Recurrent posterior dislocation following primary posterior-stabilized total knee arthroplasty

In our series of 136 patients with primary total knee arthroplasty using posterior-stabilized prosthesis, a female patient with Parkinson disease developed posterior dislocation of the knee 9 months after surgery. Eventually, the dislocation became recurrent, occurring several times a day. The patient made the reposition always by herself. Two months after the first dislocation, we performed the revision of the polyethylene tibial insert and found wearing of the tibial insert's cam as an hitherto unreported cause of the mechanical instability of the total knee prosthesis.     

Lid retraction etiology

The upper lid position is abnormal if it exposes a white band of sclera between the lid margin and the upper corneal limbus while the retracted lower lid lies below the inferior corneal margin and is tethered to the orbital margin. Lid retraction is a sign of many congenital and acquired diseases and is characterised by multifactorial etiology. The aim of this study was to discuss the etiology of lid retraction divided into four categories: neurogenic, myogenic, mechanical and miscellaneous, what suggests a successful differential diagnostic and therapeutic approach.     

Neuropeptide Y in the female reproductive tract of the rat. Distribution of nerve fibres and motor effects

The spontaneous firing of single neurones in the region of the lateral reticular nucleus was the subject of a pharmacological study employing microiontophoretic and systemic application of adrenoceptor agonists and antagonists. Both iontophoretic noradrenaline and systemic clonidine depressed neuronal firing. The depressions were consistently reversed by the alpha-2 antagonist RX781094. Other adrenergic antagonists, prazosin and sotalol, were ineffective. The results suggest the existence of alpha-2 receptors in this region of the brain.     

Importance of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration

Paraneoplastic neurologic syndromes are disorders of the nervous system function caused by cancer but not due to metastatic disease, vascular or metabolic deficits, infections, nutritive deficiency, nor side effects of antineoplastic drugs or irradiation. Immunologic factors probably play the crucial role in the pathogenesis of paraneoplastic neurologic syndromes, but nonimmunologic mechanisms that include metabolic abnormalities and competition for substrate are also involved. Paraneoplastic cerebellar degeneration most commonly occurs in the setting of gynecologic cancers, but it accompanies the small-cell lung cancer too. Other tumors are infrequently associated with cerebellar degeneration. Several paraneoplastic antibodies have been identified in patients with paraneoplastic cerebellar degeneration. Their association with particular cancers may help identify an occult lesion. Anti-Yo antibodies are directed against Purkinje cell antigens and occur in patients with cerebellar degeneration who have breast cancer or gynecologic tumors. A target antigen of anti-Yo antibody is CDR2 protein that is normally expressed only in the brain and testis. Patients with paraneoplastic cerebellar degeneration present with dizziness, nausea and vomiting followed by gait instability, diplopia, gait and appendicular ataxia, dysarthria and dysphagia. Therapeutic options include tumor excision, chemotherapy and/or irradiation, and adjuvant therapy with glucocorticoids, immunoglobulins and plasmapheresis. The role of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration is still uncertain. Reports of its efficacy are anecdotal. We present patient with paraneoplastic cerebellar degeneration with positive anti-Yo antibodies and tumor of the ovaries whose neurologic status significantly improved after four daily plasmaphereses, which was accompanied by a fourfold decrease in the anti-Yo antibodies titer. Further investigations are needed to define a protocol for plasmapheresis in the treatment of patients with paraneoplastic syndromes.     

Dilemmas about the antenatal use of corticosteroids for prevention of neonatal morbidity and mortality

Neonatal respiratory distress syndrome (RDS) is one of the biggest problems in modern obstetrics. The incidence of RDS is 1%-2%. RDS is a condition of insufficient surfactant production. Surfactant is a complex molecule which is responsible for maturation of fetal lungs. The most important factor for insufficient surfactant production and pulmonary immaturity is shortening of gestation, i.e. preterm delivery. Antenatal corticosteroids for maturation of fetal lungs are in use for over thirty years. Corticosteroids decrease the incidence and intensity of RDS, the severity of intracerebral hemorrhage, and overall neonatal morbidity and mortality. The mechanism of corticosteroid action is probably induction of fetal pulmonary enzyme complex that is responsible for adequate surfactant production and regulation of pulmonary interstitial fluids. In this literature review, we analyze long- and short-term benefits and risks of single and multiple antenatal corticosteroid administration.