Pericyte loss is an early pathologic feature of diabetic retinopathy, consistently present in retinae of diabetic humans and animals. Because pericyte recruitment and endothelial cell survival are controlled, in part, by the angiopoietin/Tie2 ligand/receptor system, we studied the expression of angiopoietin-2 and -1 in relation to the evolution of pericyte loss in diabetic rat retinae, using quantitative retinal morphometry, and in retinae from mice with heterozygous angiopoietin deficiency (Ang-2 LacZ knock-in mice). Finally, recombinant angiopoietin-2 was injected into eyes of nondiabetic rats, and pericyte numbers were quantitated in retinal capillaries. Angiopoietin-1 protein was present in the normal maturing retina and was upregulated 2.5-fold in diabetic retinae over 3 months of diabetes. In contrast, angiopoietin-2 protein was consistently upregulated more than 30-fold in the retinae of diabetic rats, preceding the onset of pericyte loss. Heterozygous angiopoietin-2 deficiency completely prevented diabetes-induced pericyte loss and reduced the number of acellular capillary segments. Injection of angiopoietin-2 into the eyes of normal rats induced a dose-dependent pericyte loss. These data show that upregulation of angiopoietin-2 plays a critical role in the loss of pericytes in the diabetic retina. Diabetes 53

Aims-To develop appropriate methods of eye muscle surgery in highly myopic patients with esotropia and hypotropia, with respect to the pathological findings in high resolution magnetic resonance imaging (MRI). Methods-35 patients with unilateral or bilateral high myopia and strabismusthat is, axial length of the globe averaged 29.4 mm. Multiple coronal, transverse, and parasagittal MRI image planes were obtained using a Siemens Magnetom 1.5 tesla MRI scanner. In 15 patients with a pathological plane of recti extraocular muscles found by MRI and confirmed intraoperatively, a new technique of eye muscle surgery was performed to reestablish the physiological muscle plane. This was checked postoperatively in addition to the measurement of alignment and motility by MRI. Results-The new MRI finding of a dislocation of the lateral rectus (LR) into the temporocaudal quadrant by 3.4 mm requires new surgical techniques. Only fixing the LR in the physiological meridian at the equator with a silicone loop ('guide pulley') or a non-absorbable suture is a causal therapy. This yields alignment and improves abduction and elevation. Conclusions-If the described misalignment of the LR is detected by MRI, a common high dosage recess-resect procedure for esotropia may even aggravate the deviation. The most important aim of eye muscle surgery is to normalise the pathological path of the LR. The restoration of the physiological function of the dislocated LR is remarkable. (Br J Ophthalmol 1997;81:625-630)

No abstract

Superior oblique myokymia (SOM) is a rare eye movement disorder presenting as uniocular rotatory microtremor due to intermittent contractions of the superior oblique muscle. Medical treatment usually fails to provide long-term benefit for the patient and has considerable side effects. Surgical alternatives including tenotomy or partial tenectomy of the superior oblique tendon often result in incomplete resolution of the visual symptoms. The authors report a patient who experienced immediate cessation of disabling SOM following microvascular decompression of the fourth nerve at the root exit zone. Temporary double vision at downgaze resolved 5 months after surgery. There was no recurrence of oscillopsia during a follow-up of 22 months to date. From this single observation it appears likely that vascular compression of the trochlear nerve could be a significant pathophysiological factor contributing to SOM. In the hands of an experienced surgeon, microvascular decompression at the brainstem exit zone of this nerve may evolve as the method of choice for selected cases of disabling SOM.

Superior oblique myokymia (SOM) is an ocular motility disorder characterized by oscillopsia, vertical or torsional diplopia, sometimes combined with pressure sensation. Although the pathophysiological basis is unclear, isolated case reports have documented its association with intracranial pathological processes. We present a case of SOM associated with a vascular compression of the fourth nerve at the root exit zone. Following microneurosurgical decompression, SOM completely resolved and paralysis of the fourth nerve occurred. This was less disturbing.