In the literature the persistence of cerebrospinal Liquorrhea after temporal bone fractures is a rare event. Between 1989 and 1992 four cases of temporal bone fractures with dural involvement were operated at the University ENT Department Mainz. These temporal bone fractures showed delayed or persistent symptoms of dural lacerations between three and sixty months after head injury. During operation we found larger bone-dura defects (1-1.5 cm in diameter) and brain herniations in all cases. Strohm stated that only in rare cases a temporal bone fracture produced a larger gap in the tegmen tympani or antri. Therefore, we assumed that in our cases such larger bone-dura defects were caused by a gradual widening of the bony gap by a local elevation of intracranial pressure. Ferguson described this phenomenon in cases with spontaneous cerebrospinal Liquorrhea. Our cases showed that the cessation of cerebrospinal Liquorrhea is not a reliable sign of a healed dura defect. Therefore we propose that temporal bone fractures should be controlled closely in the first twelve months after trauma even if the dura defect seems to close spontaneously.

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The intraluminal surface of interposition connectos which are introduced for the quick vascular connection of microsurgical free flaps was coated by heparin. This heparin coating proved to be stable at the polyurethane wall until the intraluminal surface of the interposition connectors with a length of 15 mm was coated by a layer of endothelial cells. 90% of the experimental venous connections didn't show a thrombus formation and were open for the blood flow 10 days postoperatively. The experimental free flaps which were connected by this way had survived 21 days postoperatively and showed a regular healing.

23 patients with unilateral hearing loss and presence of TEOAE on both ears were examined with regard to the association between contralateral acoustic stimulation and evoked otoacoustic emissions. Contralateral white noise of 40 dB HL, 50 dB HL and 60 dB HL decreases the amplitude of TEOAE both at the ear with and without hearing loss. In comparison with a group of subjects with normal hearing, the decrease in the amplitude of TEOAE was less in the group of patients with hearing loss. Two paradoxical cases were found with an increase in the TEOAE amplitude in the ear with hearing loss during contralateral stimulation. It is assumed that impairment of the efferent synapses on the outer hair cells or of the decussated efferent nerve fibres at the floor of the fourth ventricle contributes to the pathogenesis of hearing loss. Impairment of the efferent system at brainstem level can explain the lower decrease in the amplitude both in the diseased ear and the normal ear. The behaviour of the normal ear during stimulation of the diseased ear can also be caused by disturbance of the afferent system.