• Haining Zhang, Shuichi Okubo, Ya Hua, Richard F Keep, and Guohua Xi.
• Department of Neurosurgery, University of Michigan, 5018 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA.
• Acta Neurochir. Suppl. 2016 Jan 1; 121: 141-4.

AbstractResearch suggests that early brain injury following subarachnoid hemorrhage (SAH) is a primary therapeutic target, and early SAH-induced basal ganglia injury is not well studied. The present study examined basal ganglia injury in a rat model of SAH. Adult male Sprague-Dawley rats (n = 78) weighing 275-300 g underwent endovascular perforation to mimic aneurysmal SAH. Sham rats (n = 12) underwent the same procedure but without perforation. Magnetic resonance imaging (T2 MRI) was performed at 24 h after SAH to measure ventricle volumes and brain T2 lesion. Hydrocephalus in SAH rats was defined as a ventricular volume greater than three standard deviations above that in shams. Western blotting and immunochemistry were utilized to assess basal ganglia damage. Sixty rats survived the SAH and 40 % of those animals had T2 lesions in the basal ganglia. Twenty-six SAH rats had hydrocephalus. Rats with hydrocephalus had higher incidence of basal ganglia lesion (69 vs. 18 % in rats without hydrocephalus; p < 0.01). Basal ganglia neuronal injury was also determined by examining the levels of dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32). We found that rats with hydrocephalus had more severe basal ganglia injury with greater DARPP-32 depletion (DARPP-32/beta-actin: 0.38 ± 0.32 vs. 0.86 ± 0.45 in rats without hydrocephalus and 1.10 ± 0.28 in sham, p < 0.05). In conclusion, SAH resulted in severe basal ganglia damage, which is associated with hydrocephalus development.

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