Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A variety of transient focal neurological signs presenting at high altitude have been described without associated acute mountain sickness or other concurrent illness. We report a case series of transient global amnesia at high altitude. The term high-altitude global amnesia (HAGA) is introduced to indicate this condition, and the pathophysiology is discussed. We hypothesize that because of the highly variable ventilatory response to hypoxia and to individual cerebral vasomotor reactivity, individuals with a marked hyperventilatory response could experience significant hypocapnic cerebral vasoconstriction that in turn could cause local hypoxia or ischemia to particular regions of the brain and resulting transient focal neurological impairment.
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PMID:High-altitude global amnesia. 1073 4

In the present study, we found that complement C3a exerted central effects after intracerebroventricular administration in mice. At doses of 3 and 10 pmol/mouse, the peptide showed an antagonistic effect on analgesia induced by morphine and U-50488H, known to be mu- and kappa-opioid receptor agonists, respectively. Moreover, complement C3a improved scopolamine- and ischemia-induced amnesia at a dose of 10 pmol/mouse. Anti-analgesia was not observed by C3a des-Arg at 10 pmol/mouse. The present findings suggest that complement C3a may act as a peptide with anti-opioid activity in the central nervous system.
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PMID:Anti-analgesic and anti-amnesic effect of complement C3a. 1105 63

The transitory memory disturbance known as transient global amnesia (TGA) remains an enigma from a pathogenic point of view. In spite of its typical benign prognosis, TGA is a frightening experience for patients and their relatives. Moreover, a TGA episode usually leads to extensive investigation of patients in search of organic alterations that might be responsible for the event. Finally, TGA generates queries about therapeutic choices. In this review, we critically re-evaluate the evidence in support of and against the three main pathogenic hypotheses (i.e. ischemia, seizure discharge, and migraine), and we conclude that none of these appears completely convincing. Given the good prognosis and the lack of association with organic and instrumental abnormalities, we advance the hypothesis that TGA may be related to psychological disturbances causing transient alteration in brain metabolism and, consequently, amnesia. Our conclusion has relevant consequences in the evaluation of patients with TGA.
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PMID:Transient global amnesia: a review emphasizing pathogenic aspects. 1108 3

Complement C3a is an anti-opioid peptide, having anti-analgesic and anti-amnesic effects after intracerebroventricular administration. However, the peptide is inactive after oral administration. Orally active C3a agonist peptide was designed based on the structure of oryzatensin, a C3a agonist peptide derived from rice albumin. Tyr-Pro-Leu-Pro-Arg, a pentapeptide at the carboxyl terminus of oryzatensin is the minimally essential structure for exerting C3a activity. Due to the affinity for mu-opioid receptor, both oryzatensin and Tyr-Pro-Leu-Pro-Arg showed analgesia after intracerebroventricular administration in mice which was blocked by the opioid antagonist naloxone. Tyr-Pro-Leu-Pro-Arg lost opioid activity by substitution the amino terminus tyrosine with other hydrophobic residues. Among the newly designed peptides, Trp-Pro-Leu-Pro-Arg was found to possess the strongest C3a activity. The peptide antagonized morphine-induced analgesia at 300 mg/kg after oral administration and also improved scopolamine- and ischemia-induced amnesia in a step-through passive avoidance test.
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PMID:Designing of an orally active complement C3a agonist peptide with anti-analgesic and anti-amnesic activity. 1117 94

NNC-711 [1-(2-((diphenylmethylene)amino)oxy)ethyl)-1,2,4,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride], a gamma-aminobutyric acid (GABA) reuptake inhibitor with anticonvulsant activity, was investigated with respect to its cognition-enhancing and neuroprotective potency. In the rat, administration of NNC-711 immediately prior to training prevented amnesia for a passive avoidance task induced by the acetylcholine receptor antagonist scopolamine. NNC-711 was also effective in protecting against ischemia-induced death of CA1 pyramidal neurons in a model of bilateral common carotid artery occlusion in the gerbil. In addition to a neuroprotective activity, NNC-711 exhibited significant cognition-enhancing actions. Daily administration of NNC-711, immediately prior to a spatial learning task, significantly reduced escape latencies in the water maze paradigm in both mature (postnatal day 80) and aged (28 months) rats. All of the above actions exhibited a bell-shaped response with an optimal dose of 0.5-1.0 mg/kg. These investigations with NNC-711 and previous clinical observations on the structurally related anticonvulsant tiagabine confirm the potential of GABA reuptake inhibitors as anti-amnesia and cognition-enhancing agents.
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PMID:Anti-ischemic and cognition-enhancing properties of NNC-711, a gamma-aminobutyric acid reuptake inhibitor. 1147 Feb 58

Andropause seem to be less defined than menopause. This study on older patients describes how they perceive and understand this aging process. A noninterventional, cross-sectional study was performed to determine what men report as symptoms of andropause to ascertain if memory loss was a predominant feature. The hypothesis was that androgens such as testosterone are responsible for visual-spatial and memory development. As such the aging process of andropause, which is associated with declines in testosterone levels, would lead to memory loss. A standardized questionnaire of 22 questions was administered to 302 outpatients of a medical center. Information on patient demographics, understanding of andropause, and risk factors was collected. Of the 302 patients, 71% were above 60 years and whites predominated at 87%. Memory loss was reported in 36% of the patients who felt that they had experienced andropause. It was the third most common symptom after erectile dysfunction (46%) and general weakness (41%). Twenty-two percent of the 302 patients had a history of diabetes. Among those who reported that they had undergone andropause, diabetic patients were more likely to report memory loss (p = .03, OR = 1.9. CI = 1.1-3.4). Sixty-four percent of patients reported the onset of andropause to be between 50 and 70 years (the median age being 50-60 years). This study highlights the importance of testosterone in maintaining cognitive functions. It supports studies of testosterone replacement in men undergoing andropause and who have concomitant dementia. The results parallel recent reports of the neuroprotective effects of estrogens in preventing dementia. Diabetes is associated with memory loss because of the additional insults to cognitive function of the brain secondary to ischemia.
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PMID:Memory loss as a reported symptom of andropause. 1169 41

One of the routine memory abilities impaired in amnesic patients with temporal-lobe damage is object-recognition memory--the ability to discriminate the familiarity of previously encountered objects. Reproducing this impairment has played a central role in animal models of amnesia during the past two decades, and until recent years most of the emphasis was on describing how hippocampal damage could impair object recognition. Today most investigators are looking outside the hippocampus to explain the impairment. This paper reviews studies of object-recognition memory in rats with hippocampal damage produced by ablation, fornix transection, or forebrain ischemia. Some new perspectives on previous findings reinforce the conclusion that damage to the hippocampus has little if any impact on the ability to recognize objects, while damage in some areas outside the hippocampus is far more effective. The few circumstances in which hippocampal damage can impair performance on object-recognition tasks are situations where ancillary abilities are likely to play a significant role in supporting task performance. Some of the factors that contributed to the origins and persistence of the hippocampalcentric view of object-recognition are considered, including lesion confounds, failure to distinguish between impaired task performance and impairment of a memory ability, and disproportionate attention to a few lesion studies in monkeys, even though the hypothesis was tested far more times in rats, under a greater variety of conditions, and rejected on nearly every occasion.
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PMID:Perspectives on object-recognition memory following hippocampal damage: lessons from studies in rats. 1171 90

Sedatives continue to be used on a routine basis in critically ill patients. Although many agents are available and some approach an ideal, none are perfect. Patients require continuous reassessment of their pain and need for sedation. Pathophysiologic abnormalities that cause agitation, confusion, or delirium must be identified and treated before unilateral administration of potent sedative agents that may mask potentially lethal insufficiencies. The routine use of standardized and validated sedation scales and monitors is needed. It is hoped that reliable objective monitors of patients' level of consciousness and comfort will be forthcoming. Each sedative agent discussed in this article seems to have a place in the ICU pharmacologic armamentarium to ensure the safe and comfortable delivery of care. Etomidate is an attractive agent for short-term use to provide the rapid onset and offset of sedation in critically ill patients who are at risk for hemodynamic instability but seem to need sedation or anesthesia to perform a procedure or manipulate the airway. Ketamine administered through intramuscular injection or intravenous infusion provides quick, intense analgesia and anesthesia and allows patients to tolerate limited but painful procedures. The risk/benefit ratio associated with the use of this neuroleptic agent must be weighed carefully. Ketamine is contraindicated in patients who lack normal intracranial compliance or who have significant myocardial ischemia. Barbiturates are reserved mainly to induce coma in patients at risk for severe CNS ischemia, which frequently is associated with refractory intracranial hypertension, or in patients with status epilepticus. When administered in high doses, these drugs have prolonged sedative and depressant effects. Judicious hemodynamic monitoring is required when barbiturate coma is induced. Haloperidol is indicated in the treatment of delirium. Patients should be monitored for extrapyramidal side effects and, when they require higher doses, for potential electrocardiographic prolongation of the QT interval. Dexmedetomidine may evolve into an agent with qualities comparable with midazolam and propofol, and it may even become a drug of choice in select patients. Further study is required, however. Propofol has many of the qualities of an ideal sedative agent. Benzodiazepines and narcotics often are used in concert with propofol to provide reliable amnesia and to relieve pain, respectively. Propofol frequently causes hypotension when administered as a bolus or infusion, particularly in patients with limited cardiac reserve or hypovolemia. More data must be obtained to identify potential deleterious effects of hypertriglyceridemia, and further evaluation of the potential benefits in certain patient populations, such as neurosurgical patients, is needed.
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PMID:Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. 1176 65

The dopaminergic drugs, ropinirole and dihydroergocryptine (DHECP) were injected subcutaneously (s.c.) at doses of 0.5 and 1 mg/kg/day for 7 days into male rats of the Sprague-Dawley strain. The drug pretreatment reverted amnesia induced in rats by hypobaric hypopxia and tested in active and passive avoidance tasks. Furthermore, a partial restoration of memory retention was found in animals with a 2-month brain occlusive ischemia induced by manipulation of the four major arteries of the brain. No major changes were found in spontaneous motor activity, but drug treatment increased ambulation of animals subjected to acute or chronic experimental manipulation. In a model of kainate-induced epilepsy, ropinirole or DHECP did not affect seizure parameters, but reduced mortality rate. At the end of behavioral procedures, in all animals subjected to hypobaric hypoxia or to brain occlusive ischemia glutathione redox index (glutathione reduced/glutathione oxidized ratio) was measured in the frontal cortex, striatum and hippocampus. It was found that experimental models of brain injury were followed by a decrease of reduced glutathione content in all brain areas. The glutathione redox index was augmented by ropinirole or DHECP treatment in all brain areas. These behavioral and neurochemical findings suggest that ropinirole and DHECP may exert either protective activity (as found in animals pretreated with these drugs and exposed to hypobaric hypoxia) or reversal of brain injury (as found in animals treated after two-month occlusive brain ischemia). Thus, both drugs may be studied as therapeutic agents in brain injuries of various origin.
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PMID:Behavioral and neurochemical effects of dopaminergic drugs in models of brain injury. 1200 69

Hippocampal damage and amnesia following hypoxia and ischemia are described in the few published adult cases of suicide attempt by hanging. However, a recent review (Caine & Watson, 2000) suggests a variable pattern of brain involvement and neuropsychological impairments following hypoxic-ischemic injury that may or may not involve amnesia. To help clarify the impact of hanging on the developing brain, we examined neuropsychological functioning in two adolescents who survived suicide attempt by hanging. Despite differences in Glasgow Coma Scale (GCS), coma duration, and structural imaging findings, both patients had similar IQ (VIQ>PIQ) and presented with various combinations of deficits in expressive/receptive language, visual-constructional and perceptual ability, processing speed, attention, working memory, and/or executive functioning shortly after injury. In spite of their similarities, only one of the patients presented with classic amnesia symptoms in his early recovery. This patient was evaluated 1 year postinjury, and persistent deficits in processing speed and memory encoding were noted. Several hanging-related variables, including longer estimated hanging duration, greater weight, and severe airway edema, were thought to place this patient at increased risk for cognitive deficits. Clinical MRI scans of this patient obtained 6 weeks postinjury revealed mild volume loss as well as abnormalities in bilateral superior cortex. However, CT and MRI scans obtained throughout early recovery did not reveal overt evidence of injury to specific memory-related structures. Comprehensive neuropsychological evaluation of all adolescent survivors of suicide attempt by hanging is recommended, as a variety of postacute cognitive deficits were observed in these patients despite relatively short (<or=15 minutes) estimated hanging durations.
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PMID:Neuropsychological profile following suicide attempt by hanging: two adolescent case reports. 1605 65


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