The lack of an adequate standardized method for reporting level of hearing function in clinical trials has hampered the ability of investigators to draw comparisons across studies. Variability in data reported and presentation format inhibits meta-analysis and makes it impossible to accumulate the large patient cohorts needed for statistically significant inference. Recognizing its importance to the field and after a widely inclusive discussion, the Hearing Committee of the American Academy of Otolaryngology-Head and Neck Surgery endorsed a new minimal standard for reporting hearing results in clinical trials, consisting of a scattergram relating average pure-tone threshold to word recognition score. Investigators remain free to publish their hearing data in any format they believe is interesting and informative, as long as they include the minimal data set to facilitate interstudy comparability.
The development group made a strong recommendation that clinicians recommend intranasal steroids for patients with a clinical diagnosis of AR whose symptoms affect their quality of life. The development group also made a strong recommendation that clinicians recommend oral second-generation/less sedating antihistamines for patients with AR and primary complaints of sneezing and itching. The panel made the following recommendations: (1) Clinicians should make the clinical diagnosis of AR when patients present with a history and physical examination consistent with an allergic cause and 1 or more of the following symptoms: nasal congestion, runny nose, itchy nose, or sneezing. Findings of AR consistent with an allergic cause include, but are not limited to, clear rhinorrhea, nasal congestion, pale discoloration of the nasal mucosa, and red and watery eyes. (2) Clinicians should perform and interpret, or refer to a clinician who can perform and interpret, specific IgE (skin or blood) allergy testing for patients with a clinical diagnosis of AR who do not respond to empiric treatment, or when the diagnosis is uncertain, or when knowledge of the specific causative allergen is needed to target therapy. (3) Clinicians should assess patients with a clinical diagnosis of AR for, and document in the medical record, the presence of associated conditions such as asthma, atopic dermatitis, sleep-disordered breathing, conjunctivitis, rhinosinusitis, and otitis media. (4) Clinicians should offer, or refer to a clinician who can offer, immunotherapy (sublingual or subcutaneous) for patients with AR who have inadequate response to symptoms with pharmacologic therapy with or without environmental controls. The panel recommended against (1) clinicians routinely performing sinonasal imaging in patients presenting with symptoms consistent with a diagnosis of AR and (2) clinicians offering oral leukotriene receptor antagonists as primary therapy for patients with AR. The panel group made the following options: (1) Clinicians may advise avoidance of known allergens or may advise environmental controls (ie, removal of pets; the use of air filtration systems, bed covers, and acaricides [chemical agents formulated to kill dust mites]) in patients with AR who have identified allergens that correlate with clinical symptoms. (2) Clinicians may offer intranasal antihistamines for patients with seasonal, perennial, or episodic AR. (3) Clinicians may offer combination pharmacologic therapy in patients with AR who have inadequate response to pharmacologic monotherapy. (4) Clinicians may offer, or refer to a surgeon who can offer, inferior turbinate reduction in patients with AR with nasal airway obstruction and enlarged inferior turbinates who have failed medical management. (5) Clinicians may offer acupuncture, or refer to a clinician who can offer acupuncture, for patients with AR who are interested in nonpharmacologic therapy. The development group provided no recommendation regarding the use of herbal therapy for patients with AR.
ObjectivesTo review evidence of hearing loss as a risk factor for dementia. Data Sources: PubMed Review methods: A systematic review was conducted using the PubMed database using the search terms (hearing loss OR presbycusis) AND (dementia OR cognitive decline). Initially, 488 articles were obtained. Only those studies evaluating an association between hearing loss and incident dementia or cognitive decline were included in the analysis. This resulted in 17 articles which were thoroughly evaluated with consideration for study design, method for determining hearing loss and cognitive status, relevant covariates and confounding factors, and key findings.ResultsAll of the 17 articles meeting inclusion criteria indicate that hearing loss is associated with dementia or cognitive decline. The methods used among the studies for ascertaining hearing loss and dementia were notably varied. For hearing loss, peripheral auditory function was tested far more than central auditory function. For peripheral audition, pure tone audiometry was the most commonly reported method for defining hearing loss. Only a few studies measured central auditory function by using the Synthetic Sentence Identification with Ipsilateral Competing Message test (SSI‐ICM) and the Staggered Spondaic Word Test (SSW). Dementia was most often defined using the Mini Mental State Exam (MMSE). However, many studies used extensive batteries of tests to define cognitive status, often including a neuropsychologist. Confounding variables such as cardiovascular risk factors were measured in 17 studies and family history of dementia was only evaluated in 1 study. Overall, the methods used by studies to ascertain hearing loss, cognitive status and other variables are valid, making their evaluation appear reliable.ConclusionWhile each of the studies included in this study utilized slightly different methods for evaluating participants, each of them demonstrated that hearing loss is associated with higher incidence of dementia in older adults.Level of EvidenceLevel V, systematic review.
Objective To determine whether baseline hearing loss increases cognitive decline and risk for all-cause dementia in a population of elderly individuals. Study design Longitudinal cohort study Setting Community-based, outpatient Patients Men and women aged 65 years or older without dementia at baseline Intervention(s) All subjects completed the Modified Mini-Mental Status Exam (3MS-R) at baseline and over 3 triennial follow-up visits. Hearing loss (HL) at baseline was based on observation of hearing difficulties during testing or interview. Incident dementia was determined by clinical assessment and expert consensus. Main outcome measure(s) Dementia and 3MS-R score. Results At baseline 4,463 subjects were without dementia, 836 of whom had HL. Of those with HL, 16.3% developed dementia, compared to 12.1% of those without HL (p<0.001). Mean time to dementia was 10.3 years in the HL group vs. 11.9 years for non-HL (Log Rank test p<0.001). In Cox regression analyses controlling for gender, presence of APOE- ε4 allele, education, and baseline age, and cardiovascular risk factors, HL was an independent predictor of developing dementia (Hazard ratio = 1.27, p=0.026 (95% CI = 1.03, 1.56). Linear mixed models controlling for similar covariates showed HL was associated with faster decline on the 3MS-R, at a rate of 0.26 points/year worse than those without HL. Conclusions Elderly individuals with HL have an increased rate of developing dementia and more rapid decline on 3MS-R scores than their non-hearing impaired counterparts. These findings suggest that hearing impairment may be a marker for cognitive dysfunction in adults age 65 and older.
Objective Bell’s palsy, named after the Scottish anatomist, Sir Charles Bell, is the most common acute mono-neuropathy, or disorder affecting a single nerve, and is the most common diagnosis associated with facial nerve weakness/paralysis. Bell’s palsy is a rapid unilateral facial nerve paresis (weakness) or paralysis (complete loss of movement) of unknown cause. The condition leads to the partial or complete inability to voluntarily move facial muscles on the affected side of the face. Although typically self-limited, the facial paresis/paralysis that occurs in Bell’s palsy may cause significant temporary oral incompetence and an inability to close the eyelid, leading to potential eye injury. Additional long-term poor outcomes do occur and can be devastating to the patient. Treatments are generally designed to improve facial function and facilitate recovery. There are myriad treatment options for Bell’s palsy, and some controversy exists regarding the effectiveness of several of these options, and there are consequent variations in care. In addition, numerous diagnostic tests available are used in the evaluation of patients with Bell’s palsy. Many of these tests are of questionable benefit in Bell’s palsy. Furthermore, while patients with Bell’s palsy enter the health care system with facial paresis/paralysis as a primary complaint, not all patients with facial paresis/paralysis have Bell’s palsy. It is a concern that patients with alternative underlying etiologies may be misdiagnosed or have unnecessary delay in diagnosis. All of these quality concerns provide an important opportunity for improvement in the diagnosis and management of patients with Bell’s palsy. Purpose The primary purpose of this guideline is to improve the accuracy of diagnosis for Bell’s palsy, to improve the quality of care and outcomes for patients with Bell’s palsy, and to decrease harmful variations in the evaluation and management of Bell’s palsy. This guideline addresses these needs by encouraging accurate and efficient diagnosis and treatment and, when applicable, facilitating patient follow-up to address the management of long-term sequelae or evaluation of new or worsening symptoms not indicative of Bell’s palsy. The guideline is intended for all clinicians in any setting who are likely to diagnose and manage patients with Bell’s palsy. The target population is inclusive of both adults and children presenting with Bell’s palsy. Action Statements The development group made a strong recommendation that (a) clinicians should assess the patient using history and physical examination to exclude identifiable causes of facial paresis or paralysis in patients presenting with acute-onset unilateral facial paresis or paralysis, (b) clinicians should prescribe oral steroids within 72 hours of symptom onset for Bell’s palsy patients 16 years and older, (c) clinicians should not prescribe oral antiviral therapy alone for patients with new-onset Bell’s palsy, and (d) clinicians should implement eye protection for Bell’s palsy patients with impaired eye closure. The panel made recommendations that (a) clinicians should not obtain routine laboratory testing in patients with new-onset Bell’s palsy, (b) clinicians should not routinely perform diagnostic imaging for patients with new-onset Bell’s palsy, (c) clinicians should not perform electrodiagnostic testing in Bell’s palsy patients with incomplete facial paralysis, and (d) clinicians should reassess or refer to a facial nerve specialist those Bell’s palsy patients with (1) new or worsening neurologic findings at any point, (2) ocular symptoms developing at any point, or (3) incomplete facial recovery 3 months after initial symptom onset. The development group provided the following options: (a) clinicians may offer oral antiviral therapy in addition to oral steroids within 72 hours of symptom onset for patients with Bell’s palsy, and (b) clinicians may offer electrodiagnostic testing to Bell’s palsy patients with complete facial paralysis. The development group offered the following no recommendations: (a) no recommendation can be made regarding surgical decompression for patients with Bell’s palsy, (b) no recommendation can be made regarding the effect of acupuncture in patients with Bell’s palsy, and (c) no recommendation can be made regarding the effect of physical therapy in patients with Bell’s palsy.
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