Functions of the mastoid cell system: auto-regulation of temperature and gas pressure

This article presents a new approach to understanding the physiological functions of the mastoid cell system. It is suggested that the cell system, in combination with the continuous blood flow through the adjacent large vessels, makes up a compound functional unit that serves to protect the sensitive vestibular part of the inner ear from inadequate stimulation by external temperature changes. By virtue of the large surface area of the cell system mucosa with respect to the enclosed gas volume, the mastoid cell system may also work as a pressure regulator. Variations of the bi-directional exchange of fluid over the capillary network in the mucosa will change the size of the lumen that is available for the gas in the cell system. Volumes of gas and fluid can thus be exchanged to keep the intratympanic pressure within physiological limits. The process is most effective in a cell system with a high area-to-volume ratio.

Cerebrospinal fluid (CSF) otorhinorrhoea following vestibular schwannoma surgery treated by extended subtotal petrosectomy with obliteration

Extended subtotal petrosectomy as a treatment for persistent cerebrospinal fluid (CSF) otorhinorrhoea is presented. Four patients were successfully operated on by this technique, all previously having undergone suboccipital removal of vestibular schwannoma: other interventions used had failed to seal the fistulae. The internal auditory canal was the usual pathway for CSF leakage as well as retrosigmoid, retrolabyrinthine, retro- or perifacial cells. Total exenteration of middle ear and mastoid cell tracts, skeletonization of sigmoid sinus, jugular bulb and facial nerve, drilling out of semicircular canals, vestibule, and cochlea, and skeletonization of the internal auditory canal, followed by obliteration, are the main steps of this approach.

Hearing loss after microvascular decompression for trigeminal neuralgia

✓ Of 21 patients examined audiometrically before and after microvascular decompression of the trigeminal nerve, five (23.8%) had postoperative hearing impairment. A middle ear effusion was found in three (14.3%), probably caused by mastoid cell opening. A retrocochlear lesion in the other patients was caused by transferred pressure on the cochlear nuclei or by traction on the nerve. Vascular perfusion problems were also possible but are difficult to document.

Frequency of Pathologic Changes in the Middle Ear

One third of a total of 2,783 60-year-old males living in Gothenburg were examined to establish the frequency of pathologic changes in the middle ear. During 1973 to 1975, 767 men were examined. The eardrums were studied with otomicroscopy. Audiometric tests and x-ray of the mastoid cell system were performed. Pathologic changes were found in 37% of which 5% had chronic otitis. Hearing impairment was found in 95% of patients with chronic otitis. This group showed a significant reduction in mastoid cell area compared to males with normal tympanic membranes. There was a distinct relationship between low social class and small mastoid cell area and high frequency of noise injury.