Disease relevance of Unconsciousness

• The most common clinical finding in five patients who died after deliberately taking overdoses of disopyramide was an early loss of consciousness after an apnoeic episode [1].
• Reactive hypoglycemia was confirmed by an oral glucose tolerance test, in which plasma glucose decreased from a fasting level of 87 mg/dL to 32 mg/dL at 3 hours and 23 mg/dL at 4 hours, the last value being associated with loss of consciousness [2].
• Cardiovascular causes of loss of consciousness in patients with presumed epilepsy: a cause of the increased sudden death rate in people with epilepsy [3]?
• Propofol (2,6-diisopropylphenol) is a widely used intravenous general anesthetic, which has been reported to produce bradycardia in patients at concentrations associated with profound sedation and loss of consciousness [4].
• In 1987, changes in these regulations focused the problem on loss of consciousness and bodily control of drivers rather than on specific diagnostic entities such as epilepsy or diabetes mellitus [5].

Psychiatry related information on Unconsciousness

• We studied a 59-year-old woman with dementia, retinitis pigmentosa, sensorimotor neuropathy, and attacks of vomiting associated with blood pressure lability and loss of consciousness [6].
• Disorientation clinically similar to dissociative amnesia can occur following loss of consciousness during an episode of trichloroethylene use [7].
• Second in a series: The President's Commission for the Study of Ethical Problems in Medicine and Biomedical Behavioral Research -- "The care of patients with permanent loss of consciousness" [8].

High impact information on Unconsciousness

• HBO was not useful in patients who did not lose consciousness during carbon monoxide intoxication, irrespective of their carboxyhaemoglobin level, nor were two sessions of HBO in patients who sustained only a brief loss of consciousness [9].
• INTERVENTIONS: Before February 1985, patients received treatment with the defibrillator and amiodarone if they presented with loss of consciousness (group A) and amiodarone alone if they did not lose consciousness (group C) [10].
• Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study [11].
• The loss of consciousness and apical heart tones occurred in two young patients after protirelin injection [12].
• RESULTS: On admission, poor outcome was predicted by a low Glasgow Coma Scale score (odds ratio, 0.8; 95% confidence interval, 0.7-0.9); treatment with fluid restriction (2.5; 1.6-4.0); age over 52 (2.6; 1.7-3.9); loss of consciousness at ictus (1.7; 1.1-2.6); or a large amount of subarachnoid blood (2.0; 1.3-3.1) [13].

Chemical compound and disease context of Unconsciousness

• Rebleeding was predicted by treatment with tranexamic acid (0.4; 0.3-0.7; protective effect); age over 52 (1.9; 1.2-3.0); loss of consciousness at ictus (1.7; 1.1-2.7); or admission to a neurosurgery service (0.6; 0.3-0.9; protective effect) [13].
• The effects of fentanyl on sevoflurane requirements for loss of consciousness and skin incision [14].
• The addition of alfentanil did not affect the relation between MLAEP and loss of consciousness (P > 0.15) [15].
• BACKGROUND: This study evaluated the efficacy and safety of remifentanil, a potent mu agonist opioid with a rapid onset and offset of effect, as a sole induction agent for loss of consciousness (LOC) and compared it with alfentanil [16].
• RESULTS: The BIS at loss of consciousness and recovery of a response was not statistically different between propofol and thiopental [17].

Biological context of Unconsciousness

• The performance of electroencephalogram bispectral index and auditory evoked potential index to predict loss of consciousness during propofol infusion [18].
• Pretreatment of nonhuman primates with physostigmine (Phy) and scopolamine or physostigmine and trihexyphenidyl 25 min before exposure to 2 LD50 soman im resulted in complete survival without convulsions or loss of consciousness [19].
• A 74-year-old man received oral administration of pilsicainide, a pure sodium channel blocker with slow recovery kinetics, to convert paroxysmal atrial fibrillation to sinus rhythm and developed loss of consciousness two days later [20].
• Eye movements in loss of consciousness (stupor, coma) [21].

Anatomical context of Unconsciousness

• The initial causes for examination were: stroke (33.1%), epilepsy (20%), loss of consciousness (9%), headaches (9%), confusion (5.4%), peripheral nervous system disorders (4.4%), vertigo (4.2%), cognitive dysfunctions (4%), gait disorders (3.2%) and miscellaneous (7.1%) [22].
• During papaverine infusion into the carotid artery, he suffered loss of consciousness due to a seizure for a few minutes [23].
• A dose of 500 microg/g in 27% ethanol, injected intraperitoneally, induced loss of consciousness and tetany of all the skeletal muscles, which on the contrary appeared relaxed in animals pre-anesthetised by immersion in chlorbutol at 0.2% [24].
• A case of stable decerebrate posture in the upper limbs following sudden loss of consciousness and prolonged coma is described [25].
• Five hours after shock at levels causing transient loss of consciousness and fore and hindlimb tonic extensor seizures, major increases in ornithine decarboxylase activity were found in adrenals, hippocampus, brain stem, frontal cortex, and cerebellum, but striatal levels were unchanged [26].

Gene context of Unconsciousness

• Levels of IL-6 were significantly elevated in the plasma of those HUS patients who had external manifestations, consisting of seizures, loss of consciousness, coma and pancreatic necrosis [27].
• All 29 patients without loss of consciousness had normal S100B levels [28].
• We studied the effects of different doses of CRH and TRH given intracerebroventricularly in the urethane-anesthetized rat and a single dose of CRH in the chloral hydrate-anesthetized rat to elucidate the effects of these peptides in the unconscious state [29].
• The suggested association between edentulousness and cranial cervical dystonia may be apparent because of the confounding effect of both age at onset and head or face trauma with loss of consciousness [30].
• RESULTS: We report on a patient with an atrial septal defect, enlargement of the right heart, and incomplete right bundle branch block, who developed episodes of tachycardia, loss of consciousness, and pallor, for which he was amnesic [31].

Analytical, diagnostic and therapeutic context of Unconsciousness

• After loss of consciousness, patients were randomly allocated to receive 0.56 or 1.0 mg/kg succinylcholine or saline (control group) [32].
• Automated responsiveness test (ART) predicts loss of consciousness and adverse physiologic responses during propofol conscious sedation [33].
• In dogs anaesthetized with ketamine, morphine 15 mg kg-1 caused loss of consciousness and marked analgesia, decreased the respiratory frequency by 47%, and increased PaCO2 by 47% [34].
• After loss of consciousness, and before administration of vecuronium 0.1 mg kg(-1), a tourniquet was applied to one arm and inflated to 150 mm Hg greater than systolic pressure [35].
• Because propofol is often used for induction of general anesthesia when surgery is necessary in early pregnancy, we investigated whether early pregnancy reduces the requirement of propofol for loss of consciousness using a computer-assisted target-controlled infusion (TCI) [36].

References