Ontogenetic explanation for tegmen tympani dehiscence and superior semicircular canal dehiscence association. / Explicación ontogénica para la asociación entre dehiscencia del tegmen tympani y dehiscencia del canal semicircular superior.

OBJECTIVES: To analyze the ontogeny of the superior semicircular canal and tegmen tympani and determine if there are common embryological factors explaining both associated dehiscence. METHODS: We analyzed 77 human embryological series aged between 6 weeks and newborn. Preparations were serially cut and stained with Masson's trichrome technique. RESULTS: The tegmental prolongation of tegmen tympani and superior semicircular canal originate from the same structure, the otic capsule, and have the same type of endochondral ossification; while the extension of the squamous prolongation of tegmen tympani runs from the temporal squama and ossification is directly of intramembranous type. The nuclei of ossification of the superior and external semicircular canals and accessory of tegmen collaborate in the ossification of the tegmental extension and by growth extend to the tegmental prolongation. This fact plus the fact that both structures share a common layer of external periosteum could explain the coexistence of lack of bone coverage in tegmen and superior semicircular canal. CONCLUSION: The development of the semicircular canal and tegmen tympani could explain the causes of the association of both dehiscences.

Thickness of the bony otic capsule: etiopathogenetic perspectives on superior canal dehiscence syndrome.

The etiology of superior canal dehiscence (SCD) is controversial. An embryological perspective suggests that SCD may occur through the failure of postnatal bone formation over the superior semicircular canal (SC), whereas an acquired theory suggests that trauma or pressure from the overlying temporal lobe could break or gradually thin the SC. We infer the etiology of SCD by comparing the thickness of the bony otic capsule of the unaffected side of SCD patients with that of non-SCD participants. Twelve SCD patients (13 SCD ears and 11 normal ears) and 34 age-matched controls (68 ears) were included. The control group was subdivided into an aerated group (49 ears) and a nonaerated group (19 ears), as defined by the presence of air cells above the SC. A high-resolution temporal bone CT was performed in all participants. The thicknesses of the SC, horizontal canal (HC) and posterior canal (PC) of the unaffected ears of SCD patients were compared with those of the controls. The SC of the unaffected side in the SCD group (n = 11, 0.41 ± 0.23 mm) was significantly thinner than the one in the control group (n = 68, 0.64 ± 0.21 mm, p = 0.002). The HC and PC were also thinner in the SCD group (n = 24, 0.58 ± 0.11 and 1.39 ± 0.31 mm, respectively) than in the controls (0.70 ± 0.08 and 1.61 ± 0.32 mm; p < 0.0001 and p = 0.005, respectively). The SC, HC and PC thicknesses were also compared between the aerated and nonaerated ears within the control group. The SC was significantly thicker in the aerated group (0.73 ± 0.14 mm) than in the nonaerated group (0.60 ± 0.23 mm; p = 0.046); however, no significant difference was observed for the HC and PC thickness (aerated group, n = 49, 0.72 ± 0.07 and 1.67 ± 0.34 mm; nonaerated group, n = 19, 0.70 ± 0.09 and 1.59 ± 0.34 mm; p = 0.350 and p = 0.428, respectively). The bony otic capsule was significantly thinner in the SCD patients than in the controls. However, even within unaffected individuals, SCs lacking overlying air cells were also thinner than those with overlying air cells. These results suggest that both embryological and acquired factors affect the occurrence of SCD.

[Experimental study of the intrauterine ototoxicity of dibekacin]. / Etude expérimentale de l'ototoxicité in utero de la dibékacine.

Previous works have demonstrated that mammals are more susceptible to aminoside ototoxicity during the period of auditory development. In order to test the intrauterine ototoxicity of dibekacin, an experiment was designated in pregnant guinea pigs intoxicated during the last three weeks of gestation (100, 60 and 30 mg/kg for 8 days). Newborn guinea pigs were tested electrophysiologically by recording cochlear potentials from the round window in response to filtered clicks of various frequency. No fetal ototoxicity due to dibekacin could be detected in the 36 animals tested. This study indicates that dibekacin has a very low ototoxic effect, even during the period of increased sensitivity to antibiotics. Comparatively, kanamycin has a major ototoxic effect when it is administrated at the same dosage during the same period of time.

Observations of otoconial membranes from human infants.

The microdissection technique was used to study otoconial membrane from 30 human infants ranging from newborn to 2 years of age. Both saccular and utricular membranes were quite variable in overall shape. During the neonatal period, the gelatinous layer of the otoconial membrane appears to thicken and become less adherent to the macular surface than in the fetal period. In many infants older than 6 weeks, otoconial membranes were found at autopsy to be completely dislodged from the maculae, with abnormally large saccular otoconia present in four specimens. Fourteen of the infants studied died of sudden infant death syndrome and 16 died of other causes. The incidence of detached otoconial membranes was approximately the same in both groups. Although the majority of these membranes were apparently dislodged post mortem, the present findings suggest that otoconial membranes are susceptible to pathological alteration due to disease or head trauma.