See Ghoshal and Claassen (doi:10.1093/brain/awx226) for a scientific commentary on this article. Early cortical infarcts are common in poor-grade patients after aneurysmal subarachnoid haemorrhage. There are no animal models of these lesions and mechanisms are unknown, although mass cortical spreading depolarizations are hypothesized as a requisite mechanism and clinical marker of infarct development. Here we studied acute sequelae of subarachnoid haemorrhage in the gyrencephalic brain of propofol-anaesthetized juvenile swine using subdural electrode strips (electrocorticography) and intraparenchymal neuromonitoring probes. Subarachnoid infusion of 1–2 ml of fresh blood at 200 µl/min over cortical sulci caused clusters of spreading depolarizations (count range: 12–34) in 7/17 animals in the ipsilateral but not contralateral hemisphere in 6 h of monitoring, without meaningful changes in other variables. Spreading depolarization clusters were associated with formation of sulcal clots (P< 0.01), a high likelihood of adjacent cortical infarcts (5/7 versus 2/10, P < 0.06), and upregulation of cyclooxygenase-2 in ipsilateral cortex remote from clots/infarcts. In a second cohort, infusion of 1 ml of clotted blood into a sulcus caused spreading depolarizations in 5/6 animals (count range: 4–20 in 6 h) and persistent thick clots with patchy or extensive infarction of circumscribed cortex in all animals. Infarcts were significantly larger after blood clot infusion compared to mass effect controls using fibrin clots of equal volume. Haematoxylin and eosin staining of infarcts showed well demarcated zones of oedema and hypoxic-ischaemic neuronal injury, consistent with acute infarction. The association of spreading depolarizations with early brain injury was then investigated in 23 patients [14 female; age (median, quartiles): 57 years (47, 63)] after repair of ruptured anterior communicating artery aneurysms by clip ligation (n = 14) or coiling (n = 9). Frontal electrocorticography [duration: 54 h (34, 66)] from subdural electrode strips was analysed over Days 0–3 after initial haemorrhage and magnetic resonance imaging studies were performed at ∼ 24–48 h after aneurysm treatment. Patients with frontal infarcts only and those with frontal infarcts and/or intracerebral haemorrhage were both significantly more likely to have spreading depolarizations (6/7 and 10/12, respectively) than those without frontal brain lesions (1/11, P’s < 0.05). These results suggest that subarachnoid clots in sulci/fissures are sufficient to induce spreading depolarizations and acute infarction in adjacent cortex. We hypothesize that the cellular toxicity and vasoconstrictive effects of depolarizations act in synergy with direct ischaemic effects of haemorrhage as mechanisms of infarct development. Results further validate spreading depolarizations as a clinical marker of early brain injury and establish a clinically relevant model to investigate causal pathologic sequences and potential therapeutic interventions.

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OBJECTIVE Many low-risk unruptured intracranial aneurysms (UIAs) are followed for growth with surveillance imaging. Growth of UIAs likely increases the risk of rupture. The incidence and risk factors of UIA growth or de novo aneurysm formation require further research. The authors retrospectively identify risk factors and annual risk for UIA growth or de novo aneurysm formation in an aneurysm surveillance protocol. METHODS Over an 11.5-year period, the authors recommended surveillance imaging to 192 patients with 234 UIAs. The incidence of UIA growth and de novo aneurysm formation was assessed. With logistic regression, risk factors for UIA growth or de novo aneurysm formation and patient compliance with the surveillance protocol was assessed. RESULTS During 621 patient-years of follow-up, the incidence of aneurysm growth or de novo aneurysm formation was 5.0%/patient-year. At the 6-month examination, 5.2% of patients had aneurysm growth and 4.3% of aneurysms had grown. Four de novo aneurysms formed (0.64%/patient-year). Over 793 aneurysm-years of follow-up, the annual risk of aneurysm growth was 3.7%. Only initial aneurysm size predicted aneurysm growth (UIA < 5 mm = 1.6% vs UIA ≥ 5 mm = 8.7%, p = 0.002). Patients with growing UIAs were more likely to also have de novo aneurysms (p = 0.01). Patient compliance with this protocol was 65%, with younger age predictive of better compliance (p = 0.01). CONCLUSIONS Observation of low-risk UIAs with surveillance imaging can be implemented safely with good adherence. Aneurysm size is the only predictor of future growth. More frequent (semiannual) surveillance imaging for newly diagnosed UIAs and UIAs ≥ 5 mm is warranted.

Background:The use of anticoagulants or antiplatelet medications has become increasingly common and is a well-established risk factor for worsening of hemorrhages in trauma patients. The current study addresses the need to investigate the efficacy of point-of-care tests (POC) as an adjunct to conventional coagulation testing in traumatic brain injury (TBI) patients.Methods:A retrospective review of 190 TBI patients >18 years of age who underwent both conventional and POC testing as part of their admission coagulopathy workup was conducted. Coagulation deficiency was defined as an international normalized ratio (INR) >1.4, a reaction time (r-value) on rapid thromboelastography >50 seconds, or a VerifyNow Aspirin (VN-ASA) level of < 550 Aspirin Reaction Units.Results:Among 190 patients, 91 (48%) disclosed a history of either warfarin or antiplatelet use or had documented INR >1.4. Of the 18 (9%) patients who reported warfarin use, 83% had elevated INR and 61% had elevated r-value. However, 41% of the patients without reported anticoagulant usage revealed significantly elevated r-value consistent with a post-traumatic hypocoagulable state. Of 64 (34%) patients who reported taking ASA, 51 (80%) demonstrated therapeutic VN-ASA. Interestingly, 31 of 126 (25%) patients not reporting ASA use were also noted to have therapeutic VN-ASA suggestive of platelet dysfunction.Conclusions:The coagulopathy POC panel consisting of r-TEG and VN-ASA successfully identified a subset of TBI patients with an occult coagulopathy that would have otherwise been missed. Standardization of these POC assays on admission in TBI may help guide patient resuscitation in the acute setting.

The authors present the case of a patient that demonstrates resolution of delayed onset hypoglossal nerve palsy (HNP) subsequent to occipital condyle fracture following a motor vehicle accident. Decompression of the hypoglossal nerve and craniocervical fixation led to satisfactory long-term (>5 years) outcome. There is a scarcity of literature in recognizing HNPs following trauma and a lack of pathophysiological understanding to both a delayed presentation and to resolution versus persistence. This is the first report demonstrating long-term resolution of hypoglossal nerve injury following trauma to the craniocervical junction.