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 double-blind random study compared lorazepam with diazepam as i.m. premedicants in 84 healthy women undergoing uterine curettage. Anxiety, assessed by a self-rating test by the patient and by a trained observer, was reduced 90 min after both lorazepam (P less than 0.001) and diazepam (P less than 0.01). There was more sedation and a longer recovery time after lorazepam than after diazepam. Amnesia at 24 h after operation (lack of recall rather than lack of recognition) was greater after lorazepam. There was transient local discomfort at the site of the injection in most patients in both groups, but no serious effects. Local erythema was present in 12 patients who received lorazepam and 10 who received diazepam 90 min after the injection, disappearing after 24 h in the former group but remaining in the latter. The incidence of nausea, vomiting and headache in both groups was small and similar, but there was more restlessness and dizziness after diazepam in the early recovery period.
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PMID:Comparison of lorazepam and diazepam as premedicants. 2 39

Observations obtained by psychopathologic examination and some psychologic testing of two patients in the course of amnesic episodes (transient global amnesia) are presented and discussed. In both cases the psychopathologic findings are those of a reversible isolated amnesic syndrome, characterized by diffuse retrograde amnesia and recent memory deficit, whereas immediate and remote (personal) memory are preserved. Stereotype questions, disorientation in time, and--in one case--anxious restlessness, which accompany the amnesic syndrome, are probably due to impaired memory and the patient's awareness of it. This typical syndrome allows differentiation of amnesic episodes from other types of amnesia. In the first case, which had been under clinical observation from the beginning to the end of the amnesic episode, a special evolution of the event could be ascertained. The acute amnesic episode reached its climax with a certain delay and thereafter decreased gradually. It can be presumed that--at least during the remission phase in the second case--the ability of recall is impaired rather than that of registration and retention. Other findings obtained in the second case--and compared with observations in the literature--point out that in the phase of remission the timespan of retrieval seems to become longer and, in respect to previously applied sensory modalities, improves in a different manner.
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PMID:[Clinical observations on the psychopathology of amnesic episodes (transient global amnesia) (author's transl)]. 101 21

Reports of adverse behavioral reactions to triazolam, a triazolobenzodiazepine ultra-short-acting hypnotic, were examined in the postmarketing surveillance Spontaneous Reporting System of the Food and Drug Administration. Reports for triazolam of confusion, amnesia, bizarre behavior, agitation, and hallucinations were compared with reports of these reactions for temazepam, another short-acting hypnotic. Analysis of individual case reports from marketing through 1985 for triazolam vs temazepam showed 133 vs two for confusion, 109 vs three for amnesia, 59 vs two for bizarre behavior, 58 vs four for agitation, and 40 vs one for hallucinations. Considering extent of use, reporting rates for triazolam were 22 to 99 times those for temazepam, depending on the reaction. Reactions to triazolam tended to occur at higher doses and in older patients. This and an updated analysis of aggregate reports for the first 7 years of marketing of each drug with reporting rates and adjustment for various factors suggest a higher occurrence of these reactions with triazolam, but selection factors cannot be completely ruled out. When treating insomnia, physicians should emphasize sleep hygiene practices as alternatives to drug therapy; if drug therapy is required, they should prescribe hypnotics at the lowest recommended doses for the shortest clinically necessary durations and discontinue medication use should any adverse reactions occur.
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PMID:Adverse behavioral reactions attributed to triazolam in the Food and Drug Administration's Spontaneous Reporting System. 162 34

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

This is an account of an informal presentation of personal views and opinions concerning behavioral phenomena--anosognosia, confabulation, memory and amnesia, perseveration and agitation, plus a few interesting brief case histories that make a neurologic point. Finally, the practice of self-observation is recommended for neurologists, and a few examples from personal experience are described.
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PMID:Neurologic fragments. II. Remarks on anosognosia, confabulation, memory, and other topics; and an appendix on self-observation. 290 1

In his classic case, Alzheimer described cognitive symptoms such as amnesia, aphasia, and apraxia and noncognitive symptoms such as delusions and agitation. Recent studies have suggested that depression also occurs in Alzheimer's disease. In this study, 144 patients who met criteria for Alzheimer's disease were examined for depression on a modified version of the Present State Examination. The prevalence rate of major depression was 17%. The depressed Alzheimer's disease patients were more cognitively impaired and more disabled than the nondepressed patients. Studies are needed to clarify the etiology and treatment of depression in Alzheimer's disease.
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PMID:Depression and Alzheimer's disease. 276 95

Twenty patients scheduled for orthopaedic surgery under spinal anaesthesia received by intravenous infusion either 1% propofol or 0.1% midazolam at a rate adjusted to maintain adequate sedation as judged on a five-point scale. No other anaesthetic or analgesic drugs were given. The mean time to reach the required level of sedation was similar in both groups and the quality and ease of control of sedation were good in all patients. Mean infusion rates were 3.73 mg/kg/hour for propofol and 0.27 mg/hg/hour for midazolam. Airway maintenance was excellent and there were no side effects other than restlessness of the arms in one patient in each group. Recovery, judged by ability to open the eyes and recall date of birth, was significantly more rapid after propofol than after midazolam (2 and 10 minutes respectively after the end of infusion) and two patients in the latter group were unduly drowsy in the initial postoperative period. Pre- and postoperative amnesia were greater in the midazolam group but no patient had recall of peri-operative events. Psychometric tests showed significantly better recovery of higher mental function after propofol for up to 2 hours after surgery.
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PMID:A comparison of propofol and midazolam by infusion to provide sedation in patients who receive spinal anaesthesia. 325 11

Agitated behavior is exhibited in up to 30% of patients recovering from a traumatic brain injury. Past treatment protocols have included proactive behavioral management and major tranquilizers. We now report the use of amitriptyline for control of agitation. For a period of over 2 years, 43 male and 15 female patients with a "recent" severe brain injury were admitted for inpatient rehabilitation and subjected to traditional structured programming for treatment of post-traumatic amnesia (PTA). In 20 patients, 18 men and 2 women, where agitation persisted sufficiently to impede rehabilitation despite initiation of structure, amitriptyline was instituted. These patients were of a comparable age (29.4 years for the agitated group versus 25.6 years for the nonagitated group), but the agitated patients had a lower median Rancho Los Amigos Hospital Level of Cognitive Functioning in a comparison to nonagitated patients (V versus VI). All patients were monitored for cognitive performance by the Orientation Group Monitoring System, and a daily account of frequency, severity and type of agitation was recorded. Within 7 days of initiation of therapy, 12 of 17 patients within PTA had dramatic decrease in agitation (5/5 patients at Rancho IV; 4/8 at Rancho V; 3/4 at Rancho VI). Two of the three patients at Rancho VII had agitation that was unresponsive to amitriptyline. The amitriptyline-responsive patients were maintained on the drug through PTA, and the Orientation Group Monitoring System scale demonstrated no impedance in cognitive recovery. Thus, amitriptyline appears most useful as an adjunct for treatment of nondirected agitation; it also has a role in reducing the severity of the directed agitation that is seen during but not after PTA.
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PMID:Amitriptyline for post-traumatic agitation. 334 39

Agitation and confusion appear to be associated in the early period of recovery from traumatic head injury. Eighteen severely head-injured patients were assessed during acute rehabilitation for both the extent of agitation and level of cognitive functioning. Agitation was measured by the Agitated Behavior Scale developed by Corrigan. Simultaneous independent measurements of cognitive functioning were obtained from the Orientation Group Monitoring System and Mini-Mental State. Agitation was significantly correlated with both measures of cognitive functioning, indicating that as cognition improved, agitation diminished. Agitation was partitioned into high and low levels, and cognitive functioning was partitioned into low, middle, and high levels for each of the two measures of cognitive functioning. Chi-square analysis of the distribution of agitation and cognition indicated significant differentiation, with high agitation prevalent in low levels of cognition, and low agitation prevalent in high levels of cognition. Patients in the middle level of cognition were equally likely to demonstrate high and low agitation. Further descriptive analysis indicated that improvement from low levels of cognition preceded improved agitation, and improved agitation preceded clearing from posttraumatic amnesia. These results provide equivocal support for the long-held clinical observation that a period of pronounced confusion and agitation represents a discrete stage of recovery from traumatic head injury.
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PMID:Agitation following traumatic head injury: equivocal evidence for a discrete stage of cognitive recovery. 338 86

Sixty male and female patients, scheduled for colonoscopy were premedicated with glycopyrrolate 0.4 mg intramuscularly. Anaesthesia was induced with 2 mg/kg propofol ('Diprivan') and maintained with a continuous infusion of propofol at a rate of 3, 6 or 9 mg/kg/h randomly allocated. Patients lost consciousness within 60.6 +/- 18.7 (s.d.) s. Preservation of the hypnotic effect was infusion-rate dependent as 15, 40 and 85% of the patients were unconscious on infusion rates of 3, 6 or 9 mg/kg/h propofol, respectively. A high degree of sedation was observed in the remaining patients with an incidence of 40, 35 and 0% in the different series. Sedation was light in the remainder of the patients. To increase the acceptability of the procedure, a supplemental bolus of propofol and/or an increase in the infusion rate were required in 40, 15 and 10% of the 3, 6 and 9 mg/kg/h infusion rate groups, respectively. The incidence of amnesia was similar in all three groups (80, 90 and 95%, respectively). Recovery was significantly longer with increasing infusion rate, but remained rapid. The longest time was 7.3 +/- 4.0 min to open eyes on command and 10.6 +/- 4.6 min to answer correctly. The most important side effects were pain on injection (50%) and some restlessness during maintenance (25%). Blood pressure decreased, but heart rate was unaffected. Patients breathed room-air spontaneously. Respiratory rate slowed after induction then increased rapidly above baseline values. The incidence of apnoea was 48% with a mean duration of 51 +/- 22s (s.d.). The technique was evaluated as good or adequate in 95% of the cases. We suggest than an analgesic premedication followed by an average of 6 mg/kg/h propofol by infusion might be a simple and convenient method of achieving good conditions for colonoscopy.
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PMID:Infusion of propofol ('Diprivan') as sedative technique for colonoscopies. 387 79


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