTIVE: There is considerable controversy about delayed recall of childhood abuse. Some authors have claimed that there is a "false memory syndrome," in which therapists suggest to patients events that never actually occurred. These authors point to findings that suggest that memory traces are susceptible to modification. The purpose of this paper is to review the literature on the potential vulnerability of memory traces to modification and on the effects of stress on the neurobiology of memory. METHOD: The authors review findings on mechanisms involved in normal memory function, effects of stress on memory in normal persons, children's memory of stressful events, and alterations of memory function in psychiatric disorders. The effects of stress on specific brain regions and brain chemistry are also examined. RESULTS: Neuropeptides and neurotransmitters released during stress can modulate memory function, acting at the level of the hippocampus, amygdala, and other brain regions involved in memory. Such release may interfere with the laying down of memory traces for incidents of childhood abuse. Also, childhood abuse may result in long-term alterations in the function of these neuromodulators. CONCLUSIONS: John Nemiah pointed out several years ago that alterations in memory in the form of dissociative amnesia are an important part of exposure to traumatic stressors, such as childhood abuse. The studies reviewed here show that extreme stress has long-term effects on memory. These findings may provide a model for understanding the mechanisms involved in dissociative amnesia, as well as a rationale for phenomena such as delayed recall of childhood abuse.

Amnesia↗

Anterograde amnesia in triazolam overdose despite flumazenil treatment: a case report.

Anterograde amnesia, possibly accompanied by acute brain syndrome, is a potential side-effect of certain benzodiazepines, particularly triazolam. Flumazenil is a benzodiazepine antagonist that is highly effective in reversing the central nervous system effects of benzodiazepine overdose. We report a case of triazolam overdose resulting in anterograde amnesia after flumazenil administration had restored clear consciousness. The defect in memory may have been due to too little flumazenil being given or failure of memory consolidation affected by the character of triazolam during the induced lucent period. We feel that physicians should be aware of the potential occurrence of acute brain syndrome in patients with benzodiazepine overdose despite treatment with flumazenil.

Adolescent↗

Amnesia in relation to fugue states--distinguishing a neurological from a psychogenic basis.

A case of transient amnesia is described in which a patient reported memory loss for five days, during which he had wandered extensively. Analysis showed that he did not have selective amnesia for the public events which had occurred during the five days for which he professed memory loss. This finding was incompatible with our case having a neurologically based global memory disorder during the fugue state. These findings offer support for a distinction between personal and public episodic memory.

Adult↗

Unreliable admissions to homicide. A case of misdiagnosis of amnesia and misuse of abreaction technique.

BACKGROUND: The past decade has witnessed a recognition that unsafe criminal convictions may be occasioned by unreliable confessions. AIMS: To present a case which illustrates the dangers of using abreaction interview techniques in a legal context and demonstrate the relevance of the memory distrust syndrome to an unsafe confession to murder. METHOD: We under took a detailed assessment of a person appealing against his original murder conviction, 'the appellant', and a careful scrutiny of all the relevant papers in the case. RESULTS: The appellant served 25 years in prison before his conviction was quashed as 'unsafe' on the basis of fresh psychological and psychiatric evidence. CONCLUSIONS: Amnesia for an offence had been misdiagnosed, and the use of repeated abreaction interviews had further confused both the appellant and the original court. At the Appeal Court, the advice was that the man had experienced a form of source amnesia which resulted in an unreliable confession.

Adult↗

Unconsciousness, amnesia and psychiatric symptoms following road traffic accident injury.

BACKGROUND: Although road traffic accident injury is the most common cause of traumatic brain injury, little is known of the prevalence of psychiatric complications or the significance of unconsciousness and amnesia. AIMS: To describe amnesia and unconsciousness following a road traffic accident and to determine whether they are associated with later psychological symptoms. METHOD: Information was obtained from medical and ambulance records for 1441 consecutive attenders at an emergency department aged 17-69 who had been involved in a road traffic accident. A total of 1148 (80%) subjects completed a self-report questionnaire at baseline and were followed up at 3 months and 1 year. RESULTS: Altogether, 1.5% suffered major head (and traumatic brain) injury and 21% suffered minor head injury. Post-traumatic stress disorder (PTSD) and anxiety and depression were more common at 3 months in those who had definitely been unconscious than in those who had not, but there were no differences at 1 year. CONCLUSIONS: PTSD and other psychiatric complications are as common in those who were briefly unconscious as in those who were not.

Accidents, Traffic↗

Posttraumatic stress disorder with amnesia following asphyxiation.

We describe five cases of traumatic asphyxiation injury, each meeting diagnostic criteria for posttraumatic stress disorder (PTSD) and characterized by a range of postinjury cognitive impairment. Four patients exhibited dense retrograde amnesia, including absence of conscious memory for the traumatic event. Appreciation of these asphyxiation cases, which involve temporally extended trauma exposure, may help resolve arguments regarding the possibility of co-occurrence of PTSD and neurological amnesia based exclusively on observations of much briefer duration events (specifically, motor vehicle crashes). These five cases also provide evidence that cognitive symptoms of PTSD can develop in the absence of conscious memory for the event.

Accidents↗

High-field, T2 reversed MRI of the hippocampus in transient global amnesia.

OBJECTIVE: To investigate the fine structural integrity of the hippocampus in patients with transient global amnesia (TGA) using high-resolution T2 reversed (T2R) MRI. METHODS: The authors performed detailed structural analysis of the hippocampus in 15 patients who had recovered from an episode of TGA and 150 randomly recruited normal volunteers across the adult age spectrum using high-resolution T2R MRI obtained on a 3.0-T system. An additional 100 subjects, with stroke or tumor, were similarly studied and served as disease controls. RESULTS: The overall incidence of hippocampal cavities detected in normal volunteers increased with age but never exceeded 40%, whereas the incidence in disease control group was 31%. They were always unilateral. In contrast, cavities were found in all 15 patients with TGA (100%), an incidence higher than in normal or disease controls (p < 0.05; Ryan's multiple comparison test), and were bilateral in eight patients (53%). The cavities in all but one of the normal volunteers (99%) and all disease controls (100%) were crescent shaped and < or =2 mm in width. The cavities in 14 of 15 patients with TGA (93%) were considerably larger (>3 mm in width), and five of the patients had giant cavities (>5 mm in width). Most of the cavities in patients with TGA had a rounded shape and resembled pathologic cavities described in specimens of hypoxia-related CA1 necrosis. CONCLUSION: The data indicate that transient global amnesia may not be a benign entity. Delayed neuronal loss within CA1 area of Lorente de No may represent its important sequel.

Adolescent↗

Detection of intracranial venous reflux in patients of transient global amnesia.

BACKGROUND: The mechanism of transient global amnesia (TGA) is not clear. Attempting to support the hypothesis that retrograde venous hypertension causing cerebral venous ischemia plays a role in the pathogenesis of TGA, the authors used cranial three-dimensional time-of-flight (TOF) MR angiography (MRA) to detect a possible intracranial retrograde venous flow in TGA patients. METHODS: The frequency of abnormal venous signals on cranial three-dimensional TOF MRA was compared in 10 TGA patients with the signals in 50 age- and gender-matched normal individuals. In TGA patients with abnormal venous signals, other examinations (cerebral digital subtraction angiography, upper extremity digital subtraction venography [DSV], and thoracic inlet MRI) were performed to elucidate the etiology of these abnormal intracranial venous flow patterns. RESULTS: Abnormal venous signals on three-dimensional TOF MRA were found in five (50%) of the TGA patients and none of the control subjects (p < 0.001). Compression leading to occlusion of the left brachiocephalic vein by the sternum and aorta during regular breathing, as depicted by upper extremity DSV and thoracic inlet MRI, occurred consistently among these five TGA patients with abnormal venous signals. CONCLUSIONS: Retrograde intracranial venous flow caused by left brachiocephalic vein occlusion was found only in patients with transient global amnesia (TGA). This result suggests that TGA patients may have an underlying impairment of cerebral venous outflow that increases their vulnerability to TGA attack.

Aged↗

Musical performance during transient global amnesia.

An organist had an episode of transient global amnesia during a recital. Despite a severe immediate-memory deficit, he performed complex organ music. This case suggests that the localization of the cerebral deficit in transient global amnesia is distinct from the cerebral centers necessary for performance of instrumental music.

Aged↗

Amnesia after anterior communicating artery aneurysm rupture.

We studied 11 patients with amnesia and personality change after surgical repair of ruptured anterior communicating artery ( ACoA ) aneurysm. CT and clinical evidence suggested that infarction in the territory of the ACoA was responsible for amnesia and personality change. The medial septal nuclei, the paraventricular nucleus of the anterior hypothalamus, and the medial forebrain bundle are the primary areas of potential interest in these cases. Gross infarction in the frontal lobes is not a requirement for the syndrome.

Adult↗