Thanks for the reply Dr.
MRI findings;
01.05.2007. Rotorua Hospital booked by Musculoscelatal Specialist searching for reasons for foot numbness r/h, L Hermittes, hand paraesthesia, intermittent visual blurring, chronic cervical pain, migratory aching joints upper and lowe limbs. Neurological examination normal.
Conclusion: There is no MR evidence of myelopathy. The C7 nerve root is likely compromised by foraminal narrowing on the right at C6/C7, this is a combination of hard and soft disc.
Focal disc disease at the lumbosacral level but no sign of lumbar nerve root compromise.
03.07.2007. Midland Hamilton Hospital booked by Neurologist. L'hermitte's symptoms with dysaesthesia pains in the shoulders and arms.
Conclusion: No evidence of demyelinating syndrome with a normal MRI appearances on the brain.
The cervical cord is normal, but there is disc pathology with endplate osteophytes at the C5/C6 and C6/C7 levels slightly more prominent on the right which causes moderate forminal stenosis particularly at the C6/C7 level.
07.07.2008. Rotorua Hospital booked by Neurologist. Progressive sensory complications. Fatigue. L'hermitte's syndrome.
Findings; Since the normal Midland MRI scan of 03.07.2007, two foci of white matter hyperintensity have developed as shown on FLAIR and T2 imaging. There is a 2-3mm focal elliptical area anteriorly in the left centrum semiovale and a more confluent area of white matter hyperintensity adjacent to the lateral aspect of the atrium of the left lateral ventrilcle. This measures 11mm in maximum diameter. No ther grey matter or white matter abnormality is shown within the brain. No enhancement occurs on administration of Gadolinium. No areas of diffusion restriction. No abnormality in relation to the corpus callosum, pituitary or other midline structures. The CSF spaces appear normal and no abnormality is shown in relation to major vessel flow voids. Patchy sinsus opacity affects the ethmoid air cells bilaterally. With respect to the spine, there is a linear area of increased T2 signal within the dorsal aspect of the cervical cord at the C2 level measuring around 16 mm in length. No cord expansion is identified and there is no increased signal on post contrast T1 imaging. The remainder of the cord is normal in contour and signal. The conus terminates normally at T12/L1. This abnormality is similar to the private scan performed on 01.05.2007. There is a right paracentral protrusion of the C6/C7 disc which encroaches on the right C6/7 disc which encroaches on the right C6/7 neural foramen as previously described with no major change in severity apparent on Sagittal images only. There is osteophyte formation directed posteriorly about the C5/6 disc which mildly indents the thecal sac, but there is no evidence of cord compression or CSF effacement. Thoracic discs appear normal. There is narrowing of the L5/S1 disc with posteriorly directed osteophytes and a generalised posterior bulge of the disc which indents the thecal sac. The transiting S1 nerve roots appear deviated slightly posteriorly but there is no definite compression. Disc appearances elsewhere are satisfactory. No bone marrow signal abnormality is demonstrated apart from a small cavernous haemangioma in the T2 vertebtal body.
Summary:
Two white matter hyerintensities have developed on the left side as described since the previous scan of 12 months ago. There is a stable hyperintensity in the dorsal aspect of the cervical cord as described. No contrast enhancement. Findings are not typical of demylination and are of uncertain significance but demylination is not excluded. Degenerative changes in the lower cervical and lumbar spine similar to previously.
I must add Dr that when they injected the Gadolinium I was drawn out of the MRI the lure was already in and they injected the solution and put me immediately back in and continued Scanning. Personally I do not believe they had enough time for the dye to circulate and the last scan only took 10 mins or less.
Both MRI machine were 1.5T closed machines.
The other thought I have had is from the analogy of the balloon full of water, if it is sitting on the plug hole for the skull in my situation with my posture and leaning over and having my head up, like being on four legs would be an issue with skull design? Leaning over cars, sitting in a driving position in Jetboats, my lifting and sport choices, all points to a poor outcome for upright posture design issues?
Thanks Dr.
CCSVI and CCVBP
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uprightdoc
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Hi Dr., I would call them fluctuating more so than intermittent.
Fatigue, balance, low energy/weakness, vision disturbances, TN managed by Gabapentin, bladder frequency, cog fog, spasms, twitching, burning sensations, bubbling sensations, head aches, thoracic back pain with weakness and those are the things that are happening right now as I sit here.
Fatigue, balance, low energy/weakness, vision disturbances, TN managed by Gabapentin, bladder frequency, cog fog, spasms, twitching, burning sensations, bubbling sensations, head aches, thoracic back pain with weakness and those are the things that are happening right now as I sit here.
Dr. I have read your comments about skull position on top of the spine, a quote from your blog is below.
"Recent research shows a significant correlation between trauma and Chiari/CTE type conditions. It is my opinion, that hyperflexion type strains of the cord, in which the head and neck overstretch going forward, in a chin toward the chest direction, can traction the brainstem and pull it down toward the foramen magnum. On the way down it causes a compression deformation of the larger part of the brainstem in the foramen magnum. As the hyperflexion strain is released the brainstem then returns to normal size faster than it can return to its normal position above the foramen magnum."
Is this the type of problem I might have?
The other thought that has been lingering in my grey matter is about the injuries that happen to the cord. If there are injuries to tissue there is inflammation in the process of repair. My thought is that if there is inflammation outside the spinal canal/ structure from tissue/whiplash/tearing/, there would surely be some effect or involvement and swelling of the surrounding regions. Does the cord suffer when surrounding damage occurs?
I have always struggled with the RRMS occurrence of symptoms, could it be a form of clotting in the cord creating pressure and damaging nerves, the repair time is the remitting period?
I seems to me that if damage to tissues, veins, ligaments, muscle creates inflammation and pressure from swelling as part of that process the cord contents of the thecal sac would have a similar process in healing?
The healing could also be the cause of damage to the cord, (like the brain swelling with hemorrhaging and bruising)?
I get the impression that the cord is not thought to have pressure issues from injury damage or the repair processes.
Hope you are enjoying your day,
Nigel
"Recent research shows a significant correlation between trauma and Chiari/CTE type conditions. It is my opinion, that hyperflexion type strains of the cord, in which the head and neck overstretch going forward, in a chin toward the chest direction, can traction the brainstem and pull it down toward the foramen magnum. On the way down it causes a compression deformation of the larger part of the brainstem in the foramen magnum. As the hyperflexion strain is released the brainstem then returns to normal size faster than it can return to its normal position above the foramen magnum."
Is this the type of problem I might have?
The other thought that has been lingering in my grey matter is about the injuries that happen to the cord. If there are injuries to tissue there is inflammation in the process of repair. My thought is that if there is inflammation outside the spinal canal/ structure from tissue/whiplash/tearing/, there would surely be some effect or involvement and swelling of the surrounding regions. Does the cord suffer when surrounding damage occurs?
I have always struggled with the RRMS occurrence of symptoms, could it be a form of clotting in the cord creating pressure and damaging nerves, the repair time is the remitting period?
I seems to me that if damage to tissues, veins, ligaments, muscle creates inflammation and pressure from swelling as part of that process the cord contents of the thecal sac would have a similar process in healing?
The healing could also be the cause of damage to the cord, (like the brain swelling with hemorrhaging and bruising)?
I get the impression that the cord is not thought to have pressure issues from injury damage or the repair processes.
Hope you are enjoying your day,
Nigel
Its interesting to ponder this question. If I am to walk, I am aware that I have balance problems, if I am sitting I am not aware of balance issues. If I walk more distance the balance is a greater issue the further I walk.uprightdoc wrote:NZer1,
What are your typical and current symptoms? Are they chronic or intermittent?
So as I ponder the question more I have all the problems I listed and the longer I 'do' whatever the task is that produces the awareness of that issue the bigger that issue becomes. By the time I have finished typing by copying from an article the worse my vision and concentration is because I am repeating the task.
Listening to people talk with back ground noise, becomes more challenging the longer I try to compete with the back ground noise.
At times it seems that the mental focus on a task is the problem, the longer I do something the more concentration required and the greater the problem seems, like an overheated fuse?
So repeating a task exacerbates the symptom and increases its effect on me, and heat (both my body temp, and air temp) in itself increases the symptom(s).
Lot of words to describe this! Not easy to explain when on the internet and no feed back as I wonder through my thoughts!
Thanks for listening, Nigel
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uprightdoc
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NZer1,
You are on the right track. There is a recently published paper called Clivo-axial Angle and Brainstem Deformation. It has to do with the angle of the base of the skull. Excessive flexion of the base tractions the medulla and brainstem and compresses it against the clivus of the base. You have a similar situation in that you have flexion of the entire cervical spine foward of the gravity line. At the same time you have extension of the atlas and skull. You also have stenosis in the outlets in the lower cervical spine for the nerves to your arms and you have deformation of the vertebral bodies and cartilage in you neck and low back. It's called spondylosis. Your problems are more due to compression of neurovascular tunnels and tissues due to the spondylosis than inflammation.
You are on the right track. There is a recently published paper called Clivo-axial Angle and Brainstem Deformation. It has to do with the angle of the base of the skull. Excessive flexion of the base tractions the medulla and brainstem and compresses it against the clivus of the base. You have a similar situation in that you have flexion of the entire cervical spine foward of the gravity line. At the same time you have extension of the atlas and skull. You also have stenosis in the outlets in the lower cervical spine for the nerves to your arms and you have deformation of the vertebral bodies and cartilage in you neck and low back. It's called spondylosis. Your problems are more due to compression of neurovascular tunnels and tissues due to the spondylosis than inflammation.
Found the paper Dr. and I think I have an understanding of the issues.
Upright MRI would be required in my case I believe, as the MRI's that I have indicate mild contact and they were not looking for this specifically.
The way this problem 'MS' began was 'probably' related to lifting beams using my shoulders and head. At the time that I was seeing the Musculo Skeletal Specialist I came to the conclusion you have regarding the nerve exit compression effecting my shoulder pain. The Musculo Spec said he did not find any indication of that from trying by pressing down on my head in many, many positions that he could recreate the pains. So he said no to the possibility of compression.
Because I was having leg involvement and lower back and pelvic muscle weakness, plus balance and bladder issues he ruled out compression as the reason for the package of symptoms.
The way that my mind has put this scenario together is along the lines of stretch injury to cord in the upper cervical area compounded by lack of room for the nerve endings as they exit the cord. The 'damage' created involved the nerves to my lower body and the scaring that formed over time was seen by MRI some time later. The increase in symptom severity was due to continued aggravation of the 'scar'. The byproducts of the healing process and their spread throughout the CSF space left deposits that attached and formed further legions and scaring as seen on MRI.
(In addition when the Neurologist viewed the last MRI he found a total of eight lesions.) The big question is for me, now that there is lesions, particularly the C2 lesion on the cord will there be ongoing damage to it and further progression in the disease. This would also be based on the theory that once lesions form they spread due to movement breaking away parts of the lesion or content of the lesion and this being pumped by CSF around and collecting in specific conditions and areas.
I have the view that the lesions are live or active is a better description, so to say and that because of their location in the CSF space they can become progressive through the process of healing, whether that involves an immune system action or other action relating to CSF space/content repair.
And on top of this I have had headaches from adjustments (3rd on Thursday evening) which today have peaked, so I am off to lie down which gives me relief, CSF pressure headache? Just remembered that after having a lumbar punch I had bad headaches for 6-8 weeks, low volume or supply issues? Could CSF flow change because of atlas adjustments? Probably?
Enjoy your weekend, Nigel
Upright MRI would be required in my case I believe, as the MRI's that I have indicate mild contact and they were not looking for this specifically.
The way this problem 'MS' began was 'probably' related to lifting beams using my shoulders and head. At the time that I was seeing the Musculo Skeletal Specialist I came to the conclusion you have regarding the nerve exit compression effecting my shoulder pain. The Musculo Spec said he did not find any indication of that from trying by pressing down on my head in many, many positions that he could recreate the pains. So he said no to the possibility of compression.
Because I was having leg involvement and lower back and pelvic muscle weakness, plus balance and bladder issues he ruled out compression as the reason for the package of symptoms.
The way that my mind has put this scenario together is along the lines of stretch injury to cord in the upper cervical area compounded by lack of room for the nerve endings as they exit the cord. The 'damage' created involved the nerves to my lower body and the scaring that formed over time was seen by MRI some time later. The increase in symptom severity was due to continued aggravation of the 'scar'. The byproducts of the healing process and their spread throughout the CSF space left deposits that attached and formed further legions and scaring as seen on MRI.
(In addition when the Neurologist viewed the last MRI he found a total of eight lesions.) The big question is for me, now that there is lesions, particularly the C2 lesion on the cord will there be ongoing damage to it and further progression in the disease. This would also be based on the theory that once lesions form they spread due to movement breaking away parts of the lesion or content of the lesion and this being pumped by CSF around and collecting in specific conditions and areas.
I have the view that the lesions are live or active is a better description, so to say and that because of their location in the CSF space they can become progressive through the process of healing, whether that involves an immune system action or other action relating to CSF space/content repair.
And on top of this I have had headaches from adjustments (3rd on Thursday evening) which today have peaked, so I am off to lie down which gives me relief, CSF pressure headache? Just remembered that after having a lumbar punch I had bad headaches for 6-8 weeks, low volume or supply issues? Could CSF flow change because of atlas adjustments? Probably?
Enjoy your weekend, Nigel
Square Heads and MS
Posted on November 27, 2010 by uprightdoctor
Many years ago when I was a young boy, the carpenter’s uni0n was mostly comprised of men of Scandinavian and Norwegian descent. The other trades colloquially referred to them as the square heads. Technically, square heads are called brachycephalic, which means that the head is as wide as it is long similar to a box. The bust on the left is perfect example of a famous square head. Rather than square, some European designs are dolichocephalic. Dolichocephalic heads have relatively longer bases and narrower widths.
In contrast to Asian designs, European skulls are also prognathic. Prognathic means protruding jaws. In Europeans skulls, the muzzle which contains the nose and jaw protrudes out from the face. In round Asian skulls the jaws and nose are in line with the face. In either case, northern Europeans have a much higher incidence of multiple sclerosis than Asians. On the other hand Asians get a variant form of MS called Devic’s disease. Interestingly, African-Americans also have a low incidence of MS but likewise get a particularly aggressive form of Devic’s disease.
If you strip away the flesh the square shape of the European skull becomes more apparent. The perfect replica cast skull on the right was copied with permission from Bones Clones Inc. The most telltale signs that indicate race are in the shape of the eyes and nose. In this case the eye openings are clearly square. Even more characteristic is the triangular shape of the nose. In Asian and African-American skulls the opening for the eyes and the aperture of the nose are rounder.
The previous post contained a picture of a severely artificially deformed skull. Among other things, the shape of the head affects the pitch and layout of the base of the skull and the venous drainage system of the brain. The length and width of the base of the skull affects the position of the brain within the cranial vault.
A short length in the base from the front to the back of the cranial vault, predisposes the brain to crowding and a condition called Chiari malformations in which the cerebellum or brainstem gets pushed down into the foramen magnum. Chiari malformations can block both venous blood and cerebrospinal fluid (CSF) pathways causing CCSVI and hydrocephalus type conditions. Chiari malformations used to be considered as a childhood problem for the most part. However, recent studies show that trauma can cause Chiari malformations in adults. What’s more, Chiari malformations have also been associated with multiple sclerosis.
The graphic of the skull on the left shows the relative size of the large head compared to the relatively small human neck. In the ape the head is small and the neck is large. The body is also supported by four extremities and the head is much closer to the ground so slips and falls are less likely and the distance to the ground is much closer.
Humans on the other hand are tall and top-heavy and standing upright and balanced over a narrow base rooted in the feet is actually quite a feat. Upright posture makes it easy to fall. What’s more, the head falls further to the ground and so falls generate more force.
People living in northern climates are exposed to far more winter related whiplash type traumas than people living in southern climates. Motor vehicle accidents and winter sports and activities such as hockey, skiing and snow mobiles significantly increase the risk and the forces involved in trauma.
When it comes to MS and trauma, it’s not so much the size of the head that matters as it is how it stacks up on the cervical spine. Moreover, it is also how the brain stacks up over the large hole in the base of the skull called the foramen magnum. Brachycephalic, Asian and African designs, as well as skulls with short lengths in their base are more balanced on top of the cervical spine. On the other hand, they stack more of the brainstem over the foramen magnum. This predisposes the brainstem and cerebellum to getting pushed down, or sinking into the foramen in a Chiari malformation or and pressure cone type condition.
In brief, racial differences in the design of the skull may account for the higher incidence of classic multiple sclerosis seen in northern Europeans. It may further explain why Asian and African-Americans have a lower incidence of MS but get a more severe variant form called Devic’s disease also know as neuromyelitis optica (NMO). In the next post I will cover Asian and African-American skull designs.
Posted on November 27, 2010 by uprightdoctor
Many years ago when I was a young boy, the carpenter’s uni0n was mostly comprised of men of Scandinavian and Norwegian descent. The other trades colloquially referred to them as the square heads. Technically, square heads are called brachycephalic, which means that the head is as wide as it is long similar to a box. The bust on the left is perfect example of a famous square head. Rather than square, some European designs are dolichocephalic. Dolichocephalic heads have relatively longer bases and narrower widths.
In contrast to Asian designs, European skulls are also prognathic. Prognathic means protruding jaws. In Europeans skulls, the muzzle which contains the nose and jaw protrudes out from the face. In round Asian skulls the jaws and nose are in line with the face. In either case, northern Europeans have a much higher incidence of multiple sclerosis than Asians. On the other hand Asians get a variant form of MS called Devic’s disease. Interestingly, African-Americans also have a low incidence of MS but likewise get a particularly aggressive form of Devic’s disease.
If you strip away the flesh the square shape of the European skull becomes more apparent. The perfect replica cast skull on the right was copied with permission from Bones Clones Inc. The most telltale signs that indicate race are in the shape of the eyes and nose. In this case the eye openings are clearly square. Even more characteristic is the triangular shape of the nose. In Asian and African-American skulls the opening for the eyes and the aperture of the nose are rounder.
The previous post contained a picture of a severely artificially deformed skull. Among other things, the shape of the head affects the pitch and layout of the base of the skull and the venous drainage system of the brain. The length and width of the base of the skull affects the position of the brain within the cranial vault.
A short length in the base from the front to the back of the cranial vault, predisposes the brain to crowding and a condition called Chiari malformations in which the cerebellum or brainstem gets pushed down into the foramen magnum. Chiari malformations can block both venous blood and cerebrospinal fluid (CSF) pathways causing CCSVI and hydrocephalus type conditions. Chiari malformations used to be considered as a childhood problem for the most part. However, recent studies show that trauma can cause Chiari malformations in adults. What’s more, Chiari malformations have also been associated with multiple sclerosis.
The graphic of the skull on the left shows the relative size of the large head compared to the relatively small human neck. In the ape the head is small and the neck is large. The body is also supported by four extremities and the head is much closer to the ground so slips and falls are less likely and the distance to the ground is much closer.
Humans on the other hand are tall and top-heavy and standing upright and balanced over a narrow base rooted in the feet is actually quite a feat. Upright posture makes it easy to fall. What’s more, the head falls further to the ground and so falls generate more force.
People living in northern climates are exposed to far more winter related whiplash type traumas than people living in southern climates. Motor vehicle accidents and winter sports and activities such as hockey, skiing and snow mobiles significantly increase the risk and the forces involved in trauma.
When it comes to MS and trauma, it’s not so much the size of the head that matters as it is how it stacks up on the cervical spine. Moreover, it is also how the brain stacks up over the large hole in the base of the skull called the foramen magnum. Brachycephalic, Asian and African designs, as well as skulls with short lengths in their base are more balanced on top of the cervical spine. On the other hand, they stack more of the brainstem over the foramen magnum. This predisposes the brainstem and cerebellum to getting pushed down, or sinking into the foramen in a Chiari malformation or and pressure cone type condition.
In brief, racial differences in the design of the skull may account for the higher incidence of classic multiple sclerosis seen in northern Europeans. It may further explain why Asian and African-Americans have a lower incidence of MS but get a more severe variant form called Devic’s disease also know as neuromyelitis optica (NMO). In the next post I will cover Asian and African-American skull designs.
Dr. do you think that the differences in the CCSVI form (from Malformations of vascularture) of MS and the Chari form of MS or the trauma/injury form of MS are what we are seeing with the improvements from CCSVI treatment.
With the recovery or improvement seen in some people after angio treatment it seems to me to indicate that there is physical reason for the forms of MS e.g RRMS or episodic and SP or PPMS the progressive.
Naturally once damage to the nerves/axons has occurred the amount of of improvement or repair is limited.
Enjoyed the post on skull variances,
regards Nigel
With the recovery or improvement seen in some people after angio treatment it seems to me to indicate that there is physical reason for the forms of MS e.g RRMS or episodic and SP or PPMS the progressive.
Naturally once damage to the nerves/axons has occurred the amount of of improvement or repair is limited.
Enjoyed the post on skull variances,
regards Nigel
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uprightdoc
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There is absolutely a physical reason for the improvement, which is improved venous drainage. Pressure in the brain and cord are dynamic and misalignments and degeneration in the spine affect blood and CSF dynamics, especially compliance. See if you can locate a paper published in Cerebrospinal Fluid Research in 2008 called "A unifying theory for hydrocephalus, Chiari malformation, syringomyelia and spina bifida." The paper is about childhood conditions but the principles apply to adults as well.NZer1 wrote:Dr. do you think that the differences in the CCSVI form (from Malformations of vascularture) of MS and the Chari form of MS or the trauma/injury form of MS are what we are seeing with the improvements from CCSVI treatment.
With the recovery or improvement seen in some people after angio treatment it seems to me to indicate that there is physical reason for the forms of MS e.g RRMS or episodic and SP or PPMS the progressive.
Naturally once damage to the nerves/axons has occurred the amount of of improvement or repair is limited.
You should not be getting headaches after adjustments so let the doctor know.
http://www.biomedsearch.com/attachments ... 54-5-7.pdf
Heavy reading! It would be good if this thought had been expanded to problems when the outflows of the brain, veins are malformed.
Very thought provoking article.
My headaches appear to be related to the changing position, pivot point change of my head. I noticed yesterday a change in posture, whereby my centre of gravity had changed. My head was over the top of my spine rather than forward of my spine as before. Lost the benefit overnight and the muscle strain/ spasm in my upper back is back, probably due to the change and compensation from muscles not used to position. The head aches have gone with the return of my old posture.
I told John about the headaches at the last appointment, I didn't get any comment back from him, I was very surprised.
Hope you're having as nicer weather as we are, very hot, no wind and its the weekend.
Regards Nigel
Edited. After thought, the skull size and design differences between male and female correlate with the prevalence of MS. Interesting!!!!!!!!!
Heavy reading! It would be good if this thought had been expanded to problems when the outflows of the brain, veins are malformed.
Very thought provoking article.
My headaches appear to be related to the changing position, pivot point change of my head. I noticed yesterday a change in posture, whereby my centre of gravity had changed. My head was over the top of my spine rather than forward of my spine as before. Lost the benefit overnight and the muscle strain/ spasm in my upper back is back, probably due to the change and compensation from muscles not used to position. The head aches have gone with the return of my old posture.
I told John about the headaches at the last appointment, I didn't get any comment back from him, I was very surprised.
Hope you're having as nicer weather as we are, very hot, no wind and its the weekend.
Regards Nigel
Edited. After thought, the skull size and design differences between male and female correlate with the prevalence of MS. Interesting!!!!!!!!!
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AlmostClever
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Dear Doc,
I have been going to a chiropractor since the beginning of this year. During my Liberation procedure in August, I found out that I also had May-Thurner Syndrome. No stents were put in anywhere at the time.
I had a stent placed in my left common iliac vein on Nov. 4 to correct the M-T. (located where the right iliac artery crosses over the left iliac vein)
When (or would) it be safe to resume my chiropractic adjustments?
Thanks for all your help here on TIMS!
Best Regards,
AlmostClever
I have been going to a chiropractor since the beginning of this year. During my Liberation procedure in August, I found out that I also had May-Thurner Syndrome. No stents were put in anywhere at the time.
I had a stent placed in my left common iliac vein on Nov. 4 to correct the M-T. (located where the right iliac artery crosses over the left iliac vein)
When (or would) it be safe to resume my chiropractic adjustments?
Thanks for all your help here on TIMS!
Best Regards,
AlmostClever
If you can't explain it simply, you don't understand it well enough. - Al Einstein
[Dr. Zamboni] is conducting a new round of tests in which subjects will wear a collar fitted with a strain gauge to measure neck volume differences in the upright and prone positions. This will allow him to measure the time it takes for for blood to drain through the neck in MS vs. control subjects. This technique is called plethysmography and is less operator-dependent than Doppler ultrasound.
http://www.acceleratedcure.org:8080/node/3605
http://www.acceleratedcure.org:8080/node/3605
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uprightdoc
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Hello Almost Clever,AlmostClever wrote:Dear Doc,
I have been going to a chiropractor since the beginning of this year. During my Liberation procedure in August, I found out that I also had May-Thurner Syndrome. No stents were put in anywhere at the time.
I had a stent placed in my left common iliac vein on Nov. 4 to correct the M-T. (located where the right iliac artery crosses over the left iliac vein)
When (or would) it be safe to resume my chiropractic adjustments?
You should be able to safely resume chiropractic care at this time but you need to alert the doctor about your recent vascular surgeries. There are many low or non-force ways to work on the spine with minimal risks following even the most invasive surgeries. I worked on patients with broken bones, aneurysms, staples in their brain, strokes and open heart surgery as soon as they were out of the hospital. It can actually speed recovery. That said, the doctor needs to be aware and proceed cautiously with extra conservative care.