Posttraumatic Cerebral Infarction Research Articles

Imaging of Head Trauma

Prognostic factors affecting outcome of traumatic brain injury (TBI), despite their importance, are still under discussion. The purpose of this study was to describe risk factors of in-hospital mortality and outcome at 1 year in a homogeneously treated population of patients with moderate/severe TBI.A total of 193 consecutive patients with moderate or severe TBI (Glasgow Coma Scale [GCS] score 13–3, including patients with initial GCS score of 13 at high risk for subsequent neurologic deterioration), admitted to the intensive care unit, were retrospectively analyzed. In-hospital mortality and unfavorable outcome at 1 year, based on a Glasgow Outcome Scale–Extended score ≤4, were considered as primary and secondary outcomes.At 1 year, unfavorable outcome occurred in 47.2%, including an in-hospital mortality of 19.7%. Increasing age, GCS motor score <3, coagulation disorders, and intracranial hypertension were acute risk factors of in-hospital mortality. In the 155 remaining survivors, Oxford Handicap Scale (OHS), posttraumatic cerebral infarction, cerebrospinal fluid disturbances, and length of intensive care unit stay were associated with unfavorable outcome at 1 year, in univariate analysis. A cutoff OHS score ≥3 discriminated the probability of an unfavorable outcome (area under the curve, 0.87; P < 0.001; specificity, 74%; sensitivity, 84%). Combining the effect of acute and subacute variables in a multivariate analysis, increasing age and OHS score were independent predictors of outcome.The results of this retrospective study confirmed age as the main acute risk factor and identified OHS as new potential subacute predictor of unfavorable outcome in moderate and severe TBI.

Cerebral infarction in the caudate nucleus associated with acute epidural hematoma and diffuse brain injury in a child after severe head injury

A 6-year-old boy was admitted to our hospital 20 min after receiving a direct impact to his head in an automobile accident. He was semi-comatose on admission and computed tomography showed acute epidural hematoma in the right supratentorial region. Three hours later, his consciousness deteriorated due to the enlargement of the hematoma. Surgical removal of hematoma relieved his consciousness disturbance. Post-operative magnetic resonance imaging revealed spotty high-intensity lesions in the corpus callosum on T2-weighted images, and a solitary high-intensity lesion in the left caudate nucleus extending to the medial globus pallidum on T2-weighted and diffusion-weighted images. Magnetic resonance angiography showed no abnormality in the main arteries. These results suggested cerebral infarction in the vascular territory supplied by the recurrent artery of Heubner in association with diffuse brain injury. Post-operative course was uneventful and he was discharged without neurological deficit. Post-traumatic cerebral infarction in the caudate nucleus is extremely rare, and its association with diffuse brain injury and epidural hematoma is apparently unique.

Post-traumatic cerebral infarction. Neuroimaging findings, etiology and outcome.

To assess the radiological characteristics of post-traumatic cerebral infarctions (PTCIs), the etiology and site of infarction, and to provide neuroimaging indicators of a poor clinical outcome. A retrospective study of 16 patients with the neuroimaging-based diagnosis of PTCI was carried out. All CT, MR examinations, cerebral angiograms and medical records of the patients were reviewed. Infarcts were diagnosed in the territory of the posterior cerebral artery in 9 patients, in the middle cerebral artery in 5, in the anterior cerebral artery in 3, lenticulostriate-thalamoperforating in 2, vertebrobasilar in 3, and cortical infarcts in 2 patients. Neuroimaging studies suggested focal mass effect and/or acquired intracranial herniations as the cause of infarction in 13/16 patients (81.2%). In 3/16 patients (18.8%), PTCI was due to vascular injury of which 2 were angiographically documented (carotid artery dissection). Eight of the 16 patients in this study died or were left in a persistent vegetative state. Patients with associated subdural hematoma, brain swelling/edema and traumatic subarachnoid hemorrhage (tSAH) exhibited the worst outcome. Gross mechanical shift of the brain and herniation across the falx and/or tentorium accounted for infarction in a majority of cases in our study. The overall death rate was 43.8% and this result suggests that PTCI is an indication of a poor clinical outcome, especially among patients with associated subdural hematoma, brain swelling/edema and tSAH.

O-25-364 - Diagnostic and treatment of post-traumatic cerebral infarction. A report of 40 cases

The usefuiness of the anteroposterior (AP) radiograph of the cervical spine in contributing to the diagnosis of cervical spine injuries in the acute trauma patient was examined in a retrospective study. All cases of cervical spine fracture or dislocation seen at a level I trauma center over a 3-year period and at a rehabilitation center over a 10-year period were reviewed. The lateral radiograph, open-mouth odontoid radiograph, and AP radiograph of each case were sequentially examined by a neuroradiologist (blinded to the original diagnosis) to determine the contribution of each view in making a diagnosis of cervical spine injury. Results of these reviews showed that there were no cases of cervical spine injury evident on the AP view without an obvious corresponding abnormality on the lateral or open-mouth view. It was concluded that the AP view could be dropped from the initial screening radiographic study of the cervical spine in the trauma patient. Only an adequale lateral view and open-mouth odontoid view would then be necessary to initially evaluate the cervical spine in the trauma patient, and decisions to obtain further studies could be based safely on only the lateral and open-mouth views.

Posttraumatic cerebral infarction diagnosed by CT: prevalence, origin, and outcome.

Posttraumatic cerebral infarction is a recognized complication of craniocerebral trauma, but its frequency, cause, and influence on mortality are not well defined. To ascertain this information, all cranial CT studies demonstrating posttraumatic cerebral infarction and performed during a 40-month period at our trauma center were reviewed. Posttraumatic cerebral infarction was diagnosed by CT within 24 hr of admission (10 patients) and up to 14 days after admission (mean, 3 days) in 25 (1.9%) of 1332 patients who required cranial CT for trauma during the period. Infarcts, in well-defined arterial distributions, were diagnosed either uni- or bilaterally in the posterior cerebral (17), proximal and/or distal anterior cerebral (11), middle cerebral (11), lenticulostriate/thalamoperforating (nine), anterior choroidal (three), and/or vertebrobasilar (two) territories in 23 patients. Two other patients displayed atypical infarction patterns with sharply marginated cortical and subcortical low densities crossing typical vascular territories. CT findings suggested direct vascular compression due to mass effects from edema, contusion, and intra- or extraaxial hematoma as the cause of infarction in 24 patients; there was postmortem verification in five. In one patient, a skull-base fracture crossing the precavernous carotid canal led to occlusion of the internal carotid artery and ipsilateral cerebral infarction. Mortality in craniocerebral trauma with complicating posttraumatic cerebral infarction, 68% in this series, did not differ significantly from that in craniocerebral trauma patients without posttraumatic cerebral infarction when matched for admission Glasgow Coma Score results. Thus, aggressive management should be considered even in the presence of posttraumatic cerebral infarction.