Considerable evidence suggests that the loss of strength and muscle mass appear to be inevitable consequences of aging. Moreover, aging is associated with an increase in body fat. This study examined whether increased physical activity could prevent or reverse the losses of strength and skeletal muscle mass as well as the gain in fat in older adults. Eleven men and 31 women completed a randomized trial consisting of either a physical activity (PA; n = 22) or successful aging health educational control (SA; n = 20) group. Isokinetic knee extensor strength and computed tomography-derived midthigh skeletal muscle and adipose tissue cross-sectional areas (CSA) were assessed at baseline and at 12 mo following randomization. Total body weight and muscle CSA decreased in both groups, but these losses were not different between groups. Strength adjusted for muscle mass decreased (−20.1 ± 9.3%, P < 0.05) in SA. The loss of strength was completely prevented in PA (+2.5 ± 8.3%). In addition, there was a significant increase (18.4 ± 6.0%) in muscle fat infiltration in SA, but this gain was nearly completely prevented in PA (2.3 ± 5.7%). In conclusion, regular physical activity prevents both the age-associated loss of muscle strength and increase in muscle fat infiltration in older adults with moderate functional limitations.

Superior semicircular canal dehiscence syndrome was first reported by Lloyd Minor and colleagues in 1998. Patients with a dehiscence in the bone overlying the superior semicircular canal experience symptoms of pressure or sound-induced vertigo, bone conduction hyperacusis, and pulsatile tinnitus. The initial series of patients were diagnosed based on common symptoms, a physical examination finding of eye movements in the plane of the superior semicircular canal when ear canal pressure or loud tones were applied to the ear, and high resolution CT imaging demonstrating a dehiscence in the bone over the superior semicircular canal. Research productivity directed at understanding better methods for diagnosing and treating this condition has substantially increased over the last two decades. We now have a sound understanding of the pathophysiology of third mobile window syndromes, higher resolution imaging protocols, and several sensitive and specific diagnostic tests. Furthermore, we have a treatment (surgical occlusion of the superior semicircular canal) that has demonstrated efficacy. This review will highlight some of the fundamental insights gained in SCDS, propose diagnostic criteria, and discuss future research directions.

Profound bilateral loss of vestibular sensation disables the vestibuloocular and vestibulospinal reflexes that normally maintain stable gaze and posture. Affected individuals experience oscillopsia (illusory movement of the visible world during head movement), chronic disequilibrium, and postural instability that interfere with otherwise routine activities such as walking or driving.^1,2 Although the cause of bilateral vestibular hypofunction (BVH) is frequently unknown, ototoxicity due to gentamicin or other aminoglycosides is the most commonly identified cause of BVH; other causes include Ménière’s disease, labyrinthitis, meningitis, autoimmune disease, and iatrogenic damage due to cochlear implantation or other surgical procedures.^3-5

This paper describes the diagnostic criteria for superior semicircular canal dehiscence syndrome (SCDS) as put forth by the classification committee of the Bárány Society. In addition to the presence of a dehiscence of the superior semicircular canal on high resolution imaging, patients diagnosed with SCDS must also have symptoms and physiological tests that are both consistent with the pathophysiology of a ‘third mobile window’ syndrome and not better accounted for by another vestibular disease or disorder. The diagnosis of SCDS therefore requires a combination of A) at least one symptom consistent with SCDS and attributable to ‘third mobile window’ pathophysiology including 1) hyperacusis to bone conducted sound, 2) sound-induced vertigo and/or oscillopsia time-locked to the stimulus, 3) pressure-induced vertigo and/or oscillopsia time-locked to the stimulus, or 4) pulsatile tinnitus; B) at least 1 physiologic test or sign indicating that a ‘third mobile window’ is transmitting pressure including 1) eye movements in the plane of the affected superior semicircular canal when sound or pressure is applied to the affected ear, 2) low-frequency negative bone conduction thresholds on pure tone audiometry, or 3) enhanced vestibular-evoked myogenic potential (VEMP) responses (low cervical VEMP thresholds or elevated ocular VEMP amplitudes); and C) high resolution computed tomography (CT) scan with multiplanar reconstruction in the plane of the superior semicircular canal consistent with a dehiscence. Thus, patients who meet at least one criterion in each of the three major diagnostic categories (symptoms, physiologic tests, and imaging) are considered to have SCDS.

Vestibulo-ocular and vestibulospinal reflexes normally maintain stable gaze and posture during head movement. Individuals with bilateral vestibular deficiency (BVD) often experience oscillopsia (blurring of vision due to image slip across the retinae during head movement), disequilibrium, and postural instability that together confer a 31-fold increase in risk of falling.¹ Most individuals with unilateral vestibular deficiency (UVD) ultimately compensate for their loss by using information from the remaining labyrinth, and those with mild or moderate BVD often compensate by integrating residual labyrinthine input with other sensory cues. However, severe BVD can be devastating if adaptation and compensation strategies fail to overcome the sensory deficit.^2,3 Individuals with BVD often experience chronic imbalance and instability of vision and posture that render routine daily activities such as walking and driving difficult.