Guest post written by Rolf Tate
Lately I’ve been worried about starting my new job. Even though I have worked extremely hard with this company I did not think a promotion would come as quickly as it did. Once I was called into my boss’s office I assumed I might have done something wrong and the next thing I know he is telling me that I’m getting a promotion and the company is going to want me to move. A promotion was great news to both me and my wife but I know we were both a little bummed out that we were going to have to make a move. A friend of mine in the office recently sent me an email giving me some advice about the moving process. The best piece of advice he gave me was switching my basic cable provider to satellite TV and referred me to Satellite 911 deals Now at least I know one thing will be for sure when I end up making my move.
Friday, September 30, 2011
Family Reports That Bryan Stow Speaks
(Bay City News) Bryan Stow, the San Francisco Giants fan who suffered brain damage when he was beaten after a baseball game in Los Angeles, is making progress in his recovery and is speaking, his family said Wednesday.
In a hard-to-hear gravelly voice, Stow was been able to say the names of his children, Tabitha and Tyler, and when shown pictures of them he said, "I would like to see them soon," Stow's family said on a website they created to chronicle his progress.
In August, Stow, a 42-year-old Santa Cruz man who was attacked outside Dodger Stadium after the March 31 season opener between the Giants and the Dodgers, encountered setbacks in his recovery as he battled infections related to surgery to replace a missing part of his skull with a bone flap.
Swelling in Stow's brain had prompted Los Angeles doctors to remove a portion of his skull to relieve pressure on his brain. Doctors at San Francisco General Hospital said the procedure saved Stow's life, but that replacing the missing skull fragment has proved challenging.
Doctors have had to attempt that surgery several times in recent months because of complications. Doctors performed the most recent surgery to insert the bone flap on Aug. 10.
His temperature shot up as his body fought off a urinary tract and staph infections, according to his family, and he became less responsive. Before then, he had been showing signs of improvement, mouthing words and giving kisses to family members.
The infections had prevented doctors from performing additional necessary procedures, according to his family.
By the beginning of this month, Stow's condition had improved enough that on Sept. 13 doctors inserted a shunt to permanently divert fluid from his brain. In the week since the surgery, Stow has made facial expressions, and began talking on Wednesday, his family said.
"We are blown away with all of this," the family said in a statement on the site. "Literally one day we got some facial responses and the next, he's talking."
The doctors have been monitoring Stow closely after they also recently removed a filter that had been inserted to catch blood clots that could enter his lungs.
A full-body scan in the past week revealed clots in one of Stow's thighs, his abdomen and his shoulder. According to his family, doctors are considering blood thinners and whether to insert a permanent filter.
"Bryan's had many ups and downs, and though we see how far he has come, we try not to look too far back into these past 6 months, and we can't look too far down the road so we focus on right now," Stow's family wrote.
Before the attack, Stow worked as a paramedic in Santa Clara County. He was attacked as he left Dodger Stadium on March 31 by two suspects who first taunted him but then hit him from behind, causing him to fall.
Two men have been charged with Stow's beating--Louie Sanchez, 29, and Marivin Norwood, 30 -- and pleaded not guilty in Los Angeles County Superior Court last month to mayhem and assault charges. Sanchez and Norwood are scheduled to appear in court Sept. 30 at 8:30 a.m. for a preliminary hearing.
Bryan Stow family photo. (support4BryanStow.com)
In August, Stow, a 42-year-old Santa Cruz man who was attacked outside Dodger Stadium after the March 31 season opener between the Giants and the Dodgers, encountered setbacks in his recovery as he battled infections related to surgery to replace a missing part of his skull with a bone flap.
Swelling in Stow's brain had prompted Los Angeles doctors to remove a portion of his skull to relieve pressure on his brain. Doctors at San Francisco General Hospital said the procedure saved Stow's life, but that replacing the missing skull fragment has proved challenging.
Doctors have had to attempt that surgery several times in recent months because of complications. Doctors performed the most recent surgery to insert the bone flap on Aug. 10.
His temperature shot up as his body fought off a urinary tract and staph infections, according to his family, and he became less responsive. Before then, he had been showing signs of improvement, mouthing words and giving kisses to family members.
The infections had prevented doctors from performing additional necessary procedures, according to his family.
By the beginning of this month, Stow's condition had improved enough that on Sept. 13 doctors inserted a shunt to permanently divert fluid from his brain. In the week since the surgery, Stow has made facial expressions, and began talking on Wednesday, his family said.
"We are blown away with all of this," the family said in a statement on the site. "Literally one day we got some facial responses and the next, he's talking."
The doctors have been monitoring Stow closely after they also recently removed a filter that had been inserted to catch blood clots that could enter his lungs.
A full-body scan in the past week revealed clots in one of Stow's thighs, his abdomen and his shoulder. According to his family, doctors are considering blood thinners and whether to insert a permanent filter.
"Bryan's had many ups and downs, and though we see how far he has come, we try not to look too far back into these past 6 months, and we can't look too far down the road so we focus on right now," Stow's family wrote.
Before the attack, Stow worked as a paramedic in Santa Clara County. He was attacked as he left Dodger Stadium on March 31 by two suspects who first taunted him but then hit him from behind, causing him to fall.
Two men have been charged with Stow's beating--Louie Sanchez, 29, and Marivin Norwood, 30 -- and pleaded not guilty in Los Angeles County Superior Court last month to mayhem and assault charges. Sanchez and Norwood are scheduled to appear in court Sept. 30 at 8:30 a.m. for a preliminary hearing.
Samuel
A picture began circulating in November. It should be "The Picture of the Year,"... or perhaps, "Picture of the Decade." It won't be. In fact, unless you obtained a copy of the U.S. paper which published it, you probably would never have seen it.
The picture is that of a 21-week-old unborn baby named Samuel Alexander Armas, who is being operated on by surgeon named Joseph Bruner. The baby was diagnosed with spina bifida and would not survive if removed from his mother's womb. Little Samuel's mother, Julie Armas, is an obstetrics nurse in Atlanta. She knew of Dr. Bruner's remarkable surgical procedure. Practicing at Vanderbilt University Medical Center in Nashville, he performs these special operations while the baby is still in the womb.
During the procedure, the doctor removes the uterus via C-section and makes a small incision to operate on the baby. As Dr. Bruner completed the surgery on Samuel, the little guy reached his tiny, but fully developed hand through the incision and firmly grasped the surgeon's finger. Dr. Bruner was reported as saying that when his finger was grasped, it was the most emotional moment of his life, and that for an instant during the procedure he was just frozen, totally immobile.
The photograph captures this amazing event with perfect clarity. The editors titled the picture, "Hand of Hope." The text explaining the picture begins, "The tiny hand of 21-week-old fetus Samuel Alexander Armas emerges from the mother's uterus to grasp the finger of Dr. Joseph Bruner as if thanking the doctor for the gift of life."
Little Samuel's mother said they "wept for days" when they saw the picture. She said, "The photo reminds us pregnancy isn't about disability or an illness, it's about a little person" Samuel was born in perfect health, the operation 100 percent successful. Now see the actual picture, and it is awesome...incredible....and hey, pass it on! The world needs to see this one!See More
The picture is that of a 21-week-old unborn baby named Samuel Alexander Armas, who is being operated on by surgeon named Joseph Bruner. The baby was diagnosed with spina bifida and would not survive if removed from his mother's womb. Little Samuel's mother, Julie Armas, is an obstetrics nurse in Atlanta. She knew of Dr. Bruner's remarkable surgical procedure. Practicing at Vanderbilt University Medical Center in Nashville, he performs these special operations while the baby is still in the womb.
During the procedure, the doctor removes the uterus via C-section and makes a small incision to operate on the baby. As Dr. Bruner completed the surgery on Samuel, the little guy reached his tiny, but fully developed hand through the incision and firmly grasped the surgeon's finger. Dr. Bruner was reported as saying that when his finger was grasped, it was the most emotional moment of his life, and that for an instant during the procedure he was just frozen, totally immobile.
The photograph captures this amazing event with perfect clarity. The editors titled the picture, "Hand of Hope." The text explaining the picture begins, "The tiny hand of 21-week-old fetus Samuel Alexander Armas emerges from the mother's uterus to grasp the finger of Dr. Joseph Bruner as if thanking the doctor for the gift of life."
Little Samuel's mother said they "wept for days" when they saw the picture. She said, "The photo reminds us pregnancy isn't about disability or an illness, it's about a little person" Samuel was born in perfect health, the operation 100 percent successful. Now see the actual picture, and it is awesome...incredible....and hey, pass it on! The world needs to see this one!See More
By: Sean Keeling
Monday, September 26, 2011
Amazing things happening!
I come home from a long day and of course check on Bryan Stow. I did not expect to see an update since the sisters usually update once a week. Suddenly I got a great surprise! I'll just let you read for your self...
http://support4bryanstow.com/News-Updates/articleType/ArticleView/articleId/992/Magical
http://support4bryanstow.com/News-Updates/articleType/ArticleView/articleId/992/Magical
Sunday, September 25, 2011
Why Pepper Knows Best?
How often have you gone to my blog I have hydro, hydro doesn't have me looked up at and seen the link and wondered why is it is called "Pepper Knows Best?
Pepper is 13 years old now. I blog about my hydrocephalus Pepper is the one who took care of me through most of it.
You will find post where Pepper found me having a seizures (home alone) and pulled me out of the seizure.
When Pepper was 4 years old he had to be re- house train to use a to use the bathroom inside because he refused to leave my side because I was so sick. My dad would come in to try to get him to go out to the bathroom. Pepper would crawl over my stomach and refuse to move.
When I started blogging I could not think of a better fitting name for my blog than “Pepper Knows Best”
This is a picture of Pepper not feeling good recently. He means the world to me and my mom and dad because of the way he took care of me when I was sick. Even before that when I worked at Lowes would leave for work each day an leave him as a puppy with my dad.
When he started doing things out of character we became very worried. That night he would not sleep in the bed. He has been sleeping with me ever since the very first day I brought him home.
I thought this is my dog! My house! My bed! I was single for a reason to do what I wanted! I wanted my puppy! ~tear~ So from then on my baby would cry no more!
I had no idea the monster I was creating. He is a momma's baby. My friends online have watched messaged and text and prayed about my pepper because they know how much he means to me.
I wondered if some would think I was over reacting because to some people he may just be "just a dog" You have to realize that when you make a comment like he is "just a dog" you need to look what they have done in their life.
Much like you would before you judge a man before you convict him. Everyday that daddy had him out at the shop pepper was in and out of trucks. Helping my dad by grabbing guys that would be under cars on creepers by the hair and pull them out from under the car! LOL!
I have so many Pepper stories. I could go on for days.
But when he was not acting like himself I was sure it was a stroke. I walked into the kitchen. He stumbled and acted like he was stiff he just froze.
I knew he was in pain. My parents saw him and thought the same thing. Another system he was not making it to the bathroom. This had me convinced something really bad was happening with my baby.
Pepper is diabetic. So I keep his insulin on hand. He also has some back issues so
I keep pain medicine on hand if he needs it. Of course it is in Pepper size dose sorry Sophie Supermom
will have to talk to Dr. R for your own puppy hook up...LOL
Last night Pepper was pacing and uncomfortable. I gave him some pain medicine. I tried to get him to lay down in the bed. I felt so bad. I was crying.
I tried one last time to get him to lay down in the b ed with me. I thought he needed to be in the bed instead of the hard floor.
He came and laid his head across my stomach like he was loving on me to console me. Then he got up he wanted me to put him back in the floor.
It was 12:30am in the morning I was sure Pepper was telling me "good bye." I called and woke up my mom I was a wreck. Yep, I called her! I was crying and scared.
I had give him some medicine when he was up in the bed thinking if he was relaxed he would be more comfortable. Nope pepper was more comfortable in the floor.
I was asleep. When Pepper woke me up coming to bed an hour and half later. It was 1:30am. I was so happy.
With Pepper's back problems. We now thing that he has probably has hurt hisself jumping off the bed or couch.
Friday, September 23, 2011
The First Day of Fall
Things are so different for me than this time last year. I'm not recovering from surgery. I'm not 30 pounds heavier. It's so nice to be loosing weight.
I'm not laying in bed stressing when I'm actually going to get to have surgery.
This past summer I have enjoyed some days outside with Pepper. I want to take advantage of those days. I know my pepper is getting old. I worry this might be his last fall or summer and want every one to be special.
The first day of fall was rainy. No matter Pepper still got up and wanted to go to the shop to see Papaw after his breakfast.
I'm not laying in bed stressing when I'm actually going to get to have surgery.
This past summer I have enjoyed some days outside with Pepper. I want to take advantage of those days. I know my pepper is getting old. I worry this might be his last fall or summer and want every one to be special.
The first day of fall was rainy. No matter Pepper still got up and wanted to go to the shop to see Papaw after his breakfast.
Thursday, September 22, 2011
What's in a name?
It's been one week since Bryan's surgery. He has a raspy voice still but I know Bryan's family is thankful to hear him no matter what.
I know when Daddy said Tabatha and Tyler's name it was a big relief to the family. Can you imagine What if daddy did not know who you were...
Bryan was ask question about his kids names. He remembered both his son and daughter. He was ask some dates. He was also able to remember the dates.
Bryan is still doing physical therapy and speech therapy. Bryan has some improved movement in his left arm.
Since the shunt surgery Bryan has had trouble with swelling in his leg. It is thought it could possibly be a blood clot. The doctors are looking at possibly needing to put him on blood thinners.
To read the latest post from Bryan's family Blog go here:
Tuesday, September 20, 2011
For better or worse
So today I was opening my mail Reading I see an invitation from an old friend I was excited over the invitation for 2 days because I have lost so many of my friend over the past 11 years. They have just gone on with their lives. Forgetting about me:(
When I did not get better they seem to fade away. The friends I thought would always be there are not here anymore. I understand people have to live their own lives but a phone call would have been nice. But I do Miss some of them.
The offer of someone bringing out something to eat to help out. What really hurt is when I heard they did these things for others I worked with but not me.
About a year ago I tried to reach out to this friend. It was the first break from surgeries I had in a long time. Remember...I have had 19 in all. I really should not be the one reaching out. But I did. I even paid for dinner. I have not heard from her since.
So I invited her spur of the moment out to dinner. We met out it was a bit different since we had not seen each other in a while or been talking. But I have been sick. I hope she followes my blog and is aware of everything going on.
We worked together so she knew about how hard it was for me then. But there was so many rumors going around then.
Plus, at that time I did not realize the name of my condition. Anyway, back to the subject. The letter... Was an invitation... For 2 days I have been really excited to actually hear from an old friend again.
Then after 2 days is hit me she hasn't cared enough in the past 11 surgeries to even pick up the phone to check on me. I have not heard from her in over a year.
I guess since I'm sick now I'm just not fun anymore. I have to tell this person. I have 2 of the best friends in the world!
I Don't need some one trying to befriend me after 11 years! When I have Michelle Lee and Deanna Gentry! Plus there are about 20 women at the YWCA that love me for the person I am.
I am so thankful that this world is filled with friends like I have that surround me now. Because there is no way I would want to go back to the life I lived 10 year ago.
I heard an Evangelist yesterday say it was okay to divorce if your spouse had Alzheimer's. I just had to change the channel. What happen to in sickness and in health? I can't believe what he was saying! But this is probably why I am single.
I would not mind to meet someone but I have the fear of if I get sick again are they out the door.The guy I was engaged to could not even take care of me when I got sick. I just feel like he would have let me die if he was still around. Yes, he tried to come around... Yes my dad ran him off!!
OMG!!!As I am writing this post the mail just run.... hmmm.... what do I see??? Another innovation! Two day later for their wedding. Really?
You have not talk to me in over a year. Didn't care to do anything for me while I was sick. Now you want 2 presents.
So is is because me condition is not written on my forehead that people don't think I am sick. This is another invisible illness that is looked over once again.
I blogged so many times about how hurt I was over how many friends friends I had that I lost. I got really depressed when I was at my worst. I was friends with a woman from college then.
She suck with me through it all even though ended up pushing her away I reached out to Michelle. She helped me to start my blogging I know she will always be here. It's like we have always known each other because we had the same best friend in school Brian. He was one of my first "loves"too.
Then I can't forget Deanna she moved away for a while but she is back now. We have been friends since the 7th grade for sure. Maybe before... I am so thank to have her close again.
These 2 ladies are day and night but I would not give them up for the world. Because I get reminded daily that I had friends that didn't care enough to care.
Saturday, September 17, 2011
Man with cancer leaves his dog to friend
A Candler man is accused of beating his 20 pound dog to death because he says it attacked him. Kristopher Stroupe is being charged with cruelty to animals. Deputies says Stroupe went to Mission Hospital for dog bite wounds and claimed he had to kill the dog to stop the attack. The Buncombe County Sheriff's Office says their investigation showed no evidence to support his story and found the dog, "Bandit" had died from severe blows to the head. Stroupe is being held on a 15-thousand dollar bond.
I often worry if something happens to me or my parents what would happen to Pepper. Let's be honest. Ginger would be easy to rehome. But Pepper is 13 now. He is grumpy. He is on insulin.
I love him... My parents love him... But most people think his growling means he is going to bite When I know it is just him talking.
Reports said this guy went into the hospital for a dog bite when his story did not make since. Investigators went to the home to find that bandit had severe blows to the head from a had weight. Stroupe said Bandit had bit him and he then hit the dog. Stroupe is being held on a 15 thousand dollar bond.
Now I'm am afraid after Pepper took care of me all of these years. If someone like this hurt my Pepper I would come back from the dead! A sane person the is bit by a dog might hit the dog right then! But you don't beat it to death with a hand weight!
This breaks my heart... Bandit's owner thought he was left to a safe and loveing home. Why didn't Stroupe just find Bandit anoth home.
I often worry if something happens to me or my parents what would happen to Pepper. Let's be honest. Ginger would be easy to rehome. But Pepper is 13 now. He is grumpy. He is on insulin.
I love him... My parents love him... But most people think his growling means he is going to bite When I know it is just him talking.
Reports said this guy went into the hospital for a dog bite when his story did not make since. Investigators went to the home to find that bandit had severe blows to the head from a had weight. Stroupe said Bandit had bit him and he then hit the dog. Stroupe is being held on a 15 thousand dollar bond.
Now I'm am afraid after Pepper took care of me all of these years. If someone like this hurt my Pepper I would come back from the dead! A sane person the is bit by a dog might hit the dog right then! But you don't beat it to death with a hand weight!
This breaks my heart... Bandit's owner thought he was left to a safe and loveing home. Why didn't Stroupe just find Bandit anoth home.
Friday, September 16, 2011
My story
I was first shunted for swelling after a brain tumor surgery when I was 8 years old. I received the medication to keep the swell down before the surgery but not after.
The pressure crossed my eyes, I lost the ability to hold my bladder, and I lost all ability to stay awake or respond to comands. I also Had to learn to walk again.
My doctor had gone to Washingon to research my brain tumor it was the first of this aystrocytomia the hospital. He was gone for 9 days. During the nine days is when my eyes crossed, I was loosing bladder control, and not responding to commands. His assistants were making excuses for all of this.
When he returned he rushed me into surgery I came out of surgery Alert! I regained my bladder control after the surgery. I had to have 3 surgeries to fix my eyes. It took me a while to learn how to walk again at 8 yeas old. But I did it.
They did not tell me back then I had a condition. I found out in 2003 after a year. I had already had 2 or 3 surgeries on the shunt already. The doctors had taken out the non programmable shunt I had and put in a programmable shunt. I was getting more sick everyday.
I now blog to try to help others. to try to keep any one else from going through what I have been through.
I do think I am suppose to have this condition. I am suppose to teach others about hydrocephalus.
The pressure crossed my eyes, I lost the ability to hold my bladder, and I lost all ability to stay awake or respond to comands. I also Had to learn to walk again.
My doctor had gone to Washingon to research my brain tumor it was the first of this aystrocytomia the hospital. He was gone for 9 days. During the nine days is when my eyes crossed, I was loosing bladder control, and not responding to commands. His assistants were making excuses for all of this.
When he returned he rushed me into surgery I came out of surgery Alert! I regained my bladder control after the surgery. I had to have 3 surgeries to fix my eyes. It took me a while to learn how to walk again at 8 yeas old. But I did it.
They did not tell me back then I had a condition. I found out in 2003 after a year. I had already had 2 or 3 surgeries on the shunt already. The doctors had taken out the non programmable shunt I had and put in a programmable shunt. I was getting more sick everyday.
I now blog to try to help others. to try to keep any one else from going through what I have been through.
I do think I am suppose to have this condition. I am suppose to teach others about hydrocephalus.
Thursday, September 15, 2011
Who knew the Devils name was Elisa Baker
Elisa Baker just plead guilty in the dismemberment death of her disabled stepdaughter. She will reportedly get 15 to 18 years in prison for taking the plea.
When so many of us are struggling to live like little Zahra... This WITCH!!!saw her as too much of a burden!!! She met them online.
People! Please! be careful doing this... I know someone that wont meet anyone any other way. As you see you can't be to careful when you have children.
Stepmother of 10-year-old disabled girl Zahra pleads guilty to murdering child and dismembering her body
By Hannah RobertsLast updated at 8:17 PM on 15th September 2011
- Stepmother pleads guilty to second-degree murder
- Police found a saw that may have been used to dismember the child's body
- Baker admitted writing a fake ransom note
- Murderer is a bigamist who was already married when she tied the knot with Zahra's father
- New details about date of Zahra's death emerge
Shocking death: 10-year-old Zahra Baker disappeared in North Carolina in October 2010, sparking a massive search. Her stepmother Elisa Baker has pleaded guilty to second-degree murder and dismemberment of the child's body
Elisa Baker, 42, was sentenced to about 15 to 18 years in prison followed by emotional statements from the parents after admitting second-degree murder in the death of the child as part of a plea deal.
Baker also pleaded guilty to attempting to thwart investigators by planting a fake ransom note at the family home.
The deal comes nearly a year after the Australian girl was reported missing from her home in the western North Carolina town of Hickory.
The disappearance of the freckle-faced girl captivated communities both in the US and in Australia. Zahra's father had moved to the United States to marry Elisa after the two met online.
Zahra had a prosthetic leg after losing her limb aged five, and wore two hearing aids after an early battle with bone cancer.
The child's head, hands and parts of her arms and legs have never been found, the court heard on Thursday.
Her prosthetic leg was discovered during a mammoth search for her remains that spanned three counties.
Gitty to see Gabby!
Gabby has been doing her rehabilitation outpatient for several months since she had her last surgery to replace a skull flat and a shunt just days before her release from the hospital. She continues the weekly out patient therapy.
Wednesday, September 14, 2011
Bryan Stow was alert after shunt surgery
http://support4bryanstow.com/News-Updates/articleType/ArticleView/articleId/980/9132011-Update#Comment5947
Sept. 13, 2011
GIANTS PAGE | GIANTS VIDEO
CSNBayArea.com staff
Giants fan Bryan Stow, injured in an Opening Day attack in Los Angeles, underwent successful shunt surgery, his family announced on their website Tuesday.
According to the site, Stow's "surgery went smooth and the CT scan came back looking good." The family also reported that they saw Bryan and his eyes were open.
The Santa Cruz paramedic was attacked on Opening Day at Dodger Stadium and has been hospitalized since. Earlier this week his lawyers estimated that Stow’s medical costs would exceed $50 million.
Louie Sanchez, 29, and Marvin Norwood, 30, are charged with mayhem, assault and battery in the attack on Stow.
Prosecutors contend that Sanchez hit two of Stow's friends before chasing down Stow and punching him from behind in the side of his head.
Read more: Shunt surgery successful for Giants fan Stow
Tune to SportsNet Central at 6, 10:30 and midnight on Comcast SportsNet Bay Area for more on this story
I know this is a day to be rejoicing about Bryan and it looks like an odd place to put his offenders pictures. I figure anytime I can get these two guys seen the better.I feel like it will be like Casey Athony. If we don't keep talking this to death these fools will get off.
This is not only a hate crime it reflect back to our kids as teaches them about bulling. If these 2 men that assaulted Bryan have children. What kind of example does this set for them?
Does knocking a man down... having his head hit the pavement and bounce off the ground. While this man is bleeding. Set a good example for being a "dad."
Oh! While he was down and knocked out! Sanchez! and Norwood Started kicking a lifeless Bryan Stow while he lay there bleeding.
His friend,Matt, that has recently passed away because of a nut allergy, through his body in between Sanchez and Norwood while they were kicking Bryan after he was down. Matt is a hero!
I was so happy to here that Bryan was awake after surgery. Many of the Blog post from his blog had said he was very sleepy.
When I was 8 and I had my my first shunt I remember my parents and my physical therapist asking when I was going to start waking up more from the anesthesia. They assumed it was the surgery since I had not really woke up since I had my brain tumor removed.
After the shunt surgery I came out much like Bryan alert and and able to respond to comands. It helped my recover a good bit. Although much like Bryan I had a lot of recover to go.
GIANTS PAGE | GIANTS VIDEO
CSNBayArea.com staff
Giants fan Bryan Stow, injured in an Opening Day attack in Los Angeles, underwent successful shunt surgery, his family announced on their website Tuesday.
According to the site, Stow's "surgery went smooth and the CT scan came back looking good." The family also reported that they saw Bryan and his eyes were open.
The Santa Cruz paramedic was attacked on Opening Day at Dodger Stadium and has been hospitalized since. Earlier this week his lawyers estimated that Stow’s medical costs would exceed $50 million.
Louie Sanchez, 29, and Marvin Norwood, 30, are charged with mayhem, assault and battery in the attack on Stow.
Prosecutors contend that Sanchez hit two of Stow's friends before chasing down Stow and punching him from behind in the side of his head.
Read more: Shunt surgery successful for Giants fan Stow
Tune to SportsNet Central at 6, 10:30 and midnight on Comcast SportsNet Bay Area for more on this story
I know this is a day to be rejoicing about Bryan and it looks like an odd place to put his offenders pictures. I figure anytime I can get these two guys seen the better.I feel like it will be like Casey Athony. If we don't keep talking this to death these fools will get off.
This is not only a hate crime it reflect back to our kids as teaches them about bulling. If these 2 men that assaulted Bryan have children. What kind of example does this set for them?
Does knocking a man down... having his head hit the pavement and bounce off the ground. While this man is bleeding. Set a good example for being a "dad."
Oh! While he was down and knocked out! Sanchez! and Norwood Started kicking a lifeless Bryan Stow while he lay there bleeding.
His friend,Matt, that has recently passed away because of a nut allergy, through his body in between Sanchez and Norwood while they were kicking Bryan after he was down. Matt is a hero!
I was so happy to here that Bryan was awake after surgery. Many of the Blog post from his blog had said he was very sleepy.
When I was 8 and I had my my first shunt I remember my parents and my physical therapist asking when I was going to start waking up more from the anesthesia. They assumed it was the surgery since I had not really woke up since I had my brain tumor removed.
After the shunt surgery I came out much like Bryan alert and and able to respond to comands. It helped my recover a good bit. Although much like Bryan I had a lot of recover to go.
Tuesday, September 13, 2011
Bryan Stow shunt surgery
http://support4bryanstow.com/News-Updates/articleType/ArticleView/articleId/975/91111a-day-of-remembrance-and-kisses
I had just a quick second to post this please be thinking about Bryan today... I am praying his shunt surgery goes well today. I think this will help him in his recovery so much. It has bothered me that his sisters have not been updating the blog. I wondered if he was not improving.
I had just a quick second to post this please be thinking about Bryan today... I am praying his shunt surgery goes well today. I think this will help him in his recovery so much. It has bothered me that his sisters have not been updating the blog. I wondered if he was not improving.
Sunday, September 11, 2011
10th Anniversery of 9/11
I remember wher I was that morning. My mom had worked that night and got up to go and eat breakfast with me at my favorite placebefore I went to work.
the place we ate had Good morning America on we were talking and could not hear what the TV was saying but could see something.
What we saw was the first plane hit. I ask the waitress what happened. She only knew what I could tell from the pictures I could see.
I had to go to work by that time. I was working at Lowes. The paint department had a TV they kept on but of course I could not see or hear it from customer service.
By the time I got to work and got clocked in I was hearing from customers that a second plane had hit the towers. I was confused.... Scared....What was going on? I really did not want to be at work! I wanted to figure out what was going on!
I could not stand getting rumors of this and that from customors coming through. I called my friend at the time Staci. She said do you realize today is 9/11! We were attacked! by terrorist is what the news is saying.I thing She was the one to tell me about the Pentagon and flight 93 going down.
I know so many lives were changed that day. It still seems like it just happened in so many ways but I think back and It was also a life time ago
The only time I would have ever thought about 911 10 ago is if I need to call for an emergency. Who knew America would have had an emergency that would change the world forever.
the place we ate had Good morning America on we were talking and could not hear what the TV was saying but could see something.
What we saw was the first plane hit. I ask the waitress what happened. She only knew what I could tell from the pictures I could see.
I had to go to work by that time. I was working at Lowes. The paint department had a TV they kept on but of course I could not see or hear it from customer service.
By the time I got to work and got clocked in I was hearing from customers that a second plane had hit the towers. I was confused.... Scared....What was going on? I really did not want to be at work! I wanted to figure out what was going on!
I could not stand getting rumors of this and that from customors coming through. I called my friend at the time Staci. She said do you realize today is 9/11! We were attacked! by terrorist is what the news is saying.I thing She was the one to tell me about the Pentagon and flight 93 going down.
I know so many lives were changed that day. It still seems like it just happened in so many ways but I think back and It was also a life time ago
The only time I would have ever thought about 911 10 ago is if I need to call for an emergency. Who knew America would have had an emergency that would change the world forever.
Saturday, September 10, 2011
Yesterday right at lunch time I decided I wanted to go to Jason's Deli before swimming. I figured it would be fairly healthy and kinda on the way.
I had no way what was going to happen before I even reached the front door. I had been having a headache that morning but I did not think much about it. I had been taking medicine for it. I figured when I ate I would take something and that would help too.
I made it to the sidewalk ok as I was walking along the front of Jason's Deli my headache was getting worse. I figured it was the usual head rush. I tried to walk it off. Only this didn't walk off I started getting dizzy.
When I got dizzy I thought I was on one of those tea cup rides. I couldn't figure out where I was.
I started reaching for my mom cause I couldn't focus and I was going down because I was so dizzy I was just going to sit down to keep from falling.
When I reached for my mom I grabbed her shirt (thank goodness she had a bathing suit on underneath) I about ripped it off her.
She got me to the arm railing. The dizzy spell past. I had a headache the rest of the evening and slept really hard last night.
I wonder if the antibiotic I'm on could have caused this reaction. I am really sensitive to the side effects of medications.
I had no way what was going to happen before I even reached the front door. I had been having a headache that morning but I did not think much about it. I had been taking medicine for it. I figured when I ate I would take something and that would help too.
I made it to the sidewalk ok as I was walking along the front of Jason's Deli my headache was getting worse. I figured it was the usual head rush. I tried to walk it off. Only this didn't walk off I started getting dizzy.
When I got dizzy I thought I was on one of those tea cup rides. I couldn't figure out where I was.
I started reaching for my mom cause I couldn't focus and I was going down because I was so dizzy I was just going to sit down to keep from falling.
When I reached for my mom I grabbed her shirt (thank goodness she had a bathing suit on underneath) I about ripped it off her.
She got me to the arm railing. The dizzy spell past. I had a headache the rest of the evening and slept really hard last night.
I wonder if the antibiotic I'm on could have caused this reaction. I am really sensitive to the side effects of medications.
Thursday, September 8, 2011
Scripps rearch scientists find clue to cause of childhooh hyhrocephalus
Public release date: 7-Sep-2011[ Print | E-mail | 
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Contact: Mika Ono
mikaono@scripps.edu
858-784-2052
Scripps Research Institute
LA JOLLA, CA – September 7, 2011 – Scientists at The Scripps Research Institute have found what may be a major cause of congenital hydrocephalus, one of the most common neurological disorders of childhood that produces mental debilitation and sometimes death in premature and newborn children.
The research appears in the September 7, 2011, issue of the journal Science Translational Medicine.
Hydrocephalus, which involves excess buildup of cerebrospinal fluid in the brain, affects about 1 in 500 children in the United States. Currently only symptomatic treatment exists—the surgical placement of a shunt to drain away excess fluid. Researchers want to know the condition's causes, so they can figure out how to prevent and treat it. Scientists have known for some time that hydrocephalus was linked to bleeding events in the developing brain, but the reason for that linkage has not been clear.
The new study now suggests that hydrocephalus can be triggered by abnormal levels of lysophosphatidic acid (LPA), a blood-borne lipid that can enter the brain in high concentrations during bleeding events, with profound effects on developing brain cells. The study showed that both blood and LPA itself acted through the same receptor (receptors are proteins to which one or more specific kinds of signaling molecules bind) to produce defects in the brains of developing mice that led to severe hydrocephalus; genetic removal of a specific LPA receptor or pre-treatment with a compound that blocked the receptor largely prevented the condition.
"This provides proof of concept for the medical treatment of this disease," said Jerold Chun, MD, PhD, a professor at Scripps Research and its Dorris Neuroscience Center, and senior author of the new study, "and it also hints that this mechanism involving LPA could be relevant to other neurological conditions associated with altered brain development."
A Eureka Moment
Chun's laboratory specializes in the study of lipid-signaling molecules involved in the developing brain, including LPA. LPA is normally produced in the fast-growing fetal brain, and appears to be important for the normal development of neural "progenitor" cells. But when the researchers added abnormally high concentrations of LPA to the brains of fetal mice, they found an unexpected effect on brain development. "When we looked at their condition as newborns, we were surprised to see that they uniformly had big, fluid-filled brains," said postdoctoral fellow Yun Yung, PhD. "It was a Eureka moment, because we realized that LPA might help explain hydrocephalus."
Reviewing the medical literature on the condition, Chun and Yung noted that it was often linked to brain-bleeding events in the womb and typically also featured some improperly developed brain structures. "Our experiments with LPA connected both sets of findings," said Yung, "because LPA is involved in blood clotting and can reach very high concentrations during hemorrhages; plus, our LPA-exposed mouse brains had structural abnormalities like those reported in human cases."
Cerebrospinal fluid cushions the brain, provides it with basic nutrients, and is normally produced by the membrane-like choroid plexus within the fluid-filled chambers of the brain known as ventricles. Ependymal cells that line these ventricles have hair-like extensions that are thought to promote the normal flow of fluid. "In our LPA-exposed mice, there were patches in the ventricular lining where these ependymal cells were missing, which could have led to a disruption of the normal cerebrospinal fluid flow," said Yung. Structures in the ventricles that normally permit the proper drainage of fluid also appeared to be partly blocked by the improper overgrowth of cells, which might have further contributed to the brain-damaging fluid buildup.
The researchers were able to repeat these effects using the normal LPA-containing fluid fractions of blood, thus showing that bleeding events plausibly can lead to hydrocephalus by increasing the brain's exposure to LPA.
To investigate how LPA exerted this effect, the team produced mice that genetically lack one or both of the two receptors—LPA1 and LPA2—to which LPA can bind on ventricle-building fetal progenitor cells, finding that the LPA1 receptor was required to produce hydrocephalus. "The idea here is that excess LPA causes these ventricular progenitor cells to get the wrong developmental signals via their LPA receptors, and so the ventricles and brain develop abnormally," said Chun.
In a final demonstration, the team pre-treated normal fetal mice with a compound that blocks the activation of LPA1 receptors, and found that even after LPA exposure, their signs of hydrocephalus were greatly reduced.
Looking Ahead
LPA1-blocking drugs currently are being developed for other conditions including lung fibrosis, and the new finding from Chun's lab may lead biotech or pharmaceutical companies to study their use in hydrocephalus. "If you had an unborn baby who was at risk from an injury to the mother, an infection, or evidence of bleeding then, in principle, you could treat with a short-acting LPA1 blocker to prevent or reduce hydrocephalus," said Chun.
The discovery that excess LPA can wreak havoc in the developing brain could have broader implications as well. Abnormally high concentrations of LPA may be generated by fetal brain cells themselves, also producing abnormal LPA signaling. Moreover, schizophrenia, autism, and other developmental brain disorders have also been linked to fetal bleeding events and infections as well as ventricular abnormalities.
"It's something that we need to investigate further," said Chun, "but it may be that excess LPA exposure in an unborn child's brain can have a variety of adverse effects on development, depending on the part of the brain that's exposed, the stage of brain development, and the duration of the exposure."
This work was supported by the National Institutes of Health, the National Science Foundation, and the Hydrocephalus Association.
About The Scripps Research Institute
The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations. Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neuroscience, and vaccine development, as well as for its insights into autoimmune, cardiovascular, and infectious disease. Headquartered in La Jolla, California, the institute also includes a campus in Jupiter, Florida, where scientists focus on drug discovery and technology development in addition to basic biomedical science. Scripps Research currently employs about 3,000 scientists, staff, postdoctoral fellows, and graduate students on its two campuses. The institute's graduate program, which awards PhD degrees in biology and chemistry, is ranked among the top ten such programs in the nation. For more information, see www.scripps.edu .
Share ] [ Close Window ]Contact: Mika Ono
mikaono@scripps.edu
858-784-2052
Scripps Research Institute
Scripps research scientists find clue to cause of childhood hydrocephalus
An excess of a natural molecule can bring about the devastating ‘water on the brain’ condition in mice and blocking its action can prevent the effect
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| |   IMAGE:Jerold Chun, MD, PhD, is a professor at The Scripps Research Institute and its Dorris Neuroscience Center. | | |
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The research appears in the September 7, 2011, issue of the journal Science Translational Medicine.
Hydrocephalus, which involves excess buildup of cerebrospinal fluid in the brain, affects about 1 in 500 children in the United States. Currently only symptomatic treatment exists—the surgical placement of a shunt to drain away excess fluid. Researchers want to know the condition's causes, so they can figure out how to prevent and treat it. Scientists have known for some time that hydrocephalus was linked to bleeding events in the developing brain, but the reason for that linkage has not been clear.
The new study now suggests that hydrocephalus can be triggered by abnormal levels of lysophosphatidic acid (LPA), a blood-borne lipid that can enter the brain in high concentrations during bleeding events, with profound effects on developing brain cells. The study showed that both blood and LPA itself acted through the same receptor (receptors are proteins to which one or more specific kinds of signaling molecules bind) to produce defects in the brains of developing mice that led to severe hydrocephalus; genetic removal of a specific LPA receptor or pre-treatment with a compound that blocked the receptor largely prevented the condition.
"This provides proof of concept for the medical treatment of this disease," said Jerold Chun, MD, PhD, a professor at Scripps Research and its Dorris Neuroscience Center, and senior author of the new study, "and it also hints that this mechanism involving LPA could be relevant to other neurological conditions associated with altered brain development."
A Eureka Moment
Chun's laboratory specializes in the study of lipid-signaling molecules involved in the developing brain, including LPA. LPA is normally produced in the fast-growing fetal brain, and appears to be important for the normal development of neural "progenitor" cells. But when the researchers added abnormally high concentrations of LPA to the brains of fetal mice, they found an unexpected effect on brain development. "When we looked at their condition as newborns, we were surprised to see that they uniformly had big, fluid-filled brains," said postdoctoral fellow Yun Yung, PhD. "It was a Eureka moment, because we realized that LPA might help explain hydrocephalus."
Reviewing the medical literature on the condition, Chun and Yung noted that it was often linked to brain-bleeding events in the womb and typically also featured some improperly developed brain structures. "Our experiments with LPA connected both sets of findings," said Yung, "because LPA is involved in blood clotting and can reach very high concentrations during hemorrhages; plus, our LPA-exposed mouse brains had structural abnormalities like those reported in human cases."
Cerebrospinal fluid cushions the brain, provides it with basic nutrients, and is normally produced by the membrane-like choroid plexus within the fluid-filled chambers of the brain known as ventricles. Ependymal cells that line these ventricles have hair-like extensions that are thought to promote the normal flow of fluid. "In our LPA-exposed mice, there were patches in the ventricular lining where these ependymal cells were missing, which could have led to a disruption of the normal cerebrospinal fluid flow," said Yung. Structures in the ventricles that normally permit the proper drainage of fluid also appeared to be partly blocked by the improper overgrowth of cells, which might have further contributed to the brain-damaging fluid buildup.
The researchers were able to repeat these effects using the normal LPA-containing fluid fractions of blood, thus showing that bleeding events plausibly can lead to hydrocephalus by increasing the brain's exposure to LPA.
To investigate how LPA exerted this effect, the team produced mice that genetically lack one or both of the two receptors—LPA1 and LPA2—to which LPA can bind on ventricle-building fetal progenitor cells, finding that the LPA1 receptor was required to produce hydrocephalus. "The idea here is that excess LPA causes these ventricular progenitor cells to get the wrong developmental signals via their LPA receptors, and so the ventricles and brain develop abnormally," said Chun.
In a final demonstration, the team pre-treated normal fetal mice with a compound that blocks the activation of LPA1 receptors, and found that even after LPA exposure, their signs of hydrocephalus were greatly reduced.
Looking Ahead
LPA1-blocking drugs currently are being developed for other conditions including lung fibrosis, and the new finding from Chun's lab may lead biotech or pharmaceutical companies to study their use in hydrocephalus. "If you had an unborn baby who was at risk from an injury to the mother, an infection, or evidence of bleeding then, in principle, you could treat with a short-acting LPA1 blocker to prevent or reduce hydrocephalus," said Chun.
The discovery that excess LPA can wreak havoc in the developing brain could have broader implications as well. Abnormally high concentrations of LPA may be generated by fetal brain cells themselves, also producing abnormal LPA signaling. Moreover, schizophrenia, autism, and other developmental brain disorders have also been linked to fetal bleeding events and infections as well as ventricular abnormalities.
"It's something that we need to investigate further," said Chun, "but it may be that excess LPA exposure in an unborn child's brain can have a variety of adverse effects on development, depending on the part of the brain that's exposed, the stage of brain development, and the duration of the exposure."
###
Additional Chun lab members contributing to the study, "Lysophosphatidic Acid Signaling May Initiate Fetal Hydrocephalus," were Tetsuji Mutoh, now at the Nara Institute of Science and Technology; Mu-en Lin; Kyoko Noguchi; Richard R. Rivera; Ji Woong Choi, now at Gachon University of Medicine and Science in Korea; and Marcy A. Kingsbury, now at Indiana University.This work was supported by the National Institutes of Health, the National Science Foundation, and the Hydrocephalus Association.
About The Scripps Research Institute
The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations. Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neuroscience, and vaccine development, as well as for its insights into autoimmune, cardiovascular, and infectious disease. Headquartered in La Jolla, California, the institute also includes a campus in Jupiter, Florida, where scientists focus on drug discovery and technology development in addition to basic biomedical science. Scripps Research currently employs about 3,000 scientists, staff, postdoctoral fellows, and graduate students on its two campuses. The institute's graduate program, which awards PhD degrees in biology and chemistry, is ranked among the top ten such programs in the nation. For more information, see www.scripps.edu .
Wednesday, September 7, 2011
One of the most common side effects of hydrocephalus is insomnia. Ever since I was a little girl I have had trouble sleeping. Even before I knew I had this condition that could and would cause me problems sleeping.
For the past week I have not been sleeping. I would fall asleep for a couple of house. But then I would be wide awake to enjoy "Big Brother" on " Showtime"
I was taping it on DVD. But still. I need my sleep. This has been going on for a week or more now. I'm exhausted.
I had to go to South Carolina yesterday. I was so tired coming back with no sleep I was falling asleep in the seat. I can remember my mom's fingers on my forehead leaning my head back up.
She said my head would just flop straight over. She would have to push my head back up against the back of the seat to keep my neck from breaking.
For the past week I have not been sleeping. I would fall asleep for a couple of house. But then I would be wide awake to enjoy "Big Brother" on " Showtime"
I was taping it on DVD. But still. I need my sleep. This has been going on for a week or more now. I'm exhausted.
I had to go to South Carolina yesterday. I was so tired coming back with no sleep I was falling asleep in the seat. I can remember my mom's fingers on my forehead leaning my head back up.
She said my head would just flop straight over. She would have to push my head back up against the back of the seat to keep my neck from breaking.
Monday, September 5, 2011
ACC Hydo
Overview
Agenesis of the corpus callosum (ACC) is an anomaly that may occur in isolation or in association with other central nervous system (CNS) or systemic malformations. Because the corpus callosum may be partially or completely absent, the term dysgenesis has also been used to describe the spectrum of callosal anomalies. The normal appearance of the corpus callosum, along with the appearance on magnetic resonance imaging (MRI) of partial and complete ACC, are shown below.[1, 2, 3, 4, 5, 6]
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows the normal appearance of the corpus callosum. 
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows complete absence of the corpus callosum. The cingulate sulcus is absent, and the medial hemispheric sulci reach the third ventricle in a radial fashion. 
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the corpus callosum are visualized, whereas the posterior body, splenium, and rostrum are absent.
With partial agenesis (hypoplasia), the anterior portion (posterior genu and anterior body) is formed, but the posterior portion (posterior body and splenium) is not. The rostrum and the anterior/inferior genu are also not formed.
An atypical appearance occurs when the anterior to posterior formation is not respected.
In holoprosencephaly, callosal anomalies are atypical; for example, the splenium may be present without a genu or body. In middle interhemispheric fusion, which is a variety of holoprosencephaly, the genu and splenium may be present without the callosal body.[7]
With pseudo–corpus callosum, which involves conditions of complete or partial agenesis, the hippocampal commissure may become enlarged and appear like the posterior part of the corpus callosum.
Secondary destruction of corpus callosum occurs when the genu and anterior body are destroyed, leaving the posterior portion of the corpus callosum intact. This may occur secondary to porencephaly or schizencephaly, as a surgical complication in cases involving the transcallosal approach to the lateral and third ventricle, or with hemisection of the callosum for the treatment of seizures.
Other cerebral malformations may coexist with callosal dysgenesis. Examples of these include interhemispheric cysts; intracranial lipomas; and disorders of neuronal migration, such as neuronal heterotopias, lissencephaly, pachygyria, and, as mentioned, schizencephaly.
Antenatal diagnosis of ACC is possible from about 20 weeks' gestation. Characteristic intrauterine US findings include colpocephaly and parallel ventricular walls. Computed tomography (CT) scan findings are also diagnostic of ACC. Parallel lateral ventricles, colpocephaly, and extension of the third ventricle into the interhemispheric fissure are particularly pertinent findings. In patients with ACC who have an interhemispheric cyst, the preoperative injection of nonionic water-soluble contrast material into the cystic loculations for CT evaluation enables assessment of the ventricular system or of the communication of the cystic components with one another.
Magnetic resonance imaging (MRI) is currently the imaging procedure of choice in infants and children with ACC, even in patients who have previously undergone CT and US examinations. The multiplanar capability and high soft-tissue contrast that are possible with MRI permit confident diagnosis of ACC and its associated anomalies, especially neuronal migration anomalies or atypical forms of holoprosencephaly. These entities may be extremely subtle or indiscernible on CT or US images.
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows the normal appearance of the corpus callosum. Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows complete absence of the corpus callosum. The cingulate sulcus is absent, and the medial hemispheric sulci reach the third ventricle in a radial fashion. Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the corpus callosum are visualized, whereas the posterior body, splenium, and rostrum are absent. Spectrum of abnormalities
ACC may be complete, partial, or atypical. With complete agenesis, the corpus callosum is totally absent.With partial agenesis (hypoplasia), the anterior portion (posterior genu and anterior body) is formed, but the posterior portion (posterior body and splenium) is not. The rostrum and the anterior/inferior genu are also not formed.
An atypical appearance occurs when the anterior to posterior formation is not respected.
In holoprosencephaly, callosal anomalies are atypical; for example, the splenium may be present without a genu or body. In middle interhemispheric fusion, which is a variety of holoprosencephaly, the genu and splenium may be present without the callosal body.[7]
With pseudo–corpus callosum, which involves conditions of complete or partial agenesis, the hippocampal commissure may become enlarged and appear like the posterior part of the corpus callosum.
Secondary destruction of corpus callosum occurs when the genu and anterior body are destroyed, leaving the posterior portion of the corpus callosum intact. This may occur secondary to porencephaly or schizencephaly, as a surgical complication in cases involving the transcallosal approach to the lateral and third ventricle, or with hemisection of the callosum for the treatment of seizures.
Other cerebral malformations may coexist with callosal dysgenesis. Examples of these include interhemispheric cysts; intracranial lipomas; and disorders of neuronal migration, such as neuronal heterotopias, lissencephaly, pachygyria, and, as mentioned, schizencephaly.
Preferred examination
The diagnosis of callosal agenesis depends on neuroimaging. In the newborn, before closure of the anterior fontanelle occurs, screening ultrasonography (US) may clearly show the absence of the corpus callosum; it may also show parallel lateral ventricles, interhemispheric cysts, hydrocephalus, and other related anomalies. US was the first imaging modality to allow direct sagittal imaging of callosal dysgenesis.[8, 9, 10, 11, 12]Antenatal diagnosis of ACC is possible from about 20 weeks' gestation. Characteristic intrauterine US findings include colpocephaly and parallel ventricular walls. Computed tomography (CT) scan findings are also diagnostic of ACC. Parallel lateral ventricles, colpocephaly, and extension of the third ventricle into the interhemispheric fissure are particularly pertinent findings. In patients with ACC who have an interhemispheric cyst, the preoperative injection of nonionic water-soluble contrast material into the cystic loculations for CT evaluation enables assessment of the ventricular system or of the communication of the cystic components with one another.
Magnetic resonance imaging (MRI) is currently the imaging procedure of choice in infants and children with ACC, even in patients who have previously undergone CT and US examinations. The multiplanar capability and high soft-tissue contrast that are possible with MRI permit confident diagnosis of ACC and its associated anomalies, especially neuronal migration anomalies or atypical forms of holoprosencephaly. These entities may be extremely subtle or indiscernible on CT or US images.
Limitations of techniques
Agenesis of the corpus callosum may be depicted on CT scanning and US, but MRI is the preferred imaging modality because of its greater sensitivity for depicting associated cerebral anomalies.Computed Tomography
Axial CT scanning shows parallel ventricles and continuation of the interhemispheric fissure with the third ventricle in patients with agenesis of the corpus callosum (ACC). Colpocephaly (shown in the image below) may easily be visualized.
Corpus callosum, agenesis. Axial nonenhanced CT of the brain shows colpocephaly, caused by dilation of the atria, and occipital horns of the lateral ventricle. Note the parallel configuration of the lateral ventricles. Interdigitation of gyri from fenestration of the falx may be noted incidentally. Nonenhanced axial CT may show an interhemispheric cyst. In complex types of multilocular interhemispheric cysts associated with callosal agenesis, a CT cystogram or ventriculogram may be obtained after iohexol is introduced into the cyst to establish which of the CSF collections communicate with each other or with the ventricular system.
Corpus callosum, agenesis. Axial nonenhanced CT of the brain shows colpocephaly, caused by dilation of the atria, and occipital horns of the lateral ventricle. Note the parallel configuration of the lateral ventricles. Interdigitation of gyri from fenestration of the falx may be noted incidentally. Nonenhanced axial CT may show an interhemispheric cyst. In complex types of multilocular interhemispheric cysts associated with callosal agenesis, a CT cystogram or ventriculogram may be obtained after iohexol is introduced into the cyst to establish which of the CSF collections communicate with each other or with the ventricular system. Degree of confidence
Although CT findings may suggest the diagnosis of agenesis of the corpus callosum, MRI and US show the anatomic features of ACC better than CT does. MRI is the preferred imaging modality, especially for the diagnosis of partial agenesis and for the depiction of associated anomalies.Magnetic Resonance Imaging
The MRI findings in agenesis of the corpus callosum (ACC) are clearly demonstrated on the sagittal projection. Sagittal T1-weighted images (examples of which appear below) clearly show the exact extent of callosal dysgenesis.
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows the normal appearance of the corpus callosum. Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows complete absence of the corpus callosum. The cingulate sulcus is absent, and the medial hemispheric sulci reach the third ventricle in a radial fashion. Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the corpus callosum are visualized, whereas the posterior body, splenium, and rostrum are absent. In complete agenesis, the corpus callosum is not visualized, whereas in a hypogenetic corpus callosum, the later-forming structures are usually absent. Therefore, the corpus callosum may show a posterior genu; a posterior genu and anterior body; a genu and an entire body; or an entire genu, body, and splenium with the exception of the rostrum. The third ventricle may be high riding and interposed between the bodies of the lateral ventricles. (See the images below.)[13, 14, 15]
Corpus callosum, agenesis. Axial T1-weighted MRI shows that the lateral ventricles are parallel to each other and do not come into contact with each other as they normally should. 
Corpus callosum, agenesis. Coronal T1-weighted MRI of the brain shows absence of the normal corpus callosum. The lateral ventricles form a bull's-horn appearance and are indented medially by the Probst bundle (arrows). 
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain. Parasagittal section through the lateral ventricle shows dilatation of the atrium and occipital horn (colpocephaly). 
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly. The body and splenium of the corpus callosum are well formed, whereas the genu and rostrum are hypoplastic. 
Corpus callosum, agenesis. Axial T2-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly (same patient as in the previous image). There is fusion across the midline of the inferior basal ganglia (arrow) and the medial cortex of the frontal lobes across the interhemispheric fissure (arrowhead). Loss of the supporting function of the corpus callosum results in upward bulging of the roof of the third ventricle into the interhemispheric fissure. This upward herniation of the distended third ventricle is generally referred to as the interhemispheric cyst, but it should not be confused with a true dorsal or arachnoid cysts of the interhemispheric fissure found in some cases of callosal agenesis.
The herniated third ventricle or true cyst may be located in the midline, separating the cerebral hemispheres, or it may be located predominantly to one side of the falx or the other. The herniated third ventricle is of variable size, sometimes extending superiorly all the way to the inner table of the calvaria.
An arachnoid or dorsal cyst generally does not communicate with the third or lateral ventricles, and it may be multiseptated. Hemorrhage may occur within the cysts, markedly changing their signal intensity on MRIs.
Coronal and axial MRI sections are best for demonstrating the longitudinal callosal bundles of Probst. They represent nondecussated callosal fibers. Instead of crossing in the midline, these fibers deviate at the interhemispheric fissure to run along the medial borders of the lateral ventricles from the frontal paraolfactory cortex to the occipital region. Their volume is less than that of the fibers in the normal corpus callosum; they are of different sizes.
The anterior commissure is usually present; occasionally, it is larger or smaller than normal. It is best seen on sagittal or axial T1-weighted images. The hippocampal commissure is usually absent or hypoplastic but sometimes may be enlarged.
The lateral ventricles may have a colpocephalic appearance with a localized dilatation of the atria and occipital horns. The lateral ventricles are pressed upon superomedially by the adjacent bundles, which are more marked in the frontal regions, where the bundles are thickest. They also appear widely separated and are medially concave, with the upper corners turned up and pointed. This finding is called bull's horns or the bat-wing conformation.
The foramen of Monro may be enlarged. The cingulate gyri are not rotated, and the cingulate sulcus is absent; this results in a radial pattern of sulci in the medial surface of the cerebral hemisphere. This finding is helpful in evaluating newborns, in whom the corpus callosum is normally thin.
Often, keyhole dilatation of the temporal horns occurs secondary to incomplete inversion of the hippocampal formation. This finding indicates the intimate relationship between the development of the corpus callosum and the limbic system.
A large percentage of patients with dysgenesis of the corpus callosum have a large interhemispheric cyst, which may or may not communicate with the ventricular system. The cyst is frequently associated with hydrocephalus. The exact origin of the cyst is not known. Some suggest that it is a dilated third ventricle or a true arachnoid cyst. At autopsy, the lining of the cyst may contain ependymal or arachnoid cells. On MRIs, the cyst may have a high protein content; in these cases, the signal intensity on T1-weighted images is greater than that of CSF.
A pericallosal lipoma of the corpus callosum appears as a high–signal-intensity mass on T1-weighted images, usually dorsal to the corpus callosum; it may be associated with callosal dysgenesis.
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows the normal appearance of the corpus callosum. Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows complete absence of the corpus callosum. The cingulate sulcus is absent, and the medial hemispheric sulci reach the third ventricle in a radial fashion. Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the corpus callosum are visualized, whereas the posterior body, splenium, and rostrum are absent. In complete agenesis, the corpus callosum is not visualized, whereas in a hypogenetic corpus callosum, the later-forming structures are usually absent. Therefore, the corpus callosum may show a posterior genu; a posterior genu and anterior body; a genu and an entire body; or an entire genu, body, and splenium with the exception of the rostrum. The third ventricle may be high riding and interposed between the bodies of the lateral ventricles. (See the images below.)[13, 14, 15] Corpus callosum, agenesis. Axial T1-weighted MRI shows that the lateral ventricles are parallel to each other and do not come into contact with each other as they normally should. Corpus callosum, agenesis. Coronal T1-weighted MRI of the brain shows absence of the normal corpus callosum. The lateral ventricles form a bull's-horn appearance and are indented medially by the Probst bundle (arrows). Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain. Parasagittal section through the lateral ventricle shows dilatation of the atrium and occipital horn (colpocephaly). Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly. The body and splenium of the corpus callosum are well formed, whereas the genu and rostrum are hypoplastic. Corpus callosum, agenesis. Axial T2-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly (same patient as in the previous image). There is fusion across the midline of the inferior basal ganglia (arrow) and the medial cortex of the frontal lobes across the interhemispheric fissure (arrowhead). Loss of the supporting function of the corpus callosum results in upward bulging of the roof of the third ventricle into the interhemispheric fissure. This upward herniation of the distended third ventricle is generally referred to as the interhemispheric cyst, but it should not be confused with a true dorsal or arachnoid cysts of the interhemispheric fissure found in some cases of callosal agenesis. The herniated third ventricle or true cyst may be located in the midline, separating the cerebral hemispheres, or it may be located predominantly to one side of the falx or the other. The herniated third ventricle is of variable size, sometimes extending superiorly all the way to the inner table of the calvaria.
An arachnoid or dorsal cyst generally does not communicate with the third or lateral ventricles, and it may be multiseptated. Hemorrhage may occur within the cysts, markedly changing their signal intensity on MRIs.
Coronal and axial MRI sections are best for demonstrating the longitudinal callosal bundles of Probst. They represent nondecussated callosal fibers. Instead of crossing in the midline, these fibers deviate at the interhemispheric fissure to run along the medial borders of the lateral ventricles from the frontal paraolfactory cortex to the occipital region. Their volume is less than that of the fibers in the normal corpus callosum; they are of different sizes.
The anterior commissure is usually present; occasionally, it is larger or smaller than normal. It is best seen on sagittal or axial T1-weighted images. The hippocampal commissure is usually absent or hypoplastic but sometimes may be enlarged.
The lateral ventricles may have a colpocephalic appearance with a localized dilatation of the atria and occipital horns. The lateral ventricles are pressed upon superomedially by the adjacent bundles, which are more marked in the frontal regions, where the bundles are thickest. They also appear widely separated and are medially concave, with the upper corners turned up and pointed. This finding is called bull's horns or the bat-wing conformation.
The foramen of Monro may be enlarged. The cingulate gyri are not rotated, and the cingulate sulcus is absent; this results in a radial pattern of sulci in the medial surface of the cerebral hemisphere. This finding is helpful in evaluating newborns, in whom the corpus callosum is normally thin.
Often, keyhole dilatation of the temporal horns occurs secondary to incomplete inversion of the hippocampal formation. This finding indicates the intimate relationship between the development of the corpus callosum and the limbic system.
A large percentage of patients with dysgenesis of the corpus callosum have a large interhemispheric cyst, which may or may not communicate with the ventricular system. The cyst is frequently associated with hydrocephalus. The exact origin of the cyst is not known. Some suggest that it is a dilated third ventricle or a true arachnoid cyst. At autopsy, the lining of the cyst may contain ependymal or arachnoid cells. On MRIs, the cyst may have a high protein content; in these cases, the signal intensity on T1-weighted images is greater than that of CSF.
A pericallosal lipoma of the corpus callosum appears as a high–signal-intensity mass on T1-weighted images, usually dorsal to the corpus callosum; it may be associated with callosal dysgenesis.
Degree of confidence
With the exception of US in the sagittal projection, MRI is best for directly visualizing the anatomy of the corpus callosum. The neuropathologic abnormalities intrinsic to callosal dysgenesis, as well as the associated brain anomalies, are portrayed in exquisite detail on sagittal, axial, and coronal MRIs. Only MRI is reliable for detecting subtle partial callosal dysgenesis.False positives/negatives
The differential diagnosis of agenesis is very limited, owing to the characteristic imaging appearance. In certain cases of hydrocephalus in infants, it may sometimes be difficult to visualize a corpus callosum that is very thin. However, with careful observation of sagittal MRI images, the radial convergence of sulci that is seen with ACC is not seen, and a thin corpus may usually be identified. The midline interhemispheric cysts may be confused with midline arachnoid cysts (suprasellar, collicular) or with prominent cavum septum pellucidum and cavum vergae.Ultrasonography
Antenatal diagnosis of agenesis of the corpus callosum (ACC) is possible from about 20 weeks' gestation. Endovaginal US may contribute to the antenatal diagnosis of ACC. Findings that suggest ACC in utero are a disproportionate enlargement of the occipital horns and an abnormally parallel course of the ventricular walls. The abnormal radiating pattern may not be evident until late in the third trimester.[16, 17, 18]
In coronal sonograms, ACC findings include the following:
In coronal sonograms, ACC findings include the following:
- Enlarged atria and occipital horns
- Parallel and widely separated bodies of lateral ventricles
- An enlarged and upwardly displaced third ventricle
- Absent corpus callosum and septum pellucidum
- Frontal horns that are sharply angulated laterally and are indented medially by the Probst bundles
- Medial cerebral gyri and sulci, with a radial pattern extending to the roof of the elevated third ventricle
- Elongation of the interventricular foramen of Monro
Degree of confidence
US, especially transvaginal US, helps in the prenatal diagnosis of nonchromosomal syndromes by enabling the detection of specific morphologic findings. In rare syndromes, the index case may not be diagnosed prenatally, but with subsequent pregnancies, early diagnosis is beneficial. However, MRI has been found to be more helpful than US in the prenatal diagnosis of corpus callosal dysgenesis.[19, 20]Previous
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Contributor Information and Disclosures
Author
Manohar Aribandi, MBBS, MD Senior Consultant Radiologist, Teleradiology Solutions Manohar Aribandi, MBBS, MD is a member of the following medical societies: American Society of Neuroradiology
Disclosure: Nothing to disclose.
Specialty Editor Board
Charles M Glasier, MD Professor, Departments of Radiology and Pediatrics, University of Arkansas for Medical Sciences; Chief, Magnetic Resonance Imaging, Vice-Chief, Pediatric Radiology, Arkansas Children's Hospital Charles M Glasier, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, Radiological Society of North America, and Society for Pediatric Radiology
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
Robert M Krasny, MD Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.
Chief Editor
James G Smirniotopoulos, MD Professor of Radiology, Neurology, and Biomedical Informatics, Program Director, Diagnostic Imaging Program, Center for Neuroscience and Regenerative Medicine (CNRM), Uniformed Services University of the Health Sciences James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.
References
- Barkovich AJ. Pediatric Neuroimaging. 3rd ed. Philadelphia: Lippincott Williams & Wilkins;2000: 254-66.
- Taylor M, David AS. Agenesis of the corpus callosum: a United Kingdom series of 56 cases. J Neurol Neurosurg Psychiatry. Jan 1998;64(1):131-4. [Medline].
- Schell-Apacik CC, Wagner K, Bihler M, Ertl-Wagner B, Heinrich U, Klopocki E, et al. Agenesis and dysgenesis of the corpus callosum: clinical, genetic and neuroimaging findings in a series of 41 patients. Am J Med Genet A. Oct 1 2008;146A(19):2501-11. [Medline].
- Glass HC, Shaw GM, Ma C, Sherr EH. Agenesis of the corpus callosum in California 1983-2003: a population-based study. Am J Med Genet A. Oct 1 2008;146A(19):2495-500. [Medline].
- Paul LK, Brown WS, Adolphs R, Tyszka JM, Richards LJ, Mukherjee P, et al. Agenesis of the corpus callosum: genetic, developmental and functional aspects of connectivity. Nat Rev Neurosci. Apr 2007;8(4):287-99. [Medline].
- Dávila-Gutiérrez G. Agenesis and dysgenesis of the corpus callosum. Semin Pediatr Neurol. Dec 2002;9(4):292-301. [Medline].
- Volpe P, Campobasso G, De Robertis V, Rembouskos G. Disorders of prosencephalic development. Prenat Diagn. Apr 2009;29(4):340-54. [Medline].
- van Bon BW, Koolen DA, Borgatti R, Magee A, Garcia-Minaur S, Rooms L, et al. Clinical and molecular characteristics of 1qter microdeletion syndrome: delineating a critical region for corpus callosum agenesis/hypogenesis. J Med Genet. Jun 2008;45(6):346-54. [Medline].
- Ball WS. Pediatric Neuroradiology. Lippincott-Raven;1997: 160-7.
- Yagishita A. [Imaging of the brain malformations]. Brain Nerve. Apr 2008;60(4):453-62. [Medline].
- Vergani P, Ghidini A, Strobelt N, et al. Prognostic indicators in the prenatal diagnosis of agenesis of corpus callosum. Am J Obstet Gynecol. Mar 1994;170(3):753-8. [Medline].
- Penny SM. Agenesis of the corpus callosum: neonatal sonographic detection. Radiol Technol. Sep-Oct 2006;78(1):14-8. [Medline].
- Barkovich AJ. Apparent atypical callosal dysgenesis: analysis of MR findings and their relationship to holoprocencephaly. AJNR. 1990;11:333-339. [Medline].
- Utsunomiya H, Ogasawara T, Hayashi T, et al. Dysgenesis of the corpus callosum and associated telencephalic anomalies: MRI. Neuroradiology. Apr 1997;39(4):302-10. [Medline].
- Yoshida S, Hayakawa K, Yamamoto A, Aida N, Okano S, Matsushita H, et al. Symmetrical central tegmental tract (CTT) hyperintense lesions on magnetic resonance imaging in children. Eur Radiol. Sep 16 2008;[Medline].
- d'Ercole C, Girard N, Cravello L, et al. Prenatal diagnosis of fetal corpus callosum agenesis by ultrasonography and magnetic resonance imaging. Prenat Diagn. Mar 1998;18(3):247-53. [Medline].
- Tepper R, Zalel Y, Gaon E, et al. Antenatal ultrasonographic findings differentiating complete from partial agenesis of the corpus callosum. Am J Obstet Gynecol. Mar 1996;174(3):877-8. [Medline].
- Hagmann CF, Robertson NJ, Leung WC, Chong KW, Chitty LS. Foetal brain imaging: ultrasound or MRI. A comparison between magnetic resonance imaging and a dedicated multidisciplinary neurosonographic opinion. Acta Paediatr. Apr 2008;97(4):414-9. [Medline].
- Tang PH, Bartha AI, Norton ME, Barkovich AJ, Sherr EH, Glenn OA. Agenesis of the corpus callosum: an MR imaging analysis of associated abnormalities in the fetus. AJNR Am J Neuroradiol. Feb 2009;30(2):257-63. [Medline].
- Wright C, Sibley C, Baker P. The role of fetal magnetic resonance imaging. Arch Dis Child Fetal Neonatal Ed. Feb 10 2009;[Medline].
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows the normal appearance of the corpus callosum.
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows complete absence of the corpus callosum. The cingulate sulcus is absent, and the medial hemispheric sulci reach the third ventricle in a radial fashion.
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the corpus callosum are visualized, whereas the posterior body, splenium, and rostrum are absent.
Corpus callosum, agenesis. Axial nonenhanced CT of the brain shows colpocephaly, caused by dilation of the atria, and occipital horns of the lateral ventricle. Note the parallel configuration of the lateral ventricles. Interdigitation of gyri from fenestration of the falx may be noted incidentally.
Corpus callosum, agenesis. Axial T1-weighted MRI shows that the lateral ventricles are parallel to each other and do not come into contact with each other as they normally should.
Corpus callosum, agenesis. Coronal T1-weighted MRI of the brain shows absence of the normal corpus callosum. The lateral ventricles form a bull's-horn appearance and are indented medially by the Probst bundle (arrows).
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain. Parasagittal section through the lateral ventricle shows dilatation of the atrium and occipital horn (colpocephaly).
Corpus callosum, agenesis. Sagittal T1-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly. The body and splenium of the corpus callosum are well formed, whereas the genu and rostrum are hypoplastic.
Corpus callosum, agenesis. Axial T2-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly (same patient as in the previous image). There is fusion across the midline of the inferior basal ganglia (arrow) and the medial cortex of the frontal lobes across the interhemispheric fissure (arrowhead).
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