Pain neuroscience. I think that I “get it” and can even practice physical therapy in a complementary manner. Perhaps I have been for the past decade or so, as a function of earnestly just not being a great manual physical therapist. I have defaulted to find sensory inputs through exercise, stretch, and symmetrical motion that activated, or better yet, interrupted chronic pain messages. As Tim Flynn and Jeff Moore state in their podcast “Pain Reframed”, sometimes (suggesting often) in non-specific low back pain (NSLBP), the “issue is not the tissue”.
This has resonated with me. In an effort to digest, adopt, and apply these concepts – it struck me that there is an analogy to chronic pain, and a need for this same “neuroscience” approach in the case of Persisted Postural Perceptual Dizziness, or PPPD, referred to and spoken-aloud as “3PD”. Very briefly, PPPD can and often does develop after a true physiologic impairment in the peripheral vestibular organs or the central processing therein. By definition, PPD has lasted for 3 months or longer, to truly be classified as a persistent sense of dizziness that is perceptual and not of physiologic origin – meaning that, just as noted above – the issue is not the tissue, but rather the strong and well-formed memory of such sensation.
This primer is only intended to be a first introduction-to and suggestion-of the analogy with pain neuroscience and is not intended to be the definitive comprehensive paper. At this time, I am choosing to coin this concept, “Vestibular Neuroscience” for obvious reasons.
Consider the similarities between PPPD and chronic pain:
- Multifactorial and sometimes trauma or no evident onset
- Chronic, 3 months or longer
- A primary maladaptive sensory experience
- Heightened sensitivity to sensory inputs, with many modalities pathologically interpreted (pain/dizziness)
- Misinterpretation of normal movement-based inputs as pathologic (painful or dizziness-provoking)
Does the analogy stop there? No. Recall that we have a very strong and primitive even survival-based capacity to remember episodic memories that evoke: fear, pain, or nausea. I will not debate the evolutionary nature of these sensations, yet consider those destined to survive recall where the lion’s den is, which bush’s berries are poisonous, and what that rattling sound is at our feet. In some of these instances, we may only get one chance to experience, remember and learn. The memories are well-formed and well-preserved.
The sense of sudden, disabling, vertigo that comes on without notice or explanation can be similarly strong and well-formed episodic memory. After a few such episodes fear of another episode can and often does lead to avoidant behavior, compensation (cervical stabilization, en block movements, or concentrated gaze stabilization), or even medication. As we know from many conditions of the nervous system – avoidance can be a dangerous compensation that falls into a well of learned non-use, call it what you may – a different name for each, if you will. We now recognize that in chronic pain, as in PPPD, that learned nonuse leads to hypersensitivity to the primary and related stimuli (bending at the waist for NSPLBP or a change in direction of walking for PPPD). This cycle of fear to avoidance to learned nonuse to hypersensitivity to greater fear, is well-trodden and needs no further coverage or figure to explain it here.
There is and will be more to follow on these musings. For now, consider the “analogy of the pathology” and be ready to consider the similarities in treatment, for the next blog.