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Biomedical subjects

M Röttinger

Publications and source records attributed to M Röttinger.

5 recordsLinked to original sources
PubMed2005

Structural brain changes in tinnitus.

Tinnitus is a common but poorly understood disorder characterized by ringing or buzzing in the ear. Central mechanisms must play a crucial role in generating this auditory phantom sensation as it persists in most cases after severing the auditory nerve. One hypothesis states that tinnitus is caused by a reorganization of tonotopic maps in the auditory cortex, which leads to an overrepresentation of tinnitus frequencies. Moreover, the participation of the limbic system in generating tinnitus has been postulated. Here we aimed at identifying brain areas that display structural change in tinnitus. We compared tinnitus sufferers with healthy controls by using high-resolution magnetic resonance imaging and voxel-based morphometry. Within the auditory pathways, we found gray-matter increases only at the thalamic level. Outside the auditory system, gray-matter decrease was found in the subcallosal region including the nucleus accumbens. Our results suggest that reciprocal involvement of both sensory and emotional areas are essential in the generation of tinnitus.

Adult↗
PubMed2005

DWI in transient global amnesia and TIA: proposal for an ischaemic origin of TGA.

There are conflicting reports concerning signal intensity changes in transient global amnesia (TGA) using diffusion weighted imaging (DWI). We prospectively analysed DWI signal intensity changes in TIA and TGA patients, and compared the clinical characteristics and risk factors of both groups. Using DWI and conventional T1 and T2 weighted turbo spin echo sequences, 28 patients with acute TGA (13 men, mean age 61.5 years) and 74 TIA patients (47 men, mean age 62.4 years) were studied within 48 hours after symptom onset. Every patient underwent an intensive diagnostic investigation. In 10/28 (36%) of the TGA patients and 21/74 (28%) of the TIA patients, DWI signal intensity changes occurred. The time to DWI and the duration of symptoms were comparable in TIA and TGA patients. Overall, TIA patients showed an increased prevalence of vascular risk factors compared with TGA patients. In the TGA group, patients with abnormal DWI showed carotid atherosclerosis significantly more frequently. Based on our data, we suggest that the aetiology of TGA could be explained by an ischaemic event; due to arterial thrombembolic ischaemia in one subgroup, particularly in those patients with increased vascular risk factors, and due to venous ischaemia in another subgroup with valsalva-like activities before symptom onset.

Amnesia↗
PubMed2004

Transient ischemic attack and stroke can be differentiated by analyzing early diffusion-weighted imaging signal intensity changes.

BACKGROUND: Diffusion-weighted imaging (DWI) has been established to diagnose acute cerebral ischemia. Signal intensity changes occur not only in patients with definite stroke but also in up to 67% of transient ischemic attack (TIA) patients. We investigated the predictive value of DWI signal intensity changes to distinguish between TIA and stroke. METHODS: Clinical data, conventional magnetic resonance imaging (MRI), and DWI were collected in 60 consecutive patients with TIA and 37 consecutive patients with stroke. DWI was performed within 24 hours after symptom onset. Using an image analyzing system, we calculated the ratio of the lesion and corresponding contralateral normal tissue average signal intensity (rAI). RESULTS: Eighteen of 60 TIA patients (30%) revealed focal abnormalities on DWI. The mean duration of symptoms was 5.3 hours in TIA patients with DWI lesions and 5.2 hours in patients without lesions. The time to DWI was comparable in TIA and stroke patients. Even within 6 hours after symptom onset, the signal intensity was significantly higher (P=0.03) in stroke patients (n=13, rAI=1.26) as compared with TIA patients with DWI lesions (n=9, rAI=1.16). CONCLUSIONS: Our data indicate that already within 6 hours after symptom onset, TIA and stroke might be differentiated by analyzing the signal intensity of the lesions.

Aged↗
PubMed1999

[Surgical aortic fenestration in acute thoracoabdominal aortic dissection with abdominal malperfusion and end organ ischemia].

Intestinal, renal, spinal or peripheral arterial ischemia or failure of branch artery recanalization following initial prosthetic repair of thoracoabdominal aortic dissection is still a problem, with high morbidity and mortality. Five consecutive patients with acute thoracoabdominal aortic dissection (two type A dissections, three type B dissections) suffering from concomitant intestinal, renal, spinal and acute peripheral arterial ischemia are reported. Considering the anatomical and pathophysiological basis of thoracoabdominal aortic dissection and concomitant organ ischemia, the aortic fenestration procedure as a primary or secondary operative approach succeeded in restoring blood flow in all cases without complications. Assessment of the long-term results after 3 years revealed that all patients are doing well without any residual complaints. We conclude that in the case of persistent or secondary onset of aortic branch artery ischemia following initial prosthetic repair of either type A or type B dissection, aortic fenestration can be recommended immediately as a staged operative approach. Primary abdominal aortic fenestration is justified in acute type B dissection when end-organ ischemia becomes the focus of clinical deterioration.

Acute Disease↗