Sunday 31 August 2014

What makes MS UK far superior than MS Society,

They supply lots of alternative information based on very relevant studies, some that I have previously looked into.

CCSVI ?????????????? - MS Society???

Why the MS Society have not conducted its own comprehensive study into this subject, I do not know. CCSVI is a symptom of a misaligned Atlas. The Society raise millions and do nothing constructive with that money in regards to CCSVI research.

I ask the question WHY ?

Info on MS UK - Alison Peebles - PPMS -Korean Physiotherapy Clinic- Chongsu LeeTherapist technique - yet again I rest my case

Actress Alison Peebles has spoken of a huge improvement in her multiple sclerosis after a revolutionary new treatment.

She had been expecting the primary progressive multiple sclerosis that has blighted her life to quickly leave her dependent on the use of a wheelchair.

However, the leading Scottish actress, whose TV credits include BBC's River City and Shetland, believes a new physiotherapy has greatly improved the quality of her life – and delayed the need for a chair.

Peebles, from Wester Hailes, has been receiving treatment from the Korean Physiotherapy Clinic In Edinburgh, where therapist Chongsu Lee uses a technique that involves gentle manipulation of the spine and surrounding soft tissue to release tension.

It is claimed that as tension around the spine gradually eases off, blood and lymph circulation and nerve function improve.

"The benefits of the treatment have been quite dramatic," said Peebles, who has starred as Lady Macbeth on stage. "I was collapsing all the time as I had poor balance and strength. I was mentally and physically exhausted.

"Now, after 18 weeks of treatment, my walking, balance and vision are hugely improved and my body is much more flexible. I still use a crutch, but if I continue like this, I feel optimistic that I can keep on my feet and delay the imminent need for a wheelchair."

Peebles, 53, a co-founder of the Communicado Theatre Company, has suffered from primary progressive MS, which is characterised by a worsening of symptoms, since 2001.

She wrote and performed the 2012 theatre play My Shrinking Life as a response to her disability, and as a reflection on what it means to play a part in which she was unwillingly cast.

The actress and director continues to work. She will direct the play Bite The Bullet , by Sandy Nelson and Keith Warwick, at the Edinburgh Fringe in August. "I am more supple," I am standing straighter, and I have more energy," she added.

Scientists recently reported they may be a step closer to repairing the damage caused by MS.

Researchers at Edinburgh and Cambridge universities have pinpointed a process that helps to produce more myelin – the sheath surrounding the central nervous system.

Scotland has the highest prevalence of MS in the world, with about 10,500 people affected.

Source: heraldscotland © Copyright 2013 Herald

Info on MS UK - Bacteria and viruses - Parkinson's and MS

Bacteria and viruses

Bacteria







Anxiety or anticipation can often lead to a feeling of ‘butterflies in the stomach’ – which usually dissipates along with the source of the consternation.

But scientists have discovered that the nerve pathways between the gut and the brain that cause this phenomenon may also be linked to degenerative illnesses such as Parkinson’s disease and multiple sclerosis (MS), as well as some mental health problems.

Dr Anton Emmanuel, consultant neuro-gastroenterologist at University College London and the National Hospital for Neurology, explained: ‘The gut and brain share the same nerve chemistry and have a dialogue.

'That’s why when you feel stress and other strong emotions, such as fear, it leads to gastrointestinal symptoms, like rushing to the loo.’

A new study suggests that brain disease can be caused by an unhealthy gut because these signals also travel in the opposite direction.

The study, which was published in the journal Movement Disorders, found that sufferers of Parkinson’s disease had a higher prevalence of a condition called small intestinal bacterial overgrowth, or SIBO.

In SIBO, normally harmless bacteria proliferate in large numbers in the small intestine.

Symptoms include excess gas, abdominal bloating, diarrhoea and abdominal pain. Nobody is sure how many people have it, as it often goes undiagnosed or is confused with irritable bowel syndrome, but estimates are of up to 300,000 British sufferers.

And the researchers suggest that the bacteria may produce chemicals that affect the nerves in the gut, which pass on the damage to the brain – and result in Parkinson’s and MS. Dr Emmanuel said: ‘We now think that neurological diseases such as MS and Parkinson’s are linked to the gut being more leaky, permitting pathogens into the bloodstream and causing an antibody response. Either the pathogens, directly, or the immune response, indirectly, may damage nerve tissue.’

The damaged nerves then transmit these detrimental signals to the brain.

In Parkinson’s, a small part of the brain becomes progressively damaged over many years, something that affects mainly older people. MS is the most common neurological disease in young adults and occurs when the immune system attacks the nervous system.

The two diseases affect about 100,000 and 127,00 people in the UK respectively. Both have wide-ranging symptoms, affecting movement as well as causing tiredness, pain and depression. There are drugs that can ease symptoms, but no cure or even treatments that significantly slow down progression of the diseases.

Scientists hope that this discovery will pave the way for new treatments for both these disabling conditions.

They are now mapping the ‘bacterial genome’, which will identify the bacteria in an individual’s gut – something they hope will ultimately allow doctors to prescribe tailored treatments for leakiness of the gut, improving neurological symptoms in turn.

Until then, the doctors’ body United European Gastroenterology urges people to maintain a healthy diet, including foods that boost good bacteria and encourage efficient digestion. This may have an especially positive effect on mood disorders such as anxiety and depression.

They recommend eating plenty of fibre and probiotics such as live yogurt, as well as limiting sugar, processed foods, animal fat and the use of antibiotics, antacids and anti-inflammatories, as these cause imbalances in the gut.

Source: The Daily Mail © Associated Newspapers Ltd (23/06/14)

(info on MS UK) - People with MS may have a higher risk of developing cancer - I rest my case

Patients with MS may suffer a high risk of developing cancer - study(16/01/14)
The study reported in the European Journal of Neurology claims that people suffering from multiple sclerosis, an autoimmune disease affecting nerves in brain and spinal cord, have a higher risk of developing cancer, especially breast cancer.

Studies conducted earlier claimed that people with autoimmune disease may suffer from a greater risk of developing cancer but most of the studies detected no association between multiple sclerosis (MS) and cancer. Since this latest finding contradicts the previous findings, researchers say that additional research is required to determine whether or not there is a link between the disease and cancer.

For the study, researchers evaluated the data retrieved from the National Health Insurance System of Taiwan. They assessed the information on 1292 people who were diagnosed with MS between 1997 and 2010. They further matched each MS patient with four healthy people who were not diagnosed with the condition.

MS that is not considered as a fatal disease is a chronic and unpredictable disease. It normally affects people between the ages of 20 and 50. This autoimmune disease causes extreme fatigue, blindness, paralysis, poor coordination and more. There are more than 2.5 million people around the world living with MS.

This investigation was led by Li-Min Sun, MD, of the Zuoying Branch of Kaohsiung Armed Forces General Hospital in Kaohsiung, Taiwan.

"Our study was a nationwide population-based cohort study, and it revealed unexpected findings," said Dr. Sun

The researchers noticed that those with MS suffered 85 percent higher risk of developing cancer when compared to the control group. There was a twofold higher risk of developing breast cancer when compared to the control group.

This study suggests that those with MS should be monitored closely in order to ensure the early detection of cancer.

Unsure of why the results of this study differs from the previous studies, Dr. Sun notes says, "The underlying genetic and environmental factors in Taiwan, which differ from those of western countries, might play an undetermined role. Additional large-scale studies will help improve our understanding."

When are they going to stop chopping and changing their minds, when will they realise they have got the "ms" thing wrong

#1
Back in limbo land ? : /
Righto, a weird one this. You know about me and how over the last 2 or more years I've had MS symptoms. I had MRI, this showed lesions. Well, last month I had another MRI. I'm told by my doctor, 'I'm sorry, it's MS' ?  Well....this is where it starts getting weird.
 I had an appointment with my Crohn's disease specialist. Me and my husband told him that I wanted to come off Humira ( my Crohns treatment) as I'd been on it for 6 years and as my Crohns was fine, why not? He looked at my new MRI results. He said ' it's not MS' !!!! After bursting into tears, I asked how is that and he said, the lesions have not changed since the last MRI. The LP showed no signs, and the eye test and flashy light thing all showed negative,; this is the first time we have been told these results, some of them were done 2 years ago !
so, after the most relief I think I've EVER felt in my life, we chatted about the possibility that the Humira may have caused the lesions in my brain and the Neuro symptoms. I mean, every symptom is classic of MS ( probably why they told me I had it). So ! The upshot of it is, I am now off my injections to see if it is the injections causing it. I've been told that I should see an improvement within the month if it's the Humira. Meanwhile, I'm going to be going through the worst withdrawal until it gets out of my system. I've got 2 months without the treatment, if my condition improves...there's our answer. If not, by that time I will be seeing my Neuro. Now it's just time to wait and see.
when I last saw my Neuro, he said ' if it's not MS, it's one of 2 other things that aren't so nice'. Well, I'm hoping that that isn't the case now after the new MRI. As for my doctor who told me I have MS....he got that one wrong!
I hope this essay(lol) gives hope to others. They got it so wrong with me, despite them telling me that I have MS. Of course, I'm being objective at the same time until I hear it from my Neuro's mouth, I'm not daft. But, I do have the glimpse of hope that I've not had before.
i will keep you all updated as I hear any news, but I'm keeping my fingers crossed :)
i hope you are all alright
xxxx
OMG Beverly! That's certainly given you something to think about, hasn't it? You must have been stunned.
Hope your future news is a good, I'll keep my figers crossed too!
Rosina x
 
Thanks Rosina :) yeah, it was extremely weird, I didn't know how to feel to be quite honest. It's a mixture so 'woohoo!' and 'duh?'. I still can't believe it, but not long to go till i see my Neuro ( in November) Hopefully by then he will have an idea of what is going on. Xx thanks for your reply xx
The key thing here is the negative lumbar puncture. I just cant see how someone could be diagnosed with MS with a negative one. A negative LP shows that the immune system is active in the CSF and it shouldnt be. I have read that some neuros (including mine) will not diagnose with a negative one. Even on the Barts MS Blog the prof says that MS with an negative LP is not true MS (if at all) .I was told MS by one neuro and then another says by lesion is due the radiation therapy I had for lymphoma.
I hope that your lesions will go away when you are off the treatment.  Your first neuro probably didnt realise that your treatment can cause lesions and MS symptoms.
I hope all goes well
Moyna xx
Thanks Moyna. That's how it's weird as all my symptoms are classic MS, and he kept doing more and more tests. This is the news I got from my Crohns specialist, not the Neuro...typical! It's been a crappy 2 year ride. The other problem is that as Humira is relatively new, they don't yet fully understand it's side effects. Biological treatments aren't fully understood, but the problem I had before I went on the treatment is that the Crohns was so bad, it was that or lose the bowel : s
I hope that what I have been through is remembered for people in the future so they don't have to go through this. This is all presuming that the Humira has caused this in the first place.xx
Hi Beverly, hope it's gonna be alright and withdrawal won't be too bad! I'm stunned. But not the first time i read about a potential misdiagnosis - there are lots of stories where neuros said MS which later turned out to be neurosarcoidosis or they switched dx back and forth...
All the best and keep us posted. xx
Thanks Xenomorph. I can't believe it. It's cruel really as the process you go through to accept the MS, and all that goes with it, to then be told they've changed their minds :/ Anyway, I'm going to get through this next 2 months, the withdrawal isn't great but if I improve after it then it will be obvious it's that causing it. Thanks for the reply xx
I have MS
Hello Beverley
I notice you say you've been on Humira for six years.  As the consultant been monitoring you over the last six years, while you've been taking the drug, given that he will be aware that demyelination can be caused by this drug.   Were you made aware of  the side efects  before agreeing to take it?
Noreen xx
Thanks Blossom. The doc who put me on it sees me every 3 months. They were aware of how I was feeling and never once said it was Humira. I had every test on my Crohns and they were happy that the treatment was doing its job and not interested. I then started having heart symptoms, checked and fine so that was that. Stay on the drug and be grateful. They recently brought it regular blood tests to monitor liver function etc. my levels of inflammation are always up a bit so they always come up on the blood results.
the Neuro researched the drug and didn't say much at all. He saw my condition and results of reflexes are odd so pressed on testing. So all in all I'm just waiting to see if I improve after I've come off the drug and got over the withdrawal. I've got a backup treatment of steroids in the cupboard if the Crohns flares when I come off it and there's a new drug out if I need it. When I was recommended the Humira I had to sign a form but I cannot remember how nasty they said the side effects were, the state I was in I would have tried anything :s
the MRI (according to the doc) said no presence of demyelination , just lesions from what he could see. He did say he was no expert on brain things but it was brilliant news nonetheless . Xxx
Thanks everyone for asking and replying, I appreciate it. I'm sticking around for a while yet, I want to hear it from the horses mouth before I leave :)
i hope you are all alright and coping with the warm spell we are having, though as I'm looking out the window it looks like rain...plants won't need watering ;)
thanks again
xxxxxx
I have MS
Ok Beverley, all the best with neuro appointment smiley

Is CIDP just yet another misdiagnosis

Chronic Inflammatory Demyelinating Polyradiculoneuropathy 

  • Author: Richard A Lewis, MD; Chief Editor: Nicholas Lorenzo, MD, CPE   more...

 


Practice Essentials

The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. It can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy, the most common form of Guillain-Barré syndrome.

Signs and symptoms

CIDP typically starts insidiously and evolves slowly, in either a slowly progressive or a relapsing manner, with partial or complete recovery between recurrences; periods of worsening and improvement usually last weeks or months. Most experts consider the necessary duration of symptoms to be greater than 8 weeks for the diagnosis of CIDP to be made.
Symptoms reported include the following:
  • Preceding infection (infrequent)
  • Initial limb weakness, both proximal and distal
  • Sensory symptoms (eg, tingling and numbness of hands and feet)
  • Motor symptoms (usually predominant)
  • In about 16% of patients, a relatively acute or subacute onset of symptoms
  • In children, usually a more precipitous onset of symptoms
  • Symptoms of autonomic system dysfunction (eg, orthostatic dizziness)
Pertinent physical findings are limited to the nervous system, except when the condition is associated with other diseases. Such findings may include the following.
  • Signs of cranial nerve (CN) involvement (eg, facial muscle paralysis or diplopia)
  • Gait abnormalities
  • Motor deficits (eg, symmetric weakness of both proximal and distal muscles in upper and lower extremities)
  • Diminished or absent deep tendon reflexes
  • Sensory deficits (typically in stocking-glove distribution)
  • Impaired coordination
See Clinical Presentation for more detail.

Diagnosis

Laboratory studies that may be helpful include the following:
  • Cerebrospinal fluid analysis: Elevated protein levels are common (80% of patients); 10% of patients also have mild lymphocytic pleocytosis and increased gamma globulin
  • Complete blood count (CBC), erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA) level, biochemistry profile, and serum and urine immunoelectrophoresis (to exclude associated systemic disorders)
  • In certain instances, genetic testing
Other tests and procedures that may be warranted are as follows:
  • MRI of the spine with gadolinium enhancement
  • Electromyography (EMG) is a critical test to determine whether the disorder is truly a peripheral neuropathy and whether the neuropathy is demyelinating
  • Peripheral (sural) nerve biopsy: This is considered when the diagnosis is not completely clear, when other causes cannot be excluded, or when profound axonal involvement is observed on EMG; biopsy was once commonly recommended for most patients before immunosuppressive therapy, but current guidelines no longer recommend it
See Workup for more detail.

Management

Principles of treatment are as follows:
  • CIDP must be treated to prevent accumulating disability that necessitates physical and occupational therapy, orthotic devices, and long-term treatment
  • Close follow-up care is necessary to adjust treatment
  • Surgical and orthopedic consultation may be required for sural nerve biopsy or in severe disease with joint deformities
  • Consultation with a neurologist is warranted
  • Consultation with a physical medicine and rehabilitation specialist is appropriate for physical and occupational therapy and evaluation for orthotic devices
  • Other consultations may be necessary if associated diseases are present
  • Physical therapy and an active lifestyle should be encouraged
See Treatment and Medication for more detail.

Image library

Electron micrograph of the peripheral nerve of a pElectron micrograph of the peripheral nerve of a patient with chronic inflammatory demyelinating polyradiculoneuropathy. Note "onion bulb" formation in the myelin sheath of the nerve fibers due to continuous demyelination and remyelination. Courtesy of A. Sima, MD, Department of Pathology, Wayne State University.

Background

Chronic inflammatory demyelinating polyradiculoneuropathy is presumed to occur because of immunologic antibody-mediated reaction along with interstitial and perivascular infiltration of the endoneurium with inflammatory T cells and macrophages. The consequence is a segmental demyelination of peripheral nerves.
Human leukocyte antigens Dw3, DRw3, A1, and B8 occur more frequently in patients with CIDP than in the healthy population.
Cytoalbuminologic dissociation is a characteristic finding in cerebrospinal fluid (CSF) pointing to nerve root involvement. Occasionally, CSF studies reveal mild lymphocytic pleocytosis and elevation of gamma globulin level, but this is observed most frequently in HIV-positive patients.
The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. In many ways, CIDP can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the most common form of Guillain-Barré syndrome (GBS).
A number of variants of CIDP have been described that have immune or inflammatory aspects and electrophysiologic and/or pathologic evidence of demyelination in common. No consensus exists on the best approach to the nomenclature of these disorders. CIDP is a major subset of chronic acquired demyelinating polyneuropathies (CADP). In this context, CIDP is considered when patients have a symmetric proximal and distal motor predominant disorder.
CIDP variants include patients with predominantly sensory symptoms, those with a distal symmetric disorder (DADS), those with multifocal sensorimotor neuropathy or sensorimotor mononeuropathy multiplex with prominent conduction block (also known as Lewis-Sumner neuropathy), and those with CIDP with associated CNS demyelination or with other systemic disorders.
The following disorders are considered distinct from CIDP because they have specific pathophysiologic features and respond to treatments differently than do patients with CIDP: Demyelinating neuropathies associated with immunoglobulin M (IgM) paraproteins, including those with anti–myelin-associated glycoprotein (MAG) antibodies; polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome; and multifocal motor neuropathy.

Pathophysiology

Chronic inflammatory demyelinating polyradiculoneuropathy is presumed to occur because of immunologic antibody-mediated reaction along with interstitial and perivascular infiltration of the endoneurium with inflammatory T cells and macrophages. The consequence is a segmental demyelination of peripheral nerves.
Human leukocyte antigens Dw3, DRw3, A1, and B8 occur more frequently in patients with CIDP than in the healthy population.
Cytoalbuminologic dissociation is a characteristic finding in cerebrospinal fluid (CSF) pointing to nerve root involvement. Occasionally, CSF studies reveal mild lymphocytic pleocytosis and elevation of gamma globulin level, but this is observed most frequently in HIV-positive patients.

Frequency

International

CIDP is uncommon. The estimated prevalence of CIDP in populations from the UK, Australia, Italy, Norway, and Japan is 0.8-7.7 per 100,000. A 2009 study showed that the incidence and prevalence is variable depending on diagnostic criteria. In Rutland, UK on May 1, 2008, the prevalence of CIDP was 4.77/100,000 if the EFNS/PNS criteria were used but only 1.97 per 100,000 if the AAN criteria were used. Similarly the annual incidence was 0.7 per 100,000 using the EFNS criteria and 0.35 using the AAN criteria.[1]

Mortality/Morbidity

Chronic inflammatory demyelinating polyradiculoneuropathy most commonly has an insidious onset and either chronic progressive or relapsing course. Occasionally, complete remissions occur. Quadriplegia, respiratory failure, and death have been described but are rare.

Race

No racial predilection has been identified.

Sex

Both sexes are affected. Of CADP variants, multifocal motor neuropathy has a male predominance of at least 2:1 based on a survey of the largest case series.

Age

Chronic inflammatory demyelinating polyradiculoneuropathy may occur at any age, but it is more common in the fifth and sixth decades. Relapsing course is associated with younger age of patients (third and fourth decades). CIDP has been described in childhood.
Previous
 
 



Contributor Information and Disclosures
Author
Richard A Lewis, MD  Professor and Associate Chairman of Neurology, Department of Neurology, Wayne State University School of Medicine

Richard A Lewis, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Neurological Association, and Peripheral Nerve Society

Disclosure: GBS/CIDP FI Grant/research funds Other; Baxter Consulting fee Consulting; Baxter Grant/research funds None; CSL Behring Consulting fee Consulting
Specialty Editor Board
Dianna Quan, MD  Professor of Neurology, Director, Electromyography Laboratory, University of Colorado School of Medicine

Dianna Quan, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta Kappa

Disclosure: e-medicine Honoraria Other; Pfizer Grant/research funds Independent contractor; Alnylam Grant/research funds Independent contractor
Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment
Florian P Thomas, MD, MA, PhD, Drmed  Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, and Sigma Xi

Disclosure: Nothing to disclose.
Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Consulting; Sunovion Consulting fee None; Supernus Speaking, consulting; Upsher-Smith Grant/research funds None
Chief Editor
Nicholas Lorenzo, MD, CPE  Chairman and CEO, Neurology Specialists and Consultants; Former Senior Vice President, Founding Executive Director, Continuing Medical Education, Gannett Education (Division Gannett Healthcare Group)

Nicholas Lorenzo, MD, CPE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and American College of Physician Executives

Disclosure: Nothing to disclose.
Additional Contributors
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Marina Zvartau-Hind, MD, PhD, to the development and writing of this article.



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Electromyography of a patient with chronic inflammatory demyelinating polyradiculoneuropathy illustrating conduction block, temporal dispersion of compound muscle action potential, prolonged distal latencies, and slowed conduction.
Prolonged F wave latencies (normal is < 31).
Electron micrograph of the peripheral nerve of a patient with chronic inflammatory demyelinating polyradiculoneuropathy. Note "onion bulb" formation in the myelin sheath of the nerve fibers due to continuous demyelination and remyelination. Courtesy of A. Sima, MD, Department of Pathology, Wayne State University.



 

Atlas C-1 Twisted causing PCS symptoms

Atlas C-1 Twisted Causing PCS Symptoms


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Unread 02-15-2012, 03:59 PM   #1
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Default Atlas C-1 Twisted Causing PCS Symptoms

I have been PCS for alomost a year now has anyone ever heard of or have
any information concerning the Atlas Vertebra (C1) being out of place causing PCS related Symptoms

Thanks
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Unread 02-15-2012, 04:30 PM   #2
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Is it severely twisted or more of a misalignment?

Some threads on c1/c2 - atlas/axis adjusting - Nucca
http://neurotalk.psychcentral.com/thread164885.html
http://neurotalk.psychcentral.com/thread164957.html
http://neurotalk.psychcentral.com/post735715-15.html
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Unread 02-15-2012, 04:52 PM   #3
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Quote:
Originally Posted by crossline View Post
I have been PCS for alomost a year now has anyone ever heard of or have
any information concerning the Atlas Vertebra (C1) being out of place causing PCS related Symptoms

Thanks
C1 is right around where the brain stem is...and if it's out of place it can be causing some mild compression to your brain stem which can cause a lot of problems. Since your recovering from a head injury and it's mainly your upper cervical area your concerned with, you want to see a NUCCA specialist.

http://www.nucca.com

You can find a NUCCA chiropractor in that above link.

If you want more information about the procedure you can click that first link that Jo*mar listed...it is my thread about the success I've so far had with NUCCA.
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What happened: I was randomly assaulted from behind in June of 2011. I was knocked unconscious for an unknown amount of time (less than 30 minutes) and have no memory of the event. CT scan showed contusion and hematoma of the left frontal lobe. I spent 3 days in the hospital. Diagnosed with Post-Concussion Syndrome in September 2011. Currently have Medicaid and SSI.

Current symptoms: Brain fog, anxiety, panic attacks, memory issues, confusion, problems with spontaneity, sensitive to loud noises, trouble thinking, problems with producing speech, spacing out, word finding difficulties, tinnitus in both ears, random tingling in different parts of my head and many other things that I can't explain. I'm very easily overloaded which makes it nearly impossible to watch TV or use the computer.

Slowly but surely regaining my life back.
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Unread 02-15-2012, 08:47 PM   #4
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Any misalignment of C-1 (Atlas) can cause inflammation that can interfere with nerve function, blood flow to the brain and blood flow to the brain stem. The idea of C-1 compressing the brain stem is an over-simplification. The compression is from the inflammation, not the position of C-1.

There may also be pinching of nerve fibers but there are are not nerve fibers in or very near the joint areas (occipital condyle to Atlas) like there are near the highly moveable joints of the lower vertebra.

That is why icing the area is so valuable. Anything to reduce the inflammation is beneficial.

The blood flow being restricted is likely the cause of the PCS symptoms since they manifest from areas that are not necessarily near the C-1 structures.

An important posture issue to be aware of is moving the head laterally (rotating side to side) at the same time as moving the head up and down. In other words, don't combine Yes movements with No movements. These combined movements are most likely to cause impingement in the joint increasing inflammation.
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59 years old, retired due to disability, married 34 years, father of three, grandfather of four, Suffered a serious concussion at 10 years old (1965) stopped most driving after concussion at 46 years old (2001), Post Concussion Syndrome/Multiple Concussion/Impact Syndrome with PTSD, immediate/short term visual and auditory memory problems, slowed processing speed, visual/auditory processing difficulties, insomnia, absence seizures, OCD, 14 concussions since first concussion at 8 years old, Taking paroxetine for 14 years and gabapentin for 12 years. Added L-Tryptophan and stopped paroxetine after 3 months of tapering. I currently take 500 mgs of L-Tryptophan AM, 500 mgs noon, and 500 mgs PM.


As of Nov 15th, Due to high stress issues resulting in PTSD, docs put me on 3 meds. Clonazepam but only for 30 days ) .125 mgs twice daily (Doc presc. .25 mgs 2x daily but half a tablet is good) , citalopram (Celexa), an SSRI , and olanzapine (Zyprexa), an atypical anti-psychotic that usually causes weight gain before bed. I lost over 30 pounds since mid July. It just stopped the weight loss. Took me off the gabapentin. I am feeling better than I have in years.

This great feeling only lasted a month. Back to the same old PCS doldrums.

May 2014, I am off the olanzapine due to a 6 fold price increase. Back on 600 mgs of gabapentin before bed.

I am also taking L-Theanine to help with GABA regulation


"Be Still and Know That I am God" Psalm 46:10
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Unread 02-16-2012, 01:26 PM   #5
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Has anyone with these type of upper cervical issues felt like their necks make a grindy kind of noise when they make movements to their head, yes, no kind of movements?

Several weeks after my surgery in Dec of 2009, I recall walking and slipping off a curb with my heel landing on the street, but unfortunately in a locked leg position so I think the jolt and force of the step may have compressed some parts leading up to my brain. At least this is the closest event I remember just immediately prior to the return of my current PCS symptoms.

I've had a couple of adjustments by chiros, one of which is my current neurologist, who does a gentler adjustment. I just still don't have an immediate 'ahhhhh' feeling afterwards and wonder if more targeted adjustments are more applicable.

They've taken an upper cervical MRI which shows 'degenerative age related wear'. Yeah sure, but grindy noises? So soon after this event?

I'm debating seeing an atlas orthogonal specialist which may be closest in specialty to NUUCA adjusters and trying to evaluate the situation.

Mike
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May 31, 2009: Concussion from syncope due to low blood volume resulting from severe dehydration. Occurred after finishing my 9th marathon. 100% of symptoms cleared by August 2009.

December 15, 2009: Major surgery due to diverticulitis. 6 weeks after surgery, dizziness, fog, cognitive difficulty, anxiety, some panic, lots of headache. These symptoms largely gone, but still cannot exercise above a very low threshold otherwise resulting in severe headache and cognitive fog. Same for overwhelming odors.

Meds: Nortriptyline and Naratriptan as needed to rid severe headaches (exertional migraines).
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Unread 06-12-2014, 12:41 AM   #6
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Quote:
Originally Posted by crossline View Post
I have been PCS for alomost a year now has anyone ever heard of or have
any information concerning the Atlas Vertebra (C1) being out of place causing PCS related Symptoms

Thanks
My atlas was out of place for years, symptoms were anxiety, depression, hopelessness, neck stiffness, grinding when turning away from problem side, muscle imbalances all over the body, jaw pain (on the opposite side), TMJ, jaw clicking, lower back pain, pain mid spine on the left, trapped nerves in left trap and back, thick upper traps (from forward head posture i think) anyway, all of my symptoms disappeared after lots of research I finally cracked it (not literally).

Also I wouldnt go to a chiropractor because I've seen some of their 'corrections', all that sudden twisting can't be doing those delicate nerves in your neck any good! I guess that's why the nucca approach is the best because it's gentle.

Here's what I did to re align my c1 atlas

First, I'm not sure how misaligned you are but I'm going to assume you have muscle imbalance in the neck but either way I think the first step I'm about to right is important. If the muscles are tight on one side your head / c1 simply cant go where it's supposed to.

1. Do these stretches to loosen the neck, pay attention to imbalances ie if you can go further on one side than the other. In this case stretch twice as much and don't count, only release the stretch when the muscle has relaxed. You CAN make tighter muscles even tighter by stretching improperly.

*edit*

2. Next the hips. I'm also going to assume you have tight / limited hip movement so here's what to do.

Go for a walk, whilst walking focus on tightening you abs and your but (glutes) whilst tilting your pelvis backwards so you effectively straightening your lower back, so you're pulling the front up an pushing the back down. Hold it for as long as possible, you should feel your lower back free up almost straight away.

Necks loose and hips are loose, so that's the muscles in the top and bottom of your spine sorted, now to align the C1.

3. Perform these two simple exercises in this video. This (as he says) always works in positioning the atlas / *edit*

(Like he says repeat it every hour)

Tip: in ex.2 if you're tense try to relax and when you bring your arms to your shoulders breathe in.

Hope it helps!

Last edited by Koala77; 06-12-2014 at 05:15 AM. Reason: No links allowed for new members.
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Unread 06-12-2014, 02:07 PM   #7
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I believe that most of my long lasting issues after the initial concussion were due to neck problems.
After I started seeing an atlas orthogonal chiro about a year into my recovery, I finally started seeing good progress.
Nothing instantaneous like they claim in some of the AO videos, but definitely felt better over the course of weeks and then months. I've been seeing him for about 5 months now and a lot of my issues have either resolved or at least got way way better.
Exercise is finally an option, I'm doing 20 minutes on a stationary bike at a moderate pace and then a 2 mile walk after work.
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12/02/2012 - Light concussion at boxing practice. Ended up having PCS for about 3 months.
March 2013 - thought that since most of my symptoms resolved I could start having fun again.
Went snowmobiling once (didn't hit my head) and concussion symptoms returned and got even worse than before.
June 2013 - accidentally bumped my head against a deck railing, and had a month-long setback.
November 2013 - drove to work after a big snowstorm and the roads were very rough, ended up having another setback.
2014 - Having setbacks after coughing/sneezing too much, or someone slapping me on the back, or any other significant jarring.
Feb 2014 - Started seeing Atlas Orthogonal chiro - most helpful doc so far.
June 2014 - Started with physical therapy (also visual therapy for dizziness).

Current symptoms are: inconsistent sleep patterns, headaches, vertigo/dizziness, anxiety, mental fog, problems with computer screens.

Meds: Xanax (off), Trazodone - for sleep (off), Ambien/Lunesta