Aristotelis S. Filippidis and Kostas N. Fountas
Hans Kristian Moe, Janne Limandvik Myhr, Kent Gøran Moen, Asta Kristine Håberg, Toril Skandsen, and Anne Vik
The authors investigated the association between the cause of injury and the occurrence and grade of traumatic axonal injury (TAI) on clinical MRI in patients with moderate or severe traumatic brain injury (TBI).
Data for a total of 396 consecutive patients, aged 7–70 years, with moderate or severe TBI admitted to a level 1 trauma center were prospectively registered. Data were included for analysis from the 219 patients who had MRI performed within 35 days (median 8, IQR 4–17 days) and for whom cause of injury was known. Cause of injury was registered as road traffic accident (RTA) or fall (both with respective subcategories), alpine skiing or snowboarding accident, or violence. The MRI protocol consisted of T2*-weighted gradient echo, FLAIR, and diffusion-weighted imaging scans. TAI lesions were evaluated in a blinded manner and categorized into 3 grades, hemispheric/cerebellar white matter (grade 1), corpus callosum (grade 2), and brainstem (grade 3). The absence of TAI was analyzed as grade 0. Contusions and mass lesions on CT were also registered.
Cause of injury did not differ between included and nonincluded patients. TAI was found in 83% of patients in the included group after RTAs and 62% after falls (p < 0.001). Observed TAI grades differed between the subcategories of both RTAs (p = 0.004) and falls (p = 0.006). Pedestrians in RTAs, car drivers/passengers in RTAs, and alpine skiers had the highest prevalence of TAI (89%–100%) and the highest TAI grades (70%–82% TAI grades 2–3). TAI was found in 76% of patients after falls from > own height (45% TAI grade 2–3), 63% after falls down the stairs (26% TAI grade 2–3), and 31% after falls from ≤ own height (12% TAI grade 2–3). Moreover, 53% of patients with TAI after RTAs and 68% with TAI after falls had cortical contusions or mass lesions on CT.
This prospective study of moderate and severe TBI is to the authors’ knowledge the first clinical MRI study to demonstrate both the high prevalence and grade of TAI after most of the different types of RTAs, alpine skiing accidents, and falls from a height. Importantly, TAI was also common following more low-energy trauma such as falls down the stairs or from own height. Physicians managing TBI patients in the acute phase should be aware of the possibility of TAI no matter the cause of injury and also when the CT scan shows cortical contusions or mass lesions.
Toril Skandsen, Kjell Arne Kvistad, Ole Solheim, Ingrid Haavde Strand, Mari Folvik, and Anne Vik
In this prospective cohort study the authors examined patients with moderate to severe head injuries using MR imaging in the early phase. The objective was to explore the occurrence of diffuse axonal injury (DAI) and determine whether DAI was related to level of consciousness and patient outcome.
One hundred and fifty-nine patients (age range 5–65 years) with traumatic brain injury, who survived the acute phase, and who had a Glasgow Coma Scale (GCS) score of 3–13 were admitted between October 2004 and August 2008. Of these 159 patients, 106 were examined using MR imaging within 4 weeks postinjury. Patients were classified into 1 of 3 stages of DAI: Stage 1, in which lesions were confined to the lobar white matter; Stage 2, in which there were callosal lesions; and Stage 3, in which lesions occurred in the dorsolateral brainstem. The outcome measure used 12 months postinjury was the Glasgow Outcome Scale–Extended (GOSE).
Diffuse axonal injury was detected in 72% of the patients and a combination of DAI and contusions or hematomas was found in 50%. The GCS score was significantly lower in patients with “pure DAI” (median GCS Score 9) than in patients without DAI (median GCS Score 12; p < 0.001). The GCS score was related to outcome only in those patients with DAI (r = 0.47; p = 0.001). Patients with DAI had a median GOSE score of 7, and patients without DAI had a median GOSE score of 8 (p = 0.10). Outcome was better in patients with DAI Stage 1 (median GOSE Score 8) and DAI Stage 2 (median GOSE Score 7.5) than in patients with DAI Stage 3 (median GOSE Score 4; p < 0.001). Thus, in patients without any brainstem injury, there was no difference in good recovery between patients with DAI (67%) and patients without DAI (66%).
Diffuse axonal injury was found in almost three-quarters of the patients with moderate and severe head injury who survived the acute phase. Diffuse axonal injury influenced the level of consciousness, and only in patients with DAI was GCS score related to outcome. Finally, DAI was a negative prognostic sign only when located in the brainstem.
Nils Petter Rundhaug, Kent Gøran Moen, Toril Skandsen, Kari Schirmer-Mikalsen, Stine B. Lund, Sozaburo Hara, and Anne Vik
The influence of alcohol is assumed to reduce consciousness in patients with traumatic brain injury (TBI), but research findings are divergent. The aim of this investigation was to study the effects of different levels of blood alcohol concentration (BAC) on the Glasgow Coma Scale (GCS) scores in patients with moderate and severe TBI and to relate the findings to brain injury severity based on the admission CT scan.
In this cohort study, 265 patients (age range 16–70 years) who were admitted to St. Olavs University Hospital with moderate and severe TBI during a 7-year period were prospectively registered. Of these, 217 patients (82%) had measured BAC. Effects of 4 BAC groups on GCS score were examined with ordinal logistic regression analyses, and the GCS scores were inverted to give an OR > 1. The Rotterdam CT score based on admission CT scan was used to adjust for brain injury severity (best score 1 and worst score 6) by stratifying patients into 2 brain injury severity groups (Rotterdam CT scores of 1–3 and 4–6).
Of all patients with measured BAC, 91% had intracranial CT findings and 43% had BAC > 0 mg/dl. The median GCS score was lower in the alcohol-positive patients (6.5, interquartile range [IQR] 4–10) than in the alcohol-negative patients (9, IQR 6–13; p < 0.01). No significant differences were found between alcohol-positive and alcohol-negative patients regarding other injury severity variables. Increasing BAC was a significant predictor of lower GCS score in a dose-dependent manner in age-adjusted analyses, with OR 2.7 (range 1.4–5.0) and 3.2 (range 1.5–6.9) for the 2 highest BAC groups (p < 0.01). Subgroup analyses showed an increasing effect of BAC group on GCS scores in patients with Rotterdam CT scores of 1–3: OR 3.1 (range 1.4–6.6) and 6.7 (range 2.7–16.7) for the 2 highest BAC groups (p < 0.01). No such relationship was found in patients with Rotterdam CT scores of 4–6 (p = 0.14–0.75).
Influence of alcohol significantly reduced the GCS score in a dose-dependent manner in patients with moderate and severe TBI and with Rotterdam CT scores of 1–3. In patients with Rotterdam CT scores of 4–6, and therefore more CT findings indicating increased intracranial pressure, the brain injury itself seemed to overrun the depressing effect of the alcohol on the CNS. This finding is in agreement with the assumption of many clinicians in the emergency situation.
Hans Kristian Moe, Turid Follestad, Nada Andelic, Asta Kristine Håberg, Anne-Mari Holte Flusund, Kjell Arne Kvistad, Elin Hildrum Saksvoll, Øystein Olsen, Sebastian Abel-Grüner, Oddrun Sandrød, Toril Skandsen, Anne Vik, and Kent Gøran Moen
The aim in this study was to investigate if MRI findings of traumatic axonal injury (TAI) after traumatic brain injury (TBI) are related to the admission Glasgow Coma Scale (GCS) score and prolonged duration of posttraumatic amnesia (PTA).
A total of 490 patients with mild to severe TBI underwent brain MRI within 6 weeks of injury (mild TBI: median 2 days; moderate to severe TBI: median 8 days). The location of TAI lesions and measures of total TAI lesion burden (number and volume of lesions on FLAIR and diffusion-weighted imaging and number of lesions on T2*-weighted gradient echo or susceptibility-weighted imaging) were quantified in a blinded manner for clinical information. The volume of contusions on FLAIR was likewise recorded. Associations between GCS score and the location and burden of TAI lesions were examined with multiple linear regression, adjusted for age, Marshall CT score (which includes compression of basal cisterns, midline shift, and mass lesions), and alcohol intoxication. The predictive value of TAI lesion location and burden for duration of PTA > 28 days was analyzed with multiple logistic regression, adjusted for age and Marshall CT score. Complete-case analyses of patients with TAI were used for the regression analyses of GCS scores (n = 268) and PTA (n = 252).
TAI lesions were observed in 58% of patients: in 7% of mild, 69% of moderate, and 93% of severe TBI cases. The TAI lesion location associated with the lowest GCS scores were bilateral lesions in the brainstem (mean difference in GCS score −2.5), followed by lesions bilaterally in the thalamus, unilaterally in the brainstem, and lesions in the splenium. The volume of TAI on FLAIR was the measure of total lesion burden most strongly associated with the GCS score. Bilateral TAI lesions in the thalamus had the largest predictive value for PTA > 28 days (OR 16.2, 95% CI 3.9–87.4). Of the measures of total TAI lesion burden, the FLAIR volume of TAI predicted PTA > 28 days the best.
Bilateral TAI lesions in the brainstem and thalamus, as well as the total volume of TAI lesions on FLAIR, had the strongest association with the GCS score and prolonged PTA. The current study proposes a first step toward a modified classification of TAI, with grades ranked according to their relation to these two measures of clinical TBI severity.
Anne Vik, Torbjørn Nag, Oddrun Anita Fredriksli, Toril Skandsen, Kent Gøran Moen, Kari Schirmer-Mikalsen, and Geoffrey T. Manley
It has recently been suggested that the degree of intracranial pressure (ICP) above the treatment goal can be estimated by the area under the curve (AUC) of ICP versus time in patients with severe traumatic brain injury (TBI). The objective of this study was to determine whether the calculated “ICP dose”—the ICP AUC—is related to mortality rate, outcome, and Marshall CT classification.
Of 135 patients (age range 1–82 years) with severe TBI treated during a 5-year period at the authors' institution, 113 patients underwent ICP monitoring (84%). Ninety-three patients with a monitoring time > 24 hours were included for analysis of ICP AUC calculated using the trapezoidal method. Computed tomography scans were assessed according to the Marshall TBI classification. Patients with Glasgow Outcome Scale scores at 6 months and > 3 years were separated into 2 groups based on outcome.
Sixty patients (65%) had ICP values > 20 mm Hg, and 12 (13%) developed severe intracranial hypertension and died secondary to herniation. A multiple regression analysis adjusting for Glasgow Coma Scale score, age, pupillary abnormalities and Injury Severity Scale score demonstrated that the ICP AUC was a significant predictor of poor outcome at 6 months (p = 0.034) and of death (p = 0.035). However, it did not predict long-term outcome (p = 0.157). The ICP AUC was significantly higher in patients with Marshall head injury Categories 3 and 4 (24 patients) than in those with Category 2 (23 patients, p = 0.025) and Category 5 (46 patients, p = 0.021) TBIs using the worst CT scan obtained.
The authors found a significant relationship between the dose of ICP, the worst Marshall CT score, and patient outcome, suggesting that the AUC method may be useful in refining and improving the treatment of ICP in patients with TBI.