5Wrong Place, Wrong Path: Electrode Misplacement and Migration
An array that reaches the cochlea is not the same as an array that reaches the right place. This module covers the geometry of failure - the tip that doubles back, the array that crosses the basilar membrane into the wrong scala, the insertion that stops short, and the lead that creeps out over the years - and how each is found and fixed.
CTip fold-over: the array doubles back
In tip fold-over the leading end of the array buckles and folds back on itself near the round window/basal turn, so apical contacts end up basal to where they should be and adjacent electrodes stimulate overlapping neural populations. It is uncommon (roughly 2% in mixed series) but over-represented with precurved/perimodiolar arrays and in malformed cochleae; advancing-off-stylet and over-insertion are contributing mechanisms. Detection: a reversed or compressed spread-of-excitation (SOE) profile, electric-field imaging, abnormal impedance/telemetry patterns, and definitively intraoperative or postoperative imaging (conebeam CT, plain transorbital/Stenvers radiograph). Management when caught early is withdrawal and careful reinsertion; left in place it degrades pitch ordering and speech perception and may need revision.[2017][2018]
CScalar translocation: crossing into the wrong scala
Translocation (scalar dislocation) is when the array starts in scala tympani but tears through the basilar membrane/osseous spiral lamina into scala vestibuli, usually around the basal turn where the array must turn. Arrays fully within scala tympani give better speech outcomes; scala vestibuli location and the number of contacts in SV predict poorer CNC word recognition - electrode position explains a large share of outcome variance. Array design matters: lateral-wall straight arrays sit in scala tympani far more often (~95%) than precurved perimodiolar arrays (~49% in comparative data), which translocate more frequently on meta-analysis. Translocation also destroys residual hearing, so it is especially costly in hearing-preservation/EAS candidates; gentle, slow, round-window insertion of an appropriately sized array reduces the risk.[2008][2021]
CWrong lumen, incomplete insertion, and the malformed ear
Partial/incomplete insertion leaves apical contacts unused (deactivated), wasting frequency channels and reducing low-pitch coverage; causes include ossification, a tight cochleostomy, kinking, or premature resistance. An array can stray entirely into the wrong space - the vestibule, a semicircular canal, the internal auditory canal through a modiolar/cribriform defect, or simply outside the cochlea in a common-cavity malformation. Misplacement into non-auditory tissue or the modiolus produces non-auditory percepts (e.g. facial nerve stimulation), poor or no useful hearing, and abnormal impedances. These are precisely the situations where intraoperative imaging and electrophysiology pay off, and why malformed ears are planned with the array choice and a confirmatory image in mind.[2018][1991]
CLate migration and extrusion
Migration is later movement of an initially well-placed array - it can withdraw (extrude) from the cochlea or shift position, presenting as a delayed decline in performance, new non-auditory stimulation, or rising/changing impedances. A poorly secured lead, a dislodged cochleostomy seal (as after a gusher), head growth in young children, and trauma are recognised contributors. Telemetry, impedance trends, electrode-by-electrode percept mapping, and repeat imaging localise the migrated contacts; minor changes may be managed by reprogramming/deactivation. Significant extrusion is a surgical problem requiring revision with reinsertion and re-fixation of the lead; the functional cost is loss of the migrated channels until corrected.[1991][2013]
What is the most likely problem?
Compared with apical placement in scala tympani, an array that translocates into scala vestibuli is associated with:
Which array type is most prone to scalar translocation and tip fold-over?
A previously well-functioning recipient develops a gradual performance decline with new facial twitching and changed apical impedances months after surgery. The array is intact on telemetry. What should be suspected?