Posts Tagged Glasgow coma scale

[ARTICLE] Traumatic Brain Injury Severity, Neuropathophysiology, and Clinical Outcome: Insights from Multimodal Neuroimaging – Full Text

Background: The relationship between the acute clinical presentation of patients with traumatic brain injury (TBI), long-term changes in brain structure prompted by injury and chronic functional outcome is insufficiently understood. In this preliminary study, we investigate how acute Glasgow coma score (GCS) and epileptic seizure occurrence after TBIs are statistically related to functional outcome (as quantified using the Glasgow Outcome Score) and to the extent of cortical thinning observed 6 months after the traumatic event.

Methods: Using multivariate linear regression, the extent to which the acute GCS and epileptic seizure occurrence (predictor variables) correlate with structural brain changes (relative cortical atrophy) was examined in a group of 33 TBI patients. The statistical significance of the correlation between relative cortical atrophy and the Glasgow Outcome Score was also investigated.

Results: A statistically significant correlative relationship between cortical thinning and the predictor variables (acute GCS and seizure occurrence) was identified in the study sample. Regions where the statistical model was found to have highest statistical reliability in predicting both gray matter atrophy and neurological outcome include the frontopolar, middle frontal, postcentral, paracentral, middle temporal, angular, and lingual gyri. In addition, relative atrophy and GOS were also found to be significantly correlated over large portions of the cortex.

Conclusion: This study contributes to our understanding of the relationship between clinical descriptors of acute TBI, the extent of injury-related chronic brain changes and neurological outcome. This is partly because the brain areas where cortical thinning was found to be correlated with GCS and with seizure occurrence are implicated in executive control, sensory function, motor acuity, memory, and language, all of which may be affected by TBI. Thus, our quantification suggests the existence of a statistical relationship between acute clinical presentation, on the one hand, and structural/functional brain features which are particularly susceptible to post-injury degradation, on the other hand.

Introduction

Long-term clinical outcome after traumatic brain injury (TBI) is predicated upon a large variety of often poorly understood factors which substantially complicate the task of identifying the relationship between acute clinical variables and chronic functional deficits. Nevertheless, understanding how post-TBI cortical atrophy patterns reflect acute-stage patient presentation may help to identify cortical areas that are likely to undergo substantial atrophy, and implicitly to isolate aspects of cognitive, affective and neural function which are at highest risk for long-term degradation.

Attempts to relate TBI-related changes in brain structure to clinical variables often involve structural brain variables provided by neuroimaging methodologies, such as magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) (13). In previous studies, quantitative metrics provided by acute neuroimaging of TBI patients have been used to describe the relationship between acute injury profiles and chronic dysfunction (47). By contrast, hardly any non-neuroimaging clinical variables have been identified which can be used to elucidate the pattern of structural brain changes after TBI. Nevertheless, the ability to incorporate such non-neuroimaging clinical descriptors into outcome forecasting models is important because many such descriptors—including the Glasgow Coma Score (GCS)—are recorded routinely by clinicians and relied upon during the treatment decision-making process.

In this study, we illustrate how two important TBI severity indicators that are routinely assessed by clinicians in the acute care setting and without the use of neuroimaging can be used to relate patient presentation in the acute stage of TBI to the pattern and extent of post-TBI cortical atrophy as well as to neurological outcome. These two indicators—the GCS and the occurrence of epileptic seizures during the acute stage of TBI—can likely assist in predicting cortical atrophy patterns and in evaluating the risk for poor neurological outcome. This study additionally identifies cortical regions whose susceptibility to post-traumatic atrophy is correlated significantly and reliably—in a statistical sense—with functional outcome and with clinical descriptors of TBI severity. […]

Continue —>  Frontiers | Traumatic Brain Injury Severity, Neuropathophysiology, and Clinical Outcome: Insights from Multimodal Neuroimaging | Neurology

Figure 1. (A) Quantification of the linear model’s ability to predict cortical atrophy extent at 6 months after injury. For each gyrus and sulcus, the null hypothesis that there is no statistically significant correlation between the predictor variables and the response variable (cortical thinning, in millimeters) was tested. Values of the F2,30 statistic for each statistical test are encoded on the cortical surface, subject to the false discovery rate correction for multiple comparisons. Darker red hues indicate higher significance of the statistical test and, consequently, stronger ability to predict cortical thinning for the areas in question. Regions where the null hypothesis was not tested because less than 90% of cortical thickness data were available (see text) are drawn in black. Regions where the test statistic was lower than the threshold F statistic of the reliability analysis permutation test are drawn in white. (B) Statistical significance of the correlation between relative cortical atrophy and the GOS-E. Values of the t31 statistic for each statistical test are encoded on the cortical surface, as in panel (A). Note that all values of this statistic are negative, which confirms that greater regional atrophy is associated with lower GOS-E values (i.e., poorer functional outcome), as expected. The values of F and t statistics in (A) and (B), respectively, are associated with different statistical tests and different degrees of freedom and, therefore, they should not be compared to one another.

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[WEB SITE] Classification and Complications of Traumatic Brain Injury: Practice Essentials, Epidemiology, Pathophysiology

Practice Essentials

Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disability and mortality. It occurs when a sudden trauma damages the brain and disrupts normal brain function. TBI may have profound physical, psychological, cognitive, emotional, and social effects.

According to the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control, in the United States annually at least 1.4 million people sustain a TBI, and approximately 50,000 people die from such injuries.

See Pediatric Concussion and Other Traumatic Brain Injuries, a Critical Images slideshow, to help identify the signs and symptoms of TBI, determine the type and severity of injury, and initiate appropriate treatment.

Essential update: Metabolic biomarkers may help predict TBI severity and outcome

In a study of 256 consecutive adult patients with acute TBI and 36 control patients with acute orthopedic trauma and no acute or previous brain disorders, presented in October 2014 at the annual meeting of the Congress of Neurological Surgeons, Posti et al found 43 potential metabolic biomarkers that differed significantly in expression patterns between TBI patients and control subjects.[1] These differences were most pronounced among patients with severe TBI.

These metabolic biomarkers included small fatty acids, amino acids, and sugar derivatives.[1] Several metabolites (eg, decanoic acid, octanoic acid, glycerol serine, and 1H-indole-3-acetic acid) were significantly upregulated in cerebrospinal fluid and brain microdialysate samples from newly arrived patients with severe TBI, suggesting disruption of the blood-brain barrier. Marked intergroup differences were still evident in samples taken the day after injury. Metabolic profiles were strongly associated with outcomes, as measured by Glasgow Outcomes Scale scores.

Classification

Primary and secondary injuries

  • Primary injury: Induced by mechanical force and occurs at the moment of injury; the 2 main mechanisms that cause primary injury are contact (eg, an object striking the head or the brain striking the inside of the skull) and acceleration-deceleration [2]
  • Secondary injury: Not mechanically induced; it may be delayed from the moment of impact, and it may superimpose injury on a brain already affected by a mechanical injury [2]

Focal and diffuse injuries

These injuries are commonly found together; they are defined as follows:

  • Focal injury: Includes scalp injury, skull fracture, and surface contusions; generally caused by contact
  • Diffuse injury: Includes diffuse axonal injury (DAI), hypoxic-ischemic damage, meningitis, and vascular injury; usually caused by acceleration-deceleration forces

Measures of severity

See the list below:

  • Glasgow Coma Scale (GCS): A 3- to 15-point scale used to assess a patient’s level of consciousness and neurologic functioning [3, 4] ; scoring is based on best motor response, best verbal response, and eye opening (eg, eyes open to pain, open to command)
  • Duration of loss of consciousness: Classified as mild (mental status change or loss of consciousness [LOC] 6 hr)
  • Posttraumatic amnesia (PTA): The time elapsed from injury to the moment when patients can demonstrate continuous memory of what is happening around them [5]

Complications

Complications include the following:

  • Posttraumatic seizures: Frequently occur after moderate or severe TBI
  • Hydrocephalus
  • Deep vein thrombosis: Incidence as high as 54% [6]
  • Heterotopic ossification: Incidence of 11-76%, with a 10-20% incidence of clinically significant heterotopic ossification [7]
  • Spasticity
  • Gastrointestinal and genitourinary complications: Among the most common sequelae in patients with TBI
  • Gait abnormalities
  • Agitation: Common after TBI

Long-term physical, cognitive, and behavioral impairments are the factors that most commonly limit a patient’s reintegration into the community and his/her return to employment. They include the following:

  • Insomnia
  • Cognitive decline
  • Posttraumatic headache: Tension-type headaches are the most common form, but exacerbations of migraine-like headaches are also frequent
  • Posttraumatic depression: Depression after TBI is further associated with cognitive decline, [8, 9] anxiety disorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts

Outcome measures

The following tools are commonly used to measure outcome after TBI[10, 11] :

  • Functional Independence Measure (FIM): An 18-item scale used to assess the patient’s level of independence in mobility, self-care, and cognition
  • Glasgow Outcome Scale (GOS)
  • Disability Rating Scale (DRS): Measures general functional changes over the course of recovery after TBI (see the image below)
  • Disability Rating Scale (DRS).

Continue —>  Classification and Complications of Traumatic Brain Injury: Practice Essentials, Epidemiology, Pathophysiology.

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[ARTICLE] Predictors of On-Road Driver Performance following Traumatic Brain Injury

Conclusions

PTA duration, proved to be a better predictor of driver assessment outcome than Glasgow coma scale score and in combination with the presence of physical/visual impairment and slowed reaction times, could assist clinicians to determine referral. criteria for OT driver assessment. On-road driver rehabilitation, followed by on-road re-assessments were associated with a high probability of return to driving after TBI…

via Predictors of On-Road Driver Performance following Traumatic Brain Injury – Archives of Physical Medicine and Rehabilitation.

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