Click here to get the ‘PIVC Activation Paradox’ handout

A colleague called a couple of nights ago to discuss an article she was reading and brainstorm about activities that activate versus suppress the peri-insular vestibular cortex (PIVC).

Her curiosity derailed my plan to post “Part 5” of my EOM educational series —because the conversation focused on how neuroanatomy & physiology shape our treatment activities.

Here’s what the evidence reveals:

Visual attention actively suppresses PIVC through glutamate downregulation.

When we ask patients to attend to visual motion, we may be neurochemically inhibiting the very cortical area we’re trying to engage.

But here’s the critical distinction:

PIVC activation depends on whether the patient experiences VECTION—the perception of self-motion through space—rather than simply on exposure to visual motion.

Small-field optokinetic stimulation? Produces a BOLD signal decrease in the PIVC.

Large-field egomotion-compatible optic flow that induces vection? Activates PIVC robustly.

This changes how I think about fixation targets.

Fixation during optic flow increases fronto-temporo-parietal activation—but this reflects visual attention networks, potentially at the COST of PIVC engagement.

So, when do we use fixation, and when do we avoid it?

USE fixation when the goal is HABITUATION—reducing symptom sensitivity, building tolerance, when vection would be overwhelming.

AVOID fixation when the goal is PIVC ACTIVATION—promoting vestibular processing, sensory reweighting toward vestibular inputs.

This is where head movements change everything.

When visual and vestibular stimuli are presented simultaneously, vestibular signals DOMINATE. Adding active head movements doesn’t just “shift the balance”—it can override visual attention-mediated PIVC suppression entirely.

The emerging parameters from the literature:

→ Field size: >90° (far peripheral most effective)

→ Motion: Translational, egomotion-compatible

→ Speed: Start at 10-20°/s, progress to walking pace

→ Head movements: Rotations for canals, translations/tilts for otoliths

For patients with PPPD and visual vertigo—populations showing decreased cortical activation and absent insular responses—this reframes our approach entirely.

Are we inadvertently reinforcing maladaptive visual dependence when we use small-field, attention-demanding visual tasks?

The goal isn’t visual challenge—it’s inducing vection while adding vestibular input.

We’d genuinely like to hear from colleagues working with these populations! Join our community here and let’s continue this conversation.

What parameters are you using? What’s your clinical experience with the habituation vs. PIVC activation distinction?

By Bridgett Wallace, PT, DPT ~ 360 Neuro Health Co-Founder & Director of Clinical Education