December 3, 2002
Attorney at Law
address
Phoenix, Arizona 850__
Re: Your Requested Medical Report of Mrs. M. C.
Dear Mr. Attorney:
The above captioned patient was seen at this office on September 8, 1999 stating she had been in a vehicular accident occurring on August 14, 1999.
MECHANISM OF ACCIDENT/INJURY
Mrs. C was the seatbelted driver of her 1992 Honda Accord. She was driving north on I-17 in the far right lane about 10:15 am when traffic ahead of her stopped rapidly. She rapidly braked to a stop about a car length behind the full sized sedan stopped in front of her. It was so rapid that her small dog, in the passenger seat, was frightened and shaking/quivering. She turned her face to the right and holding onto the steering wheel with her left hand, twisting her torso and switching to her left foot on the brake pedal, reached over to console her dog by petting and talking. Her vehicle was struck from the rear by a van driven by C. D. His car hit her car so hard it was pushed into the car in front of her and it was then pushed into the car in front of it. Because of the force of the impact she assumed Mr. D must have been moving at 55 to 60 mph at the time.
SYMPTOMS
Immediately following the accident Mrs. C felt numbness on the right side of her face, headache, pain just above the elbow on the outside of her arm, and felt like she was in a state of shock. She also states that her brain was not working properly as evidenced by her addled brain function. She tried to use Mr. D’s cell phone but even though she could remember the numbers and sequence she couldn’t make her fingers push the correct buttons. So she asked Mr. D to push the buttons for her. When her daughter arrived on the scene she recognized that her mother wasn’t functioning as her normal efficient self and took over filling out all forms letting her Mother rest. However, after getting back home M was not able to rest or take her routine afternoon nap.
She states that since the accident she has continued to suffer from the preceding symptoms and has also developed the following:
Neck pain and stiffness, loss of balance (feels like wants to fall backward), dizziness, loss of memory, right temporal pain, left ankle pain, swollen right side of face, bruising on back, left forearm pain, left chest/rib pain, hands and feet feel hot, and her head feels too heavy to hold up easily, upset stomach, feeling of fatigue, tension evidenced by fear reaction on hearing sudden loud noises or being approached without warning, loss of memory, right temporal pain, left ankle pain, back spasms, pain in her right eye with the sensation of a film over it causing distorted vision necessitating closing of the right eye in order to see properly, swollen right side of face, bruising on back of left forearm and leg, pain in both knees, and left chest/breast from seatbelt. She also complained of pain in her pubic joint region and both hands in the first metacarpal joint with the wrist, just above the left elbow joint on the outside region, right ischium, left posterior hip joint, and mid to lower thoracic spine/rib regions.
She related that her pain was constant in her right temporal region and in the first metacarpal/wrist joints of her hands. The pain is on and off in the pubic bone and left ankle regions. She reports the pubic bone pain is similar to that experienced when she gave birth to her three children. The pubic bone pain is aggravated by sitting straight in a chair. The left sciatic nerve is adversely stimulated by the same sitting posture and the pain extends from the sciatic notch along the sciatic trajectory to the outside of the foot and the fifth toe.
She quantified the pain as sharp and coming in waves over the top of the skull and into the right eye, neck and mid-lower thoracic/rib spine region. She reports that her left ankle felt like it is jammed up and locked in place. On arising from sitting she feels pain and spasms in her lower back and left sciatic region.
Her most comfortable body position is lying down but if she moves it causes pain in her neck and back regions until she settles down again. After staying in any position/posture of the body for longer than a few minutes she feels the need to move to a new position/posture searching for comfort.
IMPAIRMENT
When grocery shopping prior to the accident she could easily carry a five gallon bottle of water for 50 feet (car to house) and then turn it upside down on top of the water dispenser unit. However, since the accident she reported only being able to lift 8 to 10 pounds such as one gallon of water in each hand. When lifting anything since the accident she states that she experiences pains and spasms in her upper and lower body of which some are long lasting.
She reported that since the accident walking, standing, sitting, pushing, and pulling have become painful. She further stated that bending and stooping have become limited while lifting and climbing have become difficult and painful. Further stating that reaching, gripping, kneeling, and balance have become difficult.
EXAMINATION
Based on the presenting history an examination of orthopedic, neurological, and physical medicine procedures was performed. The positive findings as shown in green throughout the initial examination form are post injury initial acute symptoms and signs.
Spinal percussion revealed increased sensitivity of the spinous processes, light to moderate pressure palpation elicited segmental tenderness, palpation also revealed paravertebral muscle splinting and paravertebral edema as marked on the chart. Additionally there is palpatory tenderness of the superior occipital nerve and the brachial plexus bilaterally. All of these symptoms and signs indicate acute nerve irritation from periosteal and tendon trauma. Tenderness of the superior, middle, and inferior cervical ganglions (nerve switching centers) bilaterally is also indicative of acute traumatic injury of the cervical structures. The cervical range of motion was not restricted but pain was present at the level of the seventh cervical vertebra (C7) on bilateral head rotation indicating intact muscle tissue but damaged joint structure. The Soto-Hall test (flexing the head anterior to approximate the chin to the chest) caused pain in the left shoulder region indicating ligament/nerve inflammation at the left C2-3 motor unit with interactions in the trapezius muscle to its mid point neuromuscular junction and through the fasciae connections from C2-3 to the fourth and fifth rib angles on the left.
Lifting her head by traction while seated decreased the neck and upper back pain indicating pressure reduction of the ligaments and other joint and spinal cord region structures. This procedure added force to the body that did not aggravate or irritate the planes of trauma of the accident.
When she was asked to turn her face to the right bringing her chin to her shoulder and then tilting her head posteriorly she complained of nausea indicating central nerve system (spinal cord pressure) involvement. The same procedure to the left was not symptomatic.
When she crossed her arms, held her head down, took a deep breath, held the breath, and bore down with her head and shoulders (Valsalva’s Test) she complained of pain in her cervical spine to her thoracic spine indicating inflammation of those structures.
She was asked to lift her arms sideways and on so doing she complained of pain in the right shoulder joint indicating inflammation of her tendon/nerve structures. (Shoulder Abduction Tendonitis-Bursitis Test)
She was asked to lift both her arms to 90 degrees and while holding them there the examiner then dropped his hands on her arms striking them downwards. She complained of spasm like pain in her deltoid muscle regions bilaterally. This indicated possible rotator cuff tearing or inflammation of the structures in the brachial plexus region. (Codman arm drop test)
When the examiner applied pressure to her coracoid/clavicle region bilaterally she complained of pain at the left joint indicating possible bursitis inflammation. (Coracoid Push Button Sign)
She was asked to raise each arm to 90 degrees with the examiner applying a firm pressure on the coracoid joint. She reported the right triceps region going numb with the pressure on the right coracoid joint which is explained by the action of the combined muscle effort raising the right arm and the examiner holding pressure raising the compressive pressure on the axillary nerve as it passed between the subscapularis muscle and the capsule of the shoulder joint blocking its cutaneous sensory function. This is due to inflammatory swelling of the tissues surrounding the nerve between the subscapularis muscle and the capsule of the shoulder joint. (Dawburn’s Test)
When she was asked to raise her arm to 90 degrees and flex the forearm on the arm to 90 degrees with the examiner then pulling the hand backward to rotate the humerous in the glenoid fossa she complained of pain in the shoulder joint when performed with the right arm. This indicates a sprain of the shoulder joint tissues in this plane of movement. (Apprehension Test)
When the left forearm was flexed 90 degrees on the arm with the forearm pointing anterior with the examiner holding the elbow stationary with a downward traction and externally rotating the humerous by pressure on the wrist she complained of pain in her left shoulder. The right side was asymptomatic. This test indicates inflammation in the anterior shoulder joint structures in this plane of movement. (Yergason’s Test)
Palpation of the upper chest wall myofascial components elicited painful reactions reported as tenderness on the left but not on the right indicating sprain of the muscle rib insertions and strain of the muscle tissue. (Cardiac Musculoskeletal Differentiation)
When her wrists were evaluated by stabilizing the forearm asking her to make a fist and flex the hand/wrist posterior towards the dorsum of the forearm with the examiner forcing the hand toward anterior flexion she complained of pain in her right wrist. Without additional tests indicating otherwise this indicated right brachial plexus neuropathic pain rather than tennis elbow or carpal tunnel syndrome. (Cozen’s Tennis Elbow Test)
The grip strength testing of this right handed woman showed a slightly variable performance but overall slight reduction in the right grip strength. She is right handed and it is expected to perform this test with approximately 10% increase of grip strength due to handedness. (Dynamometer Grip Test)
She was seated and to extend each leg sequentially bringing the lower extremity into a 90 degree configuration with her trunk. This was reported to cause a left hip joint pain indicating a sprain of the joint in that plane of motion. (Tripod Test)
Standing she was asked to bend obliquely backwards with examiners assistance. On so doing she complained of pain in the right T 7 through 10 vertebral/rib region indicating a sprain of the joint tissues in that plane of movement. (Kemp’s Test)
While standing she was asked to alternately stand on only one leg while lifting the other leg flexing the calf upon the thigh and the thigh upon the torso. In so doing the right gluteus medius was found to be weak in that it could not stabilize the sacrum and the left iliac crest was not elevated on right leg standing. This indicates a sprain in the sacroiliac joint or gluteus medius motor nerve malfunctioning. Palpation of the sacroiliac joint indicated the joint to be inflamed and assumed to be the origin of the malfunction. (Trendelenburg Test)
There was pain on palpation of the sciatic nerve in the sciatic notch of the pelvis on the left while standing. This tenderness is a sign of nerve hypersensitivity due to her left hip and pelvic joints sprain instability and/or L4-5 or L5-S1 disc ligament inflammation post trauma. It was assumed to be due to inflammation of the joints.
The range of motion of the dorsolumbar spine was carried out with no restrictions but a complaint of pain in the lumbosacral junction on forward bending was voiced supporting the previous tests indicating sprain of the sacroiliac and lumbosacral joint regions.
While lying on her back each lower extremity was raised by the examiner with the knee not bending. She complained of pain on left leg raising. This confirms inflammation of the sciatic nerve. (Lasegue’s test)
Her left lower extremity was lowered to just below the pain point and her foot was dorsiflexed. She complained of pain in the L-2,3 nerve trajectory region. This test stretches the sciatic nerve and indicated the upper branches to be tethered in some manner. (Braggard’s Test)
On raising her right lower extremity she also experienced pain on the left in the L-2, 3, & 4 radicular regions. This test result clarifies the Braggard’s test by stressing the lumbar joints on the left. They have to be swollen and narrowing the intervertebral foraman (IVF) to evoke radicular pains during the action of raising the right lower extremity in the process of stabilizing the lumbar spine for that action to take place.
When she was asked to raise each lower extremity alternately by her own muscle power with the examiner’s hand under the heel of the non active side she was able to perform the test with no downward pressure on her heels. (Hoover’s Sign)
RADIOLOGY
Based on the history and clinical examination findings x-rays of the spine and pelvis were ordered and taken with the following findings.
CERVICAL SPINE:
AP lower cervical spine shows degenerative changes in the Von Luschka joints, most notable at C4-5 on the right, C5-6 on the left and bilateral at C6-7. C5 shows a moderate rotational malposition on C6.
Lateral view of the cervical spine shows a reversal of the cervical lordotic curvature in the lower cervical spine (C4-6) as well as extensive osteophyte formation on the anterior-inferior portion of C4, 5, and 6 with mild anterior wedging of C5. This indicates prior injury with enough time elapsed for the stimulated bone to form new bone cells (osteophytes) along the planes of rotational, translational, and compressive forces. When bone tissue is stimulated it can do one of two actions i.e., grow new osteophytes or eliminate current osteophytes.
The lateral neutral view shows a 2.5 mm anterolisthesis of C2 on 3, a 3 mm anterolisthesis of C4 on 5 and a 2 mm anterolisthesis of C5 on 6. Comparing the neutral view with the flexion and extension view the following is noted: a decrease in the anterolisthesis of C2 on 3 by 1.5 mm in flexion and extension. A 1mm anterolisthesis is seen at C3 on 4 in flexion and a 2 mm retrolisthesis upon extension. C4 shows a 1 mm anterolisthesis on C5 upon flexion and C5 shows a 1 mm anterolisthesis upon C6 in extension. These findings support the diagnosis of joint instability. In a normal spine there is no listhesis (translational [lateral e.g., right-left-forward-backward] movement) present.
Oblique views show a notable decrease in the intervertebral foramen of C4-5 on the right and bilateral at C5-6 and C6-7. This is due to an overgrowth of stimulated bone tissue at the insertion of the joint ligaments that were previously sprained.
Rotational views show the majority of motion occurring in the mid cervical spine with very little motion visualized in the upper cervical spine. This is due to edema stimulating the ligament nerves creating reflexive muscle splinting of the edematous joints.
Open mouth views with lateral flexion shows lateral translation bilaterally of the C1 lateral mass on C2 (3 mm to the right and 4 mm to the left). This indicates both the alar ligaments at C1-2 attaching the odontoid to the occiput are stretched or torn.
THORACIC SPINE:
AP view shows severe degenerative changes to the mid-lower thoracic spine, most notable at T9-10. A lateral flexion malposition of T4 on 5 and T5 on 6 is noted with the open wedge to the right. This creates a left lateral list of the mid and upper thoracic spine.
Lateral view shows moderate compression of the T9 and T10 vertebral bodies.
The degenerative changes of the thoracic spine developed post prior trauma. These degenerative changes indicate the moderate compression of the T9 and T10 vertebral bodies is from prior injury. The torque of the body during the accident would not have had as severe sequels had it not been for the prior spine pathological injuries and their subsequent degenerative changes.
Bone density and trabecular patterns appear to be within normal limits. Soft tissue patterns appear to be within normal limits. Surgical staple shadows are noted at the inferior medial border of the liver, reportedly due to a cholecystectomy.
LUMBAR SPINE:
AP view shows a lateral flexion malposition of L4 on L5 with the open wedge to the right. This causes a left lateral list of the mid and upper lumbar spine.
Notable osteophyte formation is seen at the inferior portion of the left sacroiliac joint.
Lateral view shows a grade 1 anterolisthesis of L5 on S1.
Oblique views show the anterolisthesis of L5 on S1. No facet imbrication is noted. Pedicles appear to be intact.
Of note is the lack of degenerative changes surrounding the L4 on L5 vertebral segmental lesions. This lack of degenerative change and the clinical examination findings related to the lumbar spine and sciatic nerve indicate this is of recent origin, most probably due to the accident of August 14,1999.
Bone density and trabecular patterns appear to be within normal limits. Soft tissue patterns appear to be within normal limits.
AP PELVIS:
No fractures or dislocations noted. Femur heads are symmetrical and of equal height.
DIAGNOSIS
Based on the presenting history, initial clinical examination and initial x-ray findings the following diagnoses were made:
1. Hyperflexion/hyperextension traumatic injury to the right-face-rotated cervical spine with neurovascular and myofascial inflammation. (International Classification of Diseases 9th Revision [ICD-9 #847.0)
2. Traumatic injury to the torsional thoracic spine with neurovascular and myofascial inflammation. (ICD-9 #847.1)
3. Traumatic injury to the torsional lumbar spine with neurovascular and myofascial inflammation. (ICD-9 #847.2)
4. Partial dislocation C3 on C4(ICD-9 #839.03)
5. Sacroiliitis ((ICD-9 #720.2)
6. Bilateral alar and right cruciate ligament tearing (ICD-9 #839.00)
7. Mild ischemia to the brain stem and posterior brain (ICD-9 #854.0)
8. Vertebrobasilar artery syndrome (ICD-9 #435.3)
9. Traumatic spondylolisthesis of L-5 on S-1 (ICD-9 #839.2)
10. Sciatica (ICD-9 #724.3)
11. Sprain of left ankle/foot (calcanius-cuboid (ICD-9 #845.19)
12. Sprain of left foot (cuboid-metatarsal joint) (ICD-9 #845.11)
13. Right shoulder sprain (subscapularis [muscle]) (ICD-9 #840.5)
14. Right shoulder sprain (coracoclavicular (ligament)) (ICD-9 #840.1)
Based on the diagnoses a treatment regimen consisting of osteopathic manipulative medicine and physical therapy to include electrical muscle stimulation, diathermy, ultrasound were prescribed and given to appropriate body regions. Prescriptive medicine to include Ultram for nerve pain reduction, over the counter medicine to include Tylenol to assist in reducing tissue inflammation and melatonin to aid sleep, applications of ice packs to her inflamed tissues at home were also prescribed and instituted.
CLINICAL PROGRESS
She did not fill the Ultram prescription out of concern that it might have an interaction with her regular prescriptions of Prozac and Microdantin. Celebrex samples were given to evaluate their effect on her inflammatory condition.
She reported that her sleep was disturbed by the pains from the injury and therefore was only able to sleep a couple of hours at a time each night.
On September 20, 1999 glucosamine tablets were prescribed to be taken daily for their documented assistance in rebuilding the joint cartilage following damage. She was prescribed an arthritic formula of nutrients prepared for buccal absorption due to her reported poor assimilation of oral nutrients.
Massage three times a week by a masseuse was added to her therapeutic prescription on September 22, 1999 for its therapeutic and salubrious effects.
On September 24, 1999 Knox Gelatin protein was prescribed to be taken daily to aid in bone and joint recovery.
On September 29, 1999 lymphatic drainage massage to bilateral feet/ankle structures was prescribed and provided one time. Benefits could not be understood therefore the modality was not repeated.
The Celebrex was well tolerated and gave her symptom relief therefore the prescription was re-issued on October 6, 1999.
On October 15, 1999 she reported that her ophthalmologist, J. B. MD, did not have objection to her receiving manipulative or acupuncture treatments for her injuries.
Examination of her tongue showed it to be heavily scalloped on its lateral borders, the top surface to be a light purple color, and congested on the underside.. She stated that she did not have that problem prior to the accident. Therefore, it is most probably due to the stress reaction of the accident reducing the threshold of her sensitivity reaction to air born and/or food/drink substances in her body.
Comparative examination was performed on October 27, 1999. It was recorded in red on the examination form. She reported feeling much less pain during her daily activities. The pain in her right temple was listed as a 7 on a scale of 1-10 with 10 being the most intense. She stated that her right eye vision had improved slightly but it was still difficult to read.
On November 1, 1999 she reported that her ankles were feeling much improved with considerable more flexibility than just two weeks prior.
Following the office visit of 11-10-1999 she drove to Texas and returned three weeks later. She returned for evaluation and treatment continuation on December 6,1999. See the initial examination form black ink for findings. She showed continuing improvement. Frequency of treatment was reduced to observe the state of her recovery from the accident injuries.
She returned for care on January 14, 2000 stating she felt considerable lessening of pain. However, she continued to experience right eye symptoms and complain of pain in her elbows, neck, mid to upper thoracic spine and rib articulations. Motion palpation of the posterior rib cage and thoracic spine revealed it to be very tight. It appeared to this examiner that her reduction of symptoms was due to the congesting and restricting of movement of the injured joint structures with the acute neurovascular condition turning toward a chronic neurovascular inflammatory condition.
She returned on February 11, 2000 stating she had been experiencing severe flu and had been coughing often. She picked it up on traveling to Texas. Her grandmother was suffering from severe illness and it was thought she would expire. Following all of that stress Mrs. Carr states the right eye pains and rib pains have returned and has not experienced these kinds of pains after flu illness during the past 65 years of her life. She also complained of pain in her pubic bone when she stands. She reported making another appointment with an ophthalmologist to evaluate her continuing right eye pain.
Her last visit to this office for initial injury medical care was April 5, 2000. She was fearful of elevating her bill for medical services and being responsible for too large of an amount to comfortably pay.
DISCUSSION
It should be noted that the cervical spine can withstand a large amount of force when applied in the straight front to back or back to front planes of movement. When the force is applied laterally the cervical spine can withstand a moderate amount of force. However, when the face/cervical spine is rotated 45 to 50 degrees the movement occurs chiefly at the atlanto-axial joint accounting for about half of the total cervical spine rotation ability in a normal, non previously traumatized spine. If the body is then pushed suddenly and unexpectedly forward the neck is pulled into posterior flexion and extension as it begins to move the head. During consequential head rotation, because the vertebral artery is fixed at the first and second transverse cervical foramina, it is stretched, compressed and torqued. Reduction of the vertebral artery flow due to cervical spine rotation especially during posterior flexion movement has been well documented. In fact this is the preferred result of a solid landing uppercut punch in boxing that results in a knockout due to vertebral artery trauma and subsequent spasm depriving the brain of needed blood flow. If the blow is severe enough, based on the individual’s health/disease condition of the artery, the artery will tear and the person will stroke and possibly expire.
The vertebral arteries climb the cervical spine through openings (foramen) in the transverse processes. After emerging from the transverse foramen of the atlas, the vertebral arteries proceed to wind posteriorly and medially around the lateral mass of the atlas, to pass via a groove in the posterior arch of the atlas, between the atlanto-occipital joint capsule anteriorly and the posterior atlanto-occipital membrane posteriorly.
The vertebral arteries then pass through the foramen magnum and, at the lower border of the pons, unite to form the basilar artery. The basilar artery passes up the anterior surface of the brainstem and divides to become the posterior cerebral arteries.
The posterior inferior cerebellar arteries, the largest branches off the vertebral arteries leave the vertebral arteries just before the vertebral arteries join each other to form the basilar artery. The posterior inferior cerebellar arteries run a tortuous course along the lateral part of the medulla, to which they are the main blood supply. In some cases the vertebral arteries may terminate in the posterior inferior cerebellar arteries.
Research indicates that rotation is the single most effective movement producing a decrease in blood flow of the vertebral artery. Therefore compression or spasm of a vertebral artery from either the first or second cervical foramen during rotation will induce symptoms especially if compounded by posterior flexion and then by anterior flexion of the motor unit. Anterior and posterior are used to denote movement of the body forward and backward in relation to the vehicle’s impact moment of force and not anterior or posterior to the face’s rotational position.
Normally during daily head movements, occlusion due to compression does not produce a decrease in flow enough to produce ischemic signs and symptoms, or the development of infarction. In most cases the development of infarction indicates an underlying arteriopathic process, other than brief occlusion.
The time between the application of trauma in the onset of ischemic symptoms and signs can very from immediately to several days later. The interval is probably related to the mechanism of injury. When brainstem ischemia is due to vasoconstriction, symptoms would be expected immediately; whereas those (other than the pain of dissection) due to thrombus and/or embolus formation resulting from a vessel wall dissection and/or vessel occlusion would only become symptomatic after some time.
A review of 183 cases of vertebral artery flow restriction post vertebral artery injury reveals that the time between trauma and the onset of symptoms was given in 136 of the cases (74%).
Analysis showed that symptoms began:
1. 69% during trauma
2. 3% within moments or minutes of trauma
3. 9% within one hour of trauma
4. 8% 1 - 6 hours after trauma
5. 5% 7 - 24 hours after trauma
6. 6% 24 hours or more after trauma
Signs and symptoms of vertebrobasilar ischemia produced by trauma usually occur immediately.
The major signs and symptoms of vertebrobasilar ischemia are as follows:
1. Dizziness/vertigo/giddiness/light headedness
2. Drop attacks/loss of consciousness
3. Diplopia (or other visual problems/amaurosis fugax)
4. Dysarthria (speech difficulties)
5. Dysphagia
6. Ataxia of gait (walking difficulties/incoordination of the extremities/ataxia/falling to one side)
7. Nausea (with possible vomiting)
8. Numbness on one side of the face and/or body
9. Nystagmus
Dizziness is the most common symptom of vertebrobasilar ischemia and may be unaccompanied by any other symptom or sign.
An understanding of the mechanisms involved in the production of head and/or neck pain due to trauma to the pain sensitive vessel wall, or ischemic signs and symptoms due to decreased blood flow to the brainstem at the time of trauma indicates why the spine should be properly treated if signs and or symptoms develop.
It is also important to understand the pathological effect of trauma to the individual nerve cell axons, dendrites and cell bodies. Studies on experimental ischemia and compression of peripheral nerves concluded that any trauma to a nerve trunk may induce microvascular injury in the nerve. A slight trauma may cause epineurial micro-bleedings, edema, etc. Severe trauma, e.g., prolonged injury to endoneurial capillaries (blood-nerve barrier) leading to intrafascicular (space between the pathways of nerve fibers in the spinal cord) edema. The establishment of post-ischemic or post-traumatic intrafascicular edema coincides in time with severe disturbances in nerve function.
In other studies graded compression was applied directly to exposed nerve trunks by means of a “mini-cuff”. It was found that 2 hours of compression with 200 to 400 mm Hg induced break-down of the blood-nerve barrier. Local nerve compression with pressures of 50 to 400 mm Hg acutely blocked anterograde nerve cell axonal transport in sensory vagal nerve fibers. Reversal of transport blockade generally occurred within a day after compression at 50mmHg; with higher pressures recovery occurred in most cases within one week. The duration of the transport blocks was related to the magnitude (time and force) of the pressures applied.
The effect of the force of the accident impact trauma to Mrs. Carr’s nervous system was amplified by the rotation of her face/head to the right. Her initial and ongoing symptoms are explained by this traumatic pathologic effect not only on her intra-joint structures but also on the small muscles and ligaments of the inter-joint structures and the proximal neuronal and vascular structures including the pons, medulla oblongata and the posterior brain centers of vision interpretation, balance, and hand/eye coordination.
Research studies have shown that rotation of the face to the right or left and posterior extension of the head has more effect on narrowing the opening of the vertebral artery than anterior or posterior flexion in the face forward (non-rotated) posture.
Current Examination
The above captioned patient was seen at this office on November 11, 2002. She was previously evaluated and treated for injuries from September 8, 1999 through April 5, 2000.
She stated she continues to suffer from the symptoms brought on by the injuries she received during the accident of August 14, 1999.
She has been seen several times in consultation by C. E. MD and also by S. J. MD. I reviewed their reports to see if any additional insight had been discovered regarding the origins of Mrs. C. symptoms. The MRI taken on November 13, 2001 of the brain and of the cervical spine were helpful in further understandings of Mrs. C. symptoms. R. B. MD the neuroradiologist reported “Several tiny white matter hyperintensities are seen on T2 weighted images bilaterally, which likely represent small-vessel ischemic disease.” “Incidental note is made of ossification of the falx.” In my opinion this probable small vessel ischemic disease of the brain with the calcification of the falx cerebrae indicates atherosclerosis and a predisposition to poor healing from trauma of the brain is to be expected. The minimal ventral ridging of C3-4 with small central disc protrusion at C4, 5 becomes significant when one views the range of motion standard x-ray exposures taken on this examination.
A current history was taken (see “Pain and Health Questionnaire” and the Neck Pain and Low Back Pain Ostwestry Questionnaires) and based on her statements it was determined to perform examinations to compare with the original and subsequent examinations.
The clinical examination revealed that over the last two and a half years the parts of the body injured and/or made symptomatic by the accident and subsequently treated at this office with significant reduction in their acute pain status had become established as chronic pain and malfunctioning structures. This reversal of symptoms is not unusual in a person with a significant amount of joint and soft tissue injury that was treated and had become much reduced in acute sensitivity.
At the time of this injury the body showed radiological evidence of healed joint injury and new joint injury. This is supported by the changes seen in the radiological examination performed initially and compared with the radiological examination of November 11, 2002.
These changes and the clinical signs of serious spinal diarthroidial joint swelling especially in the cervical spine are significant. Her continued complaints relating to perceived neurological malfunction of vision are explainable.
CURRENT X-RAY AND INITIAL X-RAY COMPARISON
Comparison of the current x-ray studies of November 11, 2002 with the initial x-ray studies showed the following: The current resting, or upright neutral posture, posterior malposition of C-3 in relation to C-4 of 3mm and the anterior flexion posture malposition of C-3 in relation to C-4 of 2mm exceeds the maximum allowable radiological mensuration by 1mm resulting in a significant state of joint instability.
Further radiological changes of motion stability initially occurred at the occiput/C-1 motor unit articulation with C-2 on lateral head bending bilaterally indicating tearing of both the right and left alar ligaments. The current instability indicates the right cruciate ligament is either stretched or torn. This was not visualized initially due to the acute tissue swelling post initial injury splinting the structures.
MRI imaging of the cervical spine without contrast and MRI imaging of the brain without contrast was performed on November 13, 2001. The findings in the cervical spine of ventral ridging at the level of C-3,4 become medically meaningful when one merges the forward and backward flexion finding of instability of C-3 on C-4. This traumatically induced instability is due to the forces sustained in the accident of August 14, 1999. It also indicates to this examiner the level of force was sufficient to aggravate the pre-existing asymptomatic osteodegenerative arthritic changes present from a reported 1991 previous accident. The instability of the occiput/atlas (C-1) motor unit with the axis (C-2) seen initially and subsequently was due to the new accident forces being brought to bear.
When all of these radiological functional and pathological changes, both plane film and MRI, are carefully thought about with the clinical findings one can readily understand why the continuing need for the body to maintain the cervical, thoracic, and lumbar diarthroidial (freely moveable) joints in a state of congestive musculoskeletal splinting. This splinting of joint structure by muscle and increased intra-articular pressure (joint swelling) would be only of local interest if it did not occur in proximity to the circulation of the spinal nerves and spinal cord.
CURRENT DIAGNOSIS
Based on the comparative history, clinical examination, and x-ray findings the following diagnoses were made:
1. Hyperflexion/hyperextension traumatic injury to the right face rotated cervical spine with neurovascular and myofascial inflammation. (International Classification of Diseases 9th Revision [ICD-9] diagnosis number 847.0) (Moderate late effects ICD-9 #905.7)
2. Traumatic injury to the torsional thoracic spine with neurovascular and myofascial inflammation. (ICD-9 #847.1) (moderate late effects ICD-9 #905.7)
3. Traumatic injury to the torsional lumbar spine with neurovascular and myofascial inflammation. (ICD-9 #847.2) (moderate late effects ICD-9 #905.7)
4. Partial dislocation C3 on C4(ICD-9 #839.03) (moderate late effects ICD-9 #905.7)
5. Left alar and right cruciate ligament tearing (ICD-9 #839.00) (moderate late effects ICD-9 #905.7)
6. Mild ischemia to the brain stem and posterior brain (ICD-9 #854.0) (moderate late effects ICD-9 #905.7)
7. Vertebrobasilar artery syndrome (ICD-9 #435.3) (moderate late effects ICD-9 #905.7)
8. Traumatic spondylolisthesis of L-5 on S-1 (ICD-9 #839.2) (moderate late effects ICD-9 #905.7)
9. Sacroiliitis ((ICD-9 #720.2) (moderate late effects ICD-9 #905.7)
10.Sciatica (ICD-9 #724.3) (moderate late effects ICD-9 #905.7)
11.Sprain of left ankle/foot (calcanius-cuboid (ICD-9 #845.19) (moderate late effects ICD-9 #905.7)
12.Sprain of left foot (cuboid-metatarsal joint) (ICD-9 #845.11) (moderate late effects ICD-9 #905.7)
13.Right shoulder sprain (subscapularis [muscle]) (ICD-9 #840.5) (moderate late effects ICD-9 #905.7)
14.Right shoulder sprain (coracoclavicular (ligament)) (ICD-9 #840.1) (moderate late effects ICD-9 #905.7)
15.Mild ischemia to the brain stem and posterior brain affecting vision primarily e.g., Transient cerebral ischemia due to vertebral artery syndrome (ICD-9 #435.1) (moderate late effects ICD-9 #905.7)
Due to the long term continued low back, hip joint, and left sciatic nerve trajectory pain experienced an MRI of the Lumbar spine is needed to rule out intervertebral disc disease associated with the traumatic injury she sustained.
Researchers have found that whiplash biomechanics causes injury to the spinal disc and facet joints.
The spinal disc and facet joints are the most probable source for the initiation of the perception of chronic cervical, thoracic, and/or lumbar spine whiplash pain and related dysfunction .
An appreciable amount of chronic pain afferent nerves synapse in the limbic cortex. There constant stimulation causes an abnormal psychological profile in response to the chronic pain being suffered.
This abnormal psychological profile can only be helped by successful treatment of the chronic pain.
The best treatment for the spinal disc and facet soft-tissue and bone joint surface cartilage injuries is early, persistent, controlled motion of the injured tissues allowing full circulation of blood and drainage of lymph.
Self directed controlled motion of injured extremity joints is possible because the muscles that cross those joints are primarily under the control of the voluntary motor cortex.
Self directed controlled motion of injured spinal joints is not possible because the muscles that move the individual segments are not under the primary control of the voluntary motor cortex. They are controlled primarily through the vestibular spinal tracts (descending medial longitudinal fasciculus), which is non-voluntary.
Injury to the spinal disc and facet joints causes a non-voluntary contraction of the non-voluntary segmental movers (primarily the multifidus muscle) at the level of injury and for several segments above and below the level of injury.
This non-voluntary contraction locks the motor unit into a certain parameter of position and reduced movement.
This reduction of movement does the following: Opens the pain gait which impairs the “disc pump” which accelerates disc degeneration and makes the disc more acidic which increases the firing of disc nociceptor nerve fibers which alters the quality of the synovial fluid which reduces its nutrient value which accelerates posterior joint arthrosis and pain.
Osteopathic manipulative medicine applied to the injured musculoskeletal structures does the following:
1 Segmentally fires high threshold mechanoreceptors that di-synaptically inhibit tone in the segmental spinal motor unit movers, which improves segmental spinal motion and position.
2 This controlled movement allows the injured tissues to heal better and quicker.
3 This controlled movement improves the fluid exchanges of the disc and synovial fluid, which reduces pain and joint degeneration.
4 This controlled movement initiates a neurological sequence of events that causes pain inhibition (closes the pain gate).
It is important to understand the significance of her injuries.
In recent years, the micropathology of acute soft tissue trauma has been thoroughly researched. Healing of ligaments and soft tissue injuries has been shown to occur by fibrous repair (scar tissue) and not by regeneration of the damaged tissue. The pathological process of healing has been classified into 3 phases:
1. Acute Inflammatory Phase (Reaction Phase):
Demonstrated by swelling, redness, warmth and pain.
This phase may minimally last 72 hours.
2. Repair Phase:
The repair of the tissue begins after the swelling goes away. Once begun, collagen fiber synthesis may continue up to 6 weeks.
3. Remodeling Phase (Regeneration Phase):
The period during which the collagen (in the cells) is remodeled to increase the functional capacities to withstand the stress imposed on it. This phase may last up to 12 months or more.
The remodeled tissues; however, are deficient both in content and quality in the following respects.
A. The fibrotic repair of the once injured tissues leaves those tissues permanently weaker;
B. The fibrotic repaired tissue is always less elastic than normal uninjured tissues; and
C. The once injured tissues have an anatomical increase in the number of neurofibrils in them, leaving them permanently more sensitive to the normal stresses and strains of daily activities.
In a person who has suffered with traumatically induced acute inflammatory response chronically it is important to note that the stress response evokes elaborate mechanisms by which they are able to survive and function in the hostile world. The major categories of human protective mechanisms include: physical barriers (e.g., skin), stress reactions, immune responses, inflammation, coagulation, chemical detoxification, and a widespread network of phagocytic cells in the reticuloendothelial system. The host, rather than using these modalities independently, responds to all injuries at the molecular level with a concerted constellation of host responses referred to collectively as the stress response. This response is most commonly seen in people following a number of inflammatory stimuli including: infection, trauma, burns, tissue infarction, immune-related diseases, and surgery. Characteristic changes occur involving the metabolic, endocrinologic, neurologic, and immunologic bodily functions.
Most of these changes are observed within hours or days after the onset of injury. They represent a series of local and systemic responses designed to aid survival by neutralizing the offending agent and restoring normal tissue functioning. These responses represent a major adaptive phenomenon whereby homeostasis is maintained in an altered steady state. Complete recovery occurs by a return to the normal steady state.
In general the magnitude of the stress response is related to the severity of the injured state. In cases of major injury, survival occurs only if these interactive defense responses are sufficient to compensate for the imposed stresses. Host factors are important in determining individual survival. These include: nutritional status, immune status, age, gender, and concomitant disease. In addition in many cases the return to the normal steady state can be unsuccessful, in that normal homeostasis is not achieved. Stress response changes can persist that themselves cause damage (e.g., chronic inflammatory disease such as rheumatoid arthritis or osteodegenerative arthritis).
In M's. case the new injuries have resulted in significant additional morbidity when added to her previous injuries. Taking her age, weight, prior degenerative joint changes secondary to physical trauma and the continuing molecular response to the inflammation of injury stress in her it is medically probable that therapeutic neutraceutical prescription will be necessary to give the body the building blocks and tools necessary for recovery to the point of being asymptomatic.
IMPAIRMENT
Utilization of the Fourth Edition AMA Guides to the Evaluation of Permanent Impairment the following is deduced:
Spondylolisthesis with loss of motion segment integrity at C3-4 @ 25% and at C1-2 @25% of the cervicothoracic spine equals a combined total of 44% impairment of whole person.
Left sciatic radiculopathy equals 10%.
Compression of vertebral body less than 25% of the thoracolumbar spine equals 5%.
When the effects on activities of daily living are added there is an additional 25 to 50% to be added to the above. I estimate based on her reported inability to carry out normal activities that she is at a 35% level.
Due to the new injuries she now fits the AMA criteria for a 94% whole person permanent impairment rating.
PROGNOSIS
Therefore, it is probable that M. will experience periodic symptomatic exacerbations of her initial post-trauma complaints caused by increased stresses and strains brought about by her various work and daily activities.
These exacerbations can be controlled and her symptoms minimized by reapplication of the previously prescribed, medically indicated, and patient stated effective treatment of osteopathic manipulative medicine procedures and techniques. That treatment is best complimented with the presenting body abnormality appropriate physical medicine modalities such as but not limited to specific exercise, massage, electrical muscle and nerve stimulation, traction, cold and heat, diathermy, and ultrasound. Acupuncture may be appropriate to use for re-directing the sensory input to her central nervous system affording her non-pharmacological pain/discomfort relief.
It is medically probable that this care will need to be provided at least one time per week for the next three years in order to bring her to a stationary asymptomatic state such as she was experiencing prior to this injury episode.
All opinions contained in this report are given to a reasonable degree of medical probability.
If I can be of further help to you please contact me.
Sincerely,
Treating Physician
Comprehensive Health Services, Inc.
The Ciba Collection of Medical Illustrations, Frank H. Netter MD, CIBA Pharmaceutical Company, division of CIBA-GEIGY corporation
“Acute soft tissue injuries - A review of the literature”, John Kellett, Medicine and science in Sports and Exercise, Vol. 18, No. 5, pp. 489-500 (1986).
Vertebrobasilar Stroke Following Manipulation, Allan G. J. Terrett, Faculty of Biomedical and Health Sciences RMIT University, Bundoora Australia, 1996
Foundations for Osteopathic Medicine, Robert C. Ward et. al., Williams & Wilkins, 1997
The Neurobiologic Mechanisms in Manipulative Therapy, Irvin M. Korr, Plenum Press, 1977
Managing Low back Pain, William H. Kirkaldy-Willis MD, Churchill Livingstone, 1988
A Clinical Guide to Neuropathic Pain, Bradley S. Galer, MD and Robert H. Dworkin, PhD, McGraw-Hill, 2000
Guides to the Evaluation of Permanent Impairment, Fourth Edition, American Medical Association, 1993
Whiplash Overview Lecture Notes, Dan Murphy DC, International Chiropractic Association , 2002