Spinal Subarachnoid Hemorrhage Induced Intractable Miotic Pupil: A reminder of Ciliospinal Sympathetic Center Ischemia Based Miosis: Experimental Study

Although basic pupillodilatatory function of ciliospinal center is well known, neuropathological mechanism of permanent miosis has not been adequately investigated in ciliospinal center pathologies. In this study, ischemic neurodegeneration of ciliospinal center on permanent miosis examined following SAH. 19 rabbits were examined in this study. The animals were divided into three group, as control (GI, n=5), SHAM (GII, n=5) and study group(GIII,n=9). Pupil diameters were measured after giving 0.5 cc of serum saline for SHAM, and autolog arterial blood into cervicothoracic subarachnoid space for study group. After three weeks follow up, their cervicothoracic cord and superior cervical sympathetic ganglia were taken out bilaterally. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia, degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods Results: The mean pupil diameter was 5.180±370µm, mean degenerated neuron density of ciliospinal center was 4±1/mm3in animals of control group (G1 These values were detected as 9850±610µm, 10±3/mm3, in SHAM (GII); and the 7.010±440µm and 98±21/mm3 in study group(GIII). There was an inverse relationship between degenerated neuron density of ciliospinal nuclei and pupil diameters. Although there is abroad belief about that the main cause of miosis is oculomotor nerve injuries during SAH, we shown that ciliospinal sympathetic center ischemia induced neurodegeneration may have been responsible for permanent miosis following SAH which has been reported first time.