University of Iowa Hospitals and Clinics

About: University of Iowa Hospitals and Clinics is a healthcare organization based out in Iowa City, Iowa, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 7201 authors who have published 9476 publications receiving 276995 citations. The organization is also known as: University of Iowa Hospitals & Clinics.

Canal wall reconstruction tympanomastoidectomy with mastoid obliteration.

Abstract: Objectives: This study was designed to evaluate the authors' experience with canal wall reconstruction (CWR) tympanomastoidectomy with mastoid obliteration in the treatment of chronic otitis media with cholesteatoma. Study Design: Institutional review board approved retrospective case review. Methods: Retrospective review was performed of all patients undergoing CWR tympanomastoidectomy with mastoid obliteration from 1997 to 2004. Data included pre- and postoperative audiometry, findings at second look surgery with ossiculoplasty, and postoperative complications including wound infection and canal wall displacement. Results: One hundred thirty ears in 127 adults and children underwent the procedure. Mean time postoperative was 48 (range 2-94) months. A second look ossiculoplasty was performed in 102 (78%). Percentage of ears that remain safe without evidence of recurrence was 98.5. The postoperative infection rate decreased from an initial rate of 14.3% to 4.5% for the last 88 ears after protocol modification. Recurrence occurred in two (1.5%) patients, requiring conversion to a canal wall down mastoidectomy. Conclusions: A CWR technique can provide improved intraoperative exposure of the middle ear and mastoid without creating a mastoid bowl and reduces the incidence of recurrent disease. A single procedure is used for all patients with acquired cholesteatoma, including children.

Postoperative Complications of Posterior Ankle and Hindfoot Arthroscopy

Abstract: Background: Posterior ankle and hindfoot arthroscopy, performed with use of posteromedial and posterolateral portals with the patient in the prone position, has been utilized for the treatment of various disorders. However, there is limited literature addressing the postoperative complications of this procedure. In this study, the postoperative complications in patients treated with posterior ankle and hindfoot arthroscopy were analyzed to determine the type, rate, and severity of complications. Methods: The study included 189 ankles in 186 patients (eighty-two male and 104 female; mean age, 37.1 ± 16.4 years). The minimum duration of follow-up was six months, and the mean was 17 ± 13 months. The most common preoperative intra-articular diagnoses were subtalar osteoarthritis (forty-six ankles), an osteochondral lesion of the talus (forty-two), posterior ankle impingement (thirty-four), ankle osteoarthritis (twenty), and subtalar coalition (five). The most common extra-articular diagnoses were painful os trigonum (forty-six), flexor hallucis longus tendinitis (thirty-two), and insertional Achilles tendinitis (five). Results: The most common intra-articular procedures were osteochondral lesion debridement (forty-four ankles), subtalar debridement (thirty-eight), subtalar fusion (thirty-three), ankle debridement (thirty), and partial talectomy (nine). The most common extra-articular procedures were os trigonum excision (forty-eight), tenolysis of the flexor hallucis longus tendon (thirty-eight), and endoscopic partial calcanectomy (five). Complications were noted following sixteen procedures (8.5%); four patients had plantar numbness, three had sural nerve dysesthesia, four had Achilles tendon tightness, two had complex regional pain syndrome, two had an infection, and one had a cyst at the posteromedial portal. One case of plantar numbness and one case of sural nerve dysesthesia failed to resolve. Conclusions: Our experience demonstrated that posterior ankle and hindfoot arthroscopy can be performed with a low rate of major postoperative complications. Level of Evidence: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

The neuropathology of a chromosome 17-linked autosomal dominant parkinsonism and dementia ("pallido-ponto-nigral degeneration").

Abstract: A group of similar autosomal dominant hereditary neurodegenerative disorders have been linked to chromosome 17 in thirteen kindreds One of these disorders, known as pallido-ponto-nigral degeneration (PPND), is characterized by extensive degeneration of the globus pallidus and substantia nigra as well as accumulation of abnormally phosphorylated tau proteins The authors now present comprehensive data on the cellular and molecular pathology of PPND, allowing its classification among chromosome 17-linked neurodegenerative disorders as well as its classification among sporadic and other familial tauopathies First, we showed that PPND is characterized by abundant ballooned neurons in neocortical and subcortical regions as well as by tau-rich inclusions in the cytoplasm of neurons and oligodendroglia morphologically similar to those seen in corticobasal degeneration (CBD), but in a distribution pattern resembling progressive supranuclear palsy (PSP) Second, we demonstrated that antibodies to phosphorylation-independent (Alz50, 133, 304, Tau-2, T-46) as well as phosphorylation-dependent (AT8, PHF-6, 12E8, PHF-1, T3P, pS422) epitopes in human tau proteins stain these glial and neuronal inclusions as intensely as they stain CBD or PSP inclusions Third, we probed PPND brain by Western blots using some of the same anti-tau antibodies to reveal 2 tau immunobands with molecular weights of 69 kD and 64 kD in gray and white matter extracts, as reported for both PSP and CBD Finally, electron microscopy showed that these abnormal tau proteins formed flat twisted ribbons with a maximum diameter of 20 nanometers (nm) and a periodicity of about 200 nm, resembling those reported in CBD Based on this, we conclude that PPND is a hereditary neurodegenerative disorder characterized by neuronal and glial tau-rich inclusions formed from aggregated filaments and hyperphosphorylated tau proteins and, hence, can be subcategorized into the tauopathy group of chromosome 17-linked neurodegenerative disorders Further, since the morphologic and biochemical lesions of PPND overlap with those seen in sporadic CBD and PSP, we speculate that these disorders share common pathogenetic mechanisms