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A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
Published on: June 20, 2017
MR imaging, single-photon emission CT, and neurocognitive performance after mild traumatic brain injury
P A Hofman1, S Z Stapert, M J van Kroonenburgh
1Department of Radiology, University Hospital Maastricht, The Netherlands.
Background And Purpose:
Mild traumatic brain injury (mTBI) (Glasgow Coma Scale = 14-15) is a common neurologic disorder and a common cause of neurocognitive deficits in the young population. Most patients recover fully from mTBI, but 15% to 29% of patients have persistent neurocognitive problems. Although a partially organic origin is considered likely, little brain imaging evidence exists for this assumption. The aims of the present study were to establish the prevalence of posttraumatic lesions in mTBI patients on MR images and to assess the relation between these imaging findings and posttraumatic symptoms. Secondly, we explored the value of early posttraumatic single-photon emission CT (SPECT) for the evaluation of mTBI.
Methods:
Twenty-one consecutive patients were included in the study. Patients underwent MR examination, technetium-99m hexamethylpropylene amine oxime SPECT, and neurocognitive assessment within 5 days after injury. Neurocognitive follow-up was conducted 2 and 6 months after injury, and MR imaging was repeated after 6 months. Lesion size and brain atrophy were measured on the MR studies.
Results:
Twelve (57%) of 21 patients had abnormal MR findings, and 11 (61%) of 18 had abnormal SPECT findings. Patients with abnormal MR or SPECT findings had brain atrophy at follow-up. The mean neurocognitive performance of all subjects was within normal range. There was no difference in neurocognitive performance between patients with normal and abnormal MR findings. Patients with abnormal MR findings only showed significantly slower reaction times during a reaction-time task. Seven patients had persistent neurocognitive complaints and one patient met the criteria for a postconcussional syndrome.
Conclusion:
Brain lesions are common after mTBI; up to 77% of patients may have abnormal findings either on MR images or SPECT scans, and these lesions may lead to brain atrophy. The association between hypoperfusion seen on acute SPECT and brain atrophy after 6 months suggests the possibility of (secondary) ischemic brain damage. There is only a weak correlation between neuroimaging findings and neurocognitive outcome.
Insights
Mild traumatic brain injury (mTBI) can cause persistent neurocognitive issues. Brain imaging like MRI and SPECT reveal common lesions and atrophy, though their link to cognitive deficits is weak.
Area of Science:
- Neurology
- Radiology
- Neuropsychology
Background:
- Mild traumatic brain injury (mTBI) is a frequent cause of neurocognitive deficits in young individuals.
- While most patients recover, a significant percentage experience persistent neurocognitive problems.
- Evidence linking mTBI to organic brain changes is limited.
Purpose of the Study:
- To determine the prevalence of posttraumatic lesions in mTBI patients using MRI.
- To assess the relationship between imaging findings and posttraumatic symptoms.
- To evaluate the utility of early single-photon emission CT (SPECT) in mTBI assessment.
Main Methods:
- Included 21 mTBI patients undergoing MRI, SPECT, and neurocognitive assessment within 5 days of injury.
- Follow-up assessments (neurocognitive and MRI) were conducted at 2 and 6 months.
- Measured lesion size and brain atrophy on MRI scans.
Main Results:
- Abnormal MRI findings were present in 57% of patients; abnormal SPECT in 61%.
- Patients with abnormal imaging showed brain atrophy at follow-up.
- Only reaction time was significantly slower in patients with abnormal MR findings; overall neurocognitive performance was within normal limits.
Conclusions:
- Brain lesions are common post-mTBI, detected by MRI or SPECT, and can lead to atrophy.
- Acute SPECT hypoperfusion may indicate secondary ischemic brain damage, evidenced by later atrophy.
- Neuroimaging findings show a weak correlation with neurocognitive outcomes.
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