Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Auditory sensitivity and processing ability were evaluated in a patient who suffered from hyperacusis, difficulty understanding speech, withdrawn depression, lethargy, and hypersensitivity to touch, pressure, and light. Treatment with fluvoxamine and fluoxetine (selective serotonin reuptake inhibitors) reversibly alleviated complaints. Testing while medicated and unmedicated (after voluntary withdrawal from medication for several weeks) revealed no difference in pure-tone thresholds, speech thresholds, word recognition scores, tympanograms, or acoustic reflex thresholds. Medicated SCAN-A (a screening test for central auditory processing disorders) results were normal, and unmedicated results were abnormal. Unmedicated transient otoacoustic emissions and auditory brainstem response waves I, III, and V were significantly larger bilaterally. Uncomfortable loudness levels indicated greater tolerance during the medicated condition. Central processing and vigilance were evaluated with analog-synthesized three-formant consonant-vowel syllables. While medicated, responses to stimuli at each ear revealed well-defined, labeling crossovers of about 90 msec. Vowel identification matched normal subject responses; labeling of /gE/jE/ and /bE/wE/ continua was well defined but all crossover points differed from normals (p < .0001). During unmedicated testing, responses to /gE/jE/ began at medicated levels but approached chance levels for the entire continuum within 10 min; labeling of /bE/wE/ was consistent with medicated responses throughout with earlier than normal crossover points.
 ...
PMID:Effects of selective serotonin reuptake inhibitors on auditory processing: case study. 1101 41

Tinnitus is not a single entity but a rather diverse group of disorders. Despite symptoms that indicate the ear is the site of the pathology, there is strong evidence that most forms of severe tinnitus are caused by functional changes in the central nervous system. The changes are induced through expression of neural plasticity, some of which may have been caused initially by abnormalities in the ear or the auditory nerve. The involvement of the nonclassical ascending auditory pathway with its subcortical connections to limbic structures (the amygdala) may explain some of the symptoms of some forms of tinnitus including hyperacusis and affective disorders, such as phonophobia and depression, which often accompany severe tinnitus.
 ...
PMID:Pathophysiology of tinnitus. 1285 95

Psychological and physiological habituation are major goals in the treatment of patients suffering from chronic tinnitus. This study evaluates whether sound stimulation provided by use of low level white noise generators (NG) enhances the effects of cognitive-behavioral treatment (CBT). 124 outpatients with tinnitus of >6 months received manualized group treatment and were randomly assigned to the NG/no NG conditions. Those with moderate tinnitus-related distress obtained four sessions focusing on education, while severely distressed subjects were treated according to a full 10-session CBT program. Outcome was assessed at post-treatment and at 6- and 18-month follow-up. No additive effects due to the NGs could be demonstrated. All groups improved significantly on measures of tinnitus-related distress, dysfunctional cognitions, general psychopathology, depression, hypochondriasis and psychosocial functioning. Beneficial effects of the NGs were only observed for patients with concurrent tinnitus and hyperacusis. As systematic physical stimulation of the auditory system does not further improve the effects of CBT, the importance and strength of psychological interventions are emphasized. The clinical relevance of recently developed "retraining" approaches accentuating physical stimulation should be reconsidered.
 ...
PMID:Does sound stimulation have additive effects on cognitive-behavioral treatment of chronic tinnitus? 1586 15

Progress in neuroscience research has given birth to new theories for tinnitus generation. From a point of view where cochlear dysfunctions would be considered as the origin and maintenance mechanisms, it has been introduced the important role of compensation systems from the central auditory pathways. They could act as the most relevant factor for chronic persistent tinnitus after a peripheral aggression. Unmasking of silent synapses or sprouting of new ones activate cortical reorganization for frecuencial areas nearby the non-stimulated ones through brain plasticity. Connections to associative cortex and limbic-amigdala area using the non-classical auditory system explain the presence of hyperacusis, anxiety or depression, factors that increase the severity of tinnitus. Implementation of these physiopathological theories reinforces the tinnitus neurophysiological model. The development of an aversive response through the survival reflex and the participation of negative emotional response are the responsible for signal persistence and vegetative reactions from the autonomous nervous system. Implications of this knowledge for tinnitus treatment involve the central auditory system approach through the combination of medical counselling for reduction of the aversive reaction and sound therapy to diminish its perception.
 ...
PMID:[Physiopathological mechanisms in tinnitus generation and persistence]. 1628 31

Hyperacusis is defined as unusual intolerance to ordinary environmental sounds, and is commonly reported in the general population and in association with a range of medical conditions. These include neurological deficits (e.g. migraine), psychiatric conditions (e.g. depression), and several ear, nose and throat diagnoses such as tinnitus, noise-induced hearing loss, and middle ear malfunctions. However, extreme sensitivity to noise has also been studied from a public health perspective, but with a focus on noise sensitivity in general. In this review a distinction is proposed between three different aspects of the experience of hyperacusis. The first is the sensitivity, with the pain sensations reported in association with sounds. The second is the annoyance, which can be unrelated to loudness, but still cause marked distress. The third aspect deals with the fear of being harmed by sounds, which promotes avoidance and the unmotivated use of ear protection. The natural course of hyperacusis is largely unknown and there are no published randomized outcome studies on the available treatment options for the condition. In this paper we propose that cognitive behavioral therapy, presented in a multidisciplinary setting, could be a useful treatment. This treatment includes relaxation methods, advice regarding sound, and gradual exposure to everyday sounds.
 ...
PMID:[Hyperacusis--an unexplored field. Cognitive behavior therapy can relieve problems in auditory intolerance, a condition with many questions]. 1632 50

Two distinctly different kinds of tinnitus occur: objective and subjective tinnitus. Objective tinnitus is caused by sounds generated in the body while subjective tinnitus is caused by abnormal neural activity that is not evoked by sound. This chapter discusses subjective tinnitus. Subjective tinnitus has many forms. In most forms of tinnitus the anatomical location of the physiological abnormality is in the central nervous system, although the sensation is often referred to one ear or both ears. The cause of most forms of subjective tinnitus is the changes that have occurred as a result of expression of neural plasticity, thus a form of reprogramming of the brain that is not to the benefit of the individual person. Tinnitus often occurs together with hearing loss, indicating that the expression of neural plasticity has been evoked by deprivation of input. Tinnitus is often accompanied by hyperacusis, and sometimes phonophobia and depression, indicating altered processing of auditory information or rerouting of information. Several studies have brought evidence that some forms of tinnitus are associated with an abnormal involvement of the nonclassical (extralemniscal, diffuse, or polysensory) auditory pathways that bypass the primary auditory cerebral cortex and provide subcortical connections to limbic structures among others. There is no general treatment for tinnitus, but there are several treatments that can alleviate or reduce the tinnitus in some patients.
 ...
PMID:Neural plasticity in tinnitus. 1704 76

Hyperacusis is a decreased sound tolerance. Prevalence of the disease is described in 9-15% of the population, but this percentage increases among the tinnitus patients. Pathophysiological mechanisms involve some disruptions in the amplification and regulation processes of the external hair cells or affect the central sound processing at the subcortical level. The role of the serotonin, also involved in other diseases related with hyperacusis (migraine, depression), can be crucial in this disorder. Other theories confirm the effect of the endorphins that activate the excitatory function of the glutamate, the auditory neurotransmitter, increasing its toxicity. The activation of the limbic and autonomic nervous systems produces the emotional reaction of the hyperacusis (anxiety, fear and depression). Proposed treatments are based on acoustic stimulation by a progressive introduction of sound (tinnitus retraining therapy TRT). Noise generators and hearing aids can be fitted in severe cases. The role of some drugs involved in the metabolism of the serotonin open new approaches for the management of hyperacusis.
 ...
PMID:[Mechanisms and management of hyperacusis (decreased sound tolerance)]. 1711 96

Acoustic shock is a recently recognised clinical entity: following an abrupt, intense and unanticipated acoustic stimulus, usually delivered by a telephone handset or headset, some individuals report a symptom cluster that includes otalgia, altered hearing, aural fullness, imbalance, tinnitus, dislike or even fear of loud noises, and anxiety and/or depression. Symptoms start shortly after the triggering acoustic incident and can be short-lived or can last for a considerable time. If persistent, the condition can lead to significant disability. Proposed mechanisms include involvement of the tensor tympani muscle, hyperexcitability of central auditory pathways, and a precursive state of raised anxiety or arousal. A formal treatment programme has not yet been proposed, but the potential utility of modern therapeutic techniques for tinnitus and hyperacusis are considered. Given the large number of UK residents working in telephone call centres, this condition is of considerable clinical importance.
 ...
PMID:Acoustic shock. 1730 48

Zinc is an essential trace element present in all organs, tissues, fluids, and secretions of the body and it is widely distributed in the central nervous system, including the auditory pathway in synapses of the VIII nerve and in the cochlea. Zinc is an essential component of Cu/Zn superoxide dismutase (SOD) and in certain enzymes and it is important for proper function of the immune system. Three possible mechanisms have linked zinc to tinnitus; cochlear Cu/Zn SOD activity, synaptic transmission, and depression. Evidences in the literature suggest prevalence rates of zinc deficiency in individuals with tinnitus from 2 to 69%, affecting elderly individuals more frequently. Four among five small studies indicate that administration of zinc has a beneficial effect on tinnitus but these results still have to be confirmed in clinical trials with larger samples using a cross-over design, validated tinnitus handicap questionnaires, measurements of tinnitus magnitude, and accessing the coexistence of other symptoms such as depression, phonophobia, and hyperacusis.
 ...
PMID:Zinc as a possible treatment for tinnitus. 1795 92

Tinnitus is a very frequent symptom affecting 10% of the general population. It corresponds to the perception of an internal noise that can severely impair the quality of life. Tinnitus management requires a multidisciplinary approach in which neuromodulation and neurosurgery tend to play major roles. Classification of tinnitus separates objective tinnitus (i.e., tinnitus that can be heard or recorded) from the more frequent subjective tinnitus (i.e., tinnitus only perceived by the patient). Objective tinnitus is either pulsatile synchronous with heartbeat or asynchronous. In the former, appropriate radiological testing should search for a vascular abnormality as well as other neurological diseases (intracranial hypertension, Arnold-Chiari malformation, vascular loops, etc.). Asynchronous objective tinnitus generally corresponds to muscular contractions that require specific management. The pathophysiology of subjective tinnitus is more complex, showing strong analogies with postamputation pain syndromes. After peripheral middle ear or inner ear damage, auditory deafferentation could result in hyperactivity and/or functional reorganization within central auditory and nonauditory structures. This could explain the persistence of tinnitus after total hearing amputation (e.g., translabyrinthine approach for vestibular schwannoma) and associated symptoms such as hyperacusis or anxiety and depression. This central model finds strong support in animal experiments and in functional neuroimagery (PET, fMRI, MEG). Since no etiologically based therapies are currently available, severe subjective tinnitus management only targets tinnitus tolerance with sound enrichment or cognitive behavior therapy. However, in the near future better knowledge of tinnitus pathophysiology and innovative therapeutic tools could emerge from neuromodulation techniques such as repeated transcranial magnetic or epidural electric stimulation.
 ...
PMID:[Tinnitus treatment: neurosurgical management]. 1930 13


1 2 3 Next >>