This is an excerpt from Clinical Guide to Positional Release by Timothy Speicher.
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland’s classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
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