Question
Hello. I am a 27 year old female.  In June 2008, I was in a car accident where I was the driver (I was alone).  I was stopped behind a vehicle making a left hand turn, when the vehicle behind me struck me and forced me into the car in front of me.  I was initially fine, except some burns and pain from the airbags deploying.  The next morning I was in horrible pain, I could barely move, hold anything, turn a door knob, stand, sit, walk, etc... I have been seeing a chiropractor 3 times a week since a week after my accident.  I have had x-rays, MRIs, etc... X-rays of my hands, wrists, neck and back showed normal.  MRI of neck and lower back showed normal.  My pain management doctor suggested that I may have a pinched nerve (but I haven't had any tests for nerve damage to date).

I went to see my Primary Care Physician recently and I explained to her that there is something seriously wrong with the left side of my body. So she is referring me to a neurologist to rule out MS (Multiple Sclerosis).  

A lot of my pain seems to be stemming from right near my shoulder blade on my left side, which my chiropractor has told me that is a major nerve connected there and he knows something is happening there but is not sure what.

A couple days ago, I was a passenger in a vehicle and I had crossed my legs for about 10 mins.  When I went to uncross them....I couldn't move my leg.  It seemed like my entire leg went dead.  I had to physically lift my leg out and then I couldn't walk.  I have also been having several problems like that since the accident (among other things)...I have problems with balancing, the same leg has been weakening and will give out on me, and I frequently have numbness and tingling in that foot.  I also noticed that gibberish will come out of my mouth sometimes and I won't be able to stop it.  My PCP is referring me to a neurologist to rule out Multiple Sclerosis (MS).  

I am thoroughly confused...neither I, nor any member of my family has ever had a problem with MS.  Is it possible to have MS as a result of the accident?  Or are my symptoms explainable with having a pinched nerve?  Please help.

Is it possible that I have MS as a result of the car accident?  I have never had a history of MS or anything near it and it certainly doesn't run in my family.  

Answer
Dear Trish,

There is information in the scientific literature that indicates that occupants involved in collisions are more susceptible to the development of MS post crash.  I have never personally seen this in practice, but have discussed with with clinicians who have seen it. I would encourage you to print out this response...it is lengthy and technical.  You may need to discuss this with your treating chiropractic physician, your PCP as well as the neurologist.

Even though there have been reports describing a connection between multiple sclerosis and mild traumatic brain injury (MTBI)the epidemiological link appears weak (1,2). Nevertheless, in 1996 a former policeman in England was awarded $820,000 after developing multiple sclerosis following a CAD injury sustained in the line of duty (3), although this was later taken away on appeal. The most recent and definitive word on the subject comes from the American Academy of Neurology which concludes that the evidence does not support a causal connection between trauma and MS. (4)

Therefore, I would suggest that you more likely have a diffuse axonal injury or post concussive syndrome, which are difficult to ascertain with normal imaging techniques.  We know they often occur in whiplash trauma, but the diagnosis is mostly a clinical one.  Note:  the best test for MS is usually regarded to be the Brain MRI, however, there are some techniques that may help diagnostically.

Brain Stem Auditory Evoked Responses (BAER)
Clinical Applications:  Since the brain stem is very often the source of trouble in whiplash-related MTBI, a test that evaluates this structure is quite useful. The BAER allows us to investigate the integrity of the auditory nerve, the cochlear nucleus, the superior olive, the lateral lemniscus, and the inferior colliculus. Lesions in (post concussion syndrome)PCS have been noted as centrally as the superior olive. BAER is useful in the evaluation of a number of disorders, including the following:

1) Determining the cause and reversibility of coma.
2) Detecting multiple sclerosis.
3) Early detection and localization of posterior fossa tumors.
4) Detecting evidence of PCS (5,6,7,8,9,10,11).

Procedure:  The patient wears a set of headphones. Into the ear tested is delivered a series of 60 dB clicks. The contralateral side is masked with white noise. Recordings are made over the scalp using standard EEG electrodes. The sound generates an impulse which travels through the auditory apparatus and on to its cortical target. Five distinct wave patterns, representing the auditory nerve, cochlear nucleus, superior olive, lateral lemniscus, and inferior colliculus respectively, are produced. Another way of describing it is that waves I, II and V represent the acoustic nerve, pons, and midbrain respectively. These potentials are electrically very weak and are only about 1/100 the amplitude of the background EEG. Therefore, they must be extracted, averaged, and displayed by computer.

Indications:  With regard to the evaluation of PCS, the best indication for BAER is dizziness or vertigo. Because the cause of loss of consciousness is primarily the result of trauma to the brain stem, LOC and PTA also are indications for BAER. It should be noted, however, that normal BAERs are not always an accurate indicator in trauma. It is not uncommon for head trauma patients in the ICU to die of their injuries, despite normal BAERs. There are also a number of pontine and midbrain structures that cannot be evaluated using BAER.

Visual Evoked Potentials (VEP)
There is a tendency for physicians to use the expression evoked potentials when referring to any of a number of these tests. This can lead to confusion, because there are several types of evoked potentials (visual, brain stem auditory, somatosensory, motor, etc.). It is best to be as specific as possible, particularly when speaking of somatosensory evoked potentials (SEP) and dermatomal somatosensory evoked potentials (DSEP), which sound similar, but do have their differences. A number of visual and neurologic disorders can be evaluated with VEP.

Clinical Application:  As with BAER, VEP relies on computer averaging of signals which are, in this case, evoked by various types of visual stimulation. Disorders in which the VEP is abnormal include the following:

1)  Optic neuritis.
2)  Glaucoma.
3)  Other lesions of the optic nerve or anterior visual pathway.
4)  Multiple sclerosis.
5)  BI2 deficiency.
6)  Parkinson's disease.
7)  Migraine.
8)  Down's syndrome.
9)  Cortical blindness.
10)  Occipital lobe lesions.
11)  Huntington's disease.
12)  Friedreich's ataxia.
13)  Charcot-Marie-Tooth disease.
14)  Phenylketonuria.

Indications:  There is evidence for the usefulness of VEP in certain instances of MTBI, although it is generally done as part of the brain map or brain electrical activity mapping (BEAM). VEPs were recorded in 50 patients with MTBI and the data compared to controls (12). None of the patients had visual complaints. The aim was to investigate a possible visual pathway disorder and test the usefulness of VEPs as an objective noninvasive tool in the detection of a possible subclinical affection of the visual system in MTBI. The authors' data did suggest a disturbance of the human visual pathway. They concluded that "VEP recording seems to be a useful, objective, noninvasive tool, helping to identify possible subclinical affections of the visual pathway."

REFERENCES listed in above text:
1) Poser CM: The role of trauma in the pathogenesis of multiple sclerosis: a review. Clin Neurol Neurosurg 96:103-110, 1994
2) Kurland LT: Trauma and multiple sclerosis. Ann Neurol 36:S33-S37, 1994.
3) Christie B: Multiple sclerosis linked with trauma in court case. BMJ 313:1228, 1996
4) Goodin DS, Ebers GC, Johnson KP, Rodrigues M, Sibley WA, Wolinsky JS: The relationship of MS to physical trauma and psychological stress. [Report of the therapeutics and technology assessment subcommittee of the American Academy of Neurology.] Neurology 52:1737-1745, 1999.
5) Rowe, JM, Carlson C: Brain stem auditory evoked potentials in postconcussion syndrome.  Arch Neurol 37:679-683, 1980.
6) Benna P, Bergamasco B, Bianco C, et al.: Brain stem auditory evoked potentials in postconcussion syndrome.  J Neurol Sci 3:281-287, 1982.
7) Schoenhuber R, Bortolotti P, Malavasi P, et al.: Brain stem auditory evoked potentials in early evaluation of cerebral concussion.  J Neurosurg Sci 27:157-159, 1983.
8) Ruth RA, Ringer BB: The auditory brain stem response in patients with mild head trauma.  Presented to the American Speech and Hearing Association meeting, Toronto, Canada,
1982.
9) Schoenhuber R, Bortolotti P, DiDonato G, Gentilini M, et al.: Brain stem acoustic evoked potentials in 165 patients examined within 48 hours of a minor head injury.  In Morcutti C,
Rizzo PA, (eds).  Evoked Potentials, Neurophysiological and Clinical Aspects, Amsterdam, Elsevier Science Publishers BV (Biomedical Division), 1985, pp237-241.
10) Schoenhuber R, Gentilini M: Auditory brain stem responses in the prognosis of late postconcussion symptoms and neuropsychological dysfunction after minor head injury.  
Neurosurg 19:532-534, 1986.
11) Schoenhuber R, Gentilini M, Orlando A: Prognostic value of auditory brain-stem responses for late postconcussion symptoms following minor head injury.  J Neurosurg 68:742-744,
1988.
12)Papathanasopoulos P, Konstantinou D, Flaburiari K, Bezerianos A, Papadakis N, Papapetropoulos T: Pattern reversal visual evoked potentials in minor head injury. European Neurology 34(5):268-271, 1994.

Now concerning MTBI, I have my own clinical protocols that I use in addition to outside medical imaging techniques.  Below you will find my evaluation and counseling statements in regard to how we address the patients in our clinic.  I hope you find it useful.

E/M Counseling Supplement for Patient Treatment
Traumatic Brain Injury/Mild Traumatic Brain Injury/Concussion

Motor vehicle trauma is the single most important factor in both fatal and mild brain injuries. Early reports ranged from 40% to 60% caused by motor vehicle crash (MVC) with concussion being the most common diagnosis given. (15,27,57) More recent accounts report MVC as the origin of 60% to 67% of all occurrences. (1,21)  Many of these MVC-related injuries are the result of blunt head injury, which describes contact with some object without penetration of the skull, such as striking the steering wheel, dash board or the B pillar of the doorframe. However, it has been shown that non-contact concussion is a common result of acceleration type injuries.  The term of choice today is traumatic brain injury (TBI) or mild traumatic brain injury (MTBI). (15)

Mechanism of Injury: Previously thought to be a direct shearing of axons, the actual mechanism is from abrupt acceleration and deceleration of brain tissue. (39) The initial shear effect creates the activation of a degenerative cascade. During a low speed whiplash injury, (7 mph) the head may be accelerated at 9-18g. (58)  Since the brain is a soft structure, shear strains are created as the outer part of the brain moves at a different pace than the inner part of the brain.  This is intensified as the momentum of the head changes rapidly in a sagittal direction during a whiplash trauma, and when head impact occurs inside the vehicle.  The most important factors in whiplash-induced concussion are angular acceleration, flexion/extension of the neck, and increased intracranial pressure gradients. (40,41,52)

Animal studies confirm the real issue of induced concussion from acceleration/deceleration even though animals did not lose consciousness. (32,33) Portnoy et al. reported that significant increases in intracranial pressure were measured in baboons exposed to whiplash.  Examination discoveries included suprascapular intramuscular hemorrhages. (47) Hemorrhages were not from contact. Acceleration, deceleration, and shear were mechanisms of injury.  Non-centroidal motion in the coronal plane was found to be the most injurious and non-centroidal acceleration in the sagital plane to be least injurious concerning brain injury. (22,38,56) Although this infers that lateral whiplash motions of the head are more likely to produce concussion or diffuse axonal injury (DAI) than frontal or rear impacts, MTBI and DAI have been found in both types of collisions.  

According to the work of Hinoki, the integrity of the brainstem reticular formation is largely responsible for maintaining levels of consciousness.  A study by Jane et al. proved conclusively that non-centroidal accelerations of the head (without contact) could produce damage to axons in the inferior colliculus, pons, and dorsolateral medulla, which are in close proximity to the reticular formation. (25) The authors discussed the previous work of Povlishock et al., who presented the pathogenesis of DAI.  Their proposed mechanism of trauma is not necessarily an immediate shearing of axons, but rather a reactive degeneration secondary to trauma. (48,49) Others have corroborated this concept of continuing degeneration, such as Gennerelli, in statements that MTBI should be considered a process rather than an event. (21). In addition we know that the spinal cord becomes stiffer as rates of strain increase, therefore creating a higher susceptibility to injury. (5)

Pathophysiology:  The precise nature of DAI is thought to be a reactive swelling of damaged axons and capillaries throughout the brain (29,48,49) 揇irect brain trauma results in intra-axonal changes in the 68-kd neurofilament subunit which then loses its alignment and interferes with axoplasmic transport.  This causes axonal swelling and eventual disconnection.  The neurofilament change may be the result of either direct damage to the cytoskeleton or a biomechanical event that results in neurofilament disassembly.  The temporal progression of those events is related to the severity of the injury?  (16,42)

At time of injury, the brain is subjected to massive depolarization from acceleration/deceleration, and tissues are damaged due to shear currents/forces that increase intracranial pressure and mechanically deform axons. It is postulated that such events terminate with neuronal death involving the production of free radicals, and tissue acidosis. (6,7,53) In 1997, Connor and Connor showed in the American Journal of Clinical Nutrition that free radicals amplify inflammation by up regulation of genes that encode for pro-inflammatory cytokines and adhesion molecules. It is known that free radicals damage lipids, proteins, membranes and DNA. (2,8,13,18,19,28)

Micro hemorrhages develop between 12 and 96 hours post injury, arachadonic acid is released, CSF lactic acidosis is present, and lipid peroxidation occurs from membrane disruption and squalor. Free radical scavengers such as large doses of antioxidants and iron chelators have been proposed as therapeutic devices. (59)  Antioxidant supplementation as well as Omega III fatty acid supplementation, (DHA-docosahexanoic acid & EPA-eicosapentanoic acid), inhibit the degradation of tissue by the reduction of oxidative stress.  Oxidative stress is  due to free radical damage, arachadonic acid production, lipid peroxidation/degradation, prostaglandins (pge2), and leukotrienes. (9,10,11,20,24,31,34,46,51,54) In particular, bioflavonoids play a significant role as they have been proven to act as intracellular and extra cellular antioxidants, reduce platelet aggregation, repair damage in vessel walls and have anti-inflammatory action. (12,14,17,30,35,36,44,45,50)

Even in relatively mild brain injuries, an excessive release of excitatory neurotransmitters such as acetylcholine and glutamate, contribute to the pathologic neuronal apoptosis (cell death) in the brain. The results are permanent deficits!  MTBI can produce diffuse reactions in cerebral metabolic activity and can disrupt the blood brain barrier allowing an increase of excitotoxic effects. (6,7,23)  Recent research affirms that brain injury leads to increased glutamate release, which in turn activates the NMDA (N-methyl d-aspartate) receptor in cortical neurons allowing an increased calcium influx. (26) This channel complex contributes to excitatory synaptic transmission at sites throughout the brain and the spinal cord, and is responsible for neuronal plasticity. When continually activated neuronal death and chronic pain may result.  Specific areas known to be vulnerable to injury include the parieto-occipital lobe, the temporal lobe, amygdala, anterior frontal lobe, and para-sagital sinuses.  (43)  Antioxidants, magnesium and omega III fatty acid supplementation all inhibit circulating Excitotoxins and down-regulate the NMDA receptor.

Post concussion syndrome (PCS) can develop after MTBI.  Posttraumatic headaches are exceedingly common residuals, and may last for years. (55) First headaches begin with a concussion and can continue for weeks or months. The head usually hurts where the head is struck if blunt force trauma was the mechanism of injury. Etiological factors in posttraumatic headaches are blunt head trauma, 57.3%, whiplash, 43.6%, Object hit head, 13.7%, other, 13.7%, and body shaken, 9.4%.  (3)  It has been suggested by one of the preeminent experts in this area that patients suffering from recurrent post-traumatic headaches or other elements of the PCS should be treated for migraine. (37)  Other symptoms of PCS are as follows:  Dizziness:  Light headedness, vertigo and nausea, which is caused by injury to the semicircular canals, changes in endolymph or perilymph pressure, or direct damage to the vestibular cochlear nerve.  Serious symptoms of hearing loss such as hyperacusis may occur as the result of damage to the actual hearing mechanism. Cranial nerve and brain dysfunction: Disruption of smell and taste, information speed and processing, attention, articulation, memory, new information acquisition, reaction time and sleep disturbances such as lethargy, drowsiness, and fatigue are common sequelae.  (4)

**In relation to the research above, Suncoast Healthcare Professionals uses nutritional supplementation to decrease the cyto-toxic attack on neuronal tissue after resultant concussive episodes. Due to the fragile nature of brain tissue as well as the physiological makeup, it is evident that nutritional supplementation is paramount in the treatment of mild traumatic brain injury post motor vehicle trauma.  The application of ant-inflammatory and antioxidant agents should be utilized initially and sequentially for a minimum period of 6 months post injury.  Our office procedures and this supplementation is in line and adapted from protocols used in hospitals for the preservation of brain tissue after concussion, coma, transient ishemic attack and strokes, as well as brain surgery.**  

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Listen Trish, I know this is a complex subject with a bunch of things you probably need more explanation on.  Use the internet as a tool to research the above information, and make sure to discuss it all with your current specialists.  Hope all goes well.

Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net