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The aim of the paper is to present the most important neuroanatomical and neurophysiological studies concerning the phenomenon of sound localisation in space by people. The author analysed the available literature concerning this topic. The article presents different theories explaining the phenomenon of sound localisation, such as interaural differences in time, interaural differences in sound intensity, interaural and monaural differences in phase and the anatomical and physiological basis of these processes. It also describes methods of measurement of disturbances in sound localisation which are used around the world and in Poland, also by the author of this work. The author lists a number of reports on the neurological causes of disturbances in sound localisation, especially the ones connected with vascular damage of the brain. The reports indicate that it is the temporal and parietal lobes that play the role of cortical centres of sound localisation. Also, it should be pointed out that even though having two ears indeed makes it possible for humans to localise sources of sounds, the process itself takes place in the brain. (Folia Morphol 2015; 74, 1: 9–15)
Clinical observations supplemented with imaging examination show that the large vestibular aqueduct syndrome (LVAS) is a rare developmental anomaly of the inner ear, which leads to hearing loss. The authors present a case history, results of imaging examination (high resolution CT, MRI), results of hearing acuity examinations (tonal audiometry, otoacoustic emissions, brainstem auditory evoked potentials) and results of balance examinations (videonystagmography) in an 11-year-old boy suffering from deep mixed progressive hearing loss of the right ear due to head trauma. The aim of this paper is to specify the most typical clinical, radiological and anatomopathological manifestations of this pathology of the inner ear. The authors describe the diagnostic and identification difficulties associated with the mixed hearing loss observed in this case. The article also discusses the child’s activity limitations, which should be taken into account once diagnosis of this rare labyrinthine pathology is established. (Folia Morphol 2015; 74, 2: 265–271)
Background: Frontal aslant tract (FAT) is a white matter bundle connecting the pre-supplementary motor area (pre-SMA) and the supplementary motor area (SMA) with the inferior frontal gyrus (IFG). The purpose of the present study was to evaluate the anatomical variability of FAT. Materials and methods: Total number of fibres and the lateralisation index (LI) were calculated. We attempted to find factors contributing to the diversity of FAT regarding IFG terminations to the pars opercularis (IFG-Op) and to the pars triangularis (IFG-Tr). Magnetic resonance imaging of adult patients with diffusion tensor imaging (DTI) with total number of 98 hemispheres composed a cohort. V-shaped operculum was the most common (60.5%). Results: Total number of FAT fibres had widespread and unimodal distribution (6 to 1765; median: 160). Left lateralisation was noted in 64.3% of cases and was positively correlated with total number of FAT fibres and the bundle projecting to IFG-Op (p < 0.01). LI correlated with total number of FAT fibres (r = 0.43, p < 0.01). FAT projected predominantly to IFG-Op (88.9%; 88 of 99). Only in 3 (3.1%) cases more fibres terminated in IFG-Tr than in IFG-Op. Total number of FAT fibres and number of fibres terminating at IFG-Op did not correlate with the ratio of fibre numbers: FAT/IFG-Op, FAT/IFG-Tr and IFG-Op/IFG-Tr (p > 0.05). The greater total number of fibres to IFG-Tr was, the higher were the ratios of IFG-Tr/ /FAT (r = 0.57, p < 0.01) and IFG-Tr/IFG-Op (r = 0.32, p = 0.04). Conclusions: Among the IFG, the major termination of FAT is IFG-Op. Whereas the IFG-Tr projection seems to be related to the expansion of the entire FAT bundle regardless of side, domination and handedness. Nevertheless, FAT features a significant anatomical variability which cannot be explained in terms of DTI findings. (Folia Morphol 2017; 76, 4: 574–581)
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