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At least 289 records · Page 16Linked to original sources
PubMed2004

Clinical profile and course of cognitively normal patients evaluated in memory disorders clinics.

The authors investigated 499 patients that were found to be cognitively normal at the Alzheimer's Disease Research Centers of California between 1988 and 1999. Patients reported high rates of depression (39%) and family history of dementia (51%). Thirty-six percent returned for follow-up, and of those, 65% received a diagnosis of dementia or mild cognitive impairment. Patients evaluated at memory clinics who are considered cognitively normal may merit periodic re-evaluation.

Aged↗
PubMed2005

CREB, synapses and memory disorders: past progress and future challenges.

In neurons, appropriate long-term adaptive responses to changes in the environment require the conversion of extracellular stimuli into discrete intracellular signals. Many of these signals involve the regulation of gene expression. The cAMP responsive element binding protein (CREB) is a nuclear transcription factor that modulates transcription of genes containing cAMP responsive elements (CRE sites) in their promoters. CREB is a key part of many intracellular signaling events that critically regulate many neural functions. Numerous studies on invertebrates and vertebrates demonstrate that CREB is critical for long-term memory. Here, we review the key features of CREB-dependent transcription and critically evaluate the data examining the roles of CREB in different forms of plasticity, including long-term memory in mammals. Because learning and memory have been linked to specific types of synaptic plasticity in several species, we also review studies on the role of CREB in long-term facilitation in Aplysia and in hippocampal long-term potentiation (LTP). Several human cognitive disorders have been linked to alterations of CREB-regulated gene expression. Therefore, we explore the possibility of targeting CREB function in developing novel treatment strategies. Finally, we highlight areas of research on CREB that are ripe for further advancement.

Animals↗
PubMed1991

[Traumatic amnesias. Memory disorders consecutive to head injuries].

Traumatic amnesia is a good index predictive of the disablement due sequelae of cranial injuries. The residual memory deficit, correlated with the return to work, mainly affects long-term memory, learning, verbal memory and sensitivity to interferences. The most relevant tests are Rey's 15 words--and particularly their retrieval at 30 minutes--and the verbal fluency test, but the changes in memory observed in the patient's daily life must also be evaluated. Rehabilitation tends to rely on the overall management of intellectual and behavioural disorders, as part of programmes that are specific to subjects with cranial injury.

Amnesia↗
PubMed2002

[Memory disorders after unilateral cerebral lesions].

In contrast to the amnestic syndrome, unilateral hemispheric lesions are mostly connected with selective memory deficits, which are related to either verbal or visual-spatial information. Clinical studies concerning this are mostly about patients with temporal lobe epilepsy. Almost all studies found that significantly worse verbal memory deficits appeared before or after left temporal lobectomy. In contrast to these outcomes, the results concerning right temporal lobectomy (RTL) are nonuniform. There are studies that cannot prove figurative memory deficits before or after RTL and others that ascertain a correlation between RTL and figurative memory deficits. Mean values are always compared with random samples of left and right hemispheric patients. In contrast, the presented study assumes a clinical isolated case and analyses a random sample of neurological patients with different genesis with a standardized memory test (Berlin Amnesia Test, or BAT). As a result, a significant correlation between left hemispheric lesions and verbal memory deficits as well as right hemispheric lesions and visual-spatial memory deficits can be proven. Possible reasons for these differing results with visual-spatial memory deficits are still under discussion.

Adult↗
PubMed1986

Thalamic hemorrhage with neglect and memory disorder.

A patient with right thalamic hemorrhage developed left-sided hemi-inattention, indifference, motor neglect, and hypokinesia. He also developed a severe memory deficit at the time of hemorrhage. Observations in this patient suggest that, in addition to a syndrome of neglect and hypokinesia, an amnesic syndrome can arise from unilateral lesions involving the right thalamus.

Amnesia↗
PubMedDate not supplied

[Pharmacological correction of behavioral and memory disorders in rats with vasorenal arterial hypertension given propranolol].

It was established that propranolol in a daily dose of 2 mg/kg causes disturbance of behavior of rats with arterial hypertension in the open field, deteriorates retention of memory traces in passive avoidance paradigm, and leads to the development of depression in the test for zoosocial interrelation. Administration of nootropic piracetam (200 kg/mg/24 h). as well as the original compounds ACP-94 (20 mg/kg/24 h) and PIR-87--6-0 (50-mg/kg/24 h) facilitates the correction of negative changes in the behavior and memory of hypertensive rats.

Administration, Oral↗
PubMed1993

[Encephalopathy and memory disorders during treatments with mefloquine].

Benign psychiatric side effects have been frequently associated with mefloquine therapy. On the other hand, severe psychiatric disorders due to mefloquine are rare but must be detected by physicians. Two such cases are reported. In the first case, excessive curative mefloquine therapy caused an acute psychotic state which ultimately regress without treatment. The second report concerns a transient memory failure following prophylactic mefloquine treatment. The causative role of this compound is being discussed and the importance of a differential diagnosis of neuropsychiatric disorders from toxic or parasitic origin is underlined. Circumstances aggravating such neuropsychiatric side effects and actual recommendations concerning the prescription of mefloquine are recalled.

Adult↗
PubMed1978

Memory disorder in vertebrobasilar disease.

Previous workers have clearly established that the central core limbic structures of the brain are primarily concerned in the production of amnesia of the axial or mesial type. The blood supply to these structures derives primarily from the posterior cerebral circulation. This was the rationale for Benson's work on 'amnesic stroke' in patients with posterior cerebral artery occlusion. We have extended this concept to show that a similar axial amnesia, as demonstrated by a classical response on Wechsler Memory Scale testing, exists in patients with vertebrobasilar insufficiency. Relative permanency of the amnesic syndrome was demonstrated by repeat testing at may be of assistance in the diagnosis of vertebrobasilar insufficiency.

Aged↗
PubMed1994

Bilateral temporal lobe pathology with sparing of medial temporal lobe structures: lesion profile and pattern of memory disorder.

The lesion sustained by the amnesic patient H.M. consisted of bilateral ablation of medial temporal lobe structures with relative sparing of more lateral white matter and neocortical structures. We present the first detailed report of a case where the reverse pattern of lesions predominated, namely bilateral pathology of white matter and neocortical temporal lobe structures, with spared medial temporal lobe structures. This damage, which was particularly severe in anterior loci in the temporal lobes, was sustained as a result of radionecrosis. High-resolution magnetic resonance imaging was carried out to document the distinctive anatomical profile of our patient, and this profile was compared to that reported for the patient H.M. At the anatomical level, there was an almost "mirror image" profile, with contrasting involvement of lateral and medial temporal lobe structures. At the neuropsychological level, our patient was not amnesic but showed patchy impairment on traditional tests of anterograde memory functioning, in the context of notable "semantic" memory loss for knowledge acquired before and after the onset of his illness. Our findings demonstrate that bilateral temporal lobe pathology by itself does not lead to a classical amnesic syndrome, but may result in a significant but more subtle "semantic" memory loss. Our data highlight the distinctive and dissociable contribution of lateral and medial temporal lobe structures to human memory processing, and suggest a major role for anterior-inferior neocortical temporal lobe mechanisms in aspects of knowledge acquisition, storage and retrieval.

Amnesia↗