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The disorders of perceived auditory lateralization after unilateral damage of the cerebral hemispheres were investigated by dichotic presentation of pure tones, lateralization being obtained by interaural intensity differences. Observations were made on 107 unilateral brain-damaged patients and 30 normal subjects who were required to localize the perceived position of fused sound images. The images were generated by dichotic stimuli delivered through headphones and the patients were asked to point the perceived position. A clear-cut hemispheric asymmetry was found. Whereas left brain-damaged patients and right brain-damaged patients without visual field defects were not impaired in this task in comparison with controls, the performance of right brain-damaged patients with visual field defects was defective, with a systematic directional error towards the right side, that is, the side ipsilateral to the damaged hemisphere. The defect of auditory lateralization involved both the half-space contralateral to the lesion and the ipsilateral one. Different hypotheses are discussed in order to explain the present results. It is argued that they cannot easily be interpreted in terms of defective processing of sensory information and the proposal is made that lesions of the right hemisphere may produce a distortion of the internal representation of egocentric space to the right, yielding a systematic error of auditory lateralization are discussed.

35 neonates (mean gestational age: 34.9 +/- (SD) 3.5 weeks; mean birth weight: 2,180 +/- 890 g) treated with amikacin were examined for possible ototoxicity and nephrotoxicity. Audiometric tests were performed at 14.2-30.0 months postconceptional age by cross-checking behavioural with brain stem-evoked response audiometry. Only 1 infant was found with a mild hearing loss with brain stem audiometry, which, however, could not be attributed to amikacin with certainty. The effect of the aminoglycoside on the kidney was studied both by monitoring serum creatinine and the urinary elimination of the lysosomal enzyme N-acetylglucosaminidase (NAG). No significant difference was found in serum creatinine between the group under investigation and a control group of untreated premature neonates. A transient elevation was found in NAG urinary excretion in the neonates treated with amikacin. These results lead to the conclusion that amikacin at the recommended dosages (7.5 mg/kg every 12 h) causes a subclinical and reversible tubular damage in the neonate despite the high serum concentrations of the drug. The clinical relevance of this finding is discussed.