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Petra Georgiewa

Publications and source records attributed to Petra Georgiewa.

8 recordsLinked to original sources

A model of peripherally developing hearing loss and tinnitus based on the role of hypoxia and ischemia.

The incidence of sensorineural hearing loss often caused by direct damage to the cochlear hair cells is by far more frequent and more serious than disorders affecting the external ear or the middle ear. Mechanisms that are discussed to be relevant for the genesis of tinnitus and acquired hearing impairment are hair cell loss, signal transduction disturbances in the region of the outer and inner hair cells and the spiral ganglion, impairment of cochlear blood flow, mechanical disturbance, and hypoxia and ischemia. The present model surveys the possible cellular and molecular biological causes of peripherally developing hearing loss and tinnitus. In particular, the paper discusses the roles of hypoxia and ischemia in the cochlea and in the etiology of the neurosensory types of tinnitus. Peripheral origins of hearing disturbances and tinnitus may be: (a) damage to the stereocilia and the tip links, (b) dysfunction of potassium channels or (c) modification of the glutamate release. Moreover, the hypoxia inducible factor-1 may have an important role to play as a key transcription factor in the cells' adaptation to hypoxia and ischemia. An impairment of the cochlear blood flow may be induced by the expression of target genes like nitrogen monoxide synthase and endothelin-1 resulting in tinnitus. The paper discusses consequences resulting from the present model for the medical treatment of peripherally developing tinnitus and hearing loss.

Cochlea↗

A modified version of tinnitus retraining therapy: observing long-term outcome and predictors.

Tinnitus retraining therapy (TRT) in Germany includes not only directive counseling and sound therapy but also stress management and facultative psychotherapeutic treatment. The aim of the present study was to investigate the impact of this modified version of TRT on certain tinnitus-related aspects of distress and variables that may predict treatment outcome. Clinical data from 92 patients undergoing outpatient TRT in the Charité Tinnitus Centre were evaluated retrospectively over 1 year. Treatment outcome was defined by changes in specific areas of tinnitus-related distress and assessed by the Tinnitus Questionnaire. Changes in audiometric frequency and loudness of tinnitus were examined by regular audiometric testing. The overall Tinnitus Questionnaire score was significantly reduced after 1 year. Severely affected tinnitus sufferers (decompensated tinnitus) profited more than less affected patients (compensated tinnitus). In cases of indicated psychotherapy, improvement was significant for the patients who took advantage of psychotherapeutic treatment during TRT but was not significant for those who interrupted or dismissed an indicated psychotherapy. Changes in tinnitus-specific areas of distress were most pronounced in the scales for emotional and cognitive distress and intrusiveness. Significant changes in sleep disturbances, auditory perceptual difficulties and somatic complaints were observed in patients with decompensated tinnitus. In patients with chronic tinnitus, modified TRT may lead to significant subjective improvement in certain tinnitus-related symptoms like emotional and cognitive distress and intrusiveness. Particularly patients suffering from severe tinnitus distress take advantage of therapy. Careful psychotherapeutic diagnostics and therapies and, if necessary, motivation to make use of psychotherapy seem to be essential preconditions for therapeutic success in patients with severe psychosomatic comorbidity.

Adult↗

Cerebral processing of auditory stimuli in patients with irritable bowel syndrome.

AIM: To determine by brain functional magnetic resonance imaging (fMRI) whether cerebral processing of non-visceral stimuli is altered in irritable bowel syndrome (IBS) patients compared with healthy subjects. To circumvent spinal viscerosomatic convergence mechanisms, we used auditory stimulation, and to identify a possible influence of psychological factors the stimuli differed in their emotional quality. METHODS: In 8 IBS patients and 8 controls, fMRI measurements were performed using a block design of 4 auditory stimuli of different emotional quality (pleasant sounds of chimes, unpleasant peep (2000 Hz), neutral words, and emotional words). A gradient echo T2*-weighted sequence was used for the functional scans. Statistical maps were constructed using the general linear model. RESULTS: To emotional auditory stimuli, IBS patients relative to controls responded with stronger deactivations in a greater variety of emotional processing regions, while the response patterns, unlike in controls, did not differentiate between distressing or pleasant sounds. To neutral auditory stimuli, by contrast, only IBS patients responded with large significant activations. CONCLUSION: Altered cerebral response patterns to auditory stimuli in emotional stimulus-processing regions suggest that altered sensory processing in IBS may not be specific for visceral sensation, but might reflect generalized changes in emotional sensitivity and affective reactivity, possibly associated with the psychological comorbidity often found in IBS patients.

Acoustic Stimulation↗

An integrative model of developing tinnitus based on recent neurobiological findings.

Brain imaging studies suggest that the functional connectivity of various limbic, prefrontal, and temporal brain structures can be understood as the basis for particularly intense experiences of impairment and many secondary symptoms of decompensated tinnitus. Results to date suggest cortical plasticity as a likely mechanism to be involved in the chronic progression of tinnitus. Relationships between the processing of auditory signals and neural networks associated with somatosensory, attentional, cognitive and emotional processes are relevant for the genesis of the pathology. However, the neural bases of subjective impairment in tinnitus patients are unknown. An integrative model of developing tinnitus is presented here, based on the most recent neurophysiological data in current discussion. We assume the involvement of altered brain functions in the development and maintenance of perceptions of tinnitus and outline various possibilities which could contribute to decompensation and chronic progression. The discussions surrounding present models of the generation of tinnitus and its reinforcement to the point of decompensation make it clear that a unidimensional approach in clinical interventions is insufficient. Patients with decompensated tinnitus suffer from a complex somatic and psychological disorder. The interactive processes involving emotions, behaviour and symptoms, as well as the high co-morbidity with affective and psychosomatic illnesses and the important influence of psychosocial factors (distress), make the use of stage-appropriate interdisciplinary treatments necessary.

Brain↗

Protease-activated receptor 2 expression in trigeminal neurons innervating the rat nasal mucosa.

Protease-activated receptor 2 (PAR2) is activated by trypsin and mast cell tryptase to induce widespread inflammation by unknown mechanisms. Trypsin and tryptase were shown to activate sensory neurons to release substance-P and related peptides to mediate neurogenic inflammation. In the present study, the expression of PAR2 and tachykinins were investigated in rat trigeminal neurons that were identified by retrograde labeling with rhodamine dye from the nasal mucosa by using neuronal tracing in combination with immunohistochemistry. We found that large subpopulation of all trigeminal neurons (43.5+/-2.6%) identified by the pan-neuronal marker PGP 9.5 were stained with PAR2-immunoreactivity. Of all trigeminal neurons, 7.5+/-2.1% were immunoreactive for tachykinins and PAR2, and only 3.9+/-1.7% of all trigeminal neurons expressed tachykinins, but not PAR2-immunoreactivity. The present study also found that a large number trigeminal neurons innervating the nasal mucosa expressed PAR2-immunoreactivity. Of the rhodamine-labeled trigeminal neurons, 52.5+/-1.8% were immunoreactive for only PAR2 expression, 7.3+/-1.9% contained tachykinins and PAR2, and 3.1+/-0.4 of the rhodamine-labeled trigeminal neurons were non-immunoreactive PAR2, but were positive for tachykinins-immunoreactivity. In conclusion, based on the co-localization of PAR2 and tachykinins in trigeminal sensory neurons innervating the nasal mucosa, the present study suggests that, following an activation of PAR2 receptor in tachykinergic neurons by trypsin and mast cell tryptase, there may be a triggering of tachykinin-mediated phenomena such as neurogenic inflammation in allergic or non-allergic rhinitis.

Animals↗

Phonological processing in dyslexic children: a study combining functional imaging and event related potentials.

Difficulties in phonological processing are currently considered one of the major causes for dyslexia. Nine dyslexic children and eight control children were investigated using functional magnetic resonance imaging (fMRI) during non-oral reading of German words. All subjects silently read words and pronounceable non-words in an event related potentials (ERP) investigation, as well. The fMRI showed a significant difference in the activation in the left inferior frontal gyrus between the dyslexic and control groups, resulting from a hyperactivation in the dyslexics. The ERP scalp distribution showed a significant distinction between the two groups concerning the topographic difference for left frontal electrodes in a time window 250-600 ms after stimulus onset for non-word reading. Both the fMRI and the ERP results support differences in phonological processing between dyslexic and normal-reading children.

Child↗

How to avoid spurious cluster validation? A methodological investigation on simulated and fMRI data.

This paper presents an evaluation of a common approach that has been considered as a promising option for exploratory fMRI data analyses. The approach includes two stages: creating from the data a sequence of partitions with increasing number of subsets (clustering) and selecting the one partition in this sequence that exhibits the clearest indications of an existing structure (cluster validation). In order to achieve that the selected partition is actually the best characterization of the data structure, previous studies were directed to find the most appropriate validity function(s). In our analysis protocol, we first optimize the sequence of partitions according to the given objective function. Our study showed that an insufficient optimization of the partition, for one or more numbers of clusters, can easily yield a spurious validation result which, in turn, may lead the analyst to a misleading interpretation of the fMRI experiment. However, a sufficient optimization, for each included number of clusters, provided the basis for a reliable, adequate characterization of the data Furthermore, it enabled an adequate evaluation of the validity functions. These findings were obtained independently for three clustering algorithms (representing the hard and fuzzy clustering variant) and three up-to-date cluster validity functions. The findings were derived from analyses of Gaussian clusters, simulated data sets that mimic typical fMRI response signals, andreal fMRI data. Based on our results we propose a number of options of how to configure improved clustering tools.

Algorithms↗

Multicenter P300 brain mapping of impaired attention to cues in hyperkinetic children.

OBJECTIVE: To measure specific neurophysiological attention deficits in children with hyperkinetic disorders (HD; the ICD-10 diagnosis for severe and pervasive attention-deficit/hyperactivity disorder [ADHD]). METHOD: In a multicenter sample of 148 children with HD and control children aged 8 to 14 years, event-related potential maps were recorded during a cued continuous performance test (A-X/O-X). Maps to cues (requiring attention but no response) and distractors and performance were tested for differences between age- and sex-matched HD and control groups (n = 57 each), as well as between clinics (n = 5). RESULTS: The N1, P3a, and P3b maps revealed reliable attention effects, with larger amplitudes after cues than after distractors, and only minor differences across clinics. Children with HD missed more targets, made more false alarms, and had larger N1 followed by smaller P3b amplitudes after cues than did controls. Cue-P3b amplitude correlated with detecting subsequent targets. Cue-P3b tomography indicated posterior sources that were attenuated in children with HD. CONCLUSIONS: Brain mapping indicates that children with HD attend to cues (preceding potential targets) with increased initial orienting (N1) followed by insufficient resource allocation (P3b). These multiple, condition-specific attention deficits in HD within 300 msec extend previous results on ADHD and underline the importance of high temporal resolution in mapping severe attention deficits.

Adolescent↗