Understanding PPPD
Persistent postural-perceptual dizziness is a formally defined vestibular disorder: chronic dizziness, unsteadiness, or non-spinning vertigo present on most days for three months or longer, made worse by upright posture, by active or passive motion, and by exposure to complex or moving visual environments.
Its defining feature is a mismatch between history and findings. PPPD usually begins with something identifiable — a bout of vestibular neuritis, an episode of BPPV, a vestibular migraine, a panic attack, a concussion, or a whiplash. That original trigger resolves. The dizziness does not.
Patients with PPPD are frequently among the most thoroughly investigated people we meet, and among the most poorly served by that investigation. Every test comes back normal, and the accumulating implication is that the problem must be psychological.
At Cerebral Chiropractic Center, we take a specific interest in one question the standard PPPD workup does not ask: whether a degraded signal from the upper neck is part of why the system never recalibrated.
The Established Picture
PPPD is understood as a disorder of functional adaptation. In the accepted model, the acute event provokes a reasonable short-term response — the nervous system shifts to high-gain postural control, relies more heavily on visual information, and stiffens its strategy for staying upright. That response is appropriate while the system is genuinely unreliable.
The problem is that the adaptation fails to switch back off after the trigger resolves. The high-gain strategy becomes the default, and it produces symptoms of its own: exhaustion from standing, intolerance of visually complex environments, and a persistent sense of unsteadiness that is worse the harder the person concentrates on staying balanced.
This is a real and useful model. It explains the phenomenology well, and treatments built on it — vestibular rehabilitation, visual desensitization, serotonergic medication, and cognitive behavioral therapy — have genuine evidence behind them.
What the model describes less completely is why some people fail to re-adapt while others recover uneventfully from the same trigger.
The Question We Add
Re-adaptation requires something specific: a stable, reliable signal to recalibrate around.
Vestibular compensation is well studied, and its dependence on usable peripheral input is established. A persistent peripheral deficit is a recognized obstacle to durable central compensation. If a channel feeding the system is still delivering inaccurate information, the recalibration has nothing trustworthy to lock onto — and the high-gain strategy may be a rational response to a signal that genuinely is unreliable rather than a maladaptive habit.
Cervical proprioception is one such channel, and it is not routinely assessed.
The upper cervical spine supplies the position of the head relative to the trunk, and it does so through the most spindle-dense muscles in the human body. That input is what allows the nervous system to distinguish the head moving on a stationary trunk from the whole body moving together, since both produce the same signal at the inner ear. When it is degraded, the vestibular nuclear complex cannot resolve its inputs into a single answer.
Consider how often the triggering events for PPPD are also events that load the neck. Concussion. Whiplash. A fall. Even the vestibular events that do not obviously involve the neck often occur in people with a prior injury history nobody connected to anything.
We are careful about the strength of this claim. There is no controlled trial establishing that cervical dysfunction causes or perpetuates PPPD, and we will not imply one exists. What we propose is narrower and testable: that in a subset of PPPD patients — particularly those whose onset followed physical trauma — an unaddressed peripheral signal error may be part of why compensation has not completed.
Symptoms
- Dizziness, unsteadiness, or non-spinning vertigo present most days for three months or more
- Symptoms worse when upright and better when lying down
- Worse with active movement and with passive motion such as riding in a car
- Worse in visually complex environments — supermarket aisles, patterned floors, crowds, scrolling screens
- Better with distraction, worse with concentration on balance
- Fatigue disproportionate to activity
- Anxiety about symptoms, and often avoidance of the environments that provoke them
- Frequently accompanied by neck pain, tension, or headache at the skull base
- Normal results across vestibular testing, imaging, and neurological examination
Why the Anxiety Framing Is Incomplete
Anxiety is genuinely part of the PPPD picture, and the association between vestibular dysfunction and anxiety is one of the most robustly documented in clinical medicine. Among patients presenting for evaluation of dizziness, rates of panic disorder are elevated many times above the general-population rate, and most patients with panic disorder show demonstrable signs of peripheral vestibular dysfunction.
The usual interpretation runs one direction: dizziness is frightening, so anxiety follows.
There is a mechanistic interpretation as well. Reliable knowledge of one's position in space is a precondition for survival, and the nervous system does not treat spatial uncertainty as a neutral error. It treats it as danger. On that reading, an unresolved position signal reaching the structures that generate a threat response would produce anxiety directly — not as a psychological reaction to an unpleasant sensation, but as the predictable output of a system that has concluded it cannot locate itself.
The distinction matters practically. If the anxiety is downstream of a signal error, then treating the anxiety addresses the amplifier rather than the source, which may be part of why response is so often partial.
How We Evaluate It
We do not position ourselves as replacing the standard PPPD pathway. Vestibular rehabilitation and appropriate medical management have real evidence behind them and we recommend both. What we add is an examination of the cervical contribution.
- History, focused on what preceded the trigger as well as the trigger itself — prior falls, collisions, concussions, and sport or service history.
- Position-dependent testing. Balance, leg length, and limb strength assessed with the head neutral and then rotated. Findings that change with head position implicate the neck.
- Craniocervical assessment for alignment and stability at C0–C2.
- Imaging matched to the question. Three-dimensional upright imaging or cone beam CT for bony position, and where indicated cine phase-contrast MRI for fluid dynamics at the junction.
How We Treat It
If the evaluation identifies a structural problem at the craniocervical junction, we correct it — with a low-force, imaging-calculated, instrument-delivered correction applied without rotating the head — and then re-measure both the structure and the neurological findings.
The goal is specific and modest: to restore the fidelity of one input, so that the rehabilitation that addresses the adaptation has an accurate signal to work with. In our experience, patients who have plateaued in vestibular rehabilitation sometimes progress again once that input is corrected. That is a clinical observation rather than a controlled finding, and we present it as such.
If we do not find a structural contribution, we will tell you, and we will say so plainly rather than treating you anyway.
If Everything Has Been Normal and You Are Still Dizzy
Three years of normal test results is not evidence that nothing is wrong. It is evidence that the tests performed did not cover whatever is.
A workup that has examined your inner ear, your brain, and your psychology thoroughly, and has not examined the joint your skull sits on, has left a specific and checkable question open.
Call us at (727) 677-0001 and we will check it.
References
- Popkirov S, Staab JP, Stone J. Persistent postural-perceptual dizziness (PPPD): a common, characteristic and treatable cause of chronic dizziness. Practical Neurology. 2018;18(1):5–13.
- Staab JP, Balaban CD, Furman JM. Threat assessment and locomotion: clinical applications of an integrated model of anxiety and postural control. Seminars in Neurology. 2013;33(3):297–306.
- Peng B, Yang L, Li Y, Liu T, Liu Y. Cervical proprioception impairment in neck pain: pathophysiology, clinical evaluation, and management. Pain and Therapy. 2021;10(1):143–164.
- Treleaven J. Sensorimotor disturbances in neck disorders affecting postural stability, head and eye movement control. Manual Therapy. 2008;13(1):2–11.
- Lacour M, Bernard-Demanze L. Interaction between vestibular compensation mechanisms and vestibular rehabilitation therapy. Frontiers in Neurology. 2015;5:285.
- Dutheil S, Watabe I, Sadlaoud K, Tonetto A, Tighilet B. BDNF signaling promotes vestibular compensation by increasing neurogenesis and neuronal survival in the deafferented vestibular nuclei. Journal of Neuroscience. 2016;36(23):6199–6212.
- Hall CD, Herdman SJ, Whitney SL, et al. Vestibular rehabilitation for peripheral vestibular hypofunction: an updated clinical practice guideline. Journal of Neurologic Physical Therapy. 2022;46(2):118–177.
- Furman JM, Jacob RG. A clinical taxonomy of dizziness and anxiety in the otoneurological setting. Journal of Anxiety Disorders. 2001;15(1–2):9–26.
- Balaban CD, Thayer JF. Neurological bases for balance-anxiety links. Journal of Anxiety Disorders. 2001;15(1–2):53–79.
- Indovina I, Riccelli R, Chiarella G, et al. Role of the insula and vestibular system in patients with chronic subjective dizziness: an fMRI study using sound-evoked vestibular stimulation. Frontiers in Behavioral Neuroscience. 2015;9:334.
- Barmack NH. Central vestibular system: vestibular nuclei and posterior cerebellum. Brain Research Bulletin. 2003;60(5–6):511–541.