Diagnostics of perilymphatic hypertension

Abstract

Perilymphatic hypertension is a term which is under discussion. It should be emphasized that it is more a syndrome which largely reflects an unusual wide communication between the CSF and perilymph-filled spaces or a transmission of a pathologically raised ICP to the perilymph (Paparella et al. 1988; Mangabeira-Albernaz et al. 1992). It is, thus, misleading to conclude that “hypertension” relies on an increase in absolute perilymphatic pressure (Marchbanks and Reid 1990). On the contrary, the intracranial and intracochlear (i.e. perilymphatic) pressure parallel each other (Marchbanks 1990). However, the substantial pulsation of the brain and CSF can be transferred in those patients with perilymphatic hypertension directly to the perilymph-filled spaces of the cochlea (Densert et al. 1981). There are two prominent anatomical deficits which are described to be responsible (Fig. 1 and 2), i.e. a particularly wide cochlear aquaeduct and a wide internal auditory canal or a fundus defect (Schuknecht and Reisser 1988). This results in a “gusher”-type outflow of CSF when the stapes footplate is perforated (Allen 1987). On the other hand, normal-pressure hydrocephalus, benign intracranial hypertension (pseudotumour cerebri) or any increase in intracranial pressure (ICP) have a major impact on cochleovestibular function (Sismanis 1987; Sismanis et al. 1990) by increasing the perilymphatic pressure in absolute terms at the same time. It is therefore the aim of the present paper to report on patients with “perilymphatic hypertension” and to briefly review key symptoms, its diagnostics and the alternative treatment.