Valdueza. Extrajugular pathways of human cerebral venous blood drainage assessed by duplex ultrasound.

Although acoustic overstimulation has a major pathophysiological influence on the inner ear, central components of the auditory pathway can also be affected by noise-induced hearing loss (NIHL). The present study investigates the influence of a noise-induced temporary threshold shift (TTS) and/or permanent threshold shift (PTS) on neuronal cell densities in key structures of the central auditory pathway. Mice were noise-exposed (3 h, 5-20 kHz) at 115 dB sound pressure level (SPL) under anesthesia, and were investigated immediately (TTS group, n = 5) after the exposure, or 1 week later (PTS group, n = 6). Unexposed animals were used as controls (n = 7). Frequency-specific auditory brainstem responses (ABR) were recorded to examine auditory thresholds. Cell density was determined within the dorsal (DCN) and ventral (VCN) cochlear nucleus; the central nucleus of the inferior colliculus (ICC); the dorsal, ventral, and medial subdivisions of the medial geniculate body (MGBd, MGBv, and MGBm); and layer I to VI of the primary auditory cortex (AI I-VI). ABR thresholds were significantly elevated in the TTS group (52-69 dB SPL) and in the PTS group (33-42 dB SPL) compared to controls. There was a significant decrease in cell density only in the VCN of the TTS group (-10%), most likely induced by the acute overstimulation of neurons. Cell density was significantly reduced in all investigated auditory structures at 1 week post-exposure (PTS group), except in layer II of the AI (VCN: -30% and DCN: -30% (high-frequency); -39% (low-frequency); ICC: -31%; MGBd: -31%; MGBm: -28%; MGBv: -31%; AI: -10 to 14%). Thus there were dramatic changes within the neuronal cytoarchitecture of the central auditory pathway following a single noise exposure. The present findings should help clinicians to better understand the complex psychoacoustic phenomena of NIHL.

Sound-induced vertigo can occur in cochlear implantees. This seems to be primarily caused by electrical costimulation of the sacculus as part of the otolith organs.

No abstract

Noise exposure leads to an immediate hearing loss and is followed by a long-lasting permanent threshold shift, accompanied by changes of cellular properties within the central auditory pathway. Electrophysiological recordings have demonstrated an upregulation of spontaneous neuronal activity. It is still discussed if the observed effects are related to changes of peripheral input or evoked within the central auditory system. The present study should describe the intrinsic temporal patterns of single-unit activity upon noise-induced hearing loss of the dorsal and ventral cochlear nucleus (DCN and VCN) and the inferior colliculus (IC) in adult mouse brain slices. Recordings showed a slight, but significant, elevation in spontaneous firing rates in DCN and VCN immediately after noise trauma, whereas no differences were found in IC. One week postexposure, neuronal responses remained unchanged compared to controls. At 14 days after noise trauma, intrinsic long-term hyperactivity in brain slices of the DCN and the IC was detected for the first time. Therefore, increase in spontaneous activity seems to develop within the period of two weeks, but not before day 7. The results give insight into the complex temporal neurophysiological alterations after noise trauma, leading to a better understanding of central mechanisms in noise-induced hearing loss.

This study investigated the effect of systemic salicylate on central auditory and non-auditory structures in mice. Since cochlear hair cells are known to be one major target of salicylate, cochlear effects were reduced by using kanamycin to remove or impair hair cells. Neuronal brain activity was measured using the non-invasive manganese-enhanced magnetic resonance imaging technique. For all brain structures investigated, calcium-related neuronal activity was increased following systemic application of a sodium salicylate solution: probably due to neuronal hyperactivity. In addition, it was shown that the central effect of salicylate was not limited to the auditory system. A general alteration of calcium-related activity was indicated by an increase in manganese accumulation in the preoptic area of the anterior hypothalamus, as well as in the amygdala. The present data suggest that salicylate-induced activity changes in the auditory system differ from those shown in studies of noise trauma. Since salicylate action is reversible, central pharmacological effects of salicylate compared to those of (permanent) noise-induced hearing impairment and tinnitus might induce different pathophysiologies. These should therefore, be treated as different causes with the same symptoms.

Unilateral intracochlear electrical stimulation seems to facilitate the homeostasis of the network activity, since it decreases the spontaneous activity that is usually elevated upon deafferentiation. The electrical stimulation per se seems to be responsible for the bilateral changes described above, rather than the particular nature of the electrical stimulation (e.g., rate). The normalization effects of electrical stimulation found in the present study are of particular importance in cochlear implant recipients with single-sided deafness.

The purpose of the study was to evaluate transcranial Doppler ultrasonography for identifying cerebrovascular disease in neurologically asymptomatic children and young adults with sickle cell disease. A total of 47 consecutive patients with sickle cell disease (28 females, 19 males; age range 8 months to 29 years, mean age 9 years 6 months) were evaluated by transcranial color and duplex Doppler ultrasonography via transtemporal and occipital (2-MHz probe) as well as by transocular (5-MHz probe) approach. Eleven vessels (middle, posterior, anterior cerebral artery, vertebral artery, ophthalmic artery on each side and basilar artery) were analyzed in each patient. Following nine transcranial Doppler findings predictive for cerebrovascular disease, patients with one or more of those abnormal sonographic findings underwent MR imaging and MR angiography. In 8 patients with abnormal transcranial Doppler the MR angiography was normal. Thirty-one patients demonstrated normal results. In 15 of 16 patients with one or more abnormal Doppler findings (34% of all studied patients) MR imaging and MR angiography were performed. The MR angiography disclosed cerebrovascular stenosis in 7 patients (15% of all patients, 44% of those with pathological transcranial Doppler findings). In one of those patients MR imaging revealed silent peripheral ischemic infarction as well. Our findings indicate the usefulness of transcranial Doppler ultrasonography to reveal occult cerebrovascular lesions in neurologically asymptomatic patients with sickle cell disease. It should regularly be performed in all sickle cell patients in order to detect patients at risk for later stroke. Patients with homozygous disease and a high frequency of preceding sickle cell crises should be followed most closely.