Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 6 de 6
Filter
Add more filters










Database
Publication year range
1.
HNO ; 67(Suppl 2): 46-50, 2019 Jun.
Article in English | MEDLINE | ID: mdl-30927015

ABSTRACT

BACKGROUND: Tinnitus frequently occurs alongside psychological comorbidities whose assessment is important for treatment planning and -success. The selection of suitable questionnaires is thus crucial. The present study aims to investigate the ICD-10 Symptom Rating (ISR) to this regard. METHODS: The current study investigated tinnitus burden and psychological comorbidities in a sample of N = 311 patients with chronic tinnitus. All participants completed an intensive 7­day multimodal tinnitus-specific therapy. Tinnitus burden was measured using the German version of the Tinnitus Questionnaire (TQ). Psychological comorbidities were measured using the ISR (total score, depressive disorder, anxiety disorder, obsessive-compulsive disorder, somatoform disorder, and eating disorder), the Perceived Stress Questionnaire (PSQ; total score, tension, worries, joy, and demands), and the General Depression Scale (Allgemeine Depressionsskala, ADS). RESULTS: Sixty-five percent of participants suffered from psychological comorbidities. Treatment response comprised improvements in the TQ, ISQ, PSQ and ADS. At baseline, tinnitus-burden correlated with the ISR-total, ISR-obsessive-compulsive disorder and PSQ-tension scores. Post treatment, the-now reduced-tinnitus burden was additionally predicted by ISR-depressive and eating disorder scores. CONCLUSION: The ISR is a useful tool for measuring psychological comorbidities in patients with chronic tinnitus as well as short-term treatment response. Therapeutic approaches for chronic tinnitus should address stress-related tension, depressive symptomatology and coping strategies such as maladaptive eating behaviours.


Subject(s)
International Classification of Diseases , Tinnitus , Comorbidity , Depression/psychology , Humans , Psychiatric Status Rating Scales , Somatoform Disorders/psychology , Stress, Psychological/psychology , Surveys and Questionnaires , Tinnitus/diagnosis , Tinnitus/psychology
2.
HNO ; 67(3): 178-183, 2019 Mar.
Article in German | MEDLINE | ID: mdl-30806717

ABSTRACT

BACKGROUND: Psychological comorbidities are frequent in tinnitus patients and their diagnosis is important for both interventions as well as treatment success. The selection of suitable questionnaires is thus crucial. The present study aimed to investigate the ICD-10 Symptom Rating (ISR) questionnaire for the diagnosis of psychological comorbidities. METHODS: The current study investigated tinnitus burden and psychological comorbidities in a sample of n = 311 patients with chronic tinnitus. All participants completed an intensive 7­day multimodal tinnitus-specific therapy. Tinnitus burden was measured using the German version of the Tinnitus Questionnaire (TQ). Psychological comorbidities were measured using the ISR (total score, depressive disorder, anxiety disorder, obsessive-compulsive disorder, somatoform disorder, and eating disorder), the Perceived Stress Questionnaire (PSQ; total score, tension, worries, joy, and demands), and the General Depression Scale (Allgemeine Depressionsskala, ADS). RESULTS: Psychological comorbidities were suffered by 65% of participants. Treatment response comprised improvements in TQ, ISR, PSQ, and ADS. At baseline, tinnitus burden correlated with the ISR total, ISR obsessive-compulsive disorder, and PSQ tension scores. Post-treatment, the now reduced tinnitus burden was also predicted by the ISR depressive and eating disorder scores. CONCLUSION: The ISR is a useful tool for measuring psychological comorbidities in patients with chronic tinnitus as well as for assessing short-term treatment response. Therapeutic approaches for chronic tinnitus should also consider stress-related tension, depressive symptomatology, and coping strategies such as maladaptive eating behaviors.


Subject(s)
Mental Disorders , Tinnitus , Comorbidity , Depressive Disorder , Humans , International Classification of Diseases , Mental Disorders/epidemiology , Mental Disorders/psychology , Psychiatric Status Rating Scales , Surveys and Questionnaires , Tinnitus/epidemiology , Tinnitus/psychology
3.
Physiol Res ; 58(6): 895-902, 2009.
Article in English | MEDLINE | ID: mdl-19093732

ABSTRACT

Ischemia can contribute to the inner ear pathology and hearing loss. To determine the susceptibility of inner and outer hair cells (IHCs/OHCs) to ischemic and post-ischemic period, we used organotypic cultures of the organ of Corti isolated from P3 rats as an in vitro model of inner ear ischemia (oxygen-glucose deprivation, OGD). We identified the hair cells (HCs) by phalloidin staining. The cells with damaged cellular membrane integrity were identified by propidium iodide (PI)-exclusion assay. The cells with fragmented chromosomal DNA were detected by TUNEL assay. Organotypic cultures were subjected to a mild (3 h duration) or severe (4 h duration) OGD, followed by a recovery period of 21 h and 20 h, respectively. Mild OGD induced a loss of 10-20% HCs, whereas severe OGD induced loss of 35% HCs. We confirmed that OHCs are less vulnerable to OGD than IHCs. Of all missing OHCs, 80-90% was lost during the OGD period and 10-20% during the recovery period. In contrast, the loss of IHCs was equal during both experimental periods. The OGD period was mainly associated with PI-positive nuclei. TUNEL-positive nuclei were a minor fraction during the OGD period and increased during the recovery period, indicating the progression of DNA fragmentation. Our results implicate a differential susceptibility of IHCs and OHCs during and after ischemia-like insult, which may be of therapeutic consequence.


Subject(s)
Glucose/metabolism , Hair Cells, Auditory, Inner/metabolism , Hair Cells, Auditory, Outer/metabolism , Hyperglycemia/metabolism , Oxygen/metabolism , Animals , Animals, Newborn , Apoptosis , Cell Hypoxia , Cell Membrane Permeability , DNA Fragmentation , Hair Cells, Auditory, Inner/pathology , Hair Cells, Auditory, Outer/pathology , Hyperglycemia/pathology , In Situ Nick-End Labeling , Organ Culture Techniques , Rats , Rats, Wistar , Staining and Labeling/methods , Time Factors
4.
Prague Med Rep ; 110(4): 310-31, 2009.
Article in English | MEDLINE | ID: mdl-20059883

ABSTRACT

Recently we have demonstrated that recombinant human erythropoietin (EPO) protects neurosensory hair cells in the organotypic culture of the organ of Corti by reducing apoptosis and necrosis. In the present study, we tested the hypothesis that EPO may be involved in reparative angiogenesis. We analyzed in parallel the endogenous erythropoietin (Epo) mRNA expression and that of Epo receptor (Epor) and of genes associated with angiogenesis in the organ of Corti, the modiolus and the stria vascularis using real time reverse transcription polymerase chain reaction and microarray. We compared the expression levels of freshly prepared tissue (control) and tissue cultured for 24 h under normoxia or hypoxia. The basal expression of Epo- and Epor mRNA in controls of all regions was very low. However, after 24 h in culture, a 20-100 fold increase of these two transcripts was measured. In culture, the vascular endothelial growth factor and the Cxcr4 (the receptor for the stromal cell-derived factor-1, Sdf-1) mRNA levels, were found to be increased and the Sdf-1 mRNA level to be decreased. Changes in mRNA expression occurred in all pathways activated in non-erythroid cells by the application of EPO (phosphoinositide 3-kinase/serine-threonine protein kinase B, Janus-type protein tyrosine kinase 2/signal transducer and activator of transcription 3, and the mitogen activated protein kinase). These data suggest that the neuroprotective effect of EPO may include at least two molecular events, the decrease of hair cell death rate and the induction of angiogenic genes.


Subject(s)
Angiogenesis Inducing Agents/metabolism , Ear, Inner/metabolism , Erythropoietin/metabolism , Animals , Animals, Newborn , Cell Count , Cell Hypoxia , Cell Survival , Chemokine CXCL12/genetics , Chemokine CXCL12/metabolism , Ear, Inner/cytology , Ear, Inner/injuries , Hair Cells, Auditory , Oligonucleotide Array Sequence Analysis , Organ Culture Techniques , RNA, Messenger/metabolism , Rats , Rats, Wistar , Receptors, CXCR4/genetics , Receptors, CXCR4/metabolism , Receptors, Erythropoietin/genetics , Receptors, Erythropoietin/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Vascular Endothelial Growth Factor A/genetics , Vascular Endothelial Growth Factor A/metabolism
5.
Physiol Res ; 57(4): 631-638, 2008.
Article in English | MEDLINE | ID: mdl-17705670

ABSTRACT

An important mechanism underlying cochlear hair cell (HC) susceptibility to hypoxia/ischemia is the influx of Ca(2+). Two main ATP-dependent mechanisms contribute to maintaining low Ca(2+) levels: uptake of Ca(2+) into intracellular stores via smooth endoplasmic reticulum calcium ATPase (SERCA) and extrusion of Ca(2+) via plasma membrane calcium ATPase (PMCA). The effects of the SERCA inhibitors thapsigargin (10 nM-10 microM) and cyclopiazonic acid (CPA; 10-50 microM) and of the PMCA blockers eosin (1.5-10 microM) and o-vanadate (1-5 mM) on inner and outer hair cells (IHCs/OHCs) were examined in normoxia and ischemia using an in vitro model of the newborn rat cochlea. Exposure of the cultures to ischemia resulted in a significant loss of HCs. Thapsigargin and CPA had no effect. Eosin decreased the numbers of IHCs and OHCs by up to 25 % in normoxia and significantly aggravated the ischemia-induced damage to IHCs at 5 and 10 microM and to OHCs at 10 microM. o-Vanadate had no effect on IHC and OHC counts in normoxia, but aggravated the ischemia-induced HC loss in a dose-dependent manner. The effects of eosin and o-vanadate indicate that PMCA has an important role to play in protecting the HCs from ischemic cell death.


Subject(s)
Enzyme Inhibitors/pharmacology , Hair Cells, Auditory, Inner/drug effects , Hair Cells, Auditory, Outer/drug effects , Ischemia/enzymology , Plasma Membrane Calcium-Transporting ATPases/antagonists & inhibitors , Sarcoplasmic Reticulum Calcium-Transporting ATPases/antagonists & inhibitors , Animals , Animals, Newborn , Calcium/metabolism , Cell Survival/physiology , Eosine Yellowish-(YS)/pharmacology , In Vitro Techniques , Organ of Corti/cytology , Organ of Corti/physiology , Perilymph/physiology , Rats , Rats, Wistar , Vanadates/pharmacology
6.
HNO ; 54(9): 689-97, 2006 Sep.
Article in German | MEDLINE | ID: mdl-16479386

ABSTRACT

BACKGROUND: Transcription factor HIF-1 (hypoxia-inducible factor-1) regulates the expression of genes which are involved in glucose supply, growth, metabolism, redox reactions and blood supply. Hypoxia and ischemia play an important role in the pathogenesis of tinnitus and hearing loss. Therefore, HIF-1 activity and the expression of HIF-1 dependent genes in the cochlea were examined under ischemic and hypoxic conditions. MATERIAL AND METHODS: For the HIF-1 analysis, single-cell cultures of the organ of Corti (OC), stria vascularis (SV) and modiolus (MOD) were used. mRNA expression was analyzed in the organotypic culture using a microarray technique (RN U34-chip, Affymetrix). RESULTS: Ischemia (hypoxia without glucose) and pure hypoxia increase the HIF-1 activity identically, with the highest increase found in MOD and OC. The HIF-1 alpha mRNA levels were found to be higher in SV than in the OC and MOD. During culturing, there is a clear increase in HIF-1 alpha mRNA and the expression of a number of HIF-1 dependent genes, such as Gapdh/glyceraldehyde-3-phosphate dehydrogenase, Slc2a1/solute carrier family 2 (facilitated glucose transporter), member 1, Tf/transferrin and Tfrc/transferrin receptor, in all three regions. In SV, MOD and OC, increase in the expression of Hmox1/hemoxygenase 1, Nos2/nitric oxide synthase, inducible and Tfrc is particularly high. Hypoxia (5 h) results in an increased expression of Igf2/Insulin-like growth factor 2. CONCLUSION: The present data underline the contribution of radical forming processes to the pathogenesis of inner ear diseases. For experimental research, it is important to note that organotypic culture may be coupled with hypoxia.


Subject(s)
Cochlea/metabolism , Hypoxia-Inducible Factor 1/metabolism , Hypoxia/metabolism , Ischemia/metabolism , Animals , Animals, Newborn , Cell Hypoxia , Cells, Cultured , Gene Expression Regulation , Rats , Rats, Wistar
SELECTION OF CITATIONS
SEARCH DETAIL
...