dystonias

Pain from the brain: Study reveals how people with a severe unexplained psychological illness have abnormal activity in the brain

Psychogenic diseases, formerly known as ‘hysterical’ illnesses, can have many severe symptoms such as painful cramps or paralysis but without any physical explanation. However, new research from the University of Cambridge and UCL (University College London) suggests that individuals with psychogenic disease, that is to say physical illness that stems from emotional or mental stresses, do have brains that function differently. The research was published today, 25 February, in the journal Brain.

Psychogenic diseases may look very similar to illnesses caused by damage to nerves, the brain or the muscles, or similar to genetic diseases of the nervous system. However, unlike organic diseases, psychogenic diseases do not have any apparent physical cause, making them difficult to diagnose and even more difficult to treat.

“The processes leading to these disorders are poorly understood, complex and highly variable. As a result, treatments are also complex, often lengthy and in many cases there is poor recovery. In order to improve treatment of these disorders, it is important to first understand the underlying mechanism,” said Dr James Rowe from the University of Cambridge.

The study looked at people with either psychogenic or organic dystonia, as well as healthy people with no dystonia. Both types of dystonia caused painful and disabling muscle contractions affecting the leg. The organic patient group had a gene mutation (the DYT1 gene) that caused their dystonia. The psychogenic patients had the symptoms of dystonia but did not have any physical explanation for the disease, even after extensive investigations.

The scientists performed PET brain scans on the volunteers at UCL, to measure the blood flow and brain activity of both of the groups, and healthy volunteers. The participants were scanned with three different foot positions: resting, moving their foot, and holding their leg in a dystonic position. The electrical activity of the leg muscles was measured at the same time to determine which muscles were engaged during the scans.

The researchers found that the brain function of individuals with the psychogenic illness was not normal. The changes were, however, very different from the brains of individuals with the organic (genetic) disease. 

Dr Anette Schrag, from UCL, said: “Finding abnormalities of brain function that are very different from those in the organic form of dystonia opens up a way for researchers to learn how psychological factors can, by changing brain function, lead to physical problems.”

Dr Rowe added: “What struck me was just how very different the abnormal brain function was in patients with the genetic and the psychogenic dystonia. Even more striking was that the differences were there all the time, whether the patients were resting or trying to move.”

Additionally, the researchers found that one part of the brain previously thought to indicate psychogenic disease is unreliable: abnormal activity of the prefrontal cortex was thought to be the hallmark of psychogenic diseases.  In this study, the scientists showed that this abnormality is not unique to psychogenic disease, since activity was also present in the patients with the genetic cause of dystonia when they tried to move their foot. 

Dr Arpan Mehta, from the University of Cambridge, said: “It is interesting that, despite the differences, both types of patient had one thing in common - a problem at the front of the brain. This area controls attention to our movements and although the abnormality is not unique to psychogenic dystonia, it is part of the problem.”

This type of illness is very common. Dr Schrag said: “One in six patients that see a neurologist has a psychogenic illness. They are as ill as someone with organic disease, but with a different cause and different treatment needs. Understanding these disorders, diagnosing them early and finding the right treatment are all clearly very important. We are hopeful that these results might help doctors and patients understand the mechanism leading to this disorder, and guide better treatments.”

Why Cannabis Is the Future of Medicine

The future of medicine rests on the the fundamental right we all have to use things that spring from the Earth naturally as healing agents. Why should cannabis, used for at least 10000 years by humankind to alleviate suffering, be excluded from this inexorable mandate?

The politics of cannabis are exceedingly complex, and yet the truth is simple: this freely growing plant heals the human body – not to mention provides food, fuel, clothing and shelter, if only we will let it perform its birthright. The human body is in many ways pre-designed, or as it were, pre-loaded with a receptiveness to cannabis’ active compounds — cannabinoids — thanks to its well documented endocannabinoid system.

But the medical-industrial complex in the U.S. does not want you to use these freely growing compounds. They threaten its very business model and existence. Which is why it synergizes so naturally with the burgeoning privatized prison sector, which now has the dubious title of having the highest incarceration rate in the world. The statistics don’t lie:

“far surpassing any other nation. For every 100,000 Americans, 743 citizens sit behind bars. Presently, the prison population in America consists of more than six million people, a number exceeding the amount of prisoners held in the gulags of the former Soviet Union at any point in its history.”

According to a recent Al-Jeezera editorial, “One explanation for the boom in the prison population is the mandatory sentencing imposed for drug offences and the “tough on crime” attitude that has prevailed since the 1980s.”

Cannabis / Marijuana is presently on the DEA’s Schedule 1 list.

Since 1972, cannabis has been listed on the Schedule I of the Controlled Substances Act, the most tightly restricted category reserved for drugs which have “no currently accepted medical use”. Opioids, stimulants, psychedelics and a few antidepressants now populate this list of substances that can put you in jail for possessing without a prescription.

The notion that marijuana has no ‘medicinal benefits’ is preposterous, actually. Since time immemorial it has been used as a panacea (‘cure-all’). In fact, as far back as 2727 B.C., cannabis was recorded in the Chinese pharmacopoeia as an effective medicine, and evidence for its use as a food, textile and presumably as a healing agent stretch back even further, to 12 BC.

When it comes to cannabis’ medical applications, cannabis’ ‘healing properties’ is a loaded term. In fact, it is extremely dangerous, as far as the medical industrial complex goes, who has the FDA/FTC to enforce it’s mandate: anything that prevents, diagnoses, treats or cures a disease must be an FDA approved drug by law, i.e. pharmaceutical agents which often have 75 or more adverse effects for each marketed and approved “therapeutic” effect.

Indeed, the dominant, drug-based medical system does not even acknowledge the body’s healing abilities, opting for a view that looks at most bodily suffering as fatalistic, primarily genetically based, and resulting from dysfunction in the mechanical design of a highly entropic ‘bag of enzymes and proteins’ destined to suffer along the trajectory of time.

And so, an at least two trillion dollar a year industry stands between you and access to the disease alleviating properties of this humble plant.

As Emerson said, “a weed is an herb whose virtues have yet to be discovered,” and yet, by this definition, cannabis is not a weed, but given that is has been extensively researched and used for thousands of years for a wide range of health conditions, it should be considered and respected as a medicinal herb and food. Sadly, the fact that the whole herb is non-patentable is the main reason why it is still struggling to gain approval from the powers that be.

Let’s look at the actual, vetted, published and peer-reviewed research – bullet proof, if we are to subscribe to the ‘evidence-based’ model of medicine – which includes over 100 proven therapeutic actions of this amazing plant, featuring the following:

Multiple Sclerosis
Tourette Syndrome
Pain
Obsessive Compulsive Disorder
Brachial Plexus Neuropathies
Insomnia
Multiple Splasticity
Memory Disorders
Social Anxiety Disorders
Amyotrophic Lateral Sclerosis
Inflammatory Bowel Disease
Cancer
Opiate Addiction
Anorexia
Bladder Dysfunction
Bronchial Asthma
Chemotherapy-induced Harm
Constipation
Crack Addiction
Dementia
Fibromyalgia
Glaucoma
Heroin Addiction
Lymphoma
Nausea
Neuropathy
Obesity
Phantom Limb
Spinal Cord Injuries
Endotoxemia
Myocardia Infarction (Heart Attack)
Oxidative Stress
Diabetes: Cataract
Tremor
Cardiac Arrhythmias
Fatigue
Fulminant Liver Failure
Low Immune Function
Aging
Alcohol Toxicity
Allodynia
Arthritis: Rheumatoid
Ascites
Atherosclerosis
Diabetes Type 1
High Cholesterol
Liver Damage
Menopausal Syndrome
Morphine Dependence
Appetite Disorders
Auditory Disease
Dystonia
Epstein-Barr infections
Gynecomasia
Hepatitis
Intestinal permeability
Leukemia
Liver Fibrosis
Migraine Disorders
Oncoviruses
Psoriasis
Thymoma

Moreover, this plant’s therapeutic properties have been subdivided into the following 40+ pharmacological actions:

Analgesic (Pain Killing)
Neuroprotective
Antispasmodic
Anxiolytic
Tumor necrosis factor inhibitor
Anti-inflammatory
Antiproliferative
Apoptotic
Chempreventive
Antidepressive
Antiemetic
Bronchodilator
Anti-metastatic
Anti-neoplastic
Antioxidant
Cardioprotective
Hepatoprotective
Anti-tumor
Enzyme inhibitor
Immunomodulatory
Anti-angiogenic
Autophagy up-regulation
Acetylocholinesterase inhibitor
Anti-platelet
Calcium channel blocker
Cell cycle arrest
Cylooxygenase inhibitor
Glycine agents
Immunomodulatory: T-Cell down-regulation
Intracellular adhesion molecule-1 inducer
Matrix mettaproteinase-1 inhibitor
Neuritohgenic
Platelet Aggregration Inhibito
Vascular Endothelial Growth Factor A inhibitor
Anti-apoptotic
Anti-proliferative
Anti-psychotic
Antiviral
Caspase-3 activation
Chemosensitizer
Immunosupressive agent
Interleukin-6 upregulation

Thanks to modern scientific investigation, it is no longer considered strictly ‘theoretical’ that cannabis has a role to play in medicine. There is a growing movement to wrench back control from the powers that be, whose primary objectives appear to be the subjection of the human body in order to control the population (political motives) — what 20th century French philosopher Michel Foucault termed biopower, and not to awaken true healing powers intrinsic within the body of all self-possessed members of society.

Even the instinct towards recreational use – think of the etymology: to re-create – should be allowed, as long as those who choose to use cannabis instead of tobacco and alcohol (and prescription drugs) do not cause harm to themselves or others. How many deaths are attributed to cannabis each year versus these other societally approved recreational agents, not to mention prescription drugs, which are the 3rd leading cause of death in the developed world?

Ultimately, the politics surrounding cannabis access and the truth about its medicinal properties are so heavily a politicized issue that it is doubtful the science itself will prevail against the distorted lens of media characterizations of it as a ‘dangerous drug,’ and certainly not the iron-clad impasse represented by federal laws against its possession and use.

All we can do is to advocate for the fundamental rights we all possess as free men and women, and our inborn right towards self-possession, i.e as long as what we do does not interfere with the choices and rights of others, we should be free to use an herb/food/textile that sprouts freely and grows freely from this earth, as God/Nature as freely made available.

I think people need to be educated to the fact that marijuana is not a drug. Marijuana is an herb and a flower. God put it here. If He put it here and He wants it to grow, what gives the government the right to say that God is wrong? ~ Willie Nelson

“Why is marijuana against the law? It grows naturally upon our planet. Doesn’t the idea of making nature against the law seem to you a bit … unnatural?” – Bill Hicks

Scientists identify new protein in the neurological disorder dystonia, potential for treatments anticipated

A collaborative discovery involving Kansas State University researchers may lead to the first universal treatment for dystonia, a neurological disorder that affects nearly half a million Americans.

Michal Zolkiewski, associate professor of biochemistry and molecular biophysics at Kansas State University, and Jeffrey Brodsky at the University at Pittsburgh co-led a study that focused on a mutated protein associated with early onset torsion dystonia, or EOTD, the most severe type of dystonia that typically affects adolescents before the age of 20. Dystonia causes involuntary and sustained muscle contractions that can lead to paralysis and abnormal postures.

"It’s a painful and debilitating disease for which there is no cure or treatment that would be effective for all patients," Zolkiewski said. "There are some treatments that are being tested, but nothing is really available to those patients that would cure the symptoms completely."

In addition to Zolkiewski and Brodsky, researchers involved in the study included Hui-Chuan Wu, Kansas State University doctoral student in biochemistry and molecular biophysics, Taiwan, and colleagues at the University of Texas Southwestern Medical Center and the University of Adelaide in Australia.

The Journal of Biological Chemistry recently published the team’s study, "The BiP molecular chaperone plays multiple roles during the biogenesis of TorsinA, a AAA+ ATPase associated with the neurological disease Early-Onset Torsion Dystonia." The study was funded by the Dystonia Medical Research Foundation.

Researchers built the study on a decade-old discovery that patients with early onset torsion dystonia typically have a mutated gene that encodes the protein TorsionA.

"TorsinA is a protein that all people have in their bodies," Zolkiewski said. "It appears to perform an important role in the nervous system, but currently nobody knows what that role is. There also is no understanding of the link between the mutation and dystonia."

In order to study protein expression in a living organism, researchers used yeast — one of the simplest living systems. The yeast was engineered to produce the human protein TorsionA.

Observations revealed that a second protein named BiP — pronounced “dip” — helps process the TorsinA protein and maintain its active form. Additionally, researchers found that BiP also guides TorsinA to being destroyed by cells if the protein is defective. Humans carry the BiP protein as well as the TorsinA protein.

"BiP is a molecular chaperone that assists other proteins in maintaining their function," Zolkiewski said. "In this study we found that BiP really has a dual role. On one hand it’s helping TorsinA and on the other it’s leading to its degradation."

Future studies may focus on BiP as a target for treating dystonia, as modulating BiP in human cells would affect TorsinA, Zolkiewski said.

"Because we don’t know what exactly the function of TorsinA is, we may not be able to design a treatment based on that protein," Zolkiewski said. "We know what BiP does, however. It is a pretty well-studied chaperone, which makes it much easier to work with."

A new twist on neurological disease: U-M discovery could aid patients with dystonia, Parkinson's & more

Twist and hold your neck to the left. Now down, and over to the right, until it hurts. Now imagine your neck – or arms or legs – randomly doing that on their own, without you controlling it.

That’s a taste of what children and adults with a neurological condition called dystonia live with every day – uncontrollable twisting and stiffening of neck and limb muscles.

The mystery of why this happens, and what can prevent or treat it, has long puzzled doctors, who have struggled to help their suffering dystonia patients. Now, new research from a University of Michigan Medical School team may finally open the door to answering those questions and developing new options for patients.

In a new paper in the Journal of Clinical Investigation, the researchers describe new strains of mice they’ve developed that almost perfectly mimic a human form of the disease. They also detail new discoveries about the basic biology of dystonia, made from studying the mice.

They’ll soon make the mice available for researchers everywhere to study, to accelerate understanding of all forms of dystonia and the search for better treatments. The lack of such mice has held back research on dystonia for years.

The U-M team’s success in creating a mouse model for the disease came only after 17 years of stubborn, persistent effort – often in the face of setbacks and failure.

Led by U-M neurologist William Dauer, M.D., the team tried to figure out how and why a gene defect leads to an inherited form of dystonia that, intriguingly, doesn’t start until the pre-teen or teen years, after which it progresses for many years but then stops getting worse after the person reaches their mid-20s.

The gene defect responsible, called DYT1, causes brain cells to make a less-active form of a protein called torsinA. But despite more than a decade of effort by Dauer’s team and many others around the world, no one has been able to translate this information into an animal model with dystonia’s characteristic movements.

Using the childhood onset as a clue, Dauer and his team used cutting-edge genetic technology to severely impair torsinA function during early brain development. This novel twist caused the new mice to closely mimic the human disease: they don’t develop dystonia until they reach preteen age in “mouse years,” and their symptoms stop getting worse after a while.

With this powerful tool in hand, Dauer’s team were now able to peer into the brains of these animals to begin to unravel the mysteries of the disease.

In an unexpected development, they found that the lack of torsinA in the brains of dystonic mice led to the death of neurons – a process called neurodegeneration – in just a few highly localized parts of the brain that control movement. Like the dystonic movements, this neurodegeneration began in young mice, progressed for a time, and then became fixed. 

“We’ve created a model for understanding why certain parts of the brain are more vulnerable to problems from a certain genetic insult,” says Dauer, an associate professor in the U-M departments of Neurology and Cell & Developmental Biology.

“In this case, we’re showing that in dystonia, the lack of this particular protein during a critical window of time is causing cell death. Every disease is telling us something about biology — one just has to listen carefully.”

(Image caption: The brains of the mice with dystonia (shown in the right column) had much higher levels of neuron death than those without the condition (left column) — and this neurodegeneration was limited to certain areas involved in controlling muscle movements.)

More discoveries to come

Dauer and his team don’t yet know why only one-third of human DYT1 gene mutation carriers develop primary dystonia during their school years, and why those who don’t develop the disease before their early 20s will never go on to develop it.

They believe some critical events during the brain’s development in infancy and childhood may have to do with it - and they’re already working to explore that question in mice.

They also believe their mouse model will help them and other researchers understand how dystonia occurs in people who have Parkinson’s disease, Huntington’s disease, or damage caused by a stroke or brain injury. Some people develop dystonia without either a known gene defect or any of these other diagnoses – a condition called idiopathic dystonia.

In all these cases, as in people with DYT1 mutations, dystonia’s twisting and curling motions likely arise from problems in the area of the brain that controls the body’s motor control system.

In other words, something’s going wrong in the process of sending signals to the nerves that control muscles involved in movement. Studying a “pure” form of dystonia using the mice will allow researchers to understand just what’s going on.

The team’s ultimate goal is to find new treatments for all kinds of dystonia. Currently, children, teens and young adults who develop it can take medications or even opt for a form of neurosurgery called deep brain stimulation. But the drugs carry major side effects and are only partially effective – and brain surgery carries its own risks. Dauer and his team are working to screen drug candidates.

my lucky evening

please honey spend some time to read this

oh hi

let me tell you a short story (that happened with me today) in a long ass post

well at 5 pm I had done my last school activity for today and then I accidentally  decided to go for a walk. I’ve got vegetative-vascular dystonia (about which I found out recently) and as my doctor said I have to be outside as often as I can. Then the idea came to my brain that I can go to the shopping center just to look at some things and maybe buy something. I got on a bus and sat. When a conductor gave me my ticket I realized it was a double lucky ticket (lol I just came up with this term. I mean 

  1. 3 first digits are the same as 3 second digits (the order not so important)
  2. the sum of the first 3 digits is the same as the sum of second 3 digits

so that’s why this ticket is  ’double lucky’) (double lol)

Then when I was sitting in the bus and it stopped I saw a guy outside walking and this liTTLE SHIT WAS FUCKING L I K E LUKE MOTHERFUCKIN HEMMINGS. I MEAN HIS FACE WAS REALLY SIMILAR TO LUKE’S HE WAS ALL IN BLACK HE GOT SNAPBACK AND BLONDE HAIR AND HE HAD moTHERFHckING LUKE’S TURNED FUCKING UP NOSE

outfit of that boy from the outside was similar to this ↑ I SWEAR

I was about to jump on my feet and scream ‘STAY FUCKING CALM’ and run out to him. but something stopped me so I kept sitting calmly. (am I lame bc of it or what)

So after, when I was in the shopping center I bought a nice sketchbook. To say a thing, I couldn’t find any sketchbooks for over 3 months. I swear. So it was really lucky to finally buy it. 

Then I just got tired and went to a department store to buy some food. ANd there I FOUND my favourite kind of marshmallows. i was like oh this is happening lol. (my fav marshmallows became really rare so I’m happy everytime when I manage to buy it.) I was freaking glad.

Then I decided to go home by walking. (the way to home was not so close it’s about 1,5 km bUT YES I DECIDED TO WALK)

then I just looked up to the skies and it was so clear. oh god it was so beautiful.

I was walking home and I was god damn engoying. The songs in my earphones were fireproof and then no buses and I felt so free. I literally didn’t pay any attention to people around me. yes. I cought a perfect time. I was enjoying.

When I went home the sunset flooded my room. 

Look at this.

idk I just love sunrises and sunsets. And this smoothed my heart.

in the end of the day I stood on the scale and I saw something good - spending some kind of a busy day gave me -1kg. This hit me like a bus and I fucking felt happy. Like I gathered all described things into the one great thing.

I love this day. yeah. because of these little things I fucking feel happy now. finally. maybe just for a moment but finally.

appreciate the happiness caused by little things.

that’s all.

(don’t judge my sometimes broken english it’s not my first language)

3-D Computer Model May Help Refine Target for Deep Brain Stimulation Therapy for Dystonia

Although deep brain stimulation can be an effective therapy for dystonia – a potentially crippling movement disorder – the treatment isn’t always effective, or benefits may not be immediate. Precise placement of DBS electrodes is one of several factors that can affect results, but few studies have attempted to identify the “sweet spot,” where electrode placement yields the best results.

Researchers led by investigators at Cedars-Sinai, using a complex set of data from records and imaging scans of patients who have undergone successful DBS implantation, have created 3-D, computerized models that map the brain region involved in dystonia. The models identify an anatomical target for further study and provide information for neurologists and neurosurgeons to consider when planning surgery and making device programming decisions.

“We know DBS works as a treatment for dystonia, but we don’t know exactly how it works or why some patients have better, quicker results than others. Patient age, disease duration and other underlying factors have a role, and we believe electrode positioning and device programming are critical, but there is no consensus on ideal device placement and optimal programming strategies,” said Michele Tagliati, MD, director of the Movement Disorders Program in the Department of Neurology at Cedars-Sinai.

“This modeling paves the way for the construction of practical therapeutic and investigational targets,” added Tagliati, senior author of an article now available on the online edition of Annals of Neurology.

Medications usually are the first line of treatment for dystonia and several other movement disorders, but if drugs fail – as frequently happens – or side effects are excessive, neurologists and neurosurgeons may supplement them with deep brain stimulation. Electrical leads are implanted deep in the brain, and a pulse generator is placed near the collarbone. The device is later programmed with a remote, hand-held controller.

To calm the disorganized muscle contractions of dystonia, doctors generally target a brain structure called the globus pallidus, but studies on precise positioning of electrode contacts and the best programming parameters – such as the intensity and frequency of electrical stimulation – are rare and conflicting. Finding the most effective settings can take months of fine-tuning.

In this retrospective study, investigators examined a database of 94 patients with the most common genetic form of dystonia, DYT1, who had been treated with DBS for at least a year. They selected 21 patients who had good responses to treatment, compiled their demographic and treatment information, and used magnetic resonance imaging scans to create 3-D anatomical models with a fine grid to show exact location of relevant brain structures.

The investigators then simulated the placement of electrodes as they were positioned in the patients’ brains and input the actual stimulation parameters into a computer program – a “volume of tissue activation” model – which calculated detailed information specific to each patient and each electrode. The model draws on principles of neurophysiology – the way nerve cells respond to DBS – the biophysics of voltage distribution from electrodes, and the anatomy of the globus pallidus and surrounding structures.

“We found that clinicians were applying relatively large amounts of energy to wide swaths of the globus pallidus, but the area in common among most individuals was much smaller. We interpret this as being the potential ‘target within the target,’ and if our results are validated in further research and clinical practice, computer modeling may offer a physiologically-based, data-driven, visualized approach to clinical decision-making,” Tagliati said.

My 2015 Pitt Dance Marathon Story

Hello Fellow Panthers! On the outside, I probably look totally healthy. Right? However, on the inside, it’s a completely different story. Tonight, I want to share with you the amazing impact that the Children’s Hospital of Pittsburgh has had on my life.

I have been a fighter since the day I was born. I was born deaf and fitted with hearing aids at age 4. Now, fast forward to 2006, when my family moved to Pittsburgh. I was in need of a new audiologist. That was my first experience with Children’s Hospital. Through the years, my hearing became progressively worse until I was profoundly deaf in my left ear. Although I was devastated to have lost my hearing, it was at this point that I met the surgeon that would change my life forever. I underwent the placement of 2 cochlear implants during the summer of 2010.  With intense therapy, I successfully learned to hear. I was constantly amazed at my new hearing world. I could hear my mom calling me from the across the room. I could talk on the phone for the first time in my life and I was able to hear my teammates on the basketball court and the soccer field. With the increased ability to hear, my academic success improved dramatically and my confidence soared. My future was bright!

During the summer between my sophomore and junior years of high school, I injured my finger while on a mission trip and subsequently, had surgery. All seemed to be going well with my recovery until one day in October, while I was at school. I developed excruciating pain in my hand. This led to being diagnosed with Complex Regional Pain Syndrome or CRPS for short. Mine is an aggressive form of CRPS, not typically seen in kids. While I have become somewhat accustomed to living with chronic pain, there are times when I have such severe spasms in my legs that I am unable to walk. These spasms can only be alleviated by a weeklong IV treatment. I was the first patient at Children’s Hospital to undergo a special treatment that is only available in a few hospitals throughout the country. While it isn’t a cure, the treatment regimen that has been customized to treat me, has helped to alleviate some of my pain and other symptoms. Since January 2013, I have had 14 weeklong admissions for these treatments. Without this treatment, I would not have a great quality of life and I would not be the active skier and martial artist I am today. If it were not for the brilliant pain management team at Children’s Hospital, who possess the extraordinary ability to think and treat patients outside of the box, I would not be walking and standing here before you as a fellow Pitt student.

As a result of the Complex Regional Pain Syndrome, I have developed several other conditions that affect my body in various ways. Because some of these conditions are so rare and hard to treat, I have seen and continue to see several different doctors. The specialists I’ve seen at Children’s have been truly outstanding!

Here is a great example of people going the extra mile at Children’s Hospital. In April 2013, complications following a procedure led to me being admitted to the Pediatric Intensive Care Unit or PICU for short. Being in the PICU was especially scary for me because when I got there, the doctors and nurses brought me back from the brink of death and unlike the regular inpatient floors, patients in the PICU have to stay in their rooms. Honestly, that gets pretty boring after a while. One day, my nurse asked if I wanted to play a game. To my surprise, she actually came and played a couple card games with me while we listened to music and talked. She probably had a million other things to do, but for that hour, helping me to feel more comfortable was her priority. This nurse was a shining star in my unexpected PICU experience.

Children’s Hospital provides not only me but countless others hope in the face of adversity and oftentimes, overwhelming odds. Over the years, the doctors, nurses, secretaries, physical therapists, housekeeping staff and even the ladies in the gift shop have become like family. My treatments, procedures, and admissions are brutally difficult, but with so many people rallying their support, it helps to make my situation a little bit easier. I know that there are children much younger than I in very difficult and even life-threatening situations. As I walk the halls of the hospital, I am truly inspired by their fighting spirits. I can’t even begin to imagine my life without all the blessings I have received from the extraordinary staff at Children’s Hospital. Miracles do happen there and I am living proof.

We must stand up together and fight until every child is freed of hospital bracelets and every disease is cured, because no child should have to suffer. As you continue to dance, I want to leave you with these words that have served as my motto since I was four: when the going gets rough, “Keep your chin up and charge the mountain.”

For the Kids! Thank you!

I want to be the reason that your family asks you who it is when you look down at your phone and smile.
#dysautonomia #crps#chronic #pots #potssyndrome #dystonia#wheelchair #potsies#spoonies #passingout #Dysrhythmia#heart #arrhythmia #fiber #makejtthrough #salt #walker#thestruggle#icandoit #school #potsawarness #haters #selfie#spoonie#potsie #kidneys