Incidence, morbidity, and mortality of Terson syndrome in Hamilton, Ontario.

OBJECTIVE: Evaluate the incidence, neurologic morbidity, and mortality of patients with Terson syndrome. METHODS: Consecutive patients admitted to the Hamilton General Hospital from May 2012 to May 2013 with a diagnosis of spontaneous subarachnoid hemorrhage (SAH) were recruited. Funduscopic examinations were performed under pharmacological mydriasis. Outcome measures included: (1) the presence or absence of Terson syndrome; (2) The Glasgow Coma Scale (GCS), Hunt and Hess scale (H&H), and SAH Fisher score upon admission to the hospital; (3) the modified Rankin score upon discharge; and (4) and all-cause mortality. RESULTS: Forty-six patients were included and 10 had Terson syndrome (21%). The median H&H, GCS, and Fisher scores were 4, 6.5, and 4.0 for patients with Terson syndrome vs. 2, 14, and 3 for patients without Terson syndrome (p=0.0032, 0.0052, and 0.031), respectively. The median Rankin score was 6 for patients with Terson syndrome vs. 3.5 for patients without Terson syndrome (p=0.0019). The odds of all-cause mortality with Terson syndrome vs. no Terson syndrome was 12: 1 (95% confidence interval 2.33-61.7), p =0.003. Only four of the 10 patients with Terson syndrome survived. CONCLUSIONS: Based on this study, approximately one-fifth of patients admitted to the hospital with a spontaneous SAH could have Terson syndrome. Patients with Terson syndrome have significantly worse GCS and H&H scores upon admission to the hospital, lower modified Rankin scores upon discharge, and greater mortality. Thus, Terson syndrome is not rare among patients with SAH and carries a worse prognosis.

Retrograde axonal degeneration "dieback" in the corticospinal tract after transection injury of the rat spinal cord: a confocal microscopy study.

Axonal dieback is a process in which axons in spinal tracts retract away from the initial site of injury. The purpose of this project is to study the dynamics of dieback in corticospinal tract (CST) axons after various time intervals post-injury, to find the optimal spatial-temporal window for regenerative treatment. Rats received transection injuries at the T8 spinal level and were sacrificed at different time periods (1, 2, 4, 8, and 16 weeks). Three weeks prior to sacrifice, DiI crystals were implanted in the sensorimotor cortex and produced excellent CST labeling, and clear delineation of the terminal bulbs of transected axons. With DiI and confocal microscopy, we visualized axons along the entire length of the CST, and quantified the temporal and spatial features of dieback in axons of the CST based on the location of the terminal bulbs. We found that the majority of axons stopped dieing back 4 weeks after injury by which time they were approximately 2.5 mm from the site of injury. However, at 8 and 16 weeks after injury, some terminal bulbs were more than 10 and 19 mm, respectively, from the site of injury.