Dementia resulting from traumatic brain injury

Abstract

Traumatic brain injury (TBI) represents a significant public health problem in modern societies. It is primarily a consequence of traffic-related accidents and falls. Other recently recognized causes include sports injuries and indirect forces such as shock waves from battlefield explosions. TBI is an important cause of death and lifelong disability and represents the most well-established environmental risk factor for dementia. With the growing recognition that even mild head injury can lead to neurocognitive deficits, imaging of brain injury has assumed greater importance. However, there is no single imaging modality capable of characterizing TBI. Current advances, particularly in MR imaging, enable visualization and quantification of structural and functional brain changes not hitherto possible. In this review, we summarize data linking TBI with dementia, emphasizing the imaging techniques currently available in clinical practice along with some advances in medical knowledge.

Keywords: chronic traumatic encephalopathy; craniocerebral trauma; dementia; magnetic resonance; post-concussion syndrome.

Figure 1

Patient with mild cognitive decline after moderate TBI. MR Susceptibility-weighted imaging (SWI) axial images [A and B] show frontal contusion and superficial siderosis seen as cortical low signal intensity lines over the cortex due to subarachnoid hemorrhage.

Figure 2

DAI and subarachnoid hemorrhage after mild TBI. Axial SWI [A, B and C] show multiple focal lesions involving the basal ganglia and the lobar white matter at the gray-white matter interface. Note also the bilateral subarachnoid hemorrhage particularly evident in A B C the left sylvian fissure.

Figure 3

DAI involving the splenium of the corpus callosum after TBI. Axial T2-weighted [A], FLAIR [B], post-contrast T1-weighted [C], SWI [D], DWI [E] and ADC map [F] show high signal lesion T2-weighted [A] and FLAIR [B] images, with no enhancement after gadolinium administration [C], low signal on SWI [D] and restricted diffusion (high signal on DWI [E] and low signal on ADC map). MRI is the modality of choice for assessing suspected diffuse axonal injury even in patients with entirely normal CT of the brain. Note also the bilateral subgaleal haematomas.

Figure 4

Cognitive decline 8 weeks after TBI. Axial T1-weighted [A], T2-weighted [B] and FLAIR [C] images show bilateral chronic subdural hematomas with no midline shift.

Figure 5

DAI in a patient with severe TBI. Axial non-contrast CT [A and B] show multiple hyperdense lesions varying in size involving primarily the gray-white matter junction. Note that the appearance of DAI on CT depends on whether or not the lesions are hemorrhagic. Subtle or nonhemorrhagic DAI may be not detected on CT and such patients usually have relatively normal CT scans with significant unexplained neurological deficit.

Figure 6

DAI after severe TBI (motor vehicle accident) well depicted on SWI. Axial SWI [A, B and C} shows diffuse and bilateral lesions involving the basal ganglia, lobar white matter, gray-white matter junction, corpus callosum and the brainstem. SWI (or gradient echo sequences) are exquisitely sensitive to blood products and the best MR sequences for DAI detection. Note that when the DAI lesions are entirely nonhemorrhagic they will not be detected on these sequences, but the will be visible as areas of high FLAIR signal.

Figure 7

DAI involving the basal ganglia and gray-white matter junction. Axial CT [A], T2 GRE [B] and DWI [C] show hemorrhagic DAI lesions. Perfusion (dynamic susceptibility contrast) MR imaging cerebral blood volume (CBV) [D], cerebral blood flow (CBF) [E], mean transit time (MTT) [F], and time to peak (TTP) [G] maps show low perfusion at the level of the basal ganglia.