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PubMed2000

Social amnesia in mice lacking the oxytocin gene.

The development of social familiarity in rodents depends predominantly on olfactory cues and can critically influence reproductive success. Researchers have operationally defined this memory by a reliable decrease in olfactory investigation in repeated or prolonged encounters with a conspecific. Brain oxytocin (OT) and vasopressin (AVP) seem to modulate a range of social behaviour from parental care to mate guarding. Pharmacological studies indicate that AVP administration may enhance social memory, whereas OT administration may either inhibit or facilitate social memory depending on dose, route or paradigm. We found that male mice mutant for the oxytocin gene (Oxt-/-) failed to develop social memory, whereas wild-type (Oxt+/+) mice showed intact social memory. Measurement of both olfactory foraging and olfactory habituation tasks indicated that olfactory detection of non-social stimuli is intact in Oxt-/- mice. Spatial memory and behavioural inhibition measured in a Morris water-maze, Y-maze, or habituation of an acoustic startle also seemed intact. Treatment with OT but not AVP rescued social memory in Oxt-/- mice, and treatment with an OT antagonist produced a social amnesia-like effect in Oxt+/+ mice. Our data indicate that OT is necessary for the normal development of social memory in mice and support the hypothesis that social memory has a neural basis distinct from other forms of memory.

Amnesia, Retrograde↗
PubMed2005

Development of shared information in communication despite hippocampal amnesia.

This study investigated the ability of individuals with amnesia to acquire referential labels across a series of collaborative, dynamic interactions with a communication partner. Despite their inability to learn arbitrary relations in paired-associate learning, the amnesic patients showed remarkably robust collaborative learning across trials, at a rate equal to that of normal comparison subjects. The amnesic participants' learning resulted in their arriving at labels for a set of abstract shapes (tangrams), thus facilitating rapid and efficient communication. The labels generated and used by the amnesics during interactions with their partners became simpler across trials, with most labels stabilizing long before the end of training and then being used consistently throughout; moreover, they endured long after the task had ended. These findings have important implications for understanding the memory systems involved in semantic learning and in acquiring shared knowledge ('common ground') among communication partners, and the nature of hippocampal-dependent versus hippocampal-independent learning.

Adult↗
PubMedDate not supplied

Transient global amnesia after intake of tadalafil, a PDE-5 inhibitor: a possible association?

Inhibitors of phosphodiesterase type 5 (PDE-5) are well established as an oral treatment for the majority of patients with erectile dysfunction (ED). PDE-5 is found in high concentration in smooth muscle cells of the corpora cavernosa. However, enzymes of the PDE family are also expressed in various other tissues, including the brain. Little is known about its effects on the central nervous system (CNS), although it has been suggested that PDE-5 inhibitors might cross the blood-brain barrier. Side effects, such as headache, nasal congestion, flushing, nausea, are much more common. We describe a patient who had a transient global amnesia (TGA) after his first-ever use of tadalafil, a potent PDE-5 inhibitor. Despite the fact that the aetiology of TGA has not entirely been clarified at present, we consider the hypothesis of a causal relationship as tempting with respect to the current hypotheses of TGA pathophysiology. This case, together with others, suggests that PDE-5 inhibitors might be capable of exerting adverse effects in the CNS. Physicians should be aware of the possibility of neurological disturbances when prescribing PDE-5 inhibitors for ED.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2002

Myelopathy and amnesia following accidental electrical injury.

OBJECTIVE: Documentation of MRI and neurophysiological changes following accidental electrical injury. SETTING: Tertiary care referral teaching hospital at Lucknow, India. RESULTS: A 30-year-old lady developed amnesia and spastic paraparesis with loss of pin prick sensation below the second thoracic spinal segment following electrocution. Her spinal MRI was normal and cranial MRI revealed T2 hyperintensity in the right putamen. Peroneal, sural and electromyography were normal. Tibial central sensory conduction time was normal but central motor conduction time to lower limbs and right upper limb was prolonged. CONCLUSION: Neurophysiological study and MRI may help in understanding the pathophysiological basis of neurological sequelae following electrical injury.

Adult↗
PubMed2000

Quantitative single photon emission tomography analysis for the diagnosis of transient global amnesia: adaptation of statistical parametric mapping.

We report two cases of transient global amnesia (TGA) diagnosed using a clinical criteria and single photon emission tomography (SPECT) with the aid of Statistical Parametric Mapping (SPM). Both patients underwent an initial SPECT study about 20 h after the disappearance of the amnesic episode, and a second study 3 weeks after the episode. We conducted quantitative cerebral blood flow (CBF) analyses using SPM on Matlab. This revealed regions with abnormal CBF in the first studies but not in the second. This method appears to be useful for diagnosis of TGA, especially in patients with suspected TGA in whom the amnesic episode disappears within a few days.

Aged↗
PubMed2001

Reversible amnesia in a Type 1 diabetic patient and bilateral hippocampal lesions on magnetic resonance imaging (MRI).

AIMS: Intensive insulin therapy of Type 1 diabetes limits its chronic complications, but is associated with an increased risk of severe hypoglycaemia and its neuroglycopenic consequences. METHODS: Case report. RESULTS: A 24-year-old male with 15 years' history of Type 1 diabetes, who was missing for 48 h, was found at home in ketoacidosis coma. Intensive care permitted a rapid improvement revealing an unexpected severe anterograde amnesia, confirmed by neuropsychological testing. MRI performed 4 days after admission showed abnormal bilateral hyperintensity signals on T2-weighted images in the hippocampus. Three months later, the patient had nearly completely recovered and resumed work. MR images and neuropsychological testing returned to normal. CONCLUSIONS: The most likely course of events favours an initial prolonged hypoglycaemic coma following insulin overdose. The hippocampal injury may be a result of hypoglycaemia. Neuropsychological testing and MRI abnormalities were completely reversible. This case underlines the potential risks of intensive insulin therapy.

Adult↗
PubMed2003

Anomia for people's names, a restricted form of transient epileptic amnesia.

A 37-year-old man consulted after two episodes of transient anomia for people's names over a period of 6 months. The first episode lasted about 10 min and was restricted to an inability to remember his 2-year-old son's first name. The second, was limited to an inability to recall his daughter's first name for 5 min with clear abnormal experiential quality. Witnessed descriptions of the attacks confirmed the absence of any other cognitive impairment or motor automatisms. The neurological examination was normal except for hyposmia. Inter-ictal cognitive evaluation was normal apart from the anomia for people's names or retrieval of names of familiar people in his childhood on definition and on famous faces naming test. A wake electroencephalograph showed left temporal epileptiform abnormalities, following hyperpnea. On magnetic resonance imaging, quantitative analysis revealed a mildly decreased volume of the left hippocampus. The diagnosis of transient epileptic amnesia (TEA) was considered and the patient did not recur for 6 months under lamotriginum. Thus anomia for people's names may be the sole clinical manifestation of TEA. Such a clinical presentation may easily be overlooked. Treatment may prevent further recurrence and the installation of more important and permanent autobiographical memory impairment. Our observation may suggest an isolated system not only for people's knowledge, but for people's naming. It is consistent with the notion of proper name as pure referring expression.

Adult↗
PubMed1995

Characterisation of antibodies specific for chick brain neural cell adhesion molecules which cause amnesia for a passive avoidance task.

Antisera were prepared against six postsynaptic density glycoprotein fractions (150-180, 62-80, 50, 41, 33, and 28 kDa) that show enhanced fucosylation during memory formation after training day-old chicks in a one-trial passive avoidance task. Each antiserum was tested for its possible effect on memory retention. Bilateral intracranial injections of two of the antisera, R-1 and R-6, or their IgGs (IgG-1 and IgG-6), resulted in amnesia for the passive avoidance task when chicks were tested 24 h later, IgG-1 and IgG-6 antibodies were amnestic only when injected 5.5 h after training, and had no effect when injections were made 30 min before training, thus resembling an effect previously observed with polyclonal or monoclonal anti-N-CAM antibodies. IgG-1 and IgG-6 antibodies were found to be specific for protein epitopes of glycoproteins that contain a high amount of N-linked mannose and fucose, and a very low amount of polysialic acid and O-linked galactose. Absorption of IgG-6 antibodies with neural cell adhesion molecule (N-CAM) isolated from synaptic plasma membranes derived from day-old chick brain resulted in loss of amnestic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia↗
PubMed2000

Bilateral astrocytoma involving the limbic system precipitating disabling amnesia and seizures.

Astrocytomas involving the limbic system are usually unilateral in nature. We report a very unusual case where a low-grade astrocytoma originating in the left temporal lobe spread to the right hippocampus through the hippocampal commissure to cause disabling amnesia and seizures. Some improvement in the memory deficit was facilitated by identification of complex partial status epilepticus. EEG should be performed in all patients with lesions of the limbic system and neuropsychological problems if ongoing seizure activity is not to be missed.

Adult↗
PubMed2002

Transient epileptic amnesia: an under-diagnosed phenomenon? Three more cases.

Three cases of patients with transient epileptic amnesia (also known as pure amnestic seizure) are described. In two patients it was the unique seizure type and represented de novo epilepsy occurring in the elderly. In the third patient it coexisted with long standing complex partial seizure of mesial temporal lobe origin. The problems associated with the diagnosis and the main clinical features are discussed. In addition the underlining pathophysiological mechanisms are considered. It is argued that this seizure type is likely to be under-diagnosed and that further research is needed as the presence of TEA has significant implications for clinical and surgical management.

Aged↗
PubMed2000

[Posttraumatic stress disorder in patients with neurogenic amnesia for the traumatic event].

The development of symptoms of posttraumatic stress disorder (PTSD) in patients with neurogenic amnesia for the traumatic event is recorded in 2 own patients and in 19 cases from the clinical literature. With a single exception, all patients were accident victims with closed head injuries. Only about three quarters of the patients completely fulfilled DSM-III-R criteria of PTSD. Nineteen patients displayed involuntary conscious memories of aspects of the traumatic event (presenting as recurrent intrusive thoughts, images or dreams) co-existent with a complete or partial lack of voluntary conscious memories of the trauma, suggesting that different memory systems and distinct brain mechanisms subserve these phenomena. The said clinical observations are discussed against the background of current neuropsychological models of multiple memory systems. The recorded cases demonstrate that declarative episodic memory is not necessary for symptoms of PTSD to emerge, whereas preserved functions of non-declarative memory systems represent a sufficient condition for the development of PTSD symptoms.

Accidents, Occupational↗
PubMed1990

Behavioral models of memory and amnesia.

In modelling memory and amnesia, the different forms of cognition must be distinguished. For memory, distinctions between acquisition, storage, and retrieval must be made and the different kinds of memory (e.g., immediate, working, reference) identified. Other notions, such as attention, orientation, and vigilance also belong under the heading "cognition". Thus the term "cognition enhancer" is imprecise because it does not indicate which kind of cognition is to be enhanced. Animal models should be developed for each type of cognition, be based on information from the clinic, and attempt to be specific. Examples of models more specific than the passive avoidance test were discussed and included the radial maze, in which different kinds of memory could be analyzed and correlated with, for example, changes in central cholinergic activity. From the point of view of drug development an important distinction was made between "empirical" and "simulation" models. In other areas of psychopharmacology "empirical" models have been widely used because they show predictable responses to known reference compounds. In the field of cognition there are no generally recognized reference compounds and therefore no "empirical" models. There is therefore a need for "simulation" models which imitate the various aspects of cognition and its pathology. The major criterion for validating this kind of model is that it should show changes similar to those observed in humans either resulting from a particular pathology or from a particular drug treatment.

Amnesia↗
PubMed1998

[Transitory global amnesia--psychogenic origin of organic disease? Psychopathologic basis and pathogenetic considerations].

Transient global amnesia (TGA) is an acute amnestic syndrome without neurological symptoms and remitting spontaneously. Though cerebral ischemia, epilepsy, and migraine have been implicated in some cases, non of these factors could be proven responsible for most, and etiology remains unclear. Of special interest is the induction of TGA by psychological and emotional stress in about 14-29% of all cases, which is illustrated by the clinical example of a 72-year-old women who suffered an attack of TGA after discovering a burglary in her home. Psychopathological and pathogenetic aspects are discussed in the context of recent neurobiological memory research. This suggests that TGA involves transient dysfunction of a specific memory subsystem associated with hippocampal structures. Neural network modelling explains the syndrome of TGA on a pathogenetic basis allowing for heterogeneous etiology and even for psychogenic release. Thus TGA serves as a model for pathogenetic explanation in the neuro-psychiatric borderland.

Acute Disease↗
PubMed2003

Developmental amnesia: effect of age at injury.

Hypoxic-ischemic events sustained within the first year of life can result in developmental amnesia, a disorder characterized by markedly impaired episodic memory and relatively preserved semantic memory, in association with medial temporal pathology that appears to be restricted to the hippocampus. Here we compared children who had hypoxic-ischemic events before 1 year of age (early group, n = 6) with others who showed memory problems after suffering hypoxic-ischemic events between the ages of 6 and 14 years (late group, n = 5). Morphometric analyses of the whole brain revealed that, compared with age-matched controls, both groups had bilateral abnormalities in the hippocampus, putamen, and posterior thalamus, as well as in the right retrosplenial cortex. The two groups also showed similar reductions (approximately 40%) in hippocampal volumes. Neuropsychologically, the only significant differences between the two were on a few tests of immediate memory, where the early group surpassed the late group. The latter measures provided the only clear indication that very early injury can lead to greater functional sparing than injury acquired later in childhood, due perhaps to the greater plasticity of the infant brain. On measures of long-term memory, by contrast, the two groups had highly similar profiles, both showing roughly equivalent preservation of semantic memory combined with marked impairment in episodic memory. It thus appears that, if this selective memory disorder is a special syndrome related to the early occurrence of hypoxia-induced damage, then the effective age at injury for this syndrome extends from birth to puberty.

Adolescent↗
PubMed1970

Retrograde amnesia gradients by subconvulsive and high convulsive transcranial currents in chicks.

Either a subconvulsive or a high convulsive current was delivered transcranially at various intervals after a learning trial to independent groups of newly hatched chicks. The one-trial learning involves suppression of the chicks' predilection to peck at a small shiny bead. The effect of current on retention was measured one day later. Results indicate a current-sensitive memory consolidation period of about 30 seconds that cannot be appreciably prolonged by a tenfold increase in current intensity and a simultaneous twofold increase in current duration. On the other hand, at comparable trial-to-current intervals within this brief consolidation period, more retention deficit was caused by the higher current. Beyond this critical period, both currents still effected some retention deficit, but it did not seem to vary with the trial-to-current interval from one minute to 24 hours. Overt muscular convulsion was unnecessary for the retrograde amnesia effect. The subconvulsive current may be a more pure agent for consolidation studies because the high, convulsive current may affect test performance in ways other than disrupting the consolidation processes.

Amnesia↗
PubMed1971

Acetoxycycloheximide and transient amnesia in the rat.

Rats were trained during the severe inhibition of protein synthesis that follows intracerebral injection of acetoxycycloheximide. Amnesia was consistently observed 24 hours after training, but memory spontaneously returned within 6 days. There was, consequently, no evidence of interference by acetoxycycloheximide with the consolidation phase of memory, but rather a transient deficit in the retrieval phase. It is suggested that this deficit may be due to a deficiency in neurotransmitters.

Amnesia↗