Disease relevance of Coma

• Lidoflazine in the treatment of comatose survivors of cardiac arrest [1].
• We studied a case of acute lithium carbonate intoxication characterized by a prolonged comatose state, severe nephrogenic diabetes insipidus, and glucose intolerance [2].
• The study demonstrated that the administration of two single high doses 1,500 mg each of cefuroxime after the intubation of patients comatose because of head injury or medical stroke is an effective prophylactic strategy to decrease the incidence of ventilator-associated pneumonia [3].
• Plasma 3-methoxy-4-hydroxyphenylethyleneglycol concentrations were markedly elevated in subarachnoid hemorrhage patients with coma compared to those without, and the maximal concentrations observed in comatose patients never occurred in normal subjects or in patients with other neurological disorders [4].
• RESULTS: With use of logistic regression analysis, onset seizures correlated with the sum score of blood on initial CT scan (OR = 1.1, p = 0.05), but there was no significant correlation with duration of loss of consciousness at onset, Glasgow Coma Score (GCS), presence of aneurysm, or past history of hypertension or epilepsy [5].

Psychiatry related information on Coma

• Depressed level of consciousness was the most common abnormal physical finding (24 cases); 18 patients were lethargic but arousable with nonpainful stimulation and 6 patients with serum glutethimide concentrations of 10 mg/L or greater were comatose [6].

High impact information on Coma

• Chloroquine given by nasogastric tube (initial dose, 10 mg of base per kilogram) was absorbed well, even in comatose children [7].
• Benzoate treatment of four hyperammonemic comatose patients led to clinical improvement and a return of plasma ammonium levels toward normal [8].
• Patients with phenobarbital overdose who are treated only with supportive care may remain comatose for several days because of the long elimination half-life of phenobarbital [9].
• In all five patients, the comatose state was immediately reversed by the benzodiazepine-receptor antagonist flumazenil [10].
• Eliciting P300 in comatose patients [11].

Chemical compound and disease context of Coma

• The frequency of hypoglycaemia (blood glucose below 2.2 mmol/l) did not differ significantly between malarial and control patients (5.2% vs 11.2%) nor between the comatose (11.1% vs 18.8%) and conscious (1.6% vs 7.0%) malarial and control subgroups [12].
• Since the average number of hours from the beginning of vomiting to admission was no different in non-comatose and comatose cases, the time at which salicylate concentration was measured in relation to the last dose was probably similar in the two groups and therefore does not account for the higher levels in children with poor outcome [13].
• In two of these cases, status seizures were stopped by intravenous pyridoxine administration, but the patients remained comatose for prolonged periods [14].
• Combined infusion of high doses of lidocaine and thiopental in a comatose patient induced major latency and amplitude BAEP changes, which progressed to complete BAEP abolition [15].
• The patient remained in a comatose state for 4 days but then showed dramatic improvement in his neurological status following continuous i.v. infusion of thymidine at 8 g/m2/day [16].

Biological context of Coma

• The TRAN group had a higher Injury Severity Score (ISS) (17.5 versus 11.0, P < 0.05), lower Glasgow Coma Score (GCS) (13.3 versus 14.1, P < 0.05), lower initial systolic blood pressure (SBP) (130 versus 140, P< 0.05), and higher mortality (10% versus 79%, P < 0.05) than the DIR group [17].
• Partial OTC deficiency also occurs in females and can be responsible for life-threatening hyperammonemic comas in heterozygotes [18].
• Median nerve somatosensory evoked potentials and the Glasgow Coma Scale as predictors of outcome in comatose patients with head injuries [19].
• After initiation of treatment with acyclovir in the early stage of the disease, the outcomes in both patients were characterized by good general recovery with persistence of deficits of speech, mastication, and swallowing, more pronounced in the patient who was comatose during the illness [20].
• In an attempt to examine the relationship between growth hormone (GH) and periarticular new bone formation (PNBF), we studied eight patients with brain lesions of different origins who were in a prolonged comatose state for 164 to 1320 days [21].

Anatomical context of Coma

• Glutamine concentrations in brainstem of comatose rats are increased a further two-fold, whereas those of cerebral cortex are unchanged [22].
• The extent of brain polyribosome disaggregation depends on the decrease of blood glucose concentration, and in comatose animals on the duration of hypoglycemia [23].
• CONCLUSION: A PET investigation using (18)F FDG demonstrated a significant difference in glucose metabolism in the thalamus, brain stem, and cerebellum between comatose and noncomatose patients acutely after TBI [24].
• The concentrations of homovanillic acid (HVA), 3-methoxy, 4-hydroxyphenylglycol (MHPG), and 5-hydroxyindolylacetic acid (5-HIAA) were measured in samples of ventricular cerebrospinal fluid (CSF) taken from 15 patients who were comatose as a result of an acute head injury, a tumour, or a cerebrovascular accident [25].
• EEGs and somatosensory evoked responses from the brachial plexus, neck and scalp were recorded in seven comatose patients on continuous thiopentone infusion [26].

Gene context of Coma

• In addition, the entire vesicle pool can be depleted in shibire comatose double mutants, demonstrating that NSF activity is not required for the fusion step itself [27].
• Regarding clinical and radiological features, elevated NGF/BDNF levels in the CSF correlated with higher incidence of seizures and prolonged comatose state and with specific radiological lesions [28].
• The ABRs already showed features which were characteristic for brain death (loss of components other than wave 1 or small wave 2) for four comatose recordings, in three of which N18 was preserved [29].
• The increment in T3 concentrations 120 min after TRH was found reduced in the comatose patients only [30].
• This was further supported by low NSE/S100B concentration ratios in serum compared to cerebrospinal fluid (CSF) of patients with comatose state, convulsive status, or intracerebral hemorrhage [31].

Analytical, diagnostic and therapeutic context of Coma

• The intravenous injection of glucose as a "therapeutic test" in comatose diabetics is reviewed in the light of evidence that it may evoke a paradoxical rise in plasma-potassium in the insulin-deprived diabetic [32].
• Survival was 83% in patients with grade 1 and 2 comas at transplantation versus 56% (p < 0.001) in those with grade 3 comas; it was 51% versus 81% (p < 0.001) in those transplanted with high risk (ABO-incompatible, split, or steatotic) and low-risk grafts, respectively [33].
• CONCLUSION: This large-scale EEG evaluation of comatose patients without clinical signs of seizure activity found that NCSE is an underrecognized cause of coma, occurring in 8% of all comatose patients without signs of seizure activity [34].
• (12) examined 13 comatose patients with advanced coma stages (Glasgow coma scale 5-10) and recorded unspecific changes in their EEG tracings [35].
• After cuprophan hemodialysis, plasma total tryptophan is lower than in normal and even comatose animals, whereas free tryptophan is normal [36].

References