In any MVA, the muscles of the head, neck, and jaw are invariably the most involved in residual long-term regional myofascial pain. Whether the mechanism of the accident involves a rear-end, head-on, or rollover impact, neck pain, headache, and jaw pain usually are inevitable. In the velocity-change, whiplash model of physical injury to these structures, the cause is felt to lie in the pendular effect of the skull on the neck. The relatively heavy skull renders the neck more vulnerable to damag-ing forces. However, this does not explain the same cluster of painful symptoms in low-velocity accidents, or when the head and neck were not subjected to unusual forces based on the particular dynamics of the accident. It also does not explain the relative absence of permanent myofascial pain in sports and competitive driv-ing pursuits. (Hint: sports participants and competitive drivers are functiondriv-ing as predators, not prey—they tend not to freeze when injured.)
Another explanation lies in the intimate neuronal connections of the locus ceruleus with sensory end organs and especially joint proprioceptors of the head and cervical spine. These sensory receptors provide the locus ceruleus with infor-mation about environmental threat through positional orientation of the head and its sensory apparatus. The orienting reflex is a gradual side-to-side rotation of the head allowing scanning of the environment for information. It utilizes all of the sense organs of the head, and is a basic and universal instinctual motor pattern for gathering sensory information in all species. Muscles of the head and neck are therefore intimately involved in sensory information in all situations, both with regard to feeding and to fight/flight survival.
Because of their intrinsic role in survival, bracing of head and neck muscles in response to threat renders them uniquely vulnerable to the conditioned incorpo-ration of this pattern of muscular holding in survival-based procedural memory, with subsequent persistent cervical myofascial pain. In addition, most of the mus-cles of the head and neck are derived from branchial arch (gill) musmus-cles of the embryo, and originally were involved in the process of respiration, also explaining their unique role in survival.
The jaw muscles have specific importance in survival. Jaw clenching (bruxing) is a primitive reflex, with its origins based on instinctual patterns involving use of the teeth and jaw in the most basic of survival activities: alimentation (eating), and as both offensive and defensive weapons. Bruxing (jaw clenching) after an MVA is part of the nonspecific protective muscular bracing patterns linked to unresolved arousal, leading to the well-known but perplexing condition of temporomandibu-lar joint (TMJ) syndrome. TMJ, therefore, may have nothing to do with injury in whiplash, but simply may reflect the primitive role of the jaw muscles in basic instinctual survival. This bruxing occurs mainly during sleep, a period of time in which the day’s experiences are integrated during dreams with old declarative and procedural memories linked to survival for the purpose of adding to one’s storehouse of survival skills. And of course bruxing at night is also a well-known symptom of nonspecific stress.
Conclusion
Clinical experience suggests that many victims involved in MVAs experience dis-sociation, or freezing, at the moment of the accident. Dissociation is known to be a major predictor of eventual development of PTSD, and is thought to reflect the freeze response seen in animals. The acculturated human species, unlike creatures in the wild, tends not to go through the stereotyped and instinctual neuromuscu-lar discharge of the freeze response in the face of trauma. This instinctual defect may relate to issues of suppressing inappropriate social behavior. The absence of the freeze discharge does not allow “completion” of the thwarted act of escape in procedural memory. The survival brain is “fooled” into thinking the threat is still present. Thereafter, resurrection of these procedural memories in the face of internal and external cues to the trauma eventually result in neurosensitization, or kindling, providing the context for the symptoms of complex PTSD, especially multiple somatic symptoms.
This model provides a unitary hypothesis for the myriad symptoms of whiplash.
It also provides a model for the concept of somatization, one of the more promi-nent co-morbid conditions seen in complex PTSD. In this model, myofascial pain is caused by inhibition of completion of the act of self-preservation through the freeze discharge after a life threatening experience. The specific distribution of the involved muscles is based on the self-protective muscular bracing response to movement patterns of the MVA, which will be stored in motor procedural memory. Those specific muscle groups will thereafter be activated to contract with any internal
or external cues to the unresolved trauma. Blood circulation to those muscles will be impaired because of autonomic dysregulation intrinsic to unresolved trauma.
Prolonged contraction with diminished circulation will lead to spasm/myofascial pain in the involved muscles. This hypothesis explains whiplash as a problem of altered brain memory circuits and false conditioned procedural memory, rather than injuries to muscles or other soft tissues. It also explains the frequent regional persistence of myofascial pain, and the only temporary benefit of treating the spine with manipulation or the muscles with massage or physical therapy.
Similarly, vestibular, auditory, visual, and autonomic symptoms of the post-concussion syndrome also represent somatic experiences of the MVA that are stored in procedural memory and linked to arousal circuitry within the amyg-dala. These symptoms will be perpetuated by any head movement reminiscent of the trauma, and also by nonspecific arousal or by declarative memory cues of the accident. For instance, many whiplash victims experience headache and neck tightening whenever they get into a car. The frequently delayed onset of symp-toms in low-velocity accidents is consistent with the development of kindling. This supports my premise that all of these symptoms are based on changes in brain physiology, not structural injury.
Although MTBI may be a cause of specific and sometimes persisting cognitive deficits in victims of MVAs, cognitive impairment in the whiplash syndrome is also explainable by the attention deficit, thought intrusions, and short-term memory deficits seen in trauma and dissociation related to the traumatic experience of the accident. In very low-velocity accidents, these alterations in brain function associated with trauma are more than likely to be the primary cause for significant persisting cognitive symptoms and impairment. Whiplash, in other words, is pre-dominantly a syndrome based on experience and the brain, rather than on injury and the tissues.
Notes
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