A Case of Acquired Brown Syndrome after Surgical Repair of a Medial Orbital Wall Fracture

A case of acquired Brown syndrome caused by surgical repair of medial orbital wall fracture is reported in the present paper. A 23-year-old man presented at the hospital with right periorbital trauma. Although the patient did not complain of any diplopia, the imaging study revealed a blow-out fracture of the medial orbital wall. Surgical repair with a calvarial bone autograft was performed at the department of plastic surgery. The patient was referred to the ophthalmologic department due to diplopia that newly developed after surgery. The prism cover test at distant fixation showed hypotropia of the right eye, which was 4 prism diopters (PD) in primary gaze, 20 PD in left gaze, while orthophoric in right gaze. Eye movement of the right eye was markedly limited on elevation in adduction with normal elevation in abduction with intorsion in the right eye present. Forced duction test of the right eye showed restricted elevation in adduction. Computerized tomography scan of the orbits showed the right superior oblique muscle was entrapped between the autografted bone fragment and posterior margin of the fracture. When repairing medial orbital wall fracture that causes Brown syndrome, surgeons should always be careful of entrapment of the superior oblique muscle if the implant is inserted without identifying the superior and posterior margin of the orbital fracture site

Discovery of Q203, a potent clinical candidate for the treatment of tuberculosis

New therapeutic strategies are needed to combat the tuberculosis pandemic and the spread of multidrug-resistant (MDR) and extensively drug-resistant (XDR) forms of the disease, which remain a serious public health challenge worldwide1, 2. The most urgent clinical need is to discover potent agents capable of reducing the duration of MDR and XDR tuberculosis therapy with a success rate comparable to that of current therapies for drug-susceptible tuberculosis. The last decade has seen the discovery of new agent classes for the management of tuberculosis3, 4, 5, several of which are currently in clinical trials6, 7, 8. However, given the high attrition rate of drug candidates during clinical development and the emergence of drug resistance, the discovery of additional clinical candidates is clearly needed. Here, we report on a promising class of imidazopyridine amide (IPA) compounds that block Mycobacterium tuberculosis growth by targeting the respiratory cytochrome bc1 complex. The optimized IPA compound Q203 inhibited the growth of MDR and XDR M. tuberculosis clinical isolates in culture broth medium in the low nanomolar range and was efficacious in a mouse model of tuberculosis at a dose less than 1 mg per kg body weight, which highlights the potency of this compound. In addition, Q203 displays pharmacokinetic and safety profiles compatible with once-daily dosing. Together, our data indicate that Q203 is a promising new clinical candidate for the treatment of tuberculosis