Post-traumatic cerebral infarction (PTCI) is one of the most severe secondary insult after traumatic brain injury (TBI), with a frequency ranging from 1.9% to 10.4%.12,19,21,22) It is occasionally associated with poor outcome and high mortality rate. Various mechanisms have been suggested for this complication, including direct vascular compression by mass effect, dissection, embolization, cerebral vasospasm, vascular injury, and systemic hypoperfusion.7,8,9,12,14,17,19,21,22) However, there were few clinical and radiological data defining early risk factors for development of PTCI. Early detection of patients who were at particularly high risk for PTCI would be very helpful in conducting management and predicting prognosis. We examined the practical incidence, and risk factors for the development of PTCI. By doing so, we can foretell the influence of PTCI on patient mortality.

The secondary effects of TBI might be more critical than the primary injuries. Brain edema, intracranial hemorrhage, vasospasm, and posttraumatic hydrocephalus are relatively common secondary brain injuries, and many studies have been conducted to explore their development following TBI.1,5,7,10,24) Cerebral infarction after brain trauma has also been recognized as a potential secondary injury, but only a few studies have reported the association between cerebral infarction and TBI. In this study, we tried to verify some factors responsible for the development of PTCI.

Of the 986 patients with TBI in this study, cerebral infarction was observed in 21 patients (2.1%) within 3 months after trauma. In one retrospective cohort study, the prevalence of cerebral infarction was 1.9%.12) Other studies revealed that prevalence of PTCI was up to 10.4%.19,21,22) These studies included only moderate or severe brain trauma patients. However, patients with TBI of all grades of severity were enrolled in this investigation. Therefore, our result showed low incidence of PTCI compared to other studies. When excluding patient with GCS score of 12 to 15, incidence of PTCI was 6.9%.

In most patients, PTCI developed early in the hospital course. In 16 (76.2%) patients, the infarction developed within 2 weeks after the injury. Therefore, we propose that CT or magnetic resonance diffusion studies are repeated within this period not to miss the diagnosis of PTCI. Cerebral infarction was rare, after two weeks from the initial TBI.

In this study, infarcts were seen most frequently in the area of the PCA, followed by the MCA. Infarcts in the small branch, such as anterior choroidal artery, lenticulostriate, and thalamoperforators were seen in four cases, respectively. These arteries have been found to be occluded against the skull base, resulting in infarction on basal ganglia after head traumas.2,4,12,13) In our study, infarction at the territory of PCA was the most common, consistent with the results of previous reports.12,21,22) Extra-axial hematoma can directly attribute to shifting or stretching of the MCA due to its mass effect or can indirectly affect MCA due to increased ICP, severe brain edema or herniation. And thus lead to MCA territory infarction.12,19,21)

PTCI can occur secondary to thrombo-embolic events from injured carotid or vertebral arteries. Vertebral artery dissection can occur in patients with head and neck trauma. In one series, 70% of vertebral artery dissections were accompanied by headache and 64% by vertebrobasilar ischemic symptoms.18) PTCI can also occur in a form of arterial vasospasm. One study by Pasqualin et al.14) reported incidence of posttraumatic angiographic vasospasm as 2% to 41%. But, due to lack of routine angiographic work up, our study has a limitation in figuring out factors affecting vertebral artery dissection in association with arterial vasospasm.

Our study suggested that increasing age (p=0.037), higher GCS at admission (p<0.01), brain herniation (p=0.044), and decompressive craniectomy (p=0.012) were risk factors for PTCI in patients with TBI. There was no statistical significance between cerebral infarction and sex (p=0.495) or abnormalities of laboratory findings.

Decompressive craniectomy has been frequently performed to control malignant brain edema by reducing ICP and resistance to cerebrospinal fluid outflow with decreased compression of cerebral vessels in cerebral infarction or trauma patients.11,20) It has long been suggested that decompressive craniectomy can improve survival rates and functional outcomes and decrease the occurrence of infarction in patients with severe brain edema when compared to medical treatment alone.3,23) But, inevitable bulging of brain tissue through the skull defect area in decompressive craniectomy can compress the brain tissue and vessels contained in the bulged area and thus can lead to cerebral infarction by inducing congestion, edema, ischemia and strangulation. Because decompressive craniectomy was performed when elevated ICPs threaten to cause lethal brain shifts, it may not simply be associated with PTCI as a risk factor. There was statistical significance between decompressive craniectomy and PTCI, however, further studies are needed to demonstrate these association.

Initial GCS score measuring post-resuscitative period was the most important factor for prediction of survival in this study. Decompressive craniectomy should be considered in patients with a GCS higher than 6, before increased ICP can contribute to an irreversible brain damage. On the other hand, the question of whether one should operate on a patient with a GCS of less than 6 or not, remains controversial. Careful selection of patients is important in order to avoid unnecessarily aggressive procedures in patients who have little chance of benefit or anticipated medical futility.

By the fact that PCA and MCA territory are the most frequently involved areas of the PTCI due to mechanical shifts, it can be suggested that posterior cerebral infarction (posterior temporal and occipital lobe) can be induced in medial temporal lobe herniation by the compression of the PCA against the rigid edge of the tentorium.17) Also, in case of ACA territory infarction, though the extent of infarction would vary by the degree of anteriorly-directed transfalcine herniation, it has been reported that the herniation of the hemisphere across the midline can cause the compression of the branches of the ipsilateral callosomarginal artery against the free edge of the falx.16)

The mortality rate in the patients of GCS 7 to 11 with PTCI in this study was 44.4%, significantly higher than in patients having TBI without PTCI (p<0.01), when matched by initial GCS. A somewhat higher mortality rate was found in PTCI group of GCS 3 to 6 and over 12, but the difference was not statistically significant (p=0.083, p=0.947). PTCI, as a complication in TBI, has been known to be an indicator of poor clinical outcome.12,15,22) Similarly, our result proved that PTCI is a direct manifestation of poor outcome. Therefore, aggressive treatment, including surgical procedure in patients with huge infarctions and refractory elevated ICP, as well as the administration of anticoagulants or calcium channel blockers, should be considered in patients with PTCI.

There are several limitations to this study. First, because this study was conducted at a single institution by a retrospective review of medical record and radiographic images, some discrepancies in the data interpretation and unexpected loss or omission of data might have been possible. To achieve external validity, multicenter prospective investigation should be required. Second, the subgroup analysis from a large population of different types of TBI patients is necessary in future because the small sample size and heterogeneity of the patient population.

In this study, PTCI occurred in 21 patients (2.1%). And PTCI results in high mortality rate and poor clinical outcome. This study suggested that increasing age, GCS at admission and brain herniation were risk factors for PTCI. Early recognition of these factors and prompt treatment may prevent PTCI, or at least minimize fatal consequences.