UPDATE: Whiplash Trauma and Multiple Sclerosis
by Daniel J. Murphy, DC, FACO
Dan Murphy graduated magna cum laude from Western States Chiropractic College in 1978, and has more than 20 years of practice experience. He received Diplomat status in Chiropractic Orthopedics in 1986. Since 1982, Dr. Murphy has served part-time as undergraduate faculty at Life Chiropractic College West, currently teaching classes to seniors in the management of spinal disorders. Dr. Murphy is on the post-graduate faculty of several chiropractic colleges. His post-graduate continuing education classes include “Whiplash and Spinal Trauma” and “Pain Neurology.” Dr. Murphy is the coordinator of a year-long certification program in “Chiropractic Spinal Trauma,” now (2000) in its twelfth year of being offered. This year, the program is being offered through the International Chiropractors Association of California. He has taught more than 700 post-graduate continuing education seminars. Dr. Murphy is a contributing author to the book Motor Vehicle Collision Injuries, published by Aspen, 1996; and to the book Pediatric Chiropractic, published by Williams & Wilkins, 1998. He writes a quarterly column in the Journal of Clinical Chiropractic. In 1987, 1991 and 1995 Dr. Murphy received the Post-graduate Educator of the Year award, given by the International Chiropractic Association. In 1997, he received The Carl S. Cleveland, Jr., Educator of the Year award, given by the International Chiropractic Association of California.
In the mid-1980s, a local neurologist referred me a patient with trauma-related multiple sclerosis. The patient, a 26 year old female, did well under our management. Her legal case went to trial, and both myself and the referring neurologist testified about the patient’s clinical status, prognosis, and causation. We lost the trial, primarily on causation issues. Since then, new information regarding multiple sclerosis and trauma has been published. I present some of that information here:
Multiple sclerosis linked with trauma in court case
British Medical Journal, Vol. 313,
November 16, 1996
Reported by Bryan Christie
A former policeman was awarded $820,875.00 in damages by a court which accepted that he developed multiple sclerosis after sustaining whiplash injures in a road accident.
Although the judgment is controversial, it is expected to give rise to further legal action from patients with multiple sclerosis who suffered injuries before the onset of their symptoms.
The 49 year old man developed symptoms within a week of injuring his neck during a crash and overturn motor vehicle accident.
Neurologists who gave evidence on behalf of the officer told the court that they had seen people in which symptoms of MS developed within weeks of suffering whiplash injuries.
One professor of neurology emphasized that such injuries could not cause MS by themselves but could bring on the condition in already susceptible individuals. He noted that the patient “might well have lived a normal life but for the injuries he sustained.”
Dr. Charles Poser of the Harvard Medical School, said: “there were hundreds of such cases, too many to be caused by chance.”
The Judge (Lord) “accepted that the historical, anecdotal and experimental evidence supported the proposition that a causative factor in some cases” of MS, noting: “the medical witnesses “had all themselves seen cases where they had accepted that the onset or recurrences of symptoms had been brought about by trauma, especially whiplash injury. In my opinion, these circumstances are far too strong to be put down mere chance.”
Trauma to the Central Nervous System May Result in Formation or Enlargement of Multiple Sclerosis Plaques Controversies
in Neurology Charles M. Poser, MD; Archives of Neurology; Vol. 57 No. 7, July 2000 Dr. Poser is from the Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass. In this article, he notes the following:
In some patients with multiple sclerosis (MS), trauma may act as a trigger for the appearance of new or recurrent symptoms. Only trauma affecting the head, neck, or upper back, which may affect the brain and/or spinal cord, can be considered significant. This premise is based on the two considerations:
1. An alteration of the blood-brain barrier (BBB) is a necessary step in the pathogenesis of the MS lesion, and
2. Trauma to the central nervous system (CNS) can result in a breach of the BBB.
The fact that an alteration of the BBB is an important step in the formation of the MS lesion has been demonstrated many times by serial magnetic resonance imaging (MRI) studies and from positron emission tomography (PET) studies.
The alteration in the permeability of the BBB for the development of MS is most frequently triggered by an inflammatory immunological phenomenon.
Poser notes others who contend:
1. Repeated episodes of asymptomatic breakdowns of the BBB eventually leads to demyelination and symptomatic relapse.
2. Without BBB penetration, myelin injury would not occur.
3. The fact that MS is focal could be explained by local breakdown of the BBB.
4. It is clear that a breakdown of the BBB is an early if not the first step in plaque generation.
“For many years, trivial head injuries such as concussion were considered to result only in physiological disruption of neural function without anatomical changes.”
However, both spontaneous and experimental concussive CNS injury can cause diffuse microscopic lesions of blood vessel walls that often escape notice on superficial examination of the brain.
“The effects of minor trauma on the CNS assume great importance because whiplash injury is a frequent result of minor vehicular accidents, in particular, the rarely mentioned minor rear-end collision.”
Other authors note:
1. “Direct impact to the head is not necessary for brain injury; whiplash injuries can also cause brain damage.”
2. “The degree of associated bone and soft tissue injury has no bearing on the extent of the spinal cord injury or neurologic deficit.”
The fact that CNS trauma affects the deep cerebral white matter has also been demonstrated by MRI, even in patients who had experienced mild head injuries. Such white matter changes indicate alteration of the BBB.
Research on monkeys has shown that a blow to the occipital area altered the BBB in the medulla and in the cervical spinal cord.
Other experiments has shown small cerebral vessels and capillary damage in animals sustaining mechanical brain injury “too slight to produce microscopic intraparenchymal hemorrhage or other neuropathological changes but strong enough to provoke a physiological concussive response.”
Others have shown a “significant increase in BBB permeability in the brains of animals subjected to whiplash injury that had had no head trauma.”
The occurrence of MS exacerbations after trauma has previously been noted.
Trauma-induced alteration of the BBB did not always result in demyelination in patients with MS.
Research has “implicated trauma as a pathogenetic factor in the formation of MS lesions in the cervical spinal cord in cases studied postmortem, as a result of the normal stretching of the tethered cord during flexion and extension of the neck, especially in the presence of cervical spondylosis.”
Others blame “repeated episodes of trauma to the cervical cord to explain the frequent clinical association between cervical spondylosis and MS. This relationship has now been well documented by MRI in many patients with MS, revealing a close anatomical correspondence between compression of the cervical spinal cord by spondylosis or herniated discs, even in the absence of external trauma, and intraspinal plaques at the same level. Such MRI changes in the spinal cord have not been seen in patients with the same degree of spinal stenosis who do not have MS.”
“Magnetic resonance images of the neck in voluntary flexion show how traumatic hyperflexion-extension augments the degree of impingement on the spinal cord, while it cannot fully reflect the much more severe impact during the actual whiplash injury.”
Some MS experts have recognized the potential role played by trauma in the alteration of the BBB in MS, noting:
1. “Although there are many potential reasons for the BBB break, a simple model of traumatic damage could account for the commoner sites of lesions being in the highly mobile optic nerve and cervical cord, especially when tethered by the dentate ligaments.
2. Any mechanism which physically destroys the components of the BBB will render the CNS open to the cellular and molecular constituents of the blood. This causes inflammatory participants to be rapidly delivered to the site of injury in a gross, nonspecific fashion.
The author concludes:
“This side of the controversy is based on clinical, neuropathological, radiological, and experimental evidence.”
This review article has 44 references.
Acute cervical hyperextension-hyperflexion injury mayprecipitate and/or exacerbate symptomatic multiple sclerosis
Eur J Neurol 2001 Nov;8(6):659-64.
Chaudhuri A, Behan PO
We report here 39 cases in which definite multiple sclerosis (MS) was precipitated or exacerbated by specific hyperextension-hyperflexion cervical cord trauma.
The worsening or onset of the symptomatic disease bore a striking temporal relationship to the focal injury.
Our data suggests that central nervous system (CNS) — specific acute physical trauma such as cervical cord hyperextension-hyperflexion injury
may aggravate latent clinical symptoms in MS.
The deterioration of MS bore no direct relationship with the severity of neck injury.
Possible pathogenic mechanisms of focal CNS-specific trauma aggravating the course of asymptomatic or benign MS are discussed.
This may have implications in improving our understanding of the factors that may modify the clinical course of MS.
THESE AUTHORS ALSO NOTE:
The cause of multiple sclerosis (MS) is unknown.
Axonal pathology from focal trauma with an increase in nitric oxide in the brain, leads to demyelinating injury.
Certain factors modify the clinical course for MS by precipitating or
aggravating the clinical symptoms, including:
(3) electrical injuries
(4) penetrating and surgical wounds of the brain
(5) acute emotional psychological stress
(6) certain vaccinations
“Breakdown in the blood-brain barrier (BBB) is an early and obligatory event in the development of acute MS lesions.”
Focal hyperextension-hyperflexion injuries to the cervical spinal cord have been shown to cause a severe disruption of the BBB both locally and generally.
These authors have documented 39 patients who developed symptomatic MS or in whom a stable disease with minimal disability was converted to a rapidly progressive form within some days to weeks after an acute hyperextension-hyperflexion injury to the cervical spinal cord.
All patients in presented within 3 months from the date of their acute cervical cord injury from automobile, industrial or environmental accidents.
Of the 39 cases, 24 of were of new onset. These cases had no previous history of neurological symptoms and were previously in excellent health. The onset of symptoms occurred within 12 hours to 12 weeks post-trauma with a peak between 2 and 3 weeks.
In another 15 cases with pre-injury mild MS, their condition rapidly accelerated to a progressive form following their injury. The worsening of their MS occurred between 1 and 12 weeks post-trauma with a peak at 1-2 weeks.
In both groups, there was no correlation between the severity of injury and the subsequent deterioration of MS symptoms. There were no cervical vertebral fractures, dislocations or spinal cord compressions.
“The role of physical trauma on MS has been debated for a number of years.”
“In this case series, all the patients had developed new symptoms of MS within 3 months following the cervical spine hyperextension-hyperflexion injury.”
“The 24 patients with the new onset of MS had been in perfect physical health with no evidence of any disturbances within the CNS.”
“Fifteen cases were considered to have previous MS symptoms but few had any major disability prior to their acute cervical cord trauma.”
“It is important to stress that the trauma was of a uniform type in all cases, i.e. an acute hyperextension-hyperflexion focal injury to the cervical spinal cord.”
The majority of cases occurred in motor car accidents.
“The severity of the soft tissue injury was mild to moderate in the vast majority of the cases.”
The authors cite 9 studies (1946, 1950, 1957, 1964, 1966, 1975, 1975, 1988, 1991, 1992) that support that specific CNS trauma may precipitate or aggravate MS. The proposed mechanism in these studies includes:
(1) specific focal trauma
(2) co-existence of cervical spondylitic myelopathy
(3) mechanical stresses communicated to the cord via the denticulate ligaments during flexion of the spine
(4) repetitive stresses that cause breakdown of the BBB
(5) electrical injuries that cause breakdown of the BBB
The critical role of changes in the BBB influencing the clinical course
of MS has been evident since 1950.
“Research has clearly established that an abnormal BBB plays a critical role in the initiation and progression of demyelination.”
“Our hypothesis is that acute hyperextension-hyperflexion injuries of the neck will at the very least produce a local breakdown of the BBB.”
Massive breakdown of the BBB of the cord and of the brain follows experimental induction of whiplash injuries in monkeys.
There are many studies showing pathologically verified new MS plaques surrounding the specific areas where the BBB had broken down.
Therefore, any external factor that can influence the integrity of the BBB of an individual will increase chances to develop MS and have the potential to trigger the disease symptoms.
“The cervical region is the commonest site of spinal cord involvement in
MS and spinal cord atrophy provides the best correlate of the degree of disability. Thus, it would only seem logical that rapid progression of disability was a direct consequence of the cervical cord disease in our cases.”
CNS-specific focal trauma has a role in “precipitating the symptoms of undeclared MS and adversely affecting the course of benign MS.”
Cervical cord hyperextension-hyperflexion injury is likely to unmask or worsen the natural course of MS in a subgroup of affected patients.
“This may be important because the prevalence of asymptomatic (‘silent’)
MS has been estimated to be about 25% of that diagnosed in vivo.” [WOW!]
“Physiologically, CNS-specific trauma produces focal breaches in the BBB
and induces metabolic changes by activating the stress response.”
Focal trauma enhances the expression of nitric oxide synthase in the CNS microvasculature.
“In susceptible individuals, these effects might unleash critical changes in the levels of pro-inflammatory cytokines and nitric oxide, thus triggering MS symptoms ab initio or aggravating symptoms of pre-existing latent disease.”
Possible mechanisms as to how specific focal trauma can aggravate
(1) Increased permeability of BBB
(2) Increased production of pro-inflammatory cytokines
(3) Increased production of nitric oxide synthetase
(4) Synergistic effect of psychological stress
(5) Direct axonal injury
KEY POINTS FROM DAN MURPHY
(1) Whiplash and other spinal trauma can initiate MS signs and symptoms in asymptomatic, perfectly healthy individuals.
(2) Of those with MS, 25% have asymptomatic “silent” MS.
(3) Whiplash and other trauma can adversely affect the course of benign MS.
(4) The initiation of MS symptoms following trauma may manifest with
hours, peaks within days to weeks, and is rare after 3 months.
(5) Breakdown in the blood-brain barrier (BBB) is an essential event in
the development of MS.
(6) Breaching of the BBB results in a pro-inflammatory cytokines immune
system response. Consequently, I suggest that a logical aspect of management is chiropractic nerve function improvement (segmental, systemic, and postural chiropractic subluxation management), and the anti-inflammatory diet (more omega-3s with antioxidants and fewer excitotoxins, trans fatty acids, omega-6s, and saturated fats).
(7) The whiplash trauma involved may be minor.
Research Holds A Key To Understanding Mechanisms of Adjustments