The relationship between traumatic axonal injury and intracranial pressure: a clinical MRI study
Master thesis
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http://hdl.handle.net/11250/2460705Utgivelsesdato
2017Metadata
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Sammendrag
Background
Elevated intracranial pressure (ICP) is common in traumatic brain injury (TBI), and can be caused by haemorrhage, contusions or brain oedema. Traumatic axonal injury (TAI) is another important type of injury in TBI, but it is not known if TAI also is an independent contribution factor to elevated ICP. Our aim is to investigate how number and volume of TAI lesions are associated with ICP in patients with moderate to severe TBI.
Methods
101 patients with moderate to severe TBI (7-70 years) with intracranial ICP monitoring device and early clinical MRI (median 13 days, range 0-35) were prospectively included. Elevated ICP values were registered as 20-25, 26-30, 31-40 and >40 mmHg based on at least three observations within 24 hours, and only if treatment for elevated ICP was given. TAI lesions were identified in T2* gradient echo (T2*GRE), T2 fluid attenuated inversion recovery (FLAIR) and diffusion weighted imaging (DWI) scans. T2*GRE lesions were registered and counted in the hemispheric white matter, corpus callosum, thalamus, basal ganglia, brain stem and cerebellum, and volume of FLAIR lesions were registered and summarized over the hemispheric white matter, corpus callosum, thalamus and basal ganglia. TAI grade was based on all three imaging sequences, and classified as No TAI, TAI grade 1 (lesions in hemispheres/cerebellum) TAI grade 2 (lesions in corpus callosum) and TAI grade 3 (lesions in brain stem).
Results
54% of the patients had ICP ≥ 20 mmHg, and 82% of all patients had TAI. There was no difference in the proportion of patients who had ICP >20 mmHg between patients with no TAI and those with TAI. Number of T2*GRE lesions, volume of FLAIR lesions or TAI grade were not associated with level of ICP in unadjusted analyses. When adjusted for the presence of multiple contusions on CT scan and evacuation of mass lesion, volume of FLAIR lesions in ccm3 in the cerebrum predicted ICP with an OR of 1.06 (IQR 1.00-1.12, p=0.036).
Conclusion
These results suggest that TAI, estimated as volume of FLAIR lesions in the cerebrum, is associated with elevated ICP in patients with moderate-severe TBI. This finding underscores the importance of TAI load for acute patient treatment, and that early brain MRI can help clinicians understand high ICP related to all types of TBI pathologies.