The immediate and subsequent impact of a first-time traumatic anterior shoulder dislocation in people aged 16-40: Results from a national cohort study.

BACKGROUND: Limited evidence exists which details changes in quality of life, shoulder activity level, kinesiophobia, shoulder pain and disability following a first-time traumatic anterior shoulder dislocation (FTASD) in people treated non-operatively. This study had three objectives: (1) to examine quality of life, pain, disability and kinesiophobia after an FTASD within 12 weeks, (2) to examine whether these variables were different in people with and without recurrent shoulder instability and (3) to assess how these variables changed over 12 months. METHODS: A prospective cohort study was undertaken in people with an FTASD aged between 16 and 40 years. Measures of quality of life, kinesiophobia, shoulder activity, shoulder pain and disability were recorded within 12 weeks of an FTASD and at 3, 6, 9 and 12 months. RESULTS: An FTASD negatively impacted quality of life, shoulder pain and function and these variables improved over time. People with recurrent shoulder instability had poorer quality of life 12 months after an FTASD. Across the entire cohort, kinesiophobia did not significantly change across time in people following an FTASD. CONCLUSIONS: Quality of life was significantly affected by an FTASD in people with recurrent shoulder instability. Across the entire cohort of people with an FTASD, kinesiophobia remained elevated in people following an FTASD. LEVEL OF EVIDENCE: Level 1 prognostic study.

In children 18 years and under, what promotes recurrent shoulder instability after traumatic anterior shoulder dislocation? A systematic review and meta-analysis of risk factors.

BACKGROUND: Skeletal maturity and age-related changes in the composition of the glenoid labrum and joint capsule may influence rates of recurrent instability in children. We systematically review risk factors which predispose children to recurrent shoulder instability. METHODS: The systematic review-concerned studies published before May 2015. Statistical analysis was undertaken to compare rates of recurrence for each extracted risk factor. Pooled ORs were analysed using random effects meta-analysis. RESULTS: 6 retrospective cohort studies met the inclusion criteria. 8 risk factors were identified across the studies including age, sex, shoulder dominance and injury side, mechanism of injury, state of physis closure, and Hill-Sachs and Bankart lesions. The rate of recurrent instability was 73%. Children aged 14-18 years were 24 times more likely to experience recurrent instability than children aged 13 years and less (93% vs 40%; OR=24.14, 95% CI (3.71 to 156.99), Z=3.33, p=0.001, I(2)=6.83%). There was a non-significant trend indicating males were 3.4 times more likely to experience recurrent instability (OR=3.44, 95% CI (0.98 to 12.06), Z=1.93, p=0.053, I(2)=0%). Analysis of one study found that children with a closed physis are 14 times more likely to experience recurrent instability compared with those with an open physis (OR=14.0, 95% CI (1.46 to 134.25), Z=2.29, p=0.02, I(2)=0%) . CONCLUSIONS: Male children aged 14 years and over had the greatest risk of recurrent shoulder instability following a first-time traumatic anterior shoulder dislocation. This meta-analysis summarises a mix of 6 acceptable and poor quality level III retrospective cohort studies. Further examination of this population with blinded prospective cohort studies will assist clinicians in the appropriate management of first-time traumatic anterior shoulder dislocation.

Risk factors which predispose first-time traumatic anterior shoulder dislocations to recurrent instability in adults: a systematic review and meta-analysis.

BACKGROUND: Recurrent instability following a first-time anterior traumatic shoulder dislocation may exceed 26%. We systematically reviewed risk factors which predispose this population to events of recurrence. METHODS: A systematic review of studies published before 1 July 2014. Risk factors which predispose recurrence following a first-time traumatic anterior shoulder dislocation were documented and rates of recurrence were compared. Pooled ORs were analysed using random-effects meta-analysis. RESULTS: Ten studies comprising 1324 participants met the criteria for inclusion. Recurrent instability following a first-time traumatic anterior shoulder dislocation was 39%. Increased risk of recurrent instability was reported in people aged 40 years and under (OR=13.46), in men (OR=3.18) and in people with hyperlaxity (OR=2.68). Decreased risk of recurrent instability was reported in people with a greater tuberosity fracture (OR=0.13). The rate of recurrent instability decreased as time from the initial dislocation increased. Other factors such as a bony Bankart lesion, nerve palsy and occupation influenced rates of recurrent instability. CONCLUSIONS: Sex, age at initial dislocation, time from initial dislocation, hyperlaxity and greater tuberosity fractures were key risk factors in at least two good quality cohort studies resulting in strong evidence as concluded in the GRADE criteria. Although bony Bankart lesions, Hill Sachs lesions, occupation, physiotherapy treatment and nerve palsy were risk factors for recurrent instability, the evidence was weak using the GRADE criteria-these findings relied on poorer quality studies or were inconsistent among studies.

Efficacy and safety of briakinumab vs. etanercept and placebo in patients with moderate to severe chronic plaque psoriasis.

BACKGROUND: The anti-interleukin-12/23p40 monoclonal antibody briakinumab has been shown in a phase II study to be effective psoriasis treatment. OBJECTIVES: The aim of the current study was to assess the efficacy, safety and tolerability of briakinumab compared with etanercept and placebo in patients with moderate to severe chronic plaque psoriasis. METHODS: In this phase III, 12-week study (M10-114, NCT00691964), 347 patients were randomized in a 2 : 2 : 1 ratio to receive 200 mg briakinumab at weeks 0 and 4 followed by 100 mg briakinumab at week 8 (n = 138); 50 mg of etanercept twice weekly 3-4 days apart at weeks 0-11 (n = 141); or placebo injections matching active treatment (n = 68). The co-primary efficacy endpoints were the proportion of patients achieving a Physician's Global Assessment (PGA) of 0/1 at week 12, and the proportion of patients achieving a Psoriasis Area and Severity Index (PASI) 75 response at week 12. RESULTS: Of the briakinumab-treated patients, 71·0% achieved a PGA of 0/1 at week 12 as compared with 39·7% of etanercept-treated patients and 2·9% of placebo-treated patients, (P < 0·001, for both comparisons). Of the briakinumab-treated patients 81·9% achieved a PASI 75 response at week 12 as compared with 56·0% of etanercept-treated and 7·4% of placebo-treated patients (P < 0·001, for both comparisons). Serious adverse event rates were reported in four (2·9%) patients receiving briakinumab, one (0·7%) patient receiving etanercept and one (1·5%) placebo-treated patient. CONCLUSIONS: In patients with moderate to severe psoriasis, briakinumab had superior efficacy to both placebo and etanercept at 12 weeks as administered in this study.

Efficacy and safety results from a phase III, randomized controlled trial comparing the safety and efficacy of briakinumab with etanercept and placebo in patients with moderate to severe chronic plaque psoriasis.

BACKGROUND: The tumour necrosis factor-α antagonist etanercept and the interleukin (IL)-12/23p40 antagonist ustekinumab have been shown to be effective psoriasis therapies. The IL-12/23p40 antagonist briakinumab was shown to be effective psoriasis treatment in a phase II study. OBJECTIVES: To assess the efficacy, safety and tolerability of briakinumab compared with etanercept and placebo in patients with moderate to severe psoriasis. METHODS: Three hundred and fifty patients were enrolled in this phase III, 12-week study (M10-315, NCT00710580) and randomized in the following 2:2:1 ratio: 139 patients received 200 mg briakinumab at weeks 0 and 4 followed by 100 mg briakinumab at week 8; 139 patients received 50 mg of etanercept twice weekly 3-4 days apart at weeks 0-11; 72 patients received placebo injections matching active treatment. The co-primary efficacy endpoints were the proportion of patients achieving a Physician's Global Assessment (PGA) of 0/1 at week 12, and the proportion of patients achieving a Psoriasis Area and Severity Index (PASI) 75 response at week 12. RESULTS: Of the briakinumab-treated patients, 72·7% achieved a PGA of 0/1 at week 12 as compared with 29·5% of etanercept-treated patients and 4·2% of placebo-treated patients (P < 0·001, for both comparisons). Of the briakinumab-treated patients, 80·6% achieved a PASI 75 response at week 12 as compared with 39·6% of etanercept-treated and 6·9% of placebo-treated patients (P < 0·001, for both comparisons). Serious adverse events were reported in two (1·4%) briakinumab-treated patients, one (0·7%) etanercept-treated patient and two (2·8%) placebo-treated patients. CONCLUSIONS: In patients with moderate to severe psoriasis, briakinumab had superior efficacy to both placebo and etanercept at 12 weeks as administered in this study.

Relation between rotation in the 6-OHDA lesioned rat and dopamine loss in striatal and substantia nigra subregions.

The relation between the rotation response to drug-induced activation of the dopamine (DA) receptor in the rat unilaterally lesioned with 6-hydroxydopamine (6-OHDA) in the substantia nigra (SN) and the loss of DA in subregions of the SN and caudate-putamen (C/PUT) is not clear. Here this relation was examined in 23 rats classified as rotators to amphetamine (5 mg/kg). After their response was characterized in terms of ipsilateral rotation, contralateral rotation, and oral stereotypy in one place, they were divided into high, medium, low, and very low rotators. The loss of DA in each group was visualized on brain sections immunoreacted to tyrosine hydroxylase (TH). The density of the TH label on the side of the lesion was compared to that on the intact side. In the ventral midbrain, the density was determined in the SN subdivided into far lateral, lateral, central, and medial subregions and also in the ventral tegmental area (VTA). In the forebrain, it was determined in the C/PUT subdivided into lateral, central, and medial subregions and also in the nucleus accumbens (ACC). These measurements led to three principal findings. The first was a positive overall correlation between rotation and loss of TH label. The second was a correlation between rotation and penetration of the loss from the lateral subregions into more medial areas. The third was a larger loss in SN and VTA (midbrain) than in C/PUT and ACC (forebrain). These findings show that rotation depended not only on the overall loss of DA but also on its distribution across subregions. The loss in the lateral subregion, always the largest regardless of the rate of rotation, may have been the first step in inducing the motor abnormality, and the loss in the central and medial subregions may have served to enhance the abnormality due to the loss in the lateral subregion.

Behavioral and anatomical effects of quinolinic acid in the striatum of the hemiparkinsonian rat.

Parkinson's disease (PD), a hypokinetic disorder, and Huntington's disease (HD), a hyperkinetic disorder, share the fact that in the motor pathways the dysfunction starts in the striatum. In PD the projection neurons are overactive due to decreased inhibitory regulation by lost dopamine afferents, while in HD the output from the striatum is insufficient due to loss of projection neurons. This study aimed to determine whether the introduction of a mild HD condition in the PD striatum can counter the hypokinetic condition. The experiment was carried out in the 6-OHDA rat model for PD in which amphetamine, 5 mg/kg, evokes an asymmetric rotation response toward the side of the 6-OHDA lesion (ipsilateral rotation). The response to amphetamine in this study was fractionated into multiple components and measured automatically. After baseline measurements, the subjects were divided into four groups. Group I was unilaterally sham-lesioned in medial, central, and lateral striatum. Group II was injected quinolinic acid (QA) 20 nM in medial, central, and lateral striatum. Group III was injected QA 60 nM in central striatum. Group IV was injected QA 120 nM in central striatum. The effects of QA were measured weekly. The sham lesions in Group I had no effects. In Group II, ipsilateral rotation was reduced and replaced by oral stereotypy, a competitive behavior. In Group III, ipsilateral rotation decreased, but to a lesser degree than in Group II. In Group IV, QA had no effects. Histological findings show a unilateral loss of tyrosine immunoreactive (TH) neurons in substantia nigra and of fibers in striatum in all subjects. In addition, in Group II the striatum was atrophied. These findings suggest that the shift in Group II from ipsilateral rotation to oral stereotypy after QA was due to reduced striatal output caused by a loss of projection neurons, a loss insufficient to induce HD symptoms, but sufficient to counter the PD condition.

Behavioral/neurophysiological investigation of effects of combining a quinolinic acid entopeduncular lesion with a fetal mesencephalic tissue transplant in striatum of the 6-OHDA hemilesioned rat.

Behavioral and electrophysiological methods were used to investigate the effects of combining a unilateral quinolinic acid lesion of the entopeduncular nucleus (QA/EP) with a striatal transplant of fetal ventral mesencephalic tissue in the 6-hydroxydopamine (6-OHDA) hemilesioned rat model for Parkinson's disease. The subjects were 6-OHDA-lesioned rats selected because their response to amphetamine treatment was a strongly biased rotation toward the side of the 6-OHDA lesion in the substantia nigra, at the expense of other evoked behaviors associated with amphetamine. Two experiments were performed. In the first, the motor effects of the QA/EP lesion alone and of the combination of QA/EP lesion with striatal transplant were determined by measuring six aspects of the motor response. In the second the electrophysiological effects of the two interventions on the responses of neurons in the subthalamic nucleus to amphetamine and apomorphine were determined in the 6-OHDA-lesioned rats. The results of the first experiment show that the QA/EP lesion by itself produced an attenuation of the rotation response and, simultaneously, an increase of oral stereotypy. They also show that the combination of QA/EP lesion with striatal transplant was more effective than the single intervention, inducing more attenuation of rotation and more oral stereotypy. The results of the second experiment show that the responses of subthalamic neurons to amphetamine in the behaving hemiparkinsonian rat with combined QA/EP lesion and transplant were larger than the responses in the hemiparkinsonian rat with the QA/EP lesion alone. However, even these larger responses in the rats with combined intervention were not as large as those recorded at the same time in the subthalamus in the opposite, intact, hemisphere. The results of the two experiments, both of which show enhanced motor and neuronal sensitivity to amphetamine after the combined intervention, suggest that such a multiple approach might prove more beneficial than a one-site intervention targeting either the EP or the striatum.

Behavioral and subthalamic effects of combining a fetal ventral mesencephalic transplant in striatum with an electrolytic lesion of the entopeduncular nucleus in the rat with a unilateral 6-OHDA lesion of substantia nigra.

Behavioral and electrophysiological methods were used to determine whether a transplant of dopamine-rich fetal tissue in striatum combined with an electrolytic lesion of the entopeduncular nucleus have additive effects in the unilaterally lesioned rat model for Parkinson's disease. The subjects were rats with the left substantia nigra lesioned with 6-hydroxydopamine (6-OHDA) and responding to systemic amphetamine with rotation toward the side of the lesion (ipsilateral rotation). The motor response to amphetamine was fractionated into six aspects, half reflecting the unilateral deafferentation in striatum and half representing those aspects of the response evoked in normal rats. After collection of baseline values, 25 rotators received a transplant of fetal ventral mesencephalic tissue in the left striatum and 20 received a transplant and, at the same time, an electrolytic lesion of the left entopeduncular nucleus. Testing for the motor response to amphetamine resumed after 4 weeks of recovery and continued at weekly intervals for 5 weeks. Upon completion of these tests, each rotator was implanted with multiple electrodes in the subthalamic nucleus. After recovery, multiunit responses to amphetamine and apomorphine were recorded from several electrodes in parallel during the motor response to the drugs. In rotators with transplant only, treatment with amphetamine evoked oral stereotypy and an attenuated ipsilateral rotation response. In rotators with combined transplant and entopeduncular lesion, ipsilateral rotation did not change or increased. Subthalamic responses to amphetamine and apomorphine were larger in rotators with combined transplant and entopeduncular lesion than in rotators with transplant alone. These findings indicate that the combination of transplant and pallidotomy in the 6-OHDA rat model for parkinsonism does not lead to additive benefits, an effect that may have been due to the nonselectivity of the electrolytic damage and/or of the lesion extending beyond the entopeduncular nucleus into the lateral hypothalamus.

Entopeduncular lesions facilitate and thalamic lesions depress spontaneous and drug-evoked motor behavior in the hemiparkinsonian rat.

Pallidotomy is a neurosurgical procedure designed to ameliorate the akinesia and bradykinesia associated with Parkinson's disease. In the present study, the effects of pallidal-like lesions on motor behavior in the hemiparkinsonian rat were compared to the effects of lesions in the ventrolateral thalamus, a target of entopeduncular projections feeding motor-related information to motor cortex. Six aspects of spontaneous and evoked behavior induced by amphetamine and apomorphine in the hemiparkinsonian rat with either bilateral electrolytic entopeduncular lesions or bilateral electrolytic ventrolateral thalamic lesions were measured for 60 min. Saline or amphetamine, 5 mg/kg, or apomorphine, 0.3 mg/kg, were administered IP 5 min before the tests. The results show that on all measures except time spent resting the hemiparkinsonian rats with the entopeduncular lesions were more active than the hemiparkinsonian rats with the thalamic lesions. The asymmetrical rotation responses to dopamine receptor stimulation evoked by amphetamine and apomorphine were influenced by the general effect on gross motor behavior, as shown by the response being very large in the entopeduncular group and very small in the thalamic group. These results are consistent with current thinking about the functional organization of the basal ganglia according to which damage of the entopeduncular nucleus reduces its inhibitory control of the thalamic motor regions, thereby promoting thalamic facilitation of motor cortex, and damage to the thalamic motor regions has the opposite effect. These effects of the lesions translate, respectively, into hyperactivity and hypoactivity without blocking the asymmetrical rotation response of the hemiparkinsonian rat.

Subthalamic responses to amphetamine and apomorphine in the behaving rat with a unilateral 6-OHDA lesion in the substantia nigra.

The activity of neurons in the subthalamic nucleus (STN) of the behaving rat, before and after a unilateral 6-OHDA lesion of the substantia nigra, was recorded with the extracellular technique to determine whether it was altered following systemic amphetamine, 5 mg/kg, apomorphine, 3 mg/kg, and apomorphine, 0.3 mg/kg, and whether in cases of altered activity, it was related to the drug-induced motor response expressed concurrently. Activity in the STN of intact rats increased dramatically after amphetamine, 5 mg/kg. This excitatory response had the same latency, similar magnitude, and the same duration as the motor response expressed in terms of locomotion and oral stereotypy. Motor and unit responses were also induced by amphetamine after the lesion with 6-hydroxydopamine (6-OHDA), but now the excitatory response was attenuated while the motor response was not. The effects of the 6-OHDA lesion were the same in all animals with loss of the nigra dopamine neurons, regardless of whether they were rotators or non-rotators. Activity in the STN of intact rats also increased after apomorphine, 3 mg/kg, and again, this increase was correlated with the increase in motor behavior, but both responses were of shorter duration than the responses to amphetamine. The increases in unit activity and motor behavior induced by apomorphine in the 6-OHDA-lesioned rats had the same magnitude but lasted longer than in the intact rats. Treatment with apomorphine, 0.3 mg/kg, of the intact rats produced small and very brief increases in the activity of the STN and in motor behavior. The same treatment given the 6-OHDA-lesioned rats produced responses of larger magnitude but no change in duration. These findings demonstrate a role for STN neurons in the mediation of the motor behaviors induced by stimulation of the dopamine receptor. The results also show that a unilateral lesion of the substantia nigra with 6-OHDA did not block these responses but altered them in a manner consistent with a dopaminergic deafferentation of the basal ganglia. The increased activity in the STN during the expression of dopamine-dependent motor behavior conflicts with the current model of basal ganglia function that assumes prejudicial effects of excessive STN activity on the expression of motor behavior. An explanation for this conflict suggests that it is more apparent than real.

Globus pallidus lesions depress the excitatory responses to apomorphine but not amphetamine in the subthalamic nucleus of the behaving rat with a 6-OHDA nigra lesion.

The role of the dopaminergic innervation of the basal ganglia on the activity in the subthalamic nucleus (STN) evoked by amphetamine and apomorphine in the behaving rat was examined. The aim was to determine the relationship between that neural activity and the movements evoked by the drugs. Bilateral electrolytic lesions of the globus pallidus (GP), superimposed on the earlier unilateral lesion in substantia nigra (SN) with 6-hydroxydopamine (6-OHDA) affected differently the excitatory responses in the STN evoked by amphetamine and apomorphine and the motor responses to the drugs recorded concurrently. Before the GP lesions, the administration of amphetamine, 5 mg/kg, to the unilaterally deafferented rat induced increased activity in the STN and simultaneously increased movement in the animal. After the GP lesions, the excitatory response to amphetamine in the STN was not different from that seen before the GP lesions. The motor response was also unchanged. In contrast, the GP lesions altered the excitatory response to apomorphine, 3 mg/kg. Before these lesions, the administration of apomorphine to the 6-OHDA lesioned animal evoked a robust and long-lasting excitatory response in the STN and, concurrently, a long-lasting motor response. After the GP lesions, both responses to apomorphine were attenuated. These differential effects of the GP lesions on the unit and motor responses to the two drugs are viewed as representing the effects of the damage in the GP on the dopaminergic innervation contributing to the regulation of activity in the STN. In the 6-OHDA animal, the dopamine afferents innervating the basal ganglia had already been dramatically reduced by 6-OHDA. The GP lesions did not significantly add to the number of these afferents previously eliminated; therefore, the excitatory and motor responses to amphetamine were not changed by the GP lesions. But the GP damage served to eliminate the dopamine receptor in the GP and thus reduced the density of the dopamine receptor in the basal ganglia available for binding to apomorphine. Therefore, the excitatory and motor responses to apomorphine were attenuated after the GP lesions compared to the responses before these lesions.

Effect of melatonin on tinnitus.

OBJECTIVE: Evaluate melatonin as a treatment for subjective tinnitus. STUDY DESIGN: Randomized, prospective, double-blind, placebo-controlled crossover trial. Patients were given 3.0 mg melatonin, which was taken nightly for 30 days followed or preceded by a placebo nightly for 30 days, with a 7-day washout period between medications. SETTING: Outpatient, private, neurotology practice. PATIENTS: Thirty patients with subjective tinnitus. MAIN OUTCOME MEASURES: Tinnitus matching, Tinnitus Handicap Inventory (THI), patient questionnaire and interview. RESULTS: The average pretreatment THI score was 33.91 as compared with 26.43 after the placebo and 26.09 after melatonin. The difference in the THI scores between melatonin and placebo treatment were not statistically significant. The average pretreatment THI score for patients who reported overall improvement with melatonin was statistically higher (P = 0.02) than the average pretreatment THI score for patients who reported no improvement with melatonin. Among subjects reporting difficulty sleeping attributable to their tinnitus, 46.7% reported an overall improvement after melatonin compared with 20.0% for placebo (P = 0.04). There was also a statistically significant difference in improvement with melatonin for those patients with bilateral tinnitus compared with those with unilateral tinnitus (P = 0.02). CONCLUSION: Melatonin has been shown to be useful in the treatment of subjective tinnitus. Patients with high THI scores and/or difficulty sleeping are most likely to benefit from treatment with melatonin. In light of its minimal side effects, melatonin should be a part of the physician's armamentarium in the treatment of tinnitus.

Dexamethasone inner ear perfusion for the treatment of Meniere's disease: a prospective, randomized, double-blind, crossover trial.

OBJECTIVE: To investigate the benefits of intratympanic administration of dexamethasone in the treatment of unilateral Meniere's disease, with particular attention to the symptoms of hearing loss and tinnitus. STUDY DESIGN: A prospective, randomized, double-blind, crossover study comparing improvements in hearing loss, tinnitus, aural fullness, and caloric vestibular response secondary to intratympanic dexamethasone and sodium hyaluronate injection versus placebo consisting of saline and sodium hyaluronate. SETTING: A private otology/neurotology practice. PATIENTS: Twenty patients diagnosed with either definite or probable Meniere's disease as defined by the American Academy of Otolaryngology Head and Neck Surgery Committee on Hearing and Equilibrium. All patients were < or =21 years old and were not receiving any other form of treatment for their Meniere's disease. Each patient's primary symptoms of concern were hearing loss, aural fullness, and roaring tinnitus. INTERVENTIONS: Three consecutive daily administrations of intratympanic dexamethasone or placebo to the involved ear. MAIN OUTCOME MEASURES: Changes in audiometric pure-tone averages, speech reception thresholds, caloric vestibular responses, scores on the tinnitus handicap inventories, questionnaires, and telephone interview responses. RESULTS: No significant changes were observed in any measured parameter. Patients were unable to consistently identify which medication was dexamethasone and which was placebo. CONCLUSIONS: Intratympanic administration of dexamethasone in a group of patients with unilateral Meniere's disease (Shea's stage IV) showed no benefit over placebo for the treatment of hearing loss and tinnitus.

A new prosthesis for reconstructing the incudostapedial joint.

OBJECTIVE: This study aimed to evaluate the hearing results obtained using the Silverstein Incus-Stapes Connection in ossicular reconstruction among patients with chronic ear disease. STUDY DESIGN: The study was performed as a retrospective review. A control group consisted of patients undergoing similar surgery but in which no prosthesis was used. SETTING: The Florida Ear and Sinus Center outpatient offices of the senior author. PATIENTS: Forty-seven patients with a mean age of 48 years comprised the treatment group. Thirty-eight patients (mean age, 49.4 years) acted as control subjects. INTERVENTION: All patients underwent surgery for chronic ear disease. Reconstruction surgery for patients requiring separation of the incudostapedial was performed with a Silverstein Incus-Stapes Connection or by reapproximating the joint capsule to allow primary healing. MAIN OUTCOME MEASURE: The patients were categorized according to how the prosthesis was used. Results comparing the preoperative air-bone gap and postoperative air-bone gap were evaluated. The change in air-bone gap was reported according to the guidelines set forth by the Committee on Hearing and Equilibrium. RESULTS: The mean postoperative air-bone gap for reconstruction with the prosthesis was 17.6 dB compared to a mean of 11.8 dB among control subjects. An air-bone gap of 16.5 dB was achieved when the prosthesis was used to bridge an area of lenticular resorption. When a composite prosthesis, made by adding cartilage to the disk, was used to bridge larger defects, an air-bone gap of 14.3 dB was seen. Finally, when the prosthesis was used as a partial ossicular replacement prosthesis and directly contacted the tympanic membrane, the air-bone gap was 9 dB. The prosthesis was found to be stable when re-exploration was required and modification of the prosthesis with cartilage was accomplished easily intraoperatively. CONCLUSION: The Silverstein Incus-Stapes Connection is a middle ear prosthesis that can provide a mechanism for overcoming incus resorption in selected cases. In addition, the prosthesis can be modified easily with the addition of cartilage when needed.

Inner ear perfusion and the role of round window patency.

OBJECTIVE: The goal of this investigation was to evaluate the degree of round window membrane obstruction in the native state. The implications for the perfusion of the inner ear via the intratympanic instillation of medications are addressed. STUDY DESIGN: This was a retrospective chart review and a prospective intraoperative observation in the setting of an outpatient office. PATIENTS: The study population was composed of 41 patients who were undergoing middle ear endoscopy before perfusion of the inner ear with medication for the treatment of Meniere's disease, sudden sensorineural hearing loss, or tinnitus. INTERVENTION: Office-based laser-assisted tympanostomy and middle ear endoscopy was carried out in each case. Lysis of adhesions overlying the round window membrane was undertaken when the underlying round window membrane could not be visualized. MAIN OUTCOME MEASURES: Evaluation of the round window niche with regard to accessibility of the round window membrane was recorded for each patient studied. RESULTS: Of the 41 cases examined, 29 of the round windows were judged to be unobstructed, 7 were obstructed partially, and 5 were obstructed completely. CONCLUSION: A significant rate of round window obstruction exists among patients who have no history of manipulation to this area. Although, intuitively, we would expect prior middle ear surgery to increase the likelihood of obstruction, this is not uniformly the outcome. If intratympanic instillation of a medication is contemplated for the treatment of an inner ear disorder, considerations for the evaluation of the round window should be made to enhance adequate diffusion into the perilymph.

Facial nerve monitoring among graduates of the Ear Research Foundation.

OBJECTIVE: This study aimed to evaluate the patterns of facial nerve monitoring among graduates of an otology fellowship in which monitoring is emphasized throughout training. STUDY DESIGN: This study involved a questionnaire administered to graduates of the Ear Research Foundation, Sarasota, Florida, U.S.A. (otology/neurotology fellowship). SETTING: The study was performed in academic and private practices of surveyed physicians. MAIN OUTCOME MEASURES: These included patterns of facial nerve monitor use and surgical results after facial nerve injuries. RESULTS: Nearly 100% of the graduates of the Ear Research Foundation continue to use facial nerve monitoring routinely in otologic surgery. Five cases of facial nerve injury in surgery for long-term disease were reported for all 15 neurotologists surveyed. CONCLUSION: Routine facial nerve monitoring is not considered the standard of care in most communities; however risk of facial nerve injury appears to be greatly reduced when this adjunctive technique is employed.

Glucose utilization of the rat vestibular end organs: a quantitative 2-deoxyglucose study.

The local metabolic rate of glucose utilization (LMRglc) for the rat vestibular end organs was determined with a modification of the [14C]deoxyglucose method. Data are expressed as micromoles per 100 g per minute +/- SEM. Results indicate that the LMRglc is similar within the utricle (40.3 +/- 3.2) and saccule (41.2 +/- 5.5) and significantly higher than that for the superior (20.1 +/- 2.9), posterior (25.4 +/- 2.0), or lateral canal (22.0 +/- 2.6) ampullae. These differences in LMRglc may be related to differences in the ratios of sensory to nonsensory cells, dark cell distributions, response to acoustic stimulation, or activity levels during the experimental period. Given the high blood flow rates reported for the vestibular end organs by Lyon and coworkers, a much higher LMRglc was expected. Together, these data would suggest that delivery of metabolites is not a primary regulating force for vestibular blood flow. Instead, the primary reason for a high blood flow rate may be waste removal, the maintenance of pH, ion balance, and/or temperature.

Dopaminergic basis for the facilitation of brain stimulation reward by the NMDA receptor antagonist, MK-801.

MK-801 (dizocilpine maleate), an antagonist of the NMDA receptor, was given alone or in combination with dopamine D1 and D2 receptor antagonists to rats self-stimulating in lateral hypothalamus to determine whether the dopamine neurons play a role in mediating the effects of MK-801. MK-801 given at a dose of 0.1 mg/kg i.p. to self-stimulators induced a prolonged facilitation of lever-pressing, but given to non-self-stimulators, the drug had no effects. Pretreatment of self-stimulators with the dopamine D1 receptor antagonist Schering 23390 (SCH 23390), 0.2 mg/kg given i.p. 15 min before MK-801, prevented the facilitation seen with MK-801, but did not suppress self-stimulation. SCH 23390 given alone suppressed self-stimulation. Pretreatment of self-stimulators with the dopamine D1/D2 receptor antagonist, haloperidol, 0.2 mg/kg given i.p. 15 min before MK-801, also prevented the facilitation of self-stimulation induced by MK-801 yet did not suppress self-stimulation. Haloperidol given alone suppressed self-stimulation. Pretreatment of self-stimulators with both SCH 23390 and haloperidol 15 min before MK-801 prevented the facilitation seen with MK-801 and suppressed self-stimulation. The combined treatment with SCH 23390 and haloperidol (without MK-801) suppressed self-stimulation, and the suppression lasted longer than the suppression seen when the two dopamine receptor antagonists were given as pretreatment, before MK-801. Pretreating self-stimulators with the combination of SCH 23390 and haloperidol 15 min before amphetamine (2 mg/kg) prevented the facilitatory response and suppressed responding for the brain reward. The suppression was of shorter duration than the suppression seen after the injection of SCH 23390 plus haloperidol. The treatment of self-stimulators with both MK-801 and amphetamine resulted in a greater and longer-lasting facilitation than the increase in responding produced by either drug alone. The similarity between the effects of MK-801 and those of amphetamine and between the effects of pretreatment with the dopamine receptor antagonists before MK-801 and before amphetamine suggests that dopaminergic activity played a significant role in the action underlying the effects of MK-801 on brain stimulation reward.