Does thrombolysis for pulmonary embolism reduce the risk of chronic complications?

We assessed the efficacy of thrombolysis in avoiding long-term complications. Notes of patients thrombolysed for PE in the 2-year period were reviewed. The initial CTPA and echocardiogram results before thrombolysis were compared to the results of follow up imaging repeated after 6 months. Twenty-two patients were thrombolysed for PE. 14 patients had sub-massive PE and 8 patients had massive PE. The right ventricle (RV) was dilated on pre-thrombolysis echocardiogram in 16 patients. On follow up echocardiography all patients with massive PE (6 studies) had a normal RV size, with pulmonary artery pressures (PAP) of 29mmHg. Follow up echocardiography of patients with submassive PE (13 studies) showed 11 patients with a normal RV, with PAP of 28 mmHg.

Voice emotion perception and production in cochlear implant users.

Voice emotion is a fundamental component of human social interaction and social development. Unfortunately, cochlear implant users are often forced to interface with highly degraded prosodic cues as a result of device constraints in extraction, processing, and transmission. As such, individuals with cochlear implants frequently demonstrate significant difficulty in recognizing voice emotions in comparison to their normal hearing counterparts. Cochlear implant-mediated perception and production of voice emotion is an important but relatively understudied area of research. However, a rich understanding of the voice emotion auditory processing offers opportunities to improve upon CI biomedical design and to develop training programs benefiting CI performance. In this review, we will address the issues, current literature, and future directions for improved voice emotion processing in cochlear implant users.

High-resolution secondary reconstructions with the use of flat panel CT in the clinical assessment of patients with cochlear implants.

Radiologic assessment of cochlear implants can be limited because of metallic streak artifacts and the high attenuation of the temporal bones. We report on 14 patients with 18 cochlear implants (17 Med-El standard 31.5-mm arrays, 1 Med-El medium 24-mm array) who underwent flat panel CT with the use of high-resolution secondary reconstruction techniques. Flat panel CT depicted the insertion site, cochlear implant course, and all 216 individual electrode contacts. The calculated mean angular insertion depth for standard arrays was 591.9° (SD = 70.9; range, 280°). High-resolution secondary reconstructions of the initial flat panel CT dataset, by use of a manually generated field of view, Hounsfield unit kernel type, and sharp image characteristics, provided high-quality images with improved spatial resolution. Flat panel CT is a promising imaging tool for the postoperative evaluation of cochlear implant placement.

Middle ear adenoma: a challenging diagnosis.

Middle ear adenomas are rare benign tumors, which can easily be mistaken for other conditions radiologically. They derive from the middle ear mucosa. We report the case of a 48-year-old man with a history of decreased left-sided hearing and intermittent pulsatile tinnitus. High-resolution CT of the temporal bones revealed a well-defined left middle ear soft-tissue attenuation abutting the head of the malleus. Surgical excision revealed a middle ear adenoma.

Benign positional vertigo after cochlear implantation.

OBJECTIVE: To identify patients who underwent cochlear implantation (CI) and who subsequently developed benign positional vertigo (BPV) after the procedure and to identify any contributing factors. STUDY DESIGN AND SETTING: Academic tertiary referral center. Cochlear implant recipients' medical records were retrospectively reviewed to identify patients with both vertigo and, more specifically, BPV. Preoperative, intraoperative, and postoperative factors were studied vis-a-vis the development of BPV. RESULTS: BPV was newly diagnosed in 12 patients after CI. The etiology of hearing loss included presbycusis (16.6%), autoimmune inner ear disease (16.6%), congenital hearing loss (41.6%), Meniere's disease (8.3%), prematurity (8.3%), and idiopathic factors (8.3%). The onset of BPV varied after the procedure (mean +/- SD, 292 +/- 309 days). BPV symptoms did not affect implant performance. All patients were treated for BPV by Epley's maneuver and vestibular exercises. Symptoms disappeared in 11 patients and persisted in 1. CONCLUSIONS: BPV is an uncommon development after CI, although it occurs more frequently than in the general population. Two theories are proposed: the introduction of bone dust into the labyrinth and the dislodging of otoconia during surgery. The diagnosis, treatment, and prognosis of BPV after CI do not differ from those for non-CI-associated BPV. SIGNIFICANCE: Dizziness after CI usually develops as a result of vestibular hypofunction. BPV, which is a hyperfunctioning form of vestibular dysfunction, should be recognized as a possible sequelae of CI.

Targeted disruption of the Kvlqt1 gene causes deafness and gastric hyperplasia in mice.

The KvLQT1 gene encodes a voltage-gated potassium channel. Mutations in KvLQT1 underlie the dominantly transmitted Ward-Romano long QT syndrome, which causes cardiac arrhythmia, and the recessively transmitted Jervell and Lange-Nielsen syndrome, which causes both cardiac arrhythmia and congenital deafness. KvLQT1 is also disrupted by balanced germline chromosomal rearrangements in patients with Beckwith-Wiedemann syndrome (BWS), which causes prenatal overgrowth and cancer. Because of the diverse human disorders and organ systems affected by this gene, we developed an animal model by inactivating the murine Kvlqt1. No electrocardiographic abnormalities were observed. However, homozygous mice exhibited complete deafness, as well as circular movement and repetitive falling, suggesting imbalance. Histochemical study revealed severe anatomic disruption of the cochlear and vestibular end organs, suggesting that Kvlqt1 is essential for normal development of the inner ear. Surprisingly, homozygous mice also displayed threefold enlargement by weight of the stomach resulting from mucous neck cell hyperplasia. Finally, there were no features of BWS, suggesting that Kvlqt1 is not responsible for BWS.

Augmentation of alimentary insulin secretion despite similar gastric inhibitory peptide (GIP) responses in juvenile obesity.

Insulin secretion rates are greater after oral glucose than after parenteral administration of an equivalent glucose load. This augmented beta-cell secretory response to an oral glucose load results from the release of mainly two gut hormones: gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1, which potentiate glucose-induced insulin secretion. Because of their insulinotropic action, their abnormal secretion may be involved in the pathogenesis of the hyperinsulinemia of childhood obesity. In this study, we used the hyperglycemic clamp with a small oral glucose load to assess the effect of childhood obesity on GIP response in seven prepubertal lean and 11 prepubertal obese children and in 14 lean adolescents and 10 obese adolescents. Plasma glucose was acutely raised to 11 mM by infusing i.v. glucose and kept at this concentration for 180 min. Each subject ingested oral glucose (30 g) at 120 min, and the glucose infusion was adjusted to maintain the plasma glucose plateau. Basal insulin and C-peptide concentrations and insulin secretion rates (calculated by the deconvolution method) were significantly greater in obese children compared with lean children (p < 0.001). Similarly, during the first 120 min of the clamp, insulin secretion rates were higher in obese than lean children. After oral glucose, plasma insulin, C-peptide, and insulin secretion rates further increased in all four groups. This incretin effect was 2-fold greater in obese versus lean adolescents (p < 0.001). Circulating plasma GIP concentrations were similar at baseline in all four groups and remained unchanged during the first 120 min of the clamp. After oral glucose, plasma GIP concentrations rose sharply in all groups (p < 0.002). Of note, the rise in GIP was similar in both lean and obese children. In conclusion, under conditions of stable hyperglycemia, the ingestion of a small amount of glucose elicited equivalent GIP responses in both lean and obese children. However, despite similar GIP responses, insulin secretion was markedly augmented in obese adolescents. Thus, in juvenile obesity, excessive alimentary beta-cell stimulation may be independent of the increased release of GIP.

Intracanalicular schwannoma of the facial nerve: a manifestation of neurofibromatosis type 2.

Primary facial nerve tumors, which are relatively uncommon, can present a diagnostic dilemma based on their location and variable pattern of symptoms. Of primary cranial nerve tumors, schwannomas of the facial nerve rank third in frequency after those of the eighth and fifth cranial nerves. We report an illustrative case of an intracanalicular schwannoma associated with several central nervous system tumors, consistent with neurofibromatosis type 2. Initially assumed to be an eighth cranial nerve tumor, the schwannoma was found intraoperatively to arise from the facial nerve. Early diagnosis and treatment enabled excision of the tumor without sacrifice of the facial nerve. Facial nerve schwannomas can resemble acoustic schwannomas in their clinical presentation. Only a heightened level of clinical vigilance will point to the correct diagnosis and result in an optimal therapeutic outcome for patients with these rare tumors.

Development of primary axosomatic endings in the anteroventral cochlear nucleus of mice.

The endbulb of Held is a large synaptic ending that arises from the myelinated auditory nerve fibers. Endbulbs exhibit an elaborate pattern of terminal branching and produce extensive contact with the postsynaptic cell body. These structural features appear to underlie the tight coupling between presynaptic activity and postsynaptic spike discharges. As a first step toward understanding the relationship between environmental sounds and the development of these neural elements, we examined the age-related changes in the morphology of endbulbs of Held in CBA/J mice, a strain known to retain good hearing throughout life. Neurobiotin was injected into the modiolus of the cochlea in CBA/J mice ranging in age from postnatal day 1 to 7 months. Light microscopic analyses suggest that endbulbs of the CBA/J mice develop from small bouton endings at birth into large, highly branched structures in adults. This increase in structural complexity occurs mostly during the second through eighth postnatal weeks, and general stages of development can be defined. In addition, we compared endbulb structure between adult CBA/J mice and adult shaker-2 mice (Myo15sh2/sh2) and heterozygous littermates (Myo15+/sh2). The shaker-2 mouse carries a mutated myosin 15 gene that results in congenital deafness, presumably due to abnormally short stereocilia in hair cell receptors. Neurobiotin was injected into the modiolus of adult CBA/J, Myo15sh2/sh2, and Myo15+/sh2 mice. Endbulbs of deaf adult Myo15sh2/sh2 mice exhibited a striking reduction in terminal branching compared with those of CBA/J and Myo15+/sh2 mice. Notably, the abnormal endbulbs of Myo15sh2/sh2 mice do not resemble immature endbulbs of normal-hearing mice, suggesting that deafness does not simply arrest development.

Comparison of optokinetic nystagmus elicited by full versus partial visual field stimulation: diagnostic implications.

Optokinetic nystagmus (OKN) testing is one method to determine central vestibular dysfunction. OKN may be elicited by partial visual field stimulation with a light bar (OKN-ENG) or by full visual field stimulation with rotating stripes in a rotational chair test booth (OKN-RVT). OKN-ENG and OKN-RVT were elicited in 36 healthy subjects and 48 patients with known peripheral or central vestibular disorders. Abnormal test results suggested central pathology in 29 of 36 healthy subjects with OKN-ENG versus 1 of 36 with OKN-RVT. Twenty-eight of 33 patients with peripheral pathology demonstrated abnormal OKN-ENG findings, whereas 4 of 33 had abnormal OKN-RVT results. Thirteen of 15 patients with central vestibular disorders had abnormal OKN-ENG, whereas 7 of 15 had abnormal OKN-RVT. Sensitivity and specificity of OKN-ENG were 86.7% and 17.4% versus 46.7% and 92.7%, respectively, for OKN-RVT. These findings were statistically significant (P < 0.00001). OKN elicited by full visual field stimulation (OKN-RVT) is a more accurate indicator of central disease than OKN elicited by partial visual field stimulation (OKN-ENG). The use of OKN-ENG to identify central vestibular dysfunction is questionable.

Acute incretin response to oral glucose is associated with stimulation of gastric inhibitory polypeptide, not glucagon-like peptide in young subjects.

Oral glucose induces a greater insulin response than i.v. glucose, a difference apparently due to the secretion of gut factors ("incretins"). Studies examining the mechanisms of this finding in human subjects are limited, however, because of differences in glucose profiles. To overcome this obstacle, we studied eight young nonobese subjects using the hyperglycemic clamp with and without superimposed ingestion of oral glucose. In both studies, glucose was acutely raised by 12.5 mg/dL above fasting values by the infusion of i.v. glucose and maintained at this level for 180 min. During the experimental study, but not the control, each subject ingested oral glucose (30 g) at 120 min, and the glucose infusion was adjusted to maintain the plasma glucose plateau. Plasma insulin responses were nearly identical during both studies until oral glucose was added. After oral glucose, both plasma insulin and C-peptide levels sharply increased by 45-55% above control values (p < 0.001), indicating a potentiation of insulin secretion rather than decreased hepatic extraction of insulin. Plasma gastric inhibitory polypeptide (GIP) levels increased significantly in response to oral glucose, whereas plasma levels of glucagon-like peptide-1 (7-37) were not affected. The time course of the rise in plasma GIP and insulin was nearly identical. We conclude that the GIP response to a modest oral glucose load may play an important physiologic role in glucose-stimulated insulin secretion in healthy young subjects.

Central adiposity and its metabolic correlates in obese adolescent girls.

To establish whether alterations in insulin action and secretion and their relationship to body fat distribution occur early in the course of developing obesity, we studied 14 obese adolescent girls [13.2 +/- 0.7 yr, body mass index (BMI) 32 +/- 1.4], 16 nonobese young women (24.0 +/- 0.6 yr, BMI 21.0 +/- 0.9). Insulin action was assessed by a sequential two-step (8 and 40 mU,m-2.min-1) euglycemic insulin clamp in combination with [1-13C]glucose and indirect calorimetry. Insulin secretion was determined by the hyperglycemic clamp technique (6.9 mmol/l). Magnetic resonance imaging was used to quantify visceral and subcutaneous abdominal fat depots. In obese girls, an impairment in glucose disposal was present with both insulin doses; at the higher dose, rates of glucose uptake were reduced by 30% in nonobese girls (240 +/- 30 vs. 340 +/- 19 mg.m-2.min-1, P < 0.05) and by an additional 29% (170 +/- 17 mg.m-2.min-1, P < 0.05) in obese girls. Insulin infusion failed to stimulate glucose oxidation and to suppress lipid oxidation only in obese girls. Suppression of free fatty acid levels, but not hepatic glucose production, was decreased in obese girls compared with controls. Fasting and glucose-stimulated insulin responses were greater in obese than in nonobese adolescents, who, in turn, had greater responses than lean women. In obese girls, visceral fat, but neither waist-to-hip circumference ratio nor subcutaneous fat, was highly correlated with basal insulin secretion (r = 0.89, P < 0.001), stimulated insulin secretion (r = 0.61, P < 0.05), and insulin resistance (r = -0.87, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Anencephaly: changes in prenatal detection and birth status, 1972 through 1990.

OBJECTIVE: We assessed at a large university hospital the effect of prenatal diagnosis on the birth of infants with anencephaly between 1972 and 1990. STUDY DESIGN: All 175 affected infants were identified by a postnatal Malformations Surveillance Program, which included stillborn infants and elective terminations in the second trimester. The affected infants were subdivided into those whose mothers had always planned delivery at this hospital (nontransfers) and those whose mothers had planned delivery elsewhere but were transferred after the prenatal detection of the fetal abnormality (transfers). RESULTS: In the 1970s half the infants were anencephaly were born alive; the average gestational age was 35.6 weeks, and only a few were diagnosed prenatally. By 1988 to 1990 all affected infants were diagnosed either by prenatal ultrasonography or as the result of maternal serum alpha-fetoprotein screening; the parents elected to terminate the pregnancies, and the average gestational age was 19.6 weeks. CONCLUSION: Prenatal detection and the selection by parents of the option of elective termination of pregnancy has altered significantly the birth status of infants with anencephaly since 1972.