Let me explain…

Three kids.  Two of them boys.  Stinky boys.  One boy thinks my car is his personal foot locker.

Gross boys.

And their friends.

To say that I had a couple days’ worth of food in the van would not be an understatement.  I took out two shopping bags of trash, two pairs of sneakers, two flashlights (noticing a trend here?), a half-eaten can of Pringles, 44,000 m&ms, 7 water bottles, two Game Boy cartridges, lots and lots of corrected homework that should have gone to recycling, a backpack (why isn’t that in school now?), a watch that was declared missing, a half-eaten Subway sandwich and popcorn salt.

I vacuumed the entire van from top to bottom, then I scrubbed all of the seats, door jams and doors.  I then washed the windows and the front dash.  I even scraped all of the sticky money out of the cupholders and have that soaking in the sink right now.

I’m so darn proud of myself.

Now, for “normal” people, that’s really not a big deal.  It took me about an hour and fifteen minutes, but for me who is exhausted just THINKING about moving, it’s HUGE and I DID IT!!!   I did it!!  I’ll have to take a nap later, but I DID it!!

Silly NMO, I won’t let you beat me down today.

Pain:  In torso from breastbone to hips – sunburn feeling.  Firm pressure brings it some comfort.  Brushing of my shirt against my skin hurts.  On a scale from 1-10 (10 being severe pain), I think I’m at about a 4-5.

Nausea:  minor, but that’s probably from all of the Easter junk I’ve been eating

Tiredness:  Scale from 1-10 where 1 is hyper and 10 is exhaustion.  I’m at around a 9 right now. Maybe a 9.5.  I’m having a hard time keeping my eyes open today after a full night’s rest and a 5-6 hour nap.

Emotional:  blah but not weepy today.

Physical:  minor limping, minor weakness in both legs – especially at the knee.  Physically very tired.  Numbness in legs and pelvic region.

Mentally:  worn out

Other:  two canker sores in my mouth.  I haven’t had these since I was in college.  Thanks Imuran!

I am taking 60mg of prednisone every other day.  It’s not long term – about six months until my Imuran kicks in.  The prednisone is protecting me (or trying to) from another attack.

To say that my life hasn’t been emotional lately would be an understatement.

I am a voracious reader, but I have found lately that my retention is nil.  I try, I really do, but I’m so darn tired that I’m not retaining information especially when it comes to learning about this disease.  I’m also trying to get as much done while I’m healthy so that “if” I start to decline, I don’t have to worry about legal things and planning for my death.

It’s been hard.

Filling out hospice paperwork is something I hope most people never have to do.   I sit at my dining room table filling it out and I have to walk away after just a few sentences.  It’s crushing to think that I could die soon and what’s more crushing is to think that my kids may not have concrete memories of their mom.  I’m trying to work on that right now (hence the Pennsylvania trip I need to post pictures of soon!)

I’m not saying that I believe I’m going to die soon.  The prognosis is variable.   In fact, I’m aiming for the age of 92 – at least that’s my goal for now.  Yet, many people DO die from this disease and I need to be prepared for that. Maybe I’m deceiving myself, but I just don’t think my life will be cut short.  Plus, research on NMO has EXPLODED in the last few years thanks to the Guthy-Jackson foundation and many dedicated researchers and physicians.  I am optimistic of my fate and confident I will live a long life.  Still, being married to a realist physician, I need to get that paperwork done and out of the way and dang, it is hard to even think about.

So I need to be prepared and I’m filling out end of life paperwork.  I’m planning my funeral (it’s all still in my head – I need to write that down), I’m doing a power of attorney for my health decisions.  This is all so new to me and I’m sure I’m not getting the terms down right.

There’s a cemetary down the road from me and believe it or not, it brings me peace knowing that’s where I’ll be.  My kids can walk down to see me, though I’ll be in heaven partying it up with Jesus.

So, all of that being said, I’m a little weepy.  I’m doing my best to keep it from my family, but apparently I’m crying in my sleep now.  My husband is worried about me, but I think I’m handling it okay – except the days after I take my prednisone.

Because I’m on every other day, every other day I am emotional.  Every other day I am hyper!  Of course, these aren’t on the same day, so I’ll have an emotional day, then a hyper day, etc.  I’m getting used to it, but I’m sure it’s driving my husband batty.

I’m also taking things VERY personally and have been told a couple of times to lighten up.  Of course, I’m taking THAT personally too.  LOL!  I’m concerned that in the next six months or so, I’m going to alienate all of my family and friends and I don’t know how to make that NOT happen.  I feel that the prednisone is making me irrational – not in a mean or crabby way, but in a “nobody loves me, everybody hates me” worm eating way.

Nobody wants to be around someone like that.  NOBODY.  And I don’t want to put anyone through that either.  I’m normally one of those happy-go-lucky people that just take everything with a grain of salt and right now, those grains are meteors!

So, if you happen to come across this blog, please tell me how you coped with prednisone.  I love my family and I don’t want to put them through any more of this!   They deserve so much better, and honestly, so do I.  I don’t like crying all of the time and just saying, “stop it” isn’t working.

My husband had a week-long conference in Lancaster, Pennsylvania and we took the boys with us.  My DD decided to stay home because she had a ton of homework to do and one of her teachers wasn’t pleased that we wanted to pull her out of school.  He assigned her an extra report, so she decided to stay home.  Thankfully, my parents were willing to stay with her.

So, last Saturday, we drove south to Lancaster. 

Pennsylvania is a beautiful state.  Even in crummy weather, it’s a beautiful state.  I don’t think I’ve ever driven through Pennsylvania before, and if I had, I was probably too young to remember.  It’s important to me to see everything I can, so I did my best to stay awake the whole ride.

My husband (I’m calling him Boris in case you haven’t figured that out yet) insisted on driving the whole time.  Normally I don’t like that, but this trip I didn’t care.  I wanted to take in the sights.  We don’t have big mountains in lower Michigan and I couldn’t wait to see them, so I was fine with him driving.

Even in the rain the mountains were beautiful.  Going through the tunnels was really cool (though intimidating knowing all of that weight was on top of us).  In what was supposed to take us 12 hours, we arrived at our resort in 10.  It was a perfect day!

Sunday we went to Mass as a family.  Anyone who knows us knows my husband doesn’t go to church, but he came with us and I’m so glad he did!!  We went to St. Anthony’s of Padua in downtown Lancaster.  The priest was wonderful and so was the music.  We then drove around a bit, went shopping at the Outlet shops, ate at Five Guys (LOVED IT) and explored the hotel and the hotel grounds with a two mile walk.  I hopped online to get directions to the Baltimore Aquarium.  I had promised the boys a fun-filled day at the aquarium and needed to plan.

In my next post I’ll go into detail about what we did each day (and I’ll even include pictures) but what I want to concentrate on with this post is how exhausted I’ve become since my NMO diagnosis.

I am someone who is go.go.go.  Nonstop movement.  I fidget.  I toss and turn.  I do NOT like to stand still.  The main trigger with my panic attacks is me being stuck somewhere.  I have to be able to move!  On every vacation I plan something to do everyday and that activity normally lasts the entire day until we all collapse in the evening.

With NMO, I can no longer do that – I found that out this week.

Monday we drove out to Baltimore where we went to the National Aquarium and then headed on over to Fort McHenry to learn all about the fort and the National Anthem.

Tuesday was planned to be a slow day.  I figured the kids would be tired from the previous day and would want to swim in the pool. Plus it was raining all day and I didn’t want to go anywhere in the rain.  The kids swam while I read for most of the day.

Wednesday I had planned to take the kids to Philadelphia to see Independence Hall.  Instead I was hit by a mack truck with extreme exhaustion.  I couldn’t get out of bed.  My husband was worrying about me and actually skipped part of the morning conference so I could nap.  I honestly don’t remember much of the day other than I slept.  Boris had a meeting in the afternoon, so after my nap I was able to take the boys out to a bakery.  We got a whoopie pie (Oh my word – heaven!) and then drove around Lancaster to see the sights.

Thursday – we went to Philadelphia to see Independence Hall.  We spent the majority of the day there arriving back at the hotel at around 6:30/7:00pm.  I went to bed at around 9:00pm with plans to go to Valley Forge the next day.

Friday – pure exhaustion.  Again, I couldn’t lift my head out of bed until NOON!  The boys played on the computer and with their new Revolutionary Army guys.  They were probably loud as can be but I slept through it all.  Boris’ conference ended at 1pm, so he took the boys mini-golfing and swimming so I could get more sleep.  I took ANOTHER nap and was finally coherant at around 6pm.

Today we drove back from Pennsylvania and I’m tired again, but not ridiculously tired like I was yesterday.

I have a theory:  the day after I take my prednisone I feel “normal.”  I took my prednisone on Sunday, so Monday was a GREAT day.  Tuesday was fine, but I’m thinking it may have been a good day because I accidently took my prednisone two days in a row (Sunday and Monday).

Wednesday was a bad day (no prednisone on Tuesday), Thursday was awesome (prednisone on Wednesday), Friday was exhausting (no prednisone on Thursday).  Today has been a fine day with the exception of major tingles when I walked across the parking lot to the Rest Area (prednisone yesterday), so I’m assuming tomorrow I’ll be exhausted again.  Now, prednisone may have nothing to do with it.  I could very well have had those great days because I had gotten rest too, but the prednisone makes me HYPER (I can feel it now – it’s 11:35 at night and I’m a little hyper).  Is it the prednisone?  I don’t know, but right now, I’m feeling like it is.  I’m concerned that once the Imuran takes full effect and I’m pulled off the prednisone, am I going to be able to function at all?

Tomorrow is Palm Sunday.  I am NOT missing Mass tomorrow.

So, I need to figure out how to overcome with this exhaustion.  Do I push through it?  Do I listen to my body and rest?  I’m not sure of what to do.  Dr. W. told me I need to get as healthy as I can and that includes exercise.  Should I start exercising regularly (of course I should) but will this help me overcome the exhaustion?  My plan is to start walking 1/2 hour a day  – just from my house to my neighbor’s house, back and forth, so if I get tired, I can just come home without worrying about getting stuck someplace.

I also plan to lift free weights.  Just 3 sets of 10 reps every other day.  Hopefully this might wake me up a bit.

I’m not ready to give in to NMO.  I know that the clock is ticking now, so I want to enjoy as much of my life as possible – especially when my kids are still young.  I don’t want them remembering their mother as “that lady who slept the day away.” 

Auto-Immune diseases – well, they just stink.

My son earned a gift card to Double JJ Ranch, http://www.doublejj.com/index.html and we decided at the last minute on Friday to head down there for the day and check it out.  There’s a huge waterpark there and I knew the kids would love it.

So we went and the kids had a blast!

Of course I brought the crummy camera with us, so my pictures won’t be great.  I’m new to WordPress, so we’ll see how this works with me posting pictures.

We got there around 2:30, checked in and immediately went to the waterpark.  The kids had a BLAST – even my little one loved the slides!  I was so proud of him for checking them out.  He doesn’t like water (we have a pool – you’d think he’d be a fish) so the fact that he enjoyed himself so much is huge!

My three rugrats even got ME to go on a waterslide.  I get extreme vertigo even in a car, but I went anyway and even though I told the kids I hated them for making me go on the slide, I LOVED it.  To make it even better, we found friends of ours down there, so we got to spend some time catching up with them.

After the waterpark, we decided to go out to dinner at the steakhouse on the property.  It was DELICIOUS!  M got a cheeseburger with fries, B got chicken strips and fries, I got fettuccini alfredo (so not on my diet!) and a huge salad and J and DH got all you can eat perch.  Let’s just say we all needed to be rolled out of there to get back to our room.

B and M enjoying their dinners.

J and DH enjoying their “all you can eat” perch.  It was delicious!

My baby boy falling asleep at the table.  He was EXHAUSTED after 7+ hours at the waterpark!

We retreated to our beautiful room (I should have taken pictures, but it was lovely!)  It had a full kitchen with dining and living room and a separate master bedroom with a hot tub.  Very nice!

The next day we went out to the ranch where we met two silly cowboys who argued over EVERYTHING. 

It got so bad, they began to brawl.  Almost every time we saw these two together, they were fighting. 

Such a bad influence on the kids, but they loved every minute of it. 

We decided to check out the local shops there and found a checkers board for the kids to play with.  B gave M a run for her money, but M ended up winning the game – even after B got a little bit of help from Mom.

J thought this was pretty cool, but I was a little creeped out by it.  He begged for the picture anyway.

I was glad to lock up the kids for a little bit.  They were wearing me out!  J even got to ride a mechanical bull and was NOT thrown from it!  I have that on video and when I figure out how to post it here, I will.

So, would I go there again?  Hands down – YES!  Even though it was an impromptu trip, and way out of our budget (oh my goodness that place was expensive), we still had a very nice time. 

It was nice to not think about NMO while we were there.  I had so much fun people watching at the waterpark, and of course, watching my little ones having fun was awesome too.  The fact that I was able to go on a slide was great as well – though the stairs were quite difficult, I’m proud that I did it!  I was a little disappointed that the kids didn’t want to go to the water park again the second day – I really wanted to give the stairs another try.  Plus, it was just so nice to see the kids having so much fun without worrying about their mom.  I’m so glad we went and I hope we can do more trips like this in the future.

Let me tell you – if the rest of the world was run as efficiently as the Mayo Clinic, we’d have world peace.  What an amazing place!

March 14th was our day to meet with Dr. Brian Weinshanker.  I was very excited and incredibly nervous to meet him.  He’s an expert in Neuromyelitis Optica (Devic’s Disease) and he would give us the answers I need.

Unfortunately, the week we were scheduled to go was the busiest week we would have all year.  My middle son had 5 basketball games scheduled.  My youngest son had piano lessons and my daughter had Science Olympiad practices and competition that week.  It was CRAZY and I had to figure out how my mom could get everyone everywhere they needed to be.

I made out a schedule for my mom.  Gave her plenty of contact numbers for those “just in case” situations.  Printed off maps so she would know how to get to the school, McDonald’s and Church (not in that order of course!)  My husband cancelled out his patient load for the week and we were all set to go.

The day before we left, I ironed all of his shirts, all of my blouses, slacks, etc.  Packed up all of our clothes, scrubbed down the bathrooms and got the house ready for my mom to move in.  Despite me being so nervous, we were ready to go!

Many people have been praying for me.  It’s obvious now that I’m sick.  I walk with a limp and I look exhausted.  I sleep through most of the day and I’m thankful for being able to be able to drive and pick up the kids from school.  Once they are home, I lay back down.  My husband is an angel and wants me to rest, but I’ve been feeling so guilty that I’m not holding my own anymore.  Going to Mayo was going to exhaust me further, but hopefully Dr. Weinshanker would have the info I need to make myself feel better.

So, Sunday, March 13th came and my husband and I took off for Rochester, MN.  It was about a 10 hour or so drive and was very beautiful.  We enjoyed every minute of it.  We finally arrived at our hotel the Kahler Grand (http://www.thekahlerhotel.com/).  It was a nice hotel – very clean but also very small.  That didn’t matter – we were there for Mayo and not the hotel and it met our needs.

The Mayo building is where I needed to be at 7:30am on Monday morning.  We decided to explore a bit before turning in for the night. What a neat place!  The Kahler and the Mayo building are connected through a whole underground city with shops, restaurants and galleries.  It was so neat to explore!

Monday morning came and I was incredibly nervous.  Those who know me well know that I suffer from extreme panic attacks and I was very concerned that I would have one while meeting with Dr. Weinshanker.  This appointment was so important to me and I didn’t want to mess it up by being so nervous!  I did my best to keep myself calm and thankfully, my husband knows how to deal with me.  He’s such a good man.

My appointment was at 7:30am on the 8th floor.  We went up there at 7:10 and by 7:30 I was already back in a patient room.  After the nurse took my blood pressure and weight, she told me that Dr. Weinshanker wouldn’t be in until 8:20am.  She offered to let me stay back in a patient room, or wait in the lobby.  We chose to wait in the lobby and went downstairs to the cafeteria to get a quick bite to eat.

By 8:00am we were back upstairs and by 8:10 we were in the patient room again.  8:20 came and Dr. Weinshanker walked right in.  What a kind man!

I was VERY nervous by this time and probably giggled like an idiot.  I was so thankful my husband was there to listen as I just don’t retain information when I’m nervous.  I’m also thankful that we had written down a list of questions and he was able to answer almost all of them.

He looked at my MRI scans of both my spine and my brain, looked at the bloodwork I had done and in a nutshell, he confirmed my earlier diagnosis of Neuromyelitis Optica.  As with all autoimmune diseases, my prognosis is variable.  I felt bad for him as he had to answer many of our questions using that word – variable.  We don’t know how this disease will affect me as every person is different.

What he was able to tell us is that I can exercise with no problems as long as I start slow and build up and listen to my body.  I’m one who tends to overdo things, so he told me to keep that in mind.  He told me to get “as healthy as you can.”  One of my major concerns is that my body will immedately have an attack and I’ll be stranded somewhere.  He told me that that probably will not happen – my symptoms will progress over a few hours to a few days.  That gave me some comfort considering all of the driving I do with my kids.  He put me on 60mg of prednisone for 6-9 months until the Imuran I’m currently on builds up, added bactrim to help me avoid pneumocystis prophylaxis (bad pneunomia), and upped my Imuran to 175mg (I was at 75 mg when I saw him).  Currently, I am at 125mg until my next blood draw sometime this week.

Dr. Weinshanker and my husband did a bunch of medical talk about how to treat me if I have an attack.  I’ll be put on 1g of IV methyl/pred for five days.  If my symptoms don’t improve, then I’ll go on plasmaphoresis.

After we discussed all of this, he said he was done.  Because I’m a confirmed case of NMO due to the IgG antibody being present in my blood, there was no reason for us to do anymore tests.  We were free to go!

After meeting with Dr. Weinshanker, we were both a little shocked that we were done so quickly!  We both had expected to be at the Mayo for a week and here it was – only 10:30am and we were done!  Dr. Wienshanker enrolled me into the Guthy-Jackson foundation blood bank and I still needed to do my blood draw, but other than that – we were done!

We actually spent more time waiting for my insurer to approve my blood draw (Dr. W. also ordered another blood test to rule out other autoimmune diseases) than it did for me to meet with the Dr. himself!  Finally, at around 2pm I was able to do the draw and then we left to go to the Mall of America and then head back home.

My thoughts on Mayo? What a wonderful place.  Dr. W. was so kind and very helpful.  He did not mince words and I appreciated that.  I wish more was known about NMO, but it is what it is.  He gave us the information we needed and a road map to help us fight this disease.  The rest is up to me and God.

Here’s a picture of me and the giant naked man at Mayo:

This describes me to a T (gift idea anyone?).  I found it in one of the shops below the Mayo Clinic:

I wish I would have bought it.  It’s totally me.

Of course, my husband was shshing me and telling me to cut it out.

I’m probably going to jump all over the place so please forgive me.

I started Copaxone on January 8th. The nurse was wonderful and the first shot hurt like heck all the way down to my fingers. Once I got used to it, it got a lot easier. In fact, the first day was the day that hurt the most.

Don’t get me wrong – EVERY shot hurt, but the first was the worst. I had a large, hollow circle around the injection site of my right arm for a few days. The other shots weren’t at all like that.

Shared Solutions gave me a calendar in which I kept track of my shots. The shots are daily and they’d rotate. The sites were the back of both arms, the tops of both thighs, both hips and the stomach, so if done properly (which I did), I did a shot once a week in each injection site.

Shared Solutions also gave me two auto-injectors. You put the shot in the injector and press a button. It will inject the medicine for you. It’s very easy. The medicine going in was always painful, but I always did it right before bedtime. Within 15 minutes the pain would lesson and I’d be okay again.

So I’d try to do my “health hour” every evening between 7:30 and 8:30pm. Soon it became 7:30-10:30pm or even 11:00. NOT GOOD. But, I was consistently taking the shots, so I guess it’s better than nothing. I would also take 1 tsp of cod liver oil with a swirl (fish oil that tastes good) chaser.

I’m sure you’re wondering why I’m talking in the past tense.

January 26th I had an MRI of my brain to see if there were any lesions there. It would only make sense that if I had lesions on my spine (one) that I would have some in my brain as well. I assumed (as a joke) that I had 52 lesions, so when the scan came back with 30, I’d be happy!

Well, the scan came back with zero. Nada. Null.

Now, you’d think this would be a good thing, but it’s not necessarily so. My neuro wanted to run one more test on me for Devic’s Disease – Neuromyelitis Optica. It’s a blood test that checks for certain antibodies.

It was sent to Mayo Clinic and two weeks later, on February 7th, it came back positive. I don’t have Multiple Sclerosis. I have Devic’s Disease. This is NOT a good thing. After a brief phone call with my neurologist I stopped my shots of Copaxone. Copaxone, from the little we know, doesn’t really help Devic’s Disease (NMO).

On Tuesday, February 8th I went to see my neurologist and he did the regular neuro tests on me. My legs are weakening. He also referred me to the Mayo Clinic to see Dr. Brian Weinshanker. He’s an expert on NMO and has seen approximately 600 cases. This is a VERY rare disease and there is no cure. It attacks the patient violently without remorse. I am now begging for MS and I’m in tears almost constantly.

I was told that Dr. Weinshanker reviews new cases once a week. Basically, I’m applying to see him. If he accepts me, it will be 4-6 weeks until the appointment at Mayo.

On Thursday, February 10th, Mayo called me! My appointment which will last from 5-7 days will begin on Monday, March 14th. I’m hoping that the reason he wants to see me is because he thinks he can do something for me. Please God – I want to live.

I’ve been cleared to take a drug called Imuran. It’s an immune suppressant drug. When I’m in a better mood, I’ll explain how it works. I’m also continuing the Swank diet. I’ve cheated a little bit, but only a little. I know I feel much better when I follow it closely.

Boris had never heard of this disease until me. My neurologist has never diagnosed it until me. I’m a wreck! A basketcase – you name it. Everyone is saying that I am so strong, but I’m anything but strong.

I’m trying to say the Rosary daily and I’m asking Fr. Solanus Casey to pray for me. I’m scare and I know that worry is from the devil, so I’m trying to stay positive.

But I also need to be realistic. I’m getting a video camera and I’m going to start videotaping me giving advice to the kids. I’m also going to get all of our paperwork in order. I’ve done some of it, but not all of it and there’s a ton to do.

I need to get a will written out and also do the hospital paperwork that of course, I can’t think of the name of, but I’ll call it the “pull the plug paperwork.” I need to buy burial plots and plan the funeral. I want all of this taken care of now just in case. Then 30 years from now we can all look back at my paranoia and laugh! GOD WILLING!

Today’s been a hard day for me. My legs are tingling very badly. I’m wobbly. The skin on my stomach hurts like it’s been burned. I’m tired but I can’t sleep. I’m emotional and crying at the drop of a hat. I’m scared.

What I need to do is get a good night’s rest and start fresh tomorrow. I need to focus on Christ and all of the blessings that were given to me. Even though my life may end up short, I need to live it through the Grace of God.

I’m very fortunate. Most people who have Devic’s Disease are misdiagnosed for several years. I was misdiagnosed for a month. I’m sure God’s hand was in that. So, I need to concentrate on His blessings, not what this disease could do to me.

It’s hard, but I can do it.

It’s been a week and a day since I’ve been on the Swank diet and I’m doing very well. I haven’t cheated at all and I even lost 3 pounds. Of course, it looks like that’s all I may lose – I’m eating between 700 and 1400 calories a day but the scale has gone UP since our last weigh-in day on Friday. Of course that’s my luck!

Yesterday, my nurse Laurie came to train me on how to give myself a shot. I had a different nurse assigned to me, but she never contacted me. This gal did after me calling Shared Solutions twice. SS called the first nurse two times (her name is Denell) but she never called either one of us back. They weren’t too happy about that. But, they called me back and assigned a second nurse – Laurie. She was great.

She came at around 11:00am yesterday morning and went through everything I needed to know about my medicine, Copaxone. Then she showed me how to use the auto-injector. It was actually kind of fun. (I was very nervous beforehand and even took a xanax just in case). So, we got to use fake shots to shoot into a sponge and then I shot myself up.

It HURT! But I survived. I had a big round circle around the injection site and even today it looks odd, but I’ll survive. We shot the upper part of my right arm.

Today Boris helped me with my hip. I couldn’t get the shot to lie at a right angle, so he did it for me. It wasn’t that bad. Tomorrow I’ll do my right thigh.

Sounds fun, doesn’t it? Aren’t you jealous?

Here it is, around 7:30pm and I’m exhausted. I even took a two hour nap today and I’m STILL exhausted!

Tomorrow I am hoping I’ll be able to walk on the treadmill or ride on the bike for just 15 minutes. Just 15 minutes is all I want. If I can do that, I’ll be very happy.

I also need to figure out what we are going to eat tomorrow. I’m getting sick of chicken. Maybe I’ll try to figure out a vegan dish. Boris is a much better cook than I am, but he already does so much around the house, so I need to figure out what we are going to eat tomorrow.

I’d like to run to Meijer to see if they have tortillas I can eat. The local grocery stores here don’t have any. I’ll be down that way on Tuesday when I get my hair done, so I’ll check for them then.

The numbness and stiffness in my legs is still pretty severe. I walk like an old lady. I’m thankful I’m able to walk though, and I’m hoping that through this diet and the Copaxone that by summer I’m able to run.

My sister wants to sign up for the MS-150. It’s a bike ride of 150 miles to raise money for MS research. She’s sick herself with Myasthenia Gravis and she wants to do this for me? I am so touched!! I wish I could do something for her, but right now I can only pray.

A friend of mine calls the conversations my sister and I have about our diseases, “Adventures in Neuropathy.” Hilarious!

I’m pooped. I’m currently reading “The MS Recovery Diet.” It goes a step further than Swank, (and is based on his work) by stating that MS can be healed by taking out known problem foods like allergies or sensitivity causing foods. After reading this so far, I’m thinking of dropping gluten for a while to see if it makes an impact.

TTYL – M.

Upright MRI

The picture on the left is from promotional  material for Fonar Corporation’s upright MRI. In this regard, my theory is that humans are predisposed to neurodegenerative diseases such as Alzheimer’s, Parkinson’s and multiple sclerosis due to the unique design of the skull, spine and circulatory system of the brain as a result of upright posture. In addition to blood flow, upright posture also changes CSF flow. Besides its added benefit in many other health conditions, when it comes to blood and CSF flow, upright MRI is the wave of the future in brain research.

Cerebrospinal fluid (CSF) flow is called the third circulation of the brain and it is the least understood. CSF production and flow is critical to brain cushioning and protection. In terms of protection CSF is important to brain support to prevent the brain from sinking in the cranial vault. Conversely, excess CSF volume compresses the brain.

CSF comes from arterial blood that has been filtered through the blood brain barrier to the point where it is mostly water. CSF leaves the brain through the venous system. Therefore, backups in the venous drainage system affect cerebrospinal fluid (CSF) flow and drainage. Although it uses other routes as well, such as cranial and spinal nerves and the lymphatic system, most of the cerebrospinal fluid (CSF) produced by the brain eventually makes its way up to the superior sagittal sinus where it empties into the venous system.

Arachnoid Granulations

The superior sagittal sinus, depicted in the graphic image on the right, is the largest dural sinus located at the top of the brain.  The superior sagittal sinus contains arachnoid granulations that act as one way check valves for the flow of CSF from the subarachnoid space to the sinus. Click on the image for a better view. The pulsatile nature and the pressure generated by the CSF outflow through the arachnoid granulations is powerful enough to scour impressions into the roof of the cranial vault.

About sixty percent of the CSF produced in the brain ends up in the spinal cord. Eventually most of the CSF in the spinal cord makes its way back up through the subarachnoid space of the cord and into the subarchnoid space of the brain. From there it travels up to the superior sagittal sinus and arachnoid granulations to exit the brain along with venous blood.

The movement of CSF is driven by cardiovascular waves arising from the heart and blood vessels. During the contraction phase of the heart cycle (systole) pressure in the arteries of the brain increases. The increase in blood pressure drives CSF out of the brain through the upper cervical spine because as blood volume rises CSF volume must decrease. During the relaxation phase (diastole) the pressure drops and CSF enters the cranial vault through the subarachnoid space of the upper cervical spine. In addition, because the veins of the vertebral venous plexus of the spine have no valves, respiratory pressure changes are transmitted to the brain and amplify the cardiovascular waves. In brief, as pressure in the chest cavity drops during inspiration, due to the diaphram moving down and the chest wall moving out, CSF is pulled out of the cranial vault. As pressure in the chest cavity increases during exhalation CSF is driven into the cranial cavity. Thus,  combined cardiorespiratory waves are important to the movement of CSF through the brain and cord.

C1 & C2 Misalignment

The CSF that leaves the brain on its way down to the cord , however, must first pass through the tight neural (spinal) canal of the the upper cervical spine. Likewise, on its return trip back to the brain, it must again pass through the neural canal of the upper cervical spine. Therefore, the upper cervical spine is a critical link in the flow of CSF between the subarachnoid space of the brain and the cord. Under normal circumstances cardiorespiratory waves move CSF through the neural canal of the upper cervical spine unimpeded with good pulsatility and continue to drive it through the subarachnoid space up to the superior sagittal sinus. 

Genetic design flaws, such as Chiari malformations, and acquired disorders from injuries or disease can impede the pulsatility and flow of CSF through the upper cervical spine. Restrictions in CSF flow that cause a decrease in its volume, can, in turn, cause Chiari malformations and pressure conus conditions. Furthermore, any condition that restricts CSF flow can lead to hydrocephalus-like conditions. It is therefore important to maintain the correct volume of CSF in order to provide sufficient brain support and protection, as well as to prevent hydrocephalus. 

The picture above shows a fairly severe rotational misalignment of the upper cervical spine to the right. Click on the image for a better view. The dart shaped structure in the upper cervical spine is the spinous process of C2. It should be in the midline. The misalignment was caused by a motorcycle accident in which the victim landed on the right side of his head causing his head to snap to the left while simultaneously shifting and twisting his upper cervical spine to the right. Misalignments, such as the one above (due to micro or macro trauma), genetic design flaws (Chiari malformations), diseases (rheumatoid arthritis) and degenerative conditons (aging) of the upper cervical spine can affect the vertebral arteries that supply the brain, as well as the vertebral veins that drain the brain during upright posture. They can also cause deformation of the subarachnoid space and consequently, they can affect CSF flow going into and out of the brain and cord. 

While CCSVI treatment can improve venous drainage, which may further relieve hydrocephalic conditions in certain cases, it cannot improve CSF flow through the subarachnoid space of the upper cervical spine. Furthermore, increasing venous drainage of the brain and consequently decreasing CSF volume without a proportionate rise in passive CSF production could compromise brain support causing it to sink in the vault resulting in a condition similar to a pressure conus or Chiari malformation. Over drainage of the brain may thus present problems similar to spinal taps which can cause headaches due to a pressure conus condition following CSF removal. Over drainage is probably less likely in younger cases where the passive CSF pressure gradient and CSF production remains strong. Older patients, on the other hand, may have a lower CSF pressure gradient and thus a decrease in passive production of CSF due to aging of the brain and chronic craniocervical back pressure against the vertebral veins and subarachnoid space.

The flow of CSF clearly plays a role in normal pressure hydrocephalus (NPH), which has been associated with Alzheimer’s and Parkinson’s disease. It also plays a role in Chiari malformations, which cause signs and symptoms similar to MS. I discuss CSF production and flow thoroughly in my book. I will be discussing it more here in future posts as well as on my new website at: http://www.upright-health.com/.

Considering the above, in addition to the foramen magnum there are other large holes in the base of the skull through which cranial nerves and blood vessels pass, as seen in the picture on the right. It is possible that the cranial nerves may herniate into the openings or come in contact with the base of the skull due to Chiari malformations in which the volume of CSF falls too low, as mentioned above. The consequence would be similar, as well, that is cause compression of nerves and circulatory routes.

The brain floats within the cranial vault. Typically, it is prevented from sinking into the foramen magnum by the cisterns of the brain which are filled with cerebrospinal fluid (CSF). The cisterns are also strategically placed to provide cushioning, support and protection from the hard bones of the cranial vault as seen in the picture on the left.

Symptoms of MS often include cranial nerves. Common complaints include dizziness, ringing in the ears or loss of hearing, trigeminal neuralgia, burning tongue and dry mouth. By far, however, the cranial nerve most commonly involved in MS is the optic nerve. Optic neuritis is, in fact, one of the most frequent symptoms of MS. Even Asians and African-Americans who, otherwise, have a much lower incidence of MS, get optic neuritis. They also get transverse myelitis, but that’s another topic entirely. I will be covering the different cranial nerve signs, as well as transverse myelitis on my new website starting with the optic nerve. 

The optic nerve is the second most superior (highest) nerve in the cranial vault. The highest cranial nerve is the olfactory nerve to the nose which is located in the anterior fossa or forehead area of the base of the skull. The optic nerve lies in the middle fossa behind the eye sockets. Most of the cranial nerves are in the posterior fossa along with the brainstem and cerebellum.

It’s position in the cranial vault and the optic canal may be the reason why optic neuritis is one of the most common signs and symptoms of MS, optic-spinal MS and Devic’s disease. Typically, the optic nerve is protected by the chiasmatic cistern, which is one of the highest cisterns in the brain. Among other things trauma and failure of the CSF support system of the brain may play a role in optic neuritis. For further information on optic neuritis click on the link below to my new website. The website can also be found in the links section of the sidebar under upright-health.

http://www.upright-health.com/optic-neuritis.html

Basically there are three distinct shapes in the design of the human skull,  European, Asian and African. Although, there are slight variations, the cranial capacity is roughly the same and varies from about 1200 to 1800 cc. Asians tend to have the largest cranial capacity followed in size by European and African designs. Regardless of size, however, humans have roughly the same amount of nerves in the brain. Larger brains simply have larger nerves and support tissues, not necessarily more nerves.

The human brain is relatively large compared to body size. The base of the skull, however, is relatively short.  This short base is due to forward migration of the foramen magnum over time toward the middle of the skull beneath the mass of the head and brain. The foramen magnum is the large hole in the base of the skull through which the brainstem passes to the cord.

In the picture on the left the front part of the base of the skull is from the back of the nose to the notch in the yellow colored bone called the sella turcica where the pituitary gland is located. Unlike the picture, it tends to slop upwards slightly. The base then bends downward at a steep angle along the back of the yellow colored bone and along the blue colored bone. Technically, together the two bones are called the clivus portion of the base. The face of the brainstem and most of the cranial nerves are located just above the clivus. The foramen magnum for the cord is at the bottom of the clivus. The rear portion of the base extends behind the foramen magnum. The rear portion of the base is also called the posterior fossa. The base of the posterior fossa also slopes upwards.

In some skulls the angle of the clivus is relatively steep. In others it is flatter. Regardless of the angle of the clivus, all humans are predisposed to the brainstem sinking into the foramen magnum due to its location beneath the skull. A Chiari malformation occurs when the brainstem sinks into the foramen magnum as seen in the brain scan to the right.

Typically, the brainstem is surrounded by cisterns filled with cerebrospinal fluid (CSF) which allows the brain to float above the foramen magnum and base of the skull thus preventing contact with the bones of the base and foramen magnum. In a Chiari malformation, it is typically the tonsillar portion of the cerebellum that gets trapped in the foramen magnum.

In this regard, among other things, the design of the posterior fossa may explain why people of European race have a much higher incidence of multiple sclerosis than people of Asian and African races. While the floor of the posterior fossa slopes slightly upwards in all races, it is considerably shorter in European skulls than it is in Asian and African ones. The rear wall of the posterior fossa in European skulls also slant outward. Thus European designs tend to crowd the cerebellum, comparatively speaking, from front to back more than Asian and African designs. They also pitch the cerebellum forward and downward toward the foramen magnum. Additionally, the design of the shorter sloped floor and slanted rear wall also affects the length, pitch and layout of the drainage system of the brain. Shorter distances and reduced angles in the base of the European skull most likely reduces curves and provides less resistance to reverse flows of venous blood in the dural sinuses.  

Lastly, in contrast to European skulls, the jaws of Asian skulls are more in line with the face which improves balance on top of the cervical spine and makes them more energy-efficient. Protruding muzzles in European designs also create greater swing weights when the head is whiplashed as in trauma. In contrast to taller and narrower European and Asian skull faces, African skulls have shorter, wider and deeper faces. The lower wider face lowers the center of gravity and swing weight, and like Asian skulls, may provide better protection to the head and neck, as well as the brain and cord in whiplash type traumas.  

In brief, the similar designs of the Asian and African posterior fossa of the rear portion of the base of the skull may provide better protection for the brain from whiplash, inversion flows and classic MS. On the other hand, it may also explain why Asian and African races tend to get a variant of MS called optic-spinal multiple sclerosis and Devic’s disease. Both conditions are associated with optic neuritis and transverse myelitis rather than classic MS lesions, signs and symptoms.

The different signs and symptoms in the above conditions may be the consequence of different points of contact and compression of the underside of the brain against the base of the vault and within the foramen magnum. The differences in contact points may be due to design differences in the base of the skull. In my next post I will discuss the location of the brainstem and cranial nerves in relationship to the base of the skull and foramen magnum. Their location makes them highly susceptible to compression by either an increase or a decrease in CSF volume in the cisterns.

For additional information on this and related topics visit my website at http://www.upright-health.com.

The roundness of the head and eye sockets is evident in the well cast skull seen above. Permission to use the  pictures of the skull in this post was granted by Bone Clones Inc. The aperture of the nose is also rounder compared to the more triangular shape of European skull design.

The head is the sound box of the human voice. The tonal quality of the voice is affected by the design of the head, especially the mouth, nose and air sinuses, called the paranasal sinuses. 

The bridge of the nose, called the glabella, sits above the opening. Behind the bridge are the ethmoid sinuses. The large maxillary sinuses lie beneath the cheek bones to the sides of the nose.  The frontal sinuses are in the forehead just above the nose. The sphenoid sinus sits behind and between the eyes. Singing resonates in the sinuses and escapes through the nose. Yoga kundalini exercise uses the AUM chant to resonate the sphenoid sinus and stimulate the pituitary gland which sits above the sphenoid sinus. The difference in shape of the nasal opening affects the escape of air like the difference in shape between f holes in violins and jazz guitars and round holes in country guitars.

In this  regard, the design of the African-American skull is a perfect shape for singing. One of the finest quality voices ever recorded was that of Nat King Cole. Rich and mellow the music would escape his head with near perfect unobstructed flow.

If you strip away the flesh it’s easy to see that the roundness of an African-American skull is closer in design  to Asian skulls. The head is not box-like as in European designs, but smoother and rounder. The eye sockets are also rounder. The nasal aperture is especially round.

The difference in the round designs versus square European designs may explain why Asians and African-Americans have a much lower incidence of MS. On the other hand, it may explain why they get a particularly devastating variant form of MS called Devic’s disease.

The floor of the base of Asian and African skulls is longer than European skulls. The back wall of the head in Asians is taller but slightly more sloped than African designs which are steeper. The longer base and steep rear wall distribute more of the weight of the brain behind the foramen. On the other hand, it positions the brainstem over the foramen magnum prediposing it to sinking into a Chiari malformation.

Chiari malformations were once considered to be a herniation of the brainstem into the foramen magnum thus compressing it. More recent research suggests that the definition should be changed to include any decrease in CSF volume which causes the brain to sink and come in contact with the bones of the cranial vault. Recent research has also linked Chiari malformations with trauma, MS and chronic fatigue syndrome among other things.

Devic’s disease is associated with neuromyelitis optica and transverse myelitis but typically has no MS-like lesions in the brain. While transverse myelitis is associated with hyperintensity signals in the cord,  the lesions differ from MS in that they are longer and tend to span several segments of the spine. Devics disease can result in blindness and muscle weakness in the arms and legs. It can also cause respiratory failure.

The optic nerve sits beneath the weight of the frontal lobes of the brain. It is protected from compression by cerebrospinal fluid (CSF) in the interchiasmatic cistern, which is the highest cistern in the brain. In round skull designs Chiari malformations most likely result in contact of the frontal lobe of the brain against the vault thus compressing the optic nerve. Herniation of the brainstem into the foramen magnum further compresses the long nerve tracts from the brain that go to the cord resulting in muscle weakness and respiratory stress.

Let’s consider a hypothetical example of a European, Asian and African-American traveling together in a car that gets into a traumatic motor vehicle accident. Soon afterwards they all develop problems with loss of vision and weakness in the legs. Brain scans show white spots in the brain of the European and in the cord of  the Asian and African-American. In this case the European person is diagnosed with MS and the Asian and African-American with Devic’s disease. In all three cases, it will be blamed on an immunolgical problem, when in fact it is simply a different response to the same traumatic cause.

For more information on this and related topics visit my website at http://www.upright-health.com

A spinal MRI of a patient with neuromyelitis optica (from BMJ.com)

Doctors classify diseases like zoologists classify animals. A new disease, discovered and described, is placed next to diseases with similar symptoms, causes, and prognosis, which helps inform physicians about the best treatments to initially try. Later, when more specific information is known about a disease, that classification may change – just as biologists have dramatically redrawn the Tree of Life thanks to genetic similarities that trumped surface comparisons.

A disease called neuromyelitis optica (NMO), or Devic’s disease, would seem like a pretty easy one to put in its proper place. Since its discovery in the late 19th century, the disease was considered to be a variant of the neurological disorder multiple sclerosis. As in MS, a patient with NMO suffers an autoimmune attack on their nervous system, with the body’s natural defense mechanisms mistakenly killing off the insulation that help neurons conduct signals.

But unlike MS, which occurs throughout the brain and spinal cord, the NMO attack is restricted to the spinal cord and optic nerve, causing the sudden onset of visual problems and muscular difficulties. Untreated cases can lead to blindness and paralysis, said Adil Javed, assistant professor of neurology at the University of Chicago Medical Center.

“The inflammation is very intense in the spinal cord and the eyes, as opposed to multiple sclerosis,” Javed said. “The patients go blind and become paralyzed very quickly as soon as the disease starts. Within a year or two, they can go from walking to a wheelchair or a stretcher.”

Yet the differences were not enough to convince doctors that NMO was anything other than a cousin to MS. Patients with NMO symptoms were sometimes misdiagnosed as suffering from multiple sclerosis, or correctly diagnosed and treated with drugs designed for MS such as interferons. However, during his time as a neurological fellow at the Medical Center, Javed and his colleagues began to notice that NMO might not be as close a relative to MS as the field had thought.

The first clue was in the treatment – “We learned over the years that the interferons, which are the standard treatment for many MS patients, doesn’t work with Devic’s disease,” Javed said. “In fact, in many cases it made them worse.” Another mystery was the symptoms NMO patients shared with another group of diseases, the rheumatological disorders of lupus and Sjogren’s disease. Symptoms of Sjogren’s, including dry eyes and mouth, joint pain, and some organ dysfunction, turned up in a high number of NMO patients, Javed noticed with interest.

“That’s pretty rare that you would have two of these diseases,” Javed said. “So we thought perhaps they are connected.”

That hunch turned out to be true, as Javed and colleagues published in 2008 that an astonishing 80 percent of their NMO patients also qualified for a diagnosis of Sjogren’s disease. And while such patients – predominantly African-American women in their 40′s or older – were unresponsive to the treatments used for MS, they showed improvement with treatments used for Sjogren’s and lupus, including steroid and chemotherapy drugs. Treating NMO as a rheumatologic disease rather than a neurological disease helped patients prevent future relapses that could leave them with permanent damage, Javed said.

“It turns out that most attacks of disease happen in the first five years, as opposed to MS, which is a long, chronic, progressive disease,” Javed said. “We do initial intense chemotherapy for 5 years, then back off to more benign drugs.”

While the intensive treatment can’t roll back the damage done by the first or second attack, it can prevent further decline in vision and motion. That makes it especially important that the proper diagnosis of NMO, rather than MS, is reached early by physicians – an assessment that can currently be made using a blood test for antibodies unique to NMO or MRI imaging.

“The damage in the disease is done if you have an attack. It’s like having heart attacks; if you give an aspirin after a heart attack it’s not going to undo the damage that was done,” Javed said. “But if you were to give a very strong drug from the get-go to prevent that second attack or the third, that’s good. Because if one attack gets you down to a cane, you don’t want to end up in a wheelchair.”

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. Interestingly, 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. In addition, 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 Bone 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 a childhood problem for the most part. Recently, however, 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 easier to fall and unfortunately in humans, the head has a further distance 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 and or pressure conus 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.

For additional information on this and related topics visit my website at http://www.upright-health.com.

In a previous post I discussed the role of the vertebral veins, also knowns as the vertebral venous plexus (VVP), in causing chronic craniocervical venous back pressure (CCVBP) and subsequent neurodegenerative conditions and diseases such as multiple sclerosis. Like CCSVI, CCVBP can lead to chronic venous backups and edema in the brain. It can also affect cerebrospinal fluid (CSF) pressure gradients and subsequent flow and volume. Correct CSF volume is essential to brain cushioning, protection and support. Consequently, in addition to MS, CCVBP may play a role in normal pressure hydrocephalus (NPH), which has been associated with Parkinson’s and Alzheimer’s disease.

verterbral arteries

I next discussed the vertebral-basilar arterial supply to the brain and its likely role in chronic ischemia which, like chronic edema from backed up veins, is one of the main suspects in demyelination and other neurodegenerative conditions and subsequent diseases. Lastly, I posted pictures of the tight neurovascular tunnels the VVP and vertebral-basilar arteries must pass through in the upper cervical spine and foramen magnum in the base of the skull on its way to the motherboard of the brain, the brainstem.

In light of the above, the picture below on the right is of Greek techno music producer, CostumeNational of fightforccsvi.com. The picture was taken with his permission from         Dr. Scalfani’s MS website forum called, ThisIsMS.com.

The forum is a wonderful group of MS patients who have provided me with a rare opportunity and unbelievable insight into the mystery of MS that they openly and gladly share. Weakened by their condition, they are nonetheless strong and quite fiery in spirit. Together they have formed a  formidable group that is shaking up scientists and researchers around the world. Their determined efforts are helping lead the way and shape future research not only for solving MS, but other devastating neurodegenerative conditions as well, such as Alzheimer’s and Parkinson’s disease, NPH, Huntington’s chorea, ALS, PLS and others too numerous to mention here.  It is invaluable, to say the least, to have so many cases to study and follow in one location. They provide a wealth of information that demands further retrospective analysis and investigation, such as I am in the process of doing, but on a much larger scale.

This particular type of picture is called an open mouth odontoid image because the odontoid process of the second cervical vertebra, called axis or C2, is in the center of the image. It’s called the odontoid process because it looks like a tooth that sticks straight up from the body of the vertebra.

The odontoid process fits neatly into a notch in its mate directly above called Atlas or C1 beneath the base of the skull. The odontoid process permits greater pivotal action in the upper cervical spine. In my opinion, the odontoid process also reduces the size of the body of the vertebra, which may help to reduce pressure in the area during head and neck movement. The red line indicates the center line of the spine. The triangular dart-like shapes pointing upward are the spinous process of the cervical vertebra. In a normal spine, they should all line up on the red line.

If you look through the open mouth you will see one of the darts is way off to one side. You will note by the marker on the film that it indicates the right side. That particular dart is the spinous process of the second cervical vertebra (C2) called axis. The degree of misalignment in this case is severe.

According to CostumeNational, about eight years ago, he was riding a motorcycle when he crashed into a car, which threw him to the ground landing on the right side of his shoulder and head. The force of the fall from the weight of his propelled body magnified by the speed he was traveling at severely snapped his neck to the left and left him unconscious.

As the x-ray evidence clearly shows, when he came to later in the hospital, although no one knew it at the time, his head and neck were no longer aligned properly. Instead it remained in the wicked tilt to the left the same as it was after impact. Eight years later he started to develop optic neuritis in his left eye on the low side of the head tilt. Head tilts cause the brain, blood and CSF inside the cranial vault to shift to the low side just like water in a glass, which can increase pressure on the optic nerve and may play a role in optic neuritis.

Interestingly, he had no lesions in the brain but he did show a hyperintensity signal precisely at the location of the kink in the upper cervical spine. The highly suspicious, characteristic symptom of optic neuritis was next followed by cerebral, as well as cord signs and symptoms identical to MS. Nonetheless, without brain lesions, his case falls into the uncertain category of cracks, a no-man’s land not considered to be classic MS.

There is a major principle in neurology when it comes to the brain and the cranial vault, called the Monroe-Kellie principle. According to the Monroe-Kellie principle there are essentially three elements inside the cranial vault which include the brain, blood and CSF. Since the cranial vault is a closed container for the most part, if the volume of one of the elements increases, then one or both of the other two elements must decrease in volume. A brain tumor for example can compress blood and CSF vessels as can Chiari malformations mentioned in previous posts. Likewise, an increase in blood or CSF volume can compress the brain.

The same principle holds true for the spine and spinal canal, which, like the cranial vault, is for the most part a closed container. In other words, there is no free space inside the spinal canal. Instead, the space between the inside walls of the spinal canal and the cord is filled with the VVP. Therefore a kink in the upper cervical spinal canal as in the case above puts a kink in the drainage system of the brain and cord. It also causes venous back pressure and hypertension around the cord. Lastly, it increases resistance to CSF flow on its way back to the brain from the cord.

 In my next post I will discuss precision line analysis used by upper cervical chiropractors to analyze mechanical strains such as the one above. After that we will then look at some of the common signs and symptoms of MS which share a lot in common with AD and PD.

For additional information on this and related topics visit my website at http://www.upright-health.com.

Image via Wikipedia

                                                                                                     Multiple Sclerosis is technically a neurodegenerative disease of the brain. Classically MS is associated with two or more supratentorial (above the covering over the cerebellum) periventricular hyperintensity signals. The lesions are the white spots on the brain scan on the right. The large shadows in the middle of the brain shaped like a butterfly are the lateral ventricles. The periventricular area surrounds the ventricles. In addition to the brain, however, some MS patients also get lesions in the cervical cord.

Demyelinating type lesions in the cervical cord without lesions in the brain are not considered to be classic signs of MS. Lesions below the cervical cord are, likewise, not considered to be MS. Instead they are given different names.

In this post I will stick to MS lesions in the cervical cord and disregard lesions of the lower cord such as those seen in amyotrophic lateral sclerosis (ALS), primary lateral sclerosis, Devic’s Disease (neuromyelitis optica) and others. I will also ignore the lesions sometimes associated scoliosis and abnormal curvatures of the spine.

According to Schelling, the lesions seen in the cervical cord in MS are due to stretch and shear stress. Many types of trauma, such as whiplash in the picture on the left, cause hyperflexion and hyperextension of the spine. The strain can occur in a front to back motion or from side to side. At the same time, whiplash type traumas also strain the spinal cord inside the spinal canal.  

 The spinal cord, like the brain has three protective coats called meninges. The outer coat is called the dura mater. The middle coat is called the subarachnoid mater and the inner coat is called the pia mater. Except for the attachment of the tail end of the cord, called the filum terminale, to the tail bone, called the coccyx, the spinal cord moves freely, unattached inside the spinal canal.

The three coats are held together by denticulate ligaments that attach the inner pia mater to the outer dura mater at the nerve roots.  Click on the image on the right for a closer look. The subarchnoid space lies between the subarchnoid mater and the pia mater and contains a significant volume of cerebrospinal fluid, called CSF. There is also lymph like fluid that serves as a lubricant between the outer coat of the dura mater and the middle coat of the subarachnoid mater. This allows the inner contents of the cord to move somewhat independently to a limited degree.

According to Schelling, mechanical strains of the spine can take the cord to extreme limits of stretch. It can also cause shear stress within the cord between the pia mater on the inside and the dura mater on the outside. The stress points occur at the attachment of the denticulate ligament. Furthermore, violent back jets of CSF in the subarachnoid space amplify the strain like a boat moored to a dock hit by hurricane force waves. The waves amplify the strain and rip the ropes and boats from their moorings. Similarly, violent waves of CSF flowing through the subarachnoid space amplify the strain acting on the denticulate ligaments. When they reach a critical threshold, engineer’s call the yeild point, the denticulate connective tissue attachments of the pia mater to the dura mater will tear. The strained tissues of the pia mater further damage the meylinated nerve tracts they cover. Click on the image above to get a closer look. This is a cross section of the cord and shows the inside. The H shape in the middle of the cord is the grey matter. The myelinated white fiber tracts surround it. The blue area is the subarachnoid space which contains CSF.

The lesions seen in the cervical cord are micro tears in the meninges and nearby myelinated nerve pathways . The tears cause scars  to form called sclerotic plaques.  Because they occur on the outside along the flanks of the cord, the tears tend to effect the outside structures of the cord.

The outside of the cord (see picture to left)contains the long myelinated high speed primary nerve pathways of the central nervous system. Primary nerves go from the brain to particular destination levels in the cord. The long white tracts on the outside of the cord contain both sensory nerves for detecting sensations related to the environment, muscle tone and balance, and motor nerves for running the muscles. Tears in the area of the denticulate ligaments thus affect nearby myelinated nerves in the cord resulting in muscle weakness and warped sensations called paresthesias.

In brief, according to Schelling, one of the likely causes of the lesions of multiple sclerosis seen in the brain are due to violent venous back jets associated with trauma.  The lesions seen in the cervical cord are due to severe overstretching and shear stresses within the cord itself magnified by hydraulic stress from CSF waves. There is still more to the story, however, that needs further exploration and explanation.  That’s where my theory may help to fill in some of the missing pieces to the puzzle.

My theory is that craniocervical syndromes can cause chronic edema (swelling), ischemia (decreased blood flow) and NPH (normal pressure hydrocephalus) conditions in the brain. Similar events can occur in the cord due to abnormal conditions of the spine. These chronic conditions can, in turn initiate neurodegenerative processes such as the glutamate cascade, which follows strokes.

In my next post I will discuss the posterior blood supply routes to the brain and circulation to the cord. The veins are not the only problem in MS. The arteries are a big part of the problem as well. In addition to MS, I suspect that certain cases of sclerosis of the long myelin tracts of the lower cord, such as ALS and PLS are probably due more to chronic ischemia. This is probably why lesions sometimes also show up in cases of abnormal curvatures of the spine such as scoliosis and kyphosis. Oxidative stress and chronic ischemia are chief suspects in the cause of demyelination and the shape of the spine, and thus the spinal canal, affect arterial and venous blood flow in the cord.

For additional information on this and related topics visit my website at http://www.upright-health.com.

When their daughter was diagnosed with neuromyelitis optica (NMO) in June 2008, the world turned upside down for cosmetics entrepreneur Victoria Jackson and infomercial pioneer Bill Guthy. The diagnosing physician told them, “you know, if this were my child, I’d be going to Mayo Clinic.” And that’s exactly what they did.

In the video below, Victoria describes their journey, including one of her first conversations with Mayo Clinic neurologist and NMO expert, Dr. Brian Weinshenker…

We went to see Dr. Brian Weinshenker at Mayo Clinic, and he really was extraordinarily kind and patient. I said, “are you doing any work in this area?” And he said, “Well, yes.” I said, “Do you have a foundation and research?” He said, “I’m wanting to, and I’ve started…I’m doing some research.” And I said, “Well, you and I are going to be working together. I’ve got the checkbook and you’ve got the brains for this. We’re going to get together and do something — we’re going to find a cure for this.”

Today, the Guthy-Jackson Charitable Foundation is dedicated to funding basic science research to find answers that will lead to the prevention, clinical trial treatment programs and a potential cure for NMO. Guthy-Jackson is currently funding several NMO studies at Mayo Clinic. For patients with NMO, the Guthy-Jackson Charitable Foundation hosts an annual patient event and an online community called Spectrum.

Other videos of Mayo Clinic physicians discussing NMO and related topics are available as well.

Like Time and Newsweek choosing the same cover story, both JAMA and the New England Journal of Medicine offered guidance on urinary incontinence last month. The New England Journal of Medicine published an evidence-based comparison of two surgical alternatives for urinary incontinence in women that finds both effective. The editorial below inquires why few women turn to this solution (and links to the study). JAMA offers a case study and evidence-based review on the treatment options, from exercises and behavior training to medication and surgery. They advise that doctors should routinely ask female patients about the problem.

RESULT: What’s Best in the Treatment of Stress Urinary Incontinence?
New England Journal of Medicine | Jun 3, 2010

RESULT: Incontinence in Older Women
JAMA | Jun 2, 2010

If your patients are anything like those in Kaiser Permanente Northwest, then during the past year more than half of the women you see (elderly or otherwise) have problems with urinary incontinence of which you are unaware. (The article below points to another study which appears as the second result in that search.)

RESULT: Prevalence of undiagnosed urinary incontinence in women is 53% in the preceding year and 39% in the preceding week in a US managed-care population
Evidence-based Nursing | Jul 1, 2010

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OTHER RECENT SEARCHES ON SEARCHMEDICA

Search: wheat allergy

The review below describes a study that asked how often wheat allergy persists into adulthood and whether its severity can be predicted.

RESULT: The Natural History of Wheat Allergy
Pediatrics | Nov 1, 2009

Search: neuromyelitis optica

A letter and the case report that inspired the response describe this rare condition that is easily mistaken for multiple sclerosis and that requires immediate intervention to prevent rapid decline in physical function.

RESULT: Thirty-one Episodes of Myelitis and Optic Neuritis in a Woman With Neuromyelitis Optica and Systemic Lupus Erythematosus
Archives of Neurology | Jun 1, 2010

Search: glioblastoma vaccine

A triumph of cancer immunotherapy: a vaccine made from a tumor antigen proves effective in treating one of the least tractable of malignancies, glioblastoma.

RESULT: Phase I/IIa trial of autologous formalin-fixed tumor vaccine for newly diagnosed glioblastoma
2010 ASCO Annual Meeting Abstracts | May 20, 2010

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SEARCH TIP: The “Cached” option

Last week someone entered the search term “Clozaril in patients with seizure disorder.” This search is a challenge, because usually a query in the form “[Intervention] in [condition]” inquires about the use of a treatment for a disease. This searcher most likely wanted to ask whether one should prescribe the antipsychotic clozapine for someone who has a seizure disorder.

The search engine can’t tell the difference between the intent in these two kinds of searches. How can a person locate the desired information?

One option is to click on the word “Cached” that often appears in the last line of the result listing. This provides the result with the search terms highlighted in different colors.

Scrolling down, it’s easy to find where a result mentions seizures. (You can also see how generic words such as “patients” and “with” confuse the search result.)

Dr. Brian Weinshenker on PRES

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Background: Posterior reversible encephalopathy syndrome (PRES) is characterized by vasogenic subcortical edema without infarction. It has been associated with hypertensive crises and with immunosuppressive medications. It has not been associated with neuromyelitis optica (NMO).

Methods: We reviewed the clinical and neuroimaging features of five NMO-IgG seropositive Caucasian women who experienced an episode of PRES and had a coexisting NMO spectrum disorder (NMOSD). We also tested for the aquaporin-4 (AQP4) water channel autoantibody (NMO-IgG) in 14 patients from an independently ascertained cohort of individuals with PRES.

Results: All five patients developed abrupt confusion and depressed consciousness consistent with PRES. The encephalopathy resolved completely within 7 days. Comorbid conditions or interventions recognized to be associated with PRES included orthostatic hypotension with supine hypertension, plasma exchange (PLEX), intravenous immunoglobulin (IVIG) treatment, and high-dose intravenous methylprednisolone (IVMP). Brain MRI studies revealed bilateral T2-weighted (T2W) hyperintense signal abnormalities, primarily in frontal, parieto-occipital and cerebellar regions. Three patients had highly symmetrical lesions and three had gadoliniumenhancing lesions. Follow-up neuroimaging revealed partial or complete disappearance of T2W hyperintensity and complete resolution of gadolinium enhancing lesions. Patients with PRES without NMOSD were uniformly NMO-IgG seronegative.

Conclusions: Brain lesions in NMOSD patients are heterogeneous and in some individuals are accompanied by vasogenic edema manifest as PRES. Water flux impairment due to AQP4 autoimmunity may predispose to PRES in NMOSD patients who experience blood pressure fluctuations or therapies that result in rapid fluid shifts.

Authors: S.M. Magaña BS1, M. Matiello MD1, S.J. Pittock MD1,2, A. McKeon MD1, V.A. Lennon MD, PhD1-3, A.A. Rabinstein MD1, E. Shuster MD4, O.H. Kantarci MD1 C.F. Lucchinetti MD1, B.G. Weinshenker MD1
Departments of Neurology1 Laboratory Medicine and Pathology2 and Immunology3, Mayo Clinic College of Medicine, Rochester, MN and Department of Neurology, Mayo Clinic Jacksonville4