The disorder

The third window

Everything about SSCD follows from one idea: a hole that should not be there. Grasp the third-window mechanism and the whole symptom list becomes predictable.

Two windows, then three

Trainee

Normally the stapes drives fluid in at the oval window and the round window relieves it — two windows. A dehiscence adds a third window at the top of the superior canal, a low-impedance path that diverts acoustic and pressure energy.1 Toggle the model:

dehiscenceoval windowround windowsound inenergy shunted ↑
With a third window, sound and pressure drive flow up through the superior canal — stimulating it (sound/pressure vertigo) — while energy diverted from the cochlea produces the low-frequency air–bone gap, and enhanced bone conduction causes autophony and bone-conduction hyperacusis.

One mechanism, two symptom clusters

The same leak produces a vestibular cluster (sound/pressure vertigo, oscillopsia, chronic imbalance) and an auditory cluster (autophony, bone-conduction hyperacusis, pulsatile tinnitus, the pseudo-conductive gap). Holding the third window in mind lets you predict which tests will be abnormal — explored in Diagnosis & tests. For the normal canal and otolith physiology this builds on, see Physiology and Anatomy.

Why the bone is missing

A temporal-bone survey found frank dehiscence in ~0.5% and critically thin bone in ~1.4%, suggesting a developmental failure of the bone to thicken after birth.2 Most authorities favour a two-hit model: a congenitally thin roof that becomes symptomatic only after a second event — head trauma, a rise in intracranial pressure, or erosion against the middle-fossa dura or superior petrosal sinus.3 The same mechanism over other sites gives the related third-window lesions.

Key points

  • SSCD adds a third window to the normal oval and round windows.
  • Shunted energy stimulates the superior canal (vertigo) and diverts sound from the cochlea (air–bone gap).
  • Enhanced bone conduction explains autophony and bone-conduction hyperacusis.
  • A congenitally thin roof plus a second hit (trauma, raised ICP) is the favoured aetiology.