Paroxysmal positional vertigo as a complication of osteotome sinus floor elevation

Paroxysmal positional vertigo (PPV) is a high prevalence, vestibular end organ disorder due to the detachment of the utricular otoconia floating in the posterior or lateral semicircular canal. Even though in the majority of cases the etiology of PPV is unknown, it may follow viral infection, vascular disorders and head trauma after different surgical procedures. The aim of this study was to investigate the correlation between PPV and the surgical trauma induced by the vibratory and percussive forces on the upper maxilla during the osteotome sinus floor elevation procedure. We performed a complete otoneurological examination on 146 patients affected by atrophic ridges before and after upper maxilla surgery. Four patients showed a PPV of the posterior semicircular canal controlateral to the implanted side 1 or 2 days after the surgical procedure, which promptly was solved with the Epley re-positioning maneuver. We hypothesize that the surgical trauma, and specifically the pressure exerted by the osteotomes, determines the detachment of the otoliths from the utricular macula while the patient head position, hyper-extended and tilted opposite to the side where the surgeon is working, favors the entry of these free-floating particles in the posterior semicircular canal of the implanted side. Although this disease is rather frequent in the normal population and it is a benign, self-limiting peripheral disorder, it should be considered by the oral surgeon as a possible complication of pre-prosthetic upper maxilla surgery, and the patient should be informed before undergoing surgery.     

Human immunodeficiency virus infection and acquired immunodeficiency syndrome dementia complex: role of cells of monocyte-macrophage lineage

The entry of human immunodeficiency virus (HIV) into the central nervous system (CNS) causes both the establishment of a lifelong viral reservoir in the brain and symptoms of neurological dysfunction that have an AIDS dementia complex (ADC) clinical appearance. Neurological dysfunction in ADC patients still remains an unresolved problem. However, ADC pathogenesis may be a multistep process that starts with HIV invasion of CNS by crossing the blood-brain barrier (BBB). It progresses by developing a chronic inflammatory status that can cause dysfunction in neurons and astrocytes that result in apoptotic death. Monocytes-macrophages (M/M) may play an important role by concealing the HIV transfer across the BBB. Furthermore, HIV-infected M/M could produce and release neurotoxic factors. In this review the main mediators and cells involved in pathogenesis and development of ADC are highlighted. A better understanding of the mechanisms involved in this process may help in a successful therapeutic approach to the neuropathogenesis of HIV infection.     

Colorectal cancer with neuroendocrine differentiation in a child

Colorectal cancer is extremely rare in children and presents with a poor prognosis because of the delay in diagnosis and lack of histological differentiation. We report a case of a sigmoid colon carcinoma with areas of neuroendocrine cells in a 12-year-old patient without familial occurrence of colorectal cancer. Symptoms at presentation were anaemia, anorexia, abdominal pain and weight loss. The patient was treated with radical resection and adjuvant chemotherapy. One year later, a local recurrence and hepatic metastases were diagnosed and she underwent chemotherapy and surgical resection. Twenty-six months from initial diagnosis she is alive with evidence of disease. The clinical presentation, diagnosis and treatment of the previously reported cases of colorectal cancer in children are also reviewed.     

Current perspective on the pathogenesis of central diabetes insipidus

Diabetes insipidus is a heterogeneous condition characterised by polyuria and polydipsia caused by a lack of secretion of vasopressin, its physiological suppression following excessive water intake, or kidney resistance to its action. The clinical and laboratory diagnosis is confirmed by standard tests, but recent advances in molecular biology and imaging techniques have shed new light on the pathophysiology of this disease. In many patients, central diabetes insipidus is caused by a germinoma or craniopharyngioma; Langerhans' cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma from surgery or accident; and, rarely, genetic defects in vasopressin biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Tumour-associated central diabetes insipidus is uncommon in children younger than 5 years old. Biopsy of enlarged pituitary stalk should be reserved for patients with hypothalamic-pituitary mass and progressive thickening of the pituitary stalk since spontaneous recovery may occur. Molecular biology in selected patients may identify those with apparently idiopathic diabetes insipidus carrying the vasopressin-neurophysin II gene mutation.     

Maternal position during non-stress test and fetal heart rate patterns

OBJECTIVE: The aim of the study was to determinate whether maternal position during the non-stress test (NST) in different weeks of pregnancy influences fetal heart rate patterns. MATERIALS AND METHODS: A total of 1055 NST lasting 30 min were performed in 368 autochthonous mothers with low-risk pregnancies. On the basis of maternal position during the test we divided into three groups: reclining, sitting, and walking. The cardiotocographic parameters considered were: number of minutes of reactive NST with minimum length, number of fetal movements, fetal heart rate baseline, number of large accelerations, number of dubious NST, and number of variable decelerations. RESULTS: Fetal heart rate patterns in low-risk pregnancies were studied using NST in different gestational ages and in different maternal positions. Differences in heart rate were found in relationship to both gestational age and maternal position. The minimum length of NST necessary to record at least three large accelerations was significantly different in relationship to both gestational age and maternal position. The number of fetal movements perceived by the mother was greater in the reclining position than in sitting or walking. Together with the progression of pregnancy, the number of dubious NST decreased in all subgroups, especially in the sitting position. The greatest number of variable decelerations was observed in the reclining position and it was increased with pregnancy progression. The NST duration did not vary greatly in the reclining position, but in the sitting position or during walking, the time taken to record the three large accelerations required to define the trace as reactive, decreased significantly with the progression of pregnancy CONCLUSIONS: Non-stress test in sitting position or during walking should be encouraged because fetal reactivity is more quickly observed.     

Prevalence and clinical significance of left atrial remodeling in competitive athletes

OBJECTIVES: In the present study we assessed the distribution and clinical significance of left atrial (LA) size in the context of athlete's heart and the differential diagnosis from structural heart disease, as well as the proclivity to supraventricular arrhythmias. BACKGROUND: The prevalence, clinical significance, and long-term arrhythmic consequences of LA enlargement in competitive athletes are unresolved. METHODS: We assessed LA dimension and the prevalence of supraventricular tachyarrhythmias in 1,777 competitive athletes (71% of whom were males), free of structural cardiovascular disease, that were participating in 38 different sports. RESULTS: The LA dimension was 23 to 50 mm (mean, 37 +/- 4 mm) in men and 20 to 46 mm (mean, 32 +/- 4 mm) in women and was enlarged (i.e., transverse dimension > or = 40 mm) in 347 athletes (20%), including 38 (2%) with marked dilation (> or = 45 mm). Of the 1,777 athletes, only 14 (0.8%) had documented, symptomatic episodes of either paroxysmal atrial fibrillation (n = 5; 0.3%) or supraventricular tachycardia (n = 9; 0.5%), which together occurred in a similar proportion in athletes with (0.9%) or without (0.8%; p = NS) LA enlargement. Multivariate regression analysis showed LA enlargement in athletes was largely explained by left ventricular cavity enlargement (R2 = 0.53) and participation in dynamic sports (such as cycling, rowing/canoeing) but minimally by body size. CONCLUSIONS: In a large population of highly trained athletes, enlarged LA dimension > or = 40 mm was relatively common (20%), with the upper limits of 45 mm in women and 50 mm in men distinguishing physiologic cardiac remodeling ("athlete's heart") from pathologic cardiac conditions. Atrial fibrillation and other supraventricular tachyarrhythmias proved to be uncommon (prevalence < 1%) and similar to that in the general population, despite the frequency of LA enlargement. Left atrial remodeling in competitive athletes may be regarded as a physiologic adaptation to exercise conditioning, largely without adverse clinical consequences.