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MeSH Review

Glasgow Coma Scale

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Disease relevance of Glasgow Coma Scale


Psychiatry related information on Glasgow Coma Scale

  • When the severity of the injury was assessed using either the Glasgow coma scale or the length of post-traumatic amnesia, the increase in the choline/creatine ratio was significant even in the mildly injured group (P = 0.008 and P = 0.04, respectively) [6].
  • CONCLUSIONS: Rudimentary neurologic functions can be readily assessed and, when viewed together with the Glasgow Coma Scale, may circumvent the "floor effect" frequently encountered when using the currently available cognitive and functional scales and, thereby, better define patients with end-stage Alzheimer's disease [7].
  • Of these, 67% use the Ramsay scale, 10% use the Sedation-Agitation Scale, 9% use the Glasgow Coma Scale, and 8% use the Motor Activity Assessment Scale [8].
  • This article explains the concepts of consciousness and intracranial pressure and what is meant by an 'altered level of consciousness'. Assessment strategies are identified and a simple alternative to the Glasgow Coma Scale is identified that can be used as an initial assessment tool [9].

High impact information on Glasgow Coma Scale

  • At admission, these patients more often had a history of vomiting (P=0.047) and a score of 12 or lower on the Glasgow Coma Scale (P=0.02) than the others; a trend toward a greater prevalence of seizures at admission was also evident in this group (P=0.07) [10].
  • The original model, using initial Glasgow Coma Scale score, hemorrhage size, and pulse pressure, accounted for mortality or survival at 30 days in 92% of patients in the Pilot Stroke Data Bank with a sensitivity of 0.84 and a specificity of 0.96 [3].
  • Factors associated with a bad outcome (GOS </= 4) were chronic debilitating diseases, low Glasgow Coma Scale Score and focal neurological deficits on admission, low CSF leucocyte counts, pneumonia, bacteraemia and meningitis-associated intracranial and systemic complications [11].
  • Patients with mean admission peak 24-hour Glasgow Coma Scale scores of 3.5, 6, and 10 had mean admission 24-hour peak serum glucose levels of 252 +/- 23.5, 219.1 +/- 19, and 185.8 +/- 21, respectively (p = 0.05) [12].
  • GH or ACTH deficiencies were not related to age, Glasgow Coma Scale score, or the presence of other pituitary hormone abnormalities (P > 0.05) [13].

Chemical compound and disease context of Glasgow Coma Scale


Biological context of Glasgow Coma Scale


Anatomical context of Glasgow Coma Scale

  • In a Cox model, only Glasgow Coma Scale score less than 7 (P = .006) and clinical signs of brain stem involvement (P = .02) were predictive of death within 3 months of admission to the ICU [24].
  • Cerebrospinal fluid samples (n = 72) were obtained from 18 infants and children on days 1 to 3 after severe TBI (Glasgow Coma Scale score < 8) and 18 controls [25].
  • PATIENTS: Fifty-three patients with massive middle cerebral artery infarction who experienced neurologic deterioration defined by a decrease in the Glasgow Coma Scale score of two or more points attributable to mass effect [26].
  • METHODS: We monitored 52 patients continuously with the BIS monitor together with assessment of neurological function (contralateral upper and lower limb strength and the verbal component of the Glasgow Coma Scale for speech) in patients undergoing awake CEA [27].
  • Although the Glasgow coma scale (GCS) does not consider the specific type of central nervous system abnormality caused by trauma, it is an accurate and accepted assessment of outcome after coma lasting longer than 6 hours [28].

Associations of Glasgow Coma Scale with chemical compounds

  • Glasgow Coma Scale (GCS) and MCA Stroke Scale (MCASS) were measured before and after mannitol administration [29].
  • F2-isoprostane, glutamate, and lactate/pyruvate, were assessed in CSF from adults (n = 68) with severe TBI (Glasgow coma scale [GCS] score </= 8) using ventricular CSF samples (n = 207) collected on days 1, 2, and 3 post-injury [30].
  • Plasma noradrenaline concentrations were higher in patients with poor outcome, particularly after the third day, but showed covariance with established predictors of outcome such as the Glasgow coma scale score on admission, the amount of extravasated blood on the initial CT, and age [31].
  • PATIENTS: Twenty patients admitted with a Glasgow Coma Scale score of < 10 who were enrolled as part of a prospective, multicenter trial to assess the impact of multiple risk factors and ranitidine prophylaxis on the development of stress-related upper gastrointestinal bleeding [32].
  • We also did not find a correlation between the amount of Glx and the initial Glasgow Coma Scale score, duration of coma, nor with changes in spectral metabolites, including N-acetyl aspartate, choline, and myoinositol [33].

Gene context of Glasgow Coma Scale

  • METHODS AND PROCEDURES: S100B, S100A1B and S100BB concentrations were examined in sera from patients with MTBI with an arrival Glasgow Coma Scale score of 15 or 14, patients with orthopaedic injuries and non-injured subjects [34].
  • RESULTS: Ninety percent of study patients had mild TBI (Glasgow Coma Scale score of 13 to 15); 18 (22.5%) had one APOE epsilon 4 and none had two epsilon 4 alleles [35].
  • Increased CSF cytochrome c was independently associated with inflicted TBI (P=0.0001) and female gender (P=0.04), but not age, Glasgow coma scale score, or survival [36].
  • Children with admission Glasgow Coma Scale (GCS) scores of 8 or less had higher IL-6 levels compared to children with GCS scores higher than 8, 4 and 12 h post-injury (p<0.01 and p<0.05, respectively) [37].
  • Interleukin-6 and interleukin-10 levels were significantly correlated with Glasgow Coma Scale score [38].

Analytical, diagnostic and therapeutic context of Glasgow Coma Scale


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