A Posterior Interosseous Nerve Syndrome Associated With Spontaneous Rupture of the Extensor Pollicis Longus Tendon

Posterior interosseous nerve entrapment syndrome and spontaneous rupture of the extensor pollicis longus tendon are rare conditions. The authors describe the bizarre combination of a spontaneous rupture of the extensor pollicis longus tendon in a 82-year-old lady with a posterior interosseous nerve syndrome. As far as the authors know, this is the first description of such an association in the literature. Surgical exploration revealed compression of the posterior interosseous nerve at the proximal portion of the supinator muscle and at Henry's leash. The nerve was freed, and the tendon of the extensor index proprius was transferred to the extensor pollicis longus. Six months after the procedure, the patient had resumed her daily activities, showing a good functional result.

Paralisia Facial: Técnicas de Reconstrução Neuro-Muscular

Several surgical procedures have been proposed through the years for the treatment of facial paralysis. The multiplicity and diversity of techniques portray the complexity and challenge represented by this pathology. Two basic dynamic options are available: -Reconstruction of nerve continuity through direct micro suture, with interposition grafts or nerve transpositions. -Regional muscular transposition, most often using the temporalis. Facial reanimation with the temporalis transfer has withstood the test of time and still is a reference technique. In a few weeks, good results can be obtained with a single and rather simple surgical procedure. Functional free flaps have been used with increasing frequency in the last two decades, most often combining a cross-facial nerve graft followed by a gracilis free flap nine months later. With this method there is a potential for restoration of spontaneous facial mimetic function. Apparently there is a limit in microsurgical technique and expertise beyond which there is no clear improvement in nerve regeneration. Current research is now actively studying and identifying nerve growth factors and pharmacological agents that might have an important and complementary role in the near future.

Lack of Spontaneous Venous Pulsation: Possible Risk Indicator in Normal Tension Glaucoma?

PURPOSE: Recently, the absence of spontaneous venous pulsation (SVP) has been suggested as a vascular risk factor for primary open-angle glaucoma (POAG). As the mechanism behind this phenomenon is still unknown, the authors have studied this vascular component using colour Doppler imaging (CDI). METHODS: A total of 236 patients were divided into three diagnostic groups: healthy controls (81), POAG (86) and normal tension glaucoma (NTG; 69). All subjects were submitted to CDI studies of the retrobulbar circulation, intraocular pressure measurements and assessment of SVP existence. Mann-Whitney, chi-square contingency tables and Spearman correlations were used to explore differences and correlations between variables in the diagnostic groups. RESULTS: Eighty-two percent of healthy controls had SVP (66/81), while a smaller numbers were registered in both glaucoma groups: POAG - 50% (43/86); NTG - 51% (35/69). In NTG patients, but not in POAG patients, the prevalence of the SVP phenomenon decreases with increased glaucoma damage (p = 0.04; p = 0.55, respectively). Overall glaucoma patients from both groups had lower central retinal vein (CRV) velocities than the healthy controls (p < 0.05). NTG patients with SVP had less severe visual field defects (mean defect -6.92 versus -11.1, p < 0.05), higher [correction added after online publication 21 September 2012; the word 'higher' has been inserted to replace the word 'lower'] peak systolic and mean flow velocities in the central retinal artery (p < 0.01; p < 0.05, respectively) as well as higher [correction added after online publication 21 September 2012; the word higher has been inserted to replace the word lower] maximal velocities and RI of the CRV (p < 0.02; p < 0.05, respectively). CONCLUSIONS: Glaucoma patients have a decrease in CRV velocities. SVP is less prevalent in glaucoma patients than in healthy individuals. This phenomenon apparently reflects different hemodynamic patterns in the central retinal vessels. This variable may be of particular importance in NTG patients, where it may be associated with more advanced functional damage.