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At least 973 records · Page 54Linked to original sources
PubMed2004

Motor cortex excitability in transient global amnesia.

OBJECTIVE: To investigate the physiology of motor cortical areas in patients with transient global amnesia (TGA). MATERIALS AND METHODS: We performed transcranial magnetic stimulation (TMS) and single photon emission computed tomography (SPECT) in 13 patients during and after the acute phase of a typical episode of TGA. Measures of cortical excitability included motor threshold (MT) to magnetic stimulation, cortical silent period (SP) duration and intracortical inhibition (ICI) using a paired-pulse TMS technique. RESULTS: We found thalamic hypoperfusion and an ipsilateral significantly decreased ICI during the acute phase of TGA. CONCLUSIONS: Reduced activity in inhibitory circuits may explain why PET studies of patients with TGA showed neocortical hypometabolism. Our findings are consistent with the hypothesis that frontal cortex dysfunction probably due to damage affecting the thalamocortical circuits may play an important role in the pathogenesis of the syndrome.

Adult↗
PubMed2005

Weather conditions and transient global amnesia. A six-year study.

OBJECTIVES: The aetiology of transient global amnesia (TGA) is still unknown. Various events or activities have been shown to trigger TGA. A common feature of these events is an increased sympathetic activity which in turn may be influenced by meteorological factors. This prompted us to evaluate the influence of climatic parameters, and their variation on the incidence of TGA. METHODS: A total of 223 cases of TGA admitted to our hospital over a six-year period were studied. The study consisted of a comparison between the climatic parameters of days with TGA and those without TGA. The meteorological database included daily values of parameters recorded at the meteorological station of the town during this period. RESULTS: The onset of TGA was significantly correlated with lower daily,monthly and seasonal temperature values. Most cases of TGA were found when the temperature was less than 6.9 degrees C,whereas the frequency of TGA was minimum when it was more than 24 degrees C (P < 0.0001). Only temperature had a significant independent effect: an increase of 1 sd = 8.4 degrees C decreases the TGA admission odds of 0.78 (95 % CI: 0.62 to 0.97), i.e -22% (95 % CI: -38% to -3 %). CONCLUSIONS: This study suggests an association between TGA occurrence and low ambient temperature. Multicentre studies taking into account climatic differences between countries are necessary to confirm our findings.

Amnesia, Transient Global↗
PubMed2005

Transient global amnesia in a patient with high and persistent levels of antiphospholipid antibodies.

Cerebrovascular disease is one of the most common symptoms associated with anticardiolipin antibodies (ACA) and lupus anticoagulant (LA), usually in the form of ischemic stroke. However, many other neurologic disorders have been described in patients with antiphospholipid syndrome or ACA. So far, the precise relation between the presence of antibodies and the development of the disease in many of these cases remain unknown. Transient global amnesia (TGA) is an infrequent neurologic disturbance whose precise pathophysiology is not known. It is characterized by a sudden inability to acquire new information, usually lasting no more than 12 h, and it is not accompanied by any other focal neurological signs or symptoms. We report a patient with TGA with persistent and high levels of ACA and LA and suggest that in patients with TGA, investigation of the possible presence of ACA and/or LA may be warranted because a higher prevalence of TGA in the patients with antiphospholipidic syndrome with respect to the general population may lead to further insights into pathogenesis of neurologic disease associated with antiphospholipidic antibodies.

Amnesia, Transient Global↗
PubMed2006

Severe amnesia following bilateral medial temporal lobe damage occurring on two distinct occasions.

A comprehensive neuropsychological assessment was performed on a 38-year-old woman with drug-resistant right temporal lobe epilepsy before temporal lobectomy, during a 2-year follow-up period, and approximately 3 years after surgery when she developed a malignant glioma in the left medial temporal lobe (MTL). Both before and after epilepsy surgery, memory function was normal. When the tumour was discovered, the patient suffered from severe retrograde and anterograde amnesia, whereas working memory and the other cognitive abilities were preserved. Compared with other cases of bilateral temporal lesion, this case is peculiar because the damage occurred on two distinct occasions. It suggests that only one MTL can allow normal memory function, or can take over the function normally subserved by a dysfunctional contralateral MTL when the dysfunction is marked and prolonged, such as in chronic epilepsy.

Adolescent↗
PubMed1985

Facilitating telephone number recall in a case of psychogenic amnesia.

In the present case study, a middle-aged woman was admitted to the hospital with no identification and no recollection of her identity. Attempts by social and police agencies to recognize, or discover some clue about the patient, were unsuccessful. The behavioral interventions of modeling, reinforcement, and progressive relaxation were designed to induce telephone dialing behavior and telephone number recall. The positive outcome of the case is discussed in terms of spontaneous remission, and the effects of relaxation therapy, a physical-motoric non-verbal procedure on the recollection process of the amnesia victim.

Adult↗
PubMed1994

BR-16A protects against ECS-induced anterograde amnesia.

BR-16A is an herbal (non allopathic) medication used in India to enhance cognition. In experiment 1, 28 Wistar rats received either BR-16A (200 mg/kg/day) or vehicle alone for 3 weeks. During the third week, the rats were tested for learning in the Hebb Williams complex maze. BR-16A-treated rats showed significantly better learning than did controls. Experiment 2 was conducted identically except that during the second week all of 32 rats additionally received six once-daily electroconvulsive shocks (ECS). An advantage for learning was again demonstrated for the BR-16A group. It is concluded that BR-16A facilitates learning, and that this effect extends to a protection against ECS-induced anterograde amnesia. Cognitive deficits induced by electroconvulsive therapy are a major disadvantage of the treatment and, to-date, no drug has been found to offer satisfactory protection against such deficits. It is suggested that BR-16A may hold promise in the containment of electroconvulsive therapy (ECT)-induced cognitive compromise.

Amnesia↗
PubMed1983

Naloxone attenuates amnesia caused by amygdaloid stimulation: the involvement of a central opioid system.

This study investigated the effect of naloxone on amnesia produced by subseizure amygdaloid stimulation. Animals were trained in an inhibitory avoidance task, and given amygdaloid stimulation following training. Immediately after training, prior to stimulation, naloxone was injected either peripherally (i.p.) or into the bed nucleus of the stria terminalis (BNST) where the Met-enkephalin-containing fibers from the amygdala terminate. Amygdaloid stimulation caused retention deficits. The deficits were attenuated by 3.0 mg/kg naloxone given peripherally or by 1.0 microgram or 0.3 microgram naloxone injected bilaterally into the BNST. The attenuative effect was anatomically and receptor specific: 0.3 microgram of naloxone injected into the caudate nucleus was ineffective; the attenuative effect of naloxone was antagonized by simultaneous injection of 1.5 or 4.5 micrograms levorphanol into the BNST. These results suggest that endogenous opioids, possibly the enkephalins of the stria terminalis released into the BNST following amygdaloid stimulation, are at least partially involved in mediating the effect of amygdaloid stimulation on memory.

Amnesia↗
PubMed1993

Dynorphin A-(1-13) attenuates basal forebrain-lesion-induced amnesia in rats.

The effects of dynorphin A-(1-13), an endogenous kappa opioid agonist, on basal forebrain (BF)-lesion-induced amnesia in rats were investigated using step-through-type passive avoidance task. The BF was lesioned by injecting the cholinergic neurotoxin ibotenic acid (6 micrograms/side). The number of rats achieving the cut-off time (600 s) of step-through latency (STL) in BF-lesioned group significantly decreased as compared with that in sham-operated group. Dynorphin A-(1-13) (0.3 micrograms) significantly increased the number of rats achieving the cut-off time of STL in BF-lesioned rats. These results suggest that dynorphins play an improving role in the impairment of memory processes in BF-lesioned rats.

Alzheimer Disease↗
PubMed1992

L-alpha-glycerylphosphorylcholine antagonizes scopolamine-induced amnesia and enhances hippocampal cholinergic transmission in the rat.

The effects of L-alpha-glycerylphosphorylcholine (alpha-GPC) on scopolamine-induced memory impairment and on brain acetylcholine (ACh) synthesis and release were investigated in rats. Oral administration of alpha-GPC 3 h before the behavioural test prevented the learning impairment induced by scopolamine given 30 min before the acquisition of a passive avoidance response. Similarly, retrograde amnesia induced by scopolamine, given immediately after acquisition training, was also completely reversed by the drug. These effects were dose-dependent with a maximum at 300 mg/kg. The mechanism of action of this compound was investigated by measuring hippocampal ACh synthesis and release both in vivo by means of the microdialysis technique and in vitro in tissue slices. alpha-GPC dose dependently increased ACh release with a maximum at 300 mg/kg. In addition, i.v. injection of [14C]alpha-GPC resulted in [14C]ACh formation. The data suggest that the behavioural effects of alpha-GPC may be related to its property to increase hippocampal ACh synthesis and release.

Acetylcholine↗
PubMed1993

5-HT1A receptor agonists induce anterograde amnesia in mice through a postsynaptic mechanism.

The effect of the 5-HT1A receptor partial agonist tandospirone on memory was investigated in mice using a single trial, step-through passive avoidance task. Tandospirone disrupted performance in a dose-dependent manner when administered before the training trial but not when injected immediately post-training. The pre-training effect was not the result of reduced responsiveness to foot shock because tandospirone did not alter current threshold intensity to elicit flinch, run and vocalization responses. The performance deficit was alleviated by treatment with d-amphetamine prior to the retention test. The memory impairment by tandospirone was mimicked by the 5-HT1A receptor agonist 8-OH-DPAT (8-hydroxy-dipropylaminotetralin HBr) and blocked by the 5-HT1A receptor antagonist BMY7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspirol-[4]- decane-7,9-dione). BMY7378 alone was ineffective. Treatment with the 5-HT synthesis inhibitor PCPA (parachlorophenylalanine) resulted in apparent enhancement rather than disruption of the avoidance behavior. However, the anterograde amnestic effects of tandospirone and 8-OH-DPAT were not affected by PCPA, and lack of interactions between PCPA and the 5-HT1A agonists revealed in the statistical analyses indicated that the effects of PCPA were not mediated by 5-HT1A receptors. It is concluded that 5-HT1A receptor agonists and partial agonists produce a reversible anterograde amnesia that is mediated by postsynaptic 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Systemic administration of dynorphin A-(1-13) markedly improves cycloheximide-induced amnesia in mice.

The effects of systemic or intracerebroventricular injection of dynorphin A-(1-13), a kappa-selective opioid receptor agonist, on cycloheximide-induced amnesia were investigated by using a step-down-type passive avoidance task in mice. The intracerebroventricular injection of dynorphin A-(1-13) (0.3-3 micrograms) before training significantly prolonged step-down latency. The systemic administration of dynorphin A-(1-13) (1, 3 and/or 10 mg/kg, i.p.) before training or retention tests markedly inhibited the cycloheximide (30 mg/kg, s.c.)-induced shortening of step-down latency, indicating antiamnesic effects of dynorphin A-(1-13). One and 3 mg/kg doses of ((+/-)trans-3, 4-dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, methanesulfonate hydrate (U-50,488H), another kappa-selective opioid receptor agonist, significantly inhibited the shortening. The anti-amnesic effects of dynorphin A-(1-13) (3 and 10 mg/kg, i.p.) were almost completely antagonized by intracerebroventricular administration of the quaternary derivative of the opioid receptor antagonist naltrexone methobromide (0.3 microgram), but not by systemic administration of the opioid receptor antagonist (1 mg/kg, s.c.), demonstrating central mediation of the anti-amnesic effects of dynorphin A-(1-13). Furthermore, the kappa-selective opioid receptor antagonist, nor-binaltorphimine (2 mg/kg, s.c.), almost completely antagonized the effects of dynorphin A-(1-13) (3 and 10 mg/kg, i.p.). These results suggest that dynorphin A-(1-13) produces anti-amnesic effects through the blood-brain barrier.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

A cell assembly theory of hippocampal amnesia.

Recent memories are more susceptible to amnesic loss than older memories, the time scale being much longer than can reasonably be explained by a passive chemical or morphological change. A possible explanation is that memories are initially sustained by "soft", easily produced but ephemoral, synaptic changes to which are later added "hard" changes that are more durable but require repeated synaptic activity over a long period to become established. "Soft" synapses are assumed to be concentrated in parts of the limbic system, "hard" synapses in the neocortex. The theory can also explain why objects encountered by patients with anterograde amnesia never become familiar to them.

Amnesia↗
PubMed1992

Actors but not scripts: the dissociation of people and events in retrograde amnesia.

We describe our further investigations of the retrograde amnesia in a single case. R.F.R. became globally amnesic following an attack of Herpes Simplex Encephalitis. He could generate and recognize superordinate level information about the vast majority of proper names including the names of people but he was very impaired at giving information about what had "happened" to these same individuals. He could also provide detailed information about family friends but he could not recall salient major personal episodes in which these same individuals had been involved. Knowledge of people appears to be represented in a different way to that of events, even when a singular event has provided the main or only opportunity for learning about the individual.

Amnesia, Retrograde↗
PubMed1993

The contribution of the anterior thalamic nuclei to anterograde amnesia.

This paper first reviews the anatomical, pathological, and neuropsychological evidence implicating the anterior thalamic nuclei in memory processes. It is concluded that there is much indirect evidence indicating that anterior thalamic dysfunction is an important factor in anterograde amnesia. More direct evidence for the involvement of the anterior thalamic nuclei in memory processes emerges from two experiments with rats that examined performance of a spatial test of working memory, delayed nonmatching-to-position. The first study revealed that neurotoxic lesions of the anterior thalamic nuclei and radiofrequency lesions of the fornix both produce equivalent performance deficits. In contrast, lesions of the mamillary bodies were without effect. A second study showed that lesions of the fornix and removal of the hippocampus produced very similar deficits. These data indicate that while the involvement of the anterior thalamic nuclei in certain memory functions depends on inputs from the hippocampus, this involvement need not depend on indirect afferents via the mamillary bodies.

Amnesia↗
PubMed1993

Encoding ability is preserved in amnesia: evidence from a direct test of encoding.

The encoding ability of 17 amnesics of mixed aetiology and 17 matched normal controls was assessed directly using a novel procedure. On two separate occasions, subjects were shown 60 complex drawings each containing six pictures. On one occasion each drawing was shown for 6 sec, and on the other occasion it was shown for 25 sec. Immediately after presentation of each drawing subjects were asked a single unpredictable question about picture colours, location, size or semantic category. Amnesics performed normally in the 6-sec exposure condition indicating that all of the tested kinds of information were encoded at a normal rate. Performance in this condition correlated with short-term, but not long-term memory in the amnesics indicating that it depended largely on encoding and short-term memory. However, the amnesics were impaired in the 25-sec condition where performance should have depended on (long-term) memory abilities at which they were impaired. The results are inconsistent with available encoding deficit accounts of amnesia.

Adult↗
PubMed1996

Transient topographical amnesia and cingulate cortex damage: a case report.

Transient topographical amnesia (TTA) is the temporary inability to find one's way in familiar or unfamiliar surroundings due to the inability to use well known environmental landmarks for route finding. The syndrome has not been described as having any obvious aetiology and has been thought to be caused by a vascular deficit in right hemispheric structures which are crucial for topographic recognition, i.e. parietal association and parahippocampal cortex. The patient described in the present study complained of several critical episodes of TTA and tonic rigidity of the left limbs. Neuropsychological assessment was normal except for a deficit in spatial memory tasks. Magnetic resonance (MR) imaging of the brain showed an angioma at the border of areas 24d and 23 of the right cingulate cortex. Because area 23 is strategically located in a network that links the parietal associative (area 7a) and parahippocampal cortices, and because these cortical areas are involved in topographical orienting processes, we suggest that a transient functional inactivation of the network caused by epileptic discharges spreading from the damaged cingulate cortex towards the parahippocampal and parietal association cortex could account for the spatial disorder. Similar discharges spreading from area 24d towards the primary motor cortex and/or the spinal cord could account for the episodes of tonic rigidity of the left limbs.

Amnesia↗
PubMed1982

Amnesia after operations on aneurysms of the anterior communicating artery.

All patients with ruptured aneurysms admitted to neurosurgical departments in Denmark after April, 1978, are the subjects in the prospective study that includes neuropsychological examinations. Data from 48 patients with aneurysms of the anterior communicating artery have been analyzed. Trapping of the aneurysm was done in 11 patients and resulted in an amnesic syndrome in 9. Thirty-seven patients were operated upon by ligation of the neck of the aneurysm or similar procedures, resulting in 6 cases of amnesia. Trapping invariably disrupts blood supply through newly described dorsal perforating branches from the anterior communicating artery. These perforating branches may supply areas of vital importance to memory function.

Amnesia↗
PubMed1989

Hypothalamic and basal forebrain germinoma presenting with amnesia and hyperphagia.

Patients harboring primary intracranial germinomas usually have had Parinaud's syndrome and hydrocephalus (with pineal tumors) or hypopituitarism, visual loss, and diabetes insipidus (with suprasellar tumors) at presentation. The few reported cases of verified intraparenchymal hypothalamic germinomas all have been in prepubertal males with progressive neurologic deficits, altered levels of consciousness, or clinically apparent panhypopituitarism. The subject of this report was an endocrinologically normal, primiparous 24-year-old woman who presented with hydrocephalus followed by worsening anterograde amnesia and hyperphagia despite having a functioning ventriculoatrial shunt. Computed tomography scanning and magnetic resonance imaging demonstrated an anterior hypothalamic, thalamic, and basal forebrain mass, which stereotactic biopsy proved to be a germinoma. Intraaxial germinomas restricted to the anterior hypothalamus or thalamus rarely have been reported. The clinical features of the current patient may be unique.

Adult↗