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)

The dopaminergic drugs, bromocriptine, cabergoline, dihydroergocryptine, pergolide and ropinirole were injected subcutaneously (s.c.) at the dose of 0.1, 0.5 and 1 mg/kg/day for 7 days into male rats of the Sprague-Dawley strain. The drug pre-treatment reverted amnesia induced in rats by hypobaric hypopxia and tested in active and passive avoidance tasks. A restoration of memory retention, as assessed in a step-through passive avoidance task, was found in animals with a 2-month brain occlusive ischemia and exposed to dopaminergic drugs for 7 days. For behavioral effects in both active and passive avoidance tests in both experimental models, the rank of relative potency was ropirinole>bromocriptine=cabergoline>pergolide>dihydroergocryptine. Spontaneous ambulation of animals with brain occlusive ischemia was increased by the higher doses of drugs. All dopaminergic drugs reduced kainate mortality rate. The rank of relative potency for this effect was ropirinole=bromocriptine=cabergoline>pergolide=dihydroergocryptine. However, no change was found in other seizure parameters (latency to first convulsion and total number of convulsions) after drug treatment. A biochemical analysis of glutathione redox index (glutathione reduced/glutathione oxidized ratio) in discrete brain areas revealed that exposure to dopaminergic drugs increased this parameter in frontal cortex, striatum and hippocampus of animals subject to hypobaric hypoxia and brain occlusive ischemia. For this effect, the relative potency rank was ropirinole>bromocriptine=cabergoline>>pergolide=dihydroergocryptine. These behavioral and biochemical findings suggest that dopaminergic drugs may counteract either behavioral or biochemical changes induced by experimental models of brain injury. This activity was found after protective activity (as found in animals pre-treated with these drugs and exposed to hypobaric hypoxia) or reversal of brain injury (as found in animals treated after 2-month occlusive brain ischemia). Their neuroprotective activity probably involves the reduction/oxidation balance of the glutathione system in the brain.
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PMID:Dopaminergic drugs may counteract behavioral and biochemical changes induced by models of brain injury. 1624 19

Transient global amnesia is a clinically well defined syndrome, characterized by transient isolated epizodes of confusion with inability to acquire new data, repetitive quieries, retrograde amnesia and absence of other neurologic symptoms or signs. Eighteen patients who presented at admission the clinical picture of transient global amnesia were, after the examination, classified in three groups: patients with symptoms or signs of transitory focal ischemia, migraine group, and miscellaneous group. The transitory global amnesia in patients suffering from atherosclerotic changes of the vascular system is usually the first manifestation of transitory ischaemic attack pointing to the vascular insufficiency of the posterior cerebral regions as the cause of attack. The typical transient global amnesia is not a rare phenomenon, but it supposes the existence of the precipitating factors. Although its "pure" form is usually benign, the appearance of other factors such as cerebral neoplasms, involved in the aetiology of transient global amnesia, requires the complete clinical examination of each individual with these symptoms.
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PMID:[Transient global amnesia--possible aetiopathogenetic mechanisms]. 1629 27

The neuroprotective properties of phenibut and piracetam were studied in rats with cerebral ischemia caused by bilateral irreversible simultaneous occlusion of carotid arteries and gravitational overload in craniocaudal vector. In addition, the effects of both drugs on microcirculation in brain cortex under ischemic injury conditions were studied. Phenibut and (to a lower extent) piracetam reduced a neuralgic deficiency, amnesia, and the degree of cerebral circulation drop, and improved the spontaneous movement and research activity deteriorated by brain ischemia.
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PMID:[Comparative evaluation of the neuroprotective activity of phenibut and piracetam under experimental cerebral ischemia conditions in rats]. 1687 92

Transient global amnesia (TGA) is characterized by sudden, temporary dysfunction of antegrade and recent retrograde memory without other neurologic deficits. Although there is sometimes a precipitating event, the origin of TGA remains controversial. We encountered a patient who developed recurrent TGA when upright, in whom the symptom promptly and regularly resolved when supine. Symptoms began about a week after cardiac surgery concurrent with marked hyperfibrinogenemia and acceleration of the erythrocyte sedimentation rate, and abated without recurrence when these laboratory abnormalities were ameliorated by anticoagulant and corticosteroid therapy. Diagnostic studies, including temporal artery biopsy and cerebral angiography, disclosed no anatomic vascular pathology. This is the first report of TGA associated with postoperative inflammation in which amnesia was provoked by orthostatic positioning. In conclusion, these observations implicate ischemia caused by hemodynamic vascular insufficiency as a possible cause of TGA.
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PMID:Recurrent orthostatic global amnesia in a patient with postoperative hyperfibrinogenemia. 1858 46

There are numerous sedatives and analgesics used in critical care medicine today; these medications are used on critically ill patients, many of whom have heart disease, including coronary artery disease or congestive heart failure. The purpose of this review is to recognize the effects of these medications on the heart. Studies that evaluated the effects of sedatives and analgesics on normal individuals or on those with heart disease were reviewed. Current choices for sustained sedation in the critically ill include the benzodiazepines, morphine, propofol, and etomidate. Each of these medications has their particular advantages and disadvantages. Benzodiazepines provide the greatest amnesia and cardiovascular safety but they can cause significant hypotension in the hemodynamically unstable patient. Morphine provides analgesia and cardioprotective activity after ischemia, although the large observational study CRUSADE showed increased mortality rate in those patients with non-ST segment elevation myocardial infarction who received morphine. Propofol is the most easily titratable drug with cardioprotective features, but its use must be accompanied with great attention to possible development of propofol infusion syndrome, which is a deadly disease, especially in patients with head injury and those with septic shock receiving vasopressors. Etomidate has a rapid onset effect and short period of action with great hemodynamic stability even in patients with shock and hypovolemia, but the incidence of adrenal insufficiency during infusion, not bolus doses, may cause deterioration in the circulatory stability. In conclusion, the sedatives and analgesics mentioned here have characteristics that give them a cardiovascular safety profile useful in critically ill patients. However, use of these drugs on an individual basis is dependent on each agent's safety and efficacy.
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PMID:Cardiovascular manifestations of sedatives and analgesics in the critical care unit. 1909 49

The medial diencephalon is vital for memory, but it is not known why. The present study tested between the predictions of current hypotheses as to why this region is critical for memory. Lesions were made in the rat mammillothalamic tract, the only diencephalic structure consistently associated with amnesia in humans after ischemia. Decreased activity, as measured by immediate-early gene expression (c-fos), was found in three key sites associated with memory function: the hippocampus, the prefrontal cortex, and the retrosplenial cortex. The specificity of these changes was confirmed by the qualitatively different patterns of immediately-early gene changes seen after amygdala lesions, e.g., hypoactivity in the hippocampus and retrosplenial cortex following mammillothalamic tract lesions but not following amygdala lesions. The mammillothalamic lesion results unify substrates linked to diencephalic and temporal lobe amnesia, and thereby support a new account of diencephalic amnesia that emphasizes multiple dysfunctions across hippocampal, retrosplenial, and prefrontal areas. This account suggests a role for the mammillary bodies that is independent of their hippocampal inputs.
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PMID:Hippocampal, retrosplenial, and prefrontal hypoactivity in a model of diencephalic amnesia: Evidence towards an interdependent subcortical-cortical memory network. 1928 Jun 62

It was established that semax and mexidol significantly reduced neurological deficiency and increased the survival in rats with model brain ischemia induced by the bilateral ligation of common carotid arteries. Mexidol exhibited a linear dose-effect relationship (in a range of doses from 30 to 120 mg/kg per day), while the effect of semax decreased with increasing dose (in a dose range from 0.3 to 1.2 mg/kg per day). Preventive course administration of semax and mexidol considerably reduced neurologic deficiency and amnesia in a step-down passive avoidance situation in rats with model brain ischemia caused by gravitation overload.
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PMID:[Effect of semax and mexidol on brain ischemia models in rats]. 1933 16

We present 3 patients with transient global amnesia (TGA). Patient 1 was a 67-year-old man who had developed TGA 5 years ago. He showed sudden onset amnesia immediately after he quarreled with his wife loudly during driving. Three-Tesla (3T) diffusion-weighted magnetic resonance imaging (DWI) taken 18 hours after onset revealed a small hyperintense signal area in the right CA1 subfield of the hippocampus. Patient 2 was a 66-year-old woman who showed sudden onset amnesia immediately after she walked for about 20 minutes holding a heavy luggage with her arms. 3T DWI taken 64 hours after onset revealed a small hyperintense signal area in the left CA1 subfield of the hippocampus. Patient 3 was a 68-year-old woman who showed sudden onset amnesia immediately after she hurriedly cleaned up her house with a cleaner. 3T DWI taken 48 hours after onset revealed small hyperintense signal areas in the left CA1 subfield and the right subiculum proper of the hippocampus. She developed TGA recurrence 6 months after the first episode of TGA. All these 3 patients had no cardiovascular diseases. Their amnesia resolved within 5-6 hours. Magnetic resonance venography (MRV) revealed hypoplasia of the left transverse sinus in Patient 1 and Patient 3, and aplasia of the left transverse sinus in Patient 2. Ultrasound studies revealed a retrograde flow component of internal jugular vein during Valsalva maneuver in Patient 2. We speculate that an increased venous pressure might have precipitated cerebral venous ischemia in the hippocampus, which is most vulnerable to ischemic insults.
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PMID:[Three patients with transient global amnesia following an increased venous pressure: a study using 3.0 Tesla diffusion-weighted magnetic resonance imaging]. 2068 Dec 64

The essential elements of anesthesia are : hypnosis, amnesia, analgesia, immobility, and inhibition of untoward reflexes. The spinal cord is responsible for the latter three. Suppression of excitatory transmission and stimulation of inhibitory transmission are the anesthetic mechanisms in the spinal cord. Each anesthetic, however, has a unique effect on the transmission systems in the spinal cord. Some exclusively suppress excitatory transmission or stimulate inhibitory transmission, and others have a dual effect. The minimum alveolar/anesthetic concentration (MAC) is spinally mediated. Furthermore neurons in the ventral horn of spinal cord seem to be more depressed by anesthetics than neurons in the dorsal horn of the spinal cord. The ventral spinal cord also has relation to spinal cord ischemia. Investigation of the neuroprotective effect against spinal ischemia as well as the anesthetic effect in the ventral spinal cord is a very important subject of research.
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PMID:[Anesthetic mechanisms in the spinal cord]. 2162 62

Acute confusional migraine (ACM) is a rare migraine variant, affecting children and adolescents, as well as adults. Between 0.45 and 7.8% of children with migraine present with ACM, but the disorder may well be underdiagnosed. ACM is an exclusion diagnosis and some dangerous causes of confusion (e.g., epilepsy, ischemia, hemorrhagia, neoplasm, intoxication and encephalitis) should be ruled out. The confusional state often manifests with a wide diversity of cortical dysfunctions, such as speech difficulties, increased alertness, agitation and amnesia. Exact history taking, clinical examination, and laboratory, radiological and electroencephalographical findings lead the practitioner towards the diagnosis. Approximately half of the cases may be triggered by mild head trauma. Transient global amnesia is an important differential diagnosis, possibly caused by similar pathophysiological mechanisms. The exact pathomechanism remains unclear, with the common hypothesis comprising of the confusional state as a complex aura phenomenon, in which the cortical spreading depression wave reaches not only the occipital, but also the temporal, parietal and frontal cortex, as well as the brainstem and the hippocampi, leading to transient hypoperfusion and dysfunction of these brain areas.
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PMID:Acute confusional migraine: our knowledge to date. 2236 29


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