Case Report of Posttraumatic Middle Cerebral Artery Territory Infarct

A 27-year-old man had severe diffuse brain injury. The patient developed malignant right MCA territory infarction on second day. Emergency decompressive craniectomy was done. He was ventilated. He developed subdural hygroma on the opposite side that was drained. He improved slowly. He had hydrocephalus. VP shunt was done. He became conscious but dependent. PEG was done for feeding. Cranioplasty was done for syndrome of trephined. The patent improved to a state of good cognition with residual motor aphasia and left hemiplegia.Posttraumatic cerebral infarction is an indicator of poor prognosis. Vasospasm, intimal dissection, and thrombosis are the mechanisms. MCA territorial infarction is rare. Usual mechanism is impact of rotational forces on relatively fixed M1 segment on the posterior margin of lower wing of sphenoid, resulting in arterial dissection or intimal damage.

Post-traumatic cerebellar infarction due to vertebral artery foramina fracture: case report

Posttraumatic cerebral infarction is an uncommon cause of morbidity and mortality and many studies have highlighted that trauma needs to considered as causative factor for cerebellar infarction. We present a case of cerebellar infarction in a 35 year old young patient secondary to vertebral fracture involving the vertebral foramen and vertebral artery injury. CT scan cervical spine showed C2-3 fracture on left side with fracture extending into the left vertebral foramen. A CT scan angiogram could not be performed because of poor neurological status. Possibly the infarction was due to left vertebral artery injury. Without surgical intervention prognosis of these patients remain poor. Prognosis of patients with traumatic cerebellar infarction depends on the neurological status of the patient, intrinsic parenchymal damage and more importantly extrinsic compression of the brainstem by the edematous cerebellar hemispheres.

Clinical and radiological outcomes following traumatic Grade 1 and 2 vertebral artery injuries: a 10-year retrospective analysis from a Level 1 trauma center

Object Screening of blunt vertebral artery (VA) injuries has increased since research has shown that they occur at a higher incidence than originally reported. Grade 1 and 2 injuries are the most common form of blunt VA injury. Proper screening, management, and follow-up of these injuries remain controversial. In this report, imaging, progression, treatment, and outcomes of Grade 1 and 2 blunt VA injuries were analyzed to better define their natural history and to establish a rational management plan based upon their risk of progression and cerebral infarct. Methods A retrospective review of all blunt traumatic carotid artery and VA injuries from December 2003 to April 2013 was performed. For the purposes of this report, focus was given to Grade 1 and 2 VA injuries. Grade 1 injuries were defined as a vessel lumen stenosis of less than 25%, and Grade 2 injuries were defined as vessel lumen stenosis between 25% and 50%. Demographic information, radiological imaging, number of images performed per individual, length of radiological follow-up, radiological outcome at the end of follow-up, treatment provided, and documentation of stroke or transient ischemic attack were recorded. Results One hundred eighty-seven Grade 1 and 2 VA injuries in 143 patients were identified. Of these 143 patients, 120 with 152 Grade 1 or 2 blunt VA injuries were available for follow-up. The mean duration of follow-up was 40 days. Repeat imaging showed that 148 (97.4%) Grade 1 or 2 blunt VA injuries were stable, improved, or resolved on final follow-up imaging. Seventy-nine patients (66%) were treated with aspirin, whereas 35 patients (29%) received no treatment. The remaining patients were treated with other antiplatelet agents or anticoagulant medication. Neuroimaging demonstrated 2 cases (1.7%) with posterior circulation infarcts that were believed to be related to their blunt VA injuries, both of which occurred during the initial hospitalization and within the first 4 days after injury. Conclusions Although follow-up imaging showed progressive worsening without radiological improvement in only a small number of patients with low-grade blunt VA injuries, these findings did not correlate with adverse clinical outcome. The posttraumatic cerebral infarction rate of 1.7% may be overestimated, and the use of acetylsalicylic acid or other antiplatelet or anticoagulant medication did not correlate with radiological changes or rate of cerebral infarction. While these data suggest the possibility that these low-grade VA injuries may not require treatment or follow-up, future prospective studies are needed to make conclusive changes related to management.

The Influence of Hemocoagulation Disorders on the Development of Posttraumatic Cerebral Infarction and Outcome in Patients with Moderate or Severe Head Trauma

Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of head injury and often leads to a poor prognosis. Hemocoagulation disorder is recognized to have important effects on hemorrhagic or ischemic damages. We sought to assess if posttraumatic hemocoagulation disorders were associated with cerebral infarction, and evaluate their influence on outcome among patients with moderate or severe head trauma. In this study, PTCI was observed in 28 (10.57%) of the 265 patients within the first week after injury. In multivariate analysis, the thrombocytopenia (odds ratio (OR) 2.210, 95% confidence interval (CI) 1.065–4.674), abnormal prothrombin time (PT) (OR 3.241, 95% CI 1.090–7.648), D-dimer (>2 mg/L) (OR 7.260, 95% CI 1.822–28.076), or disseminated intravascular coagulation (DIC) scores (≥5) (OR 4.717, 95% CI 1.778–12.517) were each independently associated with an increased risk of PTCI. Admission Glasgow Coma Scale (GCS) score, abnormal activated partial thromboplastin time (APTT) and fibrinogen, and D-dimer (>2 mg/L) and DIC scores (≥5) showed an independent predictive effect on poor outcome. In conclusion, recognition of this important treatable cause of PTCI and the associated risk factors may help identify the group at risk and tailor management of patients with TBI.