Aberrant Neural Activity Research Articles

Tinnitus in the older adult: epidemiology, pathophysiology and treatment options.

Tinnitus is the perception of sound in the absence of an apparent acoustic stimulus. More than 35 million Americans experience tinnitus, with 2-3 million severely debilitated by this distressing symptom. The prevalence increases with age and there is a high incidence associated with both noise-induced and age-related hearing loss. Although there are several theories regarding the pathophysiology of tinnitus, the precise mechanism remains to be elucidated. The most compelling of these is the hypothesis that tinnitus occurs as a result of spontaneous and aberrant neural activity at any level along the auditory axis, even after cochlear nerve transection or labyrinthine ablation. There are numerous aetiologies associated with tinnitus. Tinnitus, in clinical practice, is characterised as either objective or subjective. The distinction is relevant in terms of both aetiology and treatment. Despite a large number of therapeutic interventions and studies claiming success in treating tinnitus, a cure remains elusive. However, there are several potential treatment options that offer patients varying degrees of symptomatic improvement and enhanced quality of life. It is imperative to formulate a rational and systematic approach in evaluating an older adult with tinnitus. An individualised treatment regimen and the creation of a strong therapeutic relationship are the hallmarks of successful management of the patient with tinnitus.

Mechanisms of central pain.

Central pain is common in patients with stroke, multiple sclerosis, syringomyelia, and spinal cord injury. It frequently develops after a delay of weeks or months, is associated with sensory change involving the spinothalamic pathways, and has a poor prognosis for spontaneous remission. Hypotheses to explain the varied clinical manifestations can be divided in two categories: those stressing aberrant neural activity in the deafferented circuits and those focusing on the postlesion imbalance between facilitatory and inhibitory neural pathways. All models inherently assume a degree of specialization of cerebral structures in pain processing, which has not been proved conclusively.