I believe this letter is long overdue.
I HATE you. I HATE everything about you. I hate how you tend to hide until you become so strong as to take part of me down. You know what I am talking about--my ovary and my kidney. You think you are so smart being so tiny until you advance too often to a point where a person who has you can't recover. You aren't smart. You are a coward.
I HATE how you tried and perhaps succeeded in part to steal away a part of my childhood. I hate even more how you came back into my body six years later--right at the point where we thought I was cured and stole much of my teen years by giving me worry and grief. I let you win back then, didn't I?
I HATE that you again tried to get me in my adult years. You see--I knew in my heart you were in my breasts and I had known for a few months. Finding you there wasn't a huge surprise but it WAS a victory. I may have lost my breasts due to your existence there but guess what cancer. For that part of my body I can have replacements. Also we caught you before you invaded--when you were weak as you truly are.
I HATE that you became a part of my life even before I was born when my 49 year old grandpa lost his body to you.
I HATE that I let you have years 15-30 by worrying and wasting away life convinced you were hiding and would come back and get me. I didn't plan to live but I did. I am now double the age I was when you came back with a vengence with the 1992-1993 relapse. I guess you didn't like that so you came back in my breasts. We got you this time cancer.
I HATE that I must go through more medical testing because I am at extreme risk of you coming back in other places. You need to leave me alone. I vow not to die from you. Do you hear me cancer? I would rather suffer painful, burning death than have you win. You won't win. I will NOT die from cancer of any type. I can be sure of that. In the name of Jesus, I rebuke you abnormal cells. I asked in his name that my cells have enough protein to slow the growth of cells. Yet if it be his will that you have your way with me you STILL won't have me. My father in heaven will have me. You won't be let in there. See he hates cancer and hates seeing his children go through it as much as I do.
Most of all cancer, I HATE that you took so many of my friends before they were even able to vote in a presidental election. Remember Jonathon, cancer? My first friend to fall? Well I have some news for you. You took my 12 year old friend's body but his soul is with Jesus. That's also where Terrie, Milton, Tony, Beth, Ryan, Jamey, Jessica, and the other friends who had cancer end their lives entirely too soon are.
You see cancer. You can't possibly win. You may eventually take down my body but I'm no longer letting you have my soul. You know what else cancer? I vow to tell everyone I know who is diagnosed my experiences so that you can''t steal their childhood, adolescence, and adulthood.
You are nothing more than a left-over from the time of the dinosaurs. Taking families and tearing them apart. Making me have nightmares when you have again reared your ugly self. I hate you cancer. Absolutely despise you. From this point on, I vow to worry much less. I dare to dream of a future where I will be living and seeing my children grow up. That's right cancer. Remember when you came back stage IV ovarian and almost stole my fertility? Well, you didn't. You can't have everything. When all is said and done you may get my body but not my soul. In the name of Jesus you will have neither. So you might as well go back to where you came from.
I'm not letting you win any more. On this date --June 25, 2008 I make this vow. So you might as well run now.
You can also run from my friends Renee and Shelley who have had you visit them this year. I won't let you have them so you might as well give up. As for Carrie's little Zackary---you can forget about having him as well. He's going to live to a ripe old age and give her grandchildren. I claim that. Christ said whatever you believe if you ask in his name it will happen and I have. You have no power over us cancer so go back to Hell where you belong.
I HATE you--you evil disease. You are no longer all of who I am.
Tuesday, June 24, 2008
Friday, June 20, 2008
The beginning
I was born in June 1977--a few weeks early. This takes conception back to fall 1976. On the date of conception it was set that I would have the bizarre condition known as Cowden Syndrome...from wikipedia
Cowden syndrome is an inherited disorder characterized by multiple tumor-like growths called hamartomas and an increased risk of certain forms of cancer. Almost everyone with this condition has hamartomas. These small, noncancerous growths are most commonly found on the skin and mucous membranes (such as the lining of the mouth and nose), but can also occur in the intestinal tract and other parts of the body. People with Cowden syndrome have an increased risk of developing several types of cancer, including cancers of the breast, thyroid, and uterus. Indeed, women with Cowden syndrome have as much as a 25-50% lifetime risk of developing breast cancer. (Robbins & Cotran (2004). Pathological Basis of Disease, 7th Edition. Elsevier, 1134. ) Noncancerous breast and thyroid diseases are also common. Other signs and symptoms of Cowden syndrome can include an enlarged head, a rare noncancerous brain tumor called Lhermitte-Duclos disease.
[edit] Epidemiology
Because Cowden syndrome can be difficult to diagnose, the exact prevalence is unknown; however, it probably occurs in at least 1 in 200,000 people.
[edit] Genetics
Mutations in the PTEN gene cause Cowden syndrome. PTEN is a tumor suppressor gene, which means it helps control the growth and division of cells. Inherited mutations in the PTEN gene have been found in about 80 percent of people with Cowden syndrome. These mutations prevent the PTEN protein from effectively regulating cell survival and division, which can lead to the formation of tumors. Cowden syndrome is one of several inherited diseases caused by mutations in the PTEN gene.
In the other 20 percent of Cowden syndrome cases, the cause is not yet known. Some of these cases may be caused by mutations in a region of DNA that regulates the activity of the PTEN gene.
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, an affected person inherits the mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family. It is characterized by numerous hamartomas, among other symptoms.
The truly bizarre thing is that no one in my family has shown strong symptoms of this and even now we are just beginning to test to see which parent I inherited it from. There had been a strong history of colon cancer in my dad's family line. In late Dec 1976, my paternal grandfather died of metastic colon-rectal cancer at only 49 years old. Three weeks later my maternal grandfather died of a heart attack. My mom was pregnant with me at the time both grandfathers died. I always wondered if that caused all my weird problems---the stress she felt when she lost these important men but learning many years later that I definately have a genetic problem put those thoughts to rest.
When I was born, my neck and back muscles were very underdeveloped. Mom said it either came from my being born a little early or from being so cramped up in her uterus that I couldn't move to develop them. I also had a gigantic head. O.k., more large than gigantic but still large enough for the doctor to wonder if I had hydrocephalus
From wikipedia
Hydrocephalus (pronunciation IPA: /ˌhaɪˌdɹoʊˈsɛfələs/) is a term derived from the Greek words "hydro" meaning water, and "cephalus" meaning head, and this condition is sometimes known as "water on the brain". People with this condition have abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain. This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, and mental disability.
Hydrocephalus is usually due to blockage of CSF outflow in the ventricles or in the subarachnoid space over the brain. In a normal healthy person, CSF continuously circulates through the brain and its ventricles and the spinal cord and is continuously drained away into the circulatory system. In a hydrocephalic situation, the fluid accumulates in the ventricles, and the skull may become enlarged because of the great volume of fluid pressing against the brain and skull. Alternatively, the condition may result from an overproduction of the CSF fluid, from a congenital malformation blocking normal drainage of the fluid, or from complications of head injuries or infections.[1]
Infants and young children with hydrocephalus typically have abnormally large heads, because the pressure of the fluid causes the individual skull bones — which have yet to fuse — to bulge outward at their juncture points. Compression of the brain by the accumulating fluid eventually may cause convulsions and mental retardation. Hydrocephalus occurs in about one out of every 500 live births[2] and was routinely fatal until surgical techniques for shunting the excess fluid out of the central nervous system and into the blood or abdomen were developed.
Usually, hydrocephalus need not cause any intellectual impairment if recognized and properly treated. A massive degree of hydrocephalus rarely exists in normally functioning people, though such a rarity may occur if onset is gradual rather than sudden.[3]
Contents[hide]
1 History
2 Epidemiology
3 Pathology
4 Types of hydrocephalus and their etiologies
4.1 Communicating hydrocephalus
4.2 Non-communicating hydrocephalus
4.3 Congenital hydrocephalus
4.4 Acquired hydrocephalus
5 Symptoms
6 Effects
7 Treatment
7.1 Shunt complications
8 Shunts in Developing Countries
9 Exceptional case
10 See also
11 References
12 External links
//
[edit] History
Hydrocephalus was first described by the ancient Greek physician Hippocrates, but it remained an intractable condition until the 20th century, when shunts and other neurosurgical treatment modalities were developed. The condition has been often informally referred to as "water on the brain".
[edit] Epidemiology
Hydrocephalus affects one in every 500 live births, making it one of the most common birth defects, more common than Down syndrome or deafness.[2] According to the NIH website, there are an estimated 700,000 children and adults living with hydrocephalus, and it is the leading cause of brain surgery for children in the United States. There are over 180 different causes of the condition, one of the most common being brain hemorrhage associated with premature birth.
One of the most performed treatments for hydrocephalus, the cerebral shunt, has not changed much since it was developed in 1960. The shunt must be implanted through neurosurgery into the patient's brain, a procedure which itself may cause brain damage. An estimated 50% of all shunts fail within two years, requiring further surgery to replace the shunts. In the past 25 years, death rates associated with hydrocephalus have decreased from 54% to 5% and the occurrence of intellectual disability has decreased from 62% to 30%.
In the United States, the healthcare costs for hydrocephalus has exceeded $1 billion per year, but is still much less funded than research on other diseases including juvenile diabetes.[4]
[edit] Pathology
The elevated intracranial pressure may cause compression of the brain, leading to brain damage and other complications. Conditions among affected individual vary widely. Children who have had hydrocephalus may have very small ventricles, and presented as the "normal case". This is the problem with this condition.
If the foramina (pl.) of the fourth ventricle or the cerebral aqueduct are blocked, cereobrospinal fluid (CSF) can accumulate within the ventricles. This condition is called internal hydrocephalus and it results in increased CSF pressure. The production of CSF continues, even when the passages that normally allow it to exit the brain are blocked. Consequently, fluid builds inside the brain causing pressure that compresses the nervous tissue and dilates the ventricles. Compression of the nervous tissue usually results in irreversible brain damage. If the skull bones are not completely ossified when the hydrocephalus occurs, the pressure may also severely enlarge the head. The cerebral aqueduct may be blocked at the time of birth or may become blocked later in life because of a tumor growing in the brainstem.
Internal hydrocephalus can be successfully treated by placing a drainage tube (shunt) between the brain ventricles and abdominal cavity to eliminate the high internal pressures. There is some risk of infection being introduced into the brain through these shunts, however, and the shunts must be replaced as the person grows. A subarachnoid hemorrhage may block the return of CSF to the circulation. If CSF accumulates in the subarachnoid space, the condition is called external hydrocephalus. In this condition, pressure is applied to the brain externally, compressing neural tissues and causing brain damage. Thus resulting in further damage of the brain tissue and leading to necrotization
[edit] Types of hydrocephalus and their etiologies
Hydrocephalus can be caused by impaired cerebrospinal fluid (CSF) flow, reabsorption, or excessive CSF production.
The most common cause of hydrocephalus is CSF flow obstruction, hindering the free passage of cerebrospinal fluid through the ventricular system and subarachnoid space (e.g., stenosis of the cerebral aqueduct or obstruction of the interventricular foramina - foramina of Monro secondary to tumors, hemorrhages, infections or congenital malformations).
Hydrocephalus can also be caused by overproduction of cerebrospinal fluid (relative obstruction) (e.g., papilloma of choroid plexus).
Based on its underlying mechanisms, hydrocephalus can be classified into communicating, and non-communicating (obstructive). Both forms can be either congenital, or acquired.
[edit] Communicating hydrocephalus
Communicating hydrocephalus, also known as non-obstructive hydrocephalus, is caused by impaired cerebrospinal fluid resorption in the absence of any CSF-flow obstruction. It has been theorized that this is due to functional impairment of the arachnoid granulations, which are located along the superior sagittal sinus and is the site of cerebrospinal fluid resorption back into the venous system. Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis, Chiari malformation, and congenital absence of arachnoidal granulations (Pacchioni's granulations).
Normal pressure hydrocephalus (NPH) is a particular form of communicating hydrocephalus, characterized by enlarged cerebral ventricles, with only intermittently elevated cerebrospinal fluid pressure. The diagnosis of NPH can be established only with the help of continuous intraventricular pressure recordings (over 24 hours or even longer), since more often than not, instant measurements yield normal pressure values. Dynamic compliance studies may be also helpful. Altered compliance (elasticity) of the ventricular walls, as well as increased viscosity of the cerebrospinal fluid, may play a role in the pathogenesis of normal pressure hydrocephalus.
Main article: normal pressure hydrocephalus
Hydrocephalus ex vacuo also refers to an enlargement of cerebral ventricles and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in dementias), post-traumatic brain injuries and even in some psychiatric disorders, such as schizophrenia. As opposed to hydrocephalus, this is a compensatory enlargement of the CSF-spaces in response to brain parenchyma loss - it is not the result of increased CSF pressure.
[edit] Non-communicating hydrocephalus
Non-communicating hydrocephalus, or obstructive hydrocephalus, is caused by a CSF-flow obstruction (either due to external compression or intraventricular mass lesions).
Foramen of Monro obstruction may lead to dilation of one or, if large enough (e.g., in colloid cyst), both lateral ventricles.
The aqueduct of Sylvius, normally narrow to begin with, may be obstructed by a number of genetically or acquired lesions (e.g., atresia, ependymitis, hemorrhage, tumor) and lead to dilatation of both lateral ventricles as well as the third ventricle.
Fourth ventricle obstruction will lead to dilatation of the aqueduct as well as the lateral and third ventricles.
The foramina of Luschka and foramen of Magendie may be obstructed due to congenital failure of opening (e.g., Dandy-Walker malformation).
The subarachnoid space surrounding the brainstem may also be obstructed due to inflammatory or hemorrhagic fibrosing meningitis, leading to widespread dilatation, including the fourth ventricle.
[edit] Congenital hydrocephalus
The cranial bones fuse by the end of the third year of life. For head enlargement to occur, hydrocephalus must occur before then. The causes are usually genetic but can also be acquired and usually occur within the first few months of life, which include 1) intraventricular matrix hemorrhages in premature infants, 2) infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and stenosis, and 5) Dandy-Walker malformation.
Main articles: Arnold-Chiari malformation and Dandy-Walker malformation
In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th%. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position.
The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in his surroundings. Later on, the upper eyelids become retracted and the eyes are turned downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous. Papilledema is absent but there may be reduction of vision. The head becomes so enlarged that the child may eventually be bedridden.
About 80-90% of fetuses or newborn infants with spina bifida - often associated with meningocele or myelomeningocele - develop.[hydrocephalus.[5]
[edit] Acquired hydrocephalus
This condition is acquired as a consequence of CNS-infections, meningitis, brain tumors, head trauma, intracranial hemorrhage (subarachnoid or intraparenchymal) and is usually extremely painful for the patient.
[edit] Symptoms
Symptoms of increased intracranial pressure may include headaches, vomiting, nausea, papilledema, sleepiness, or coma. Elevated intracranial pressure may result in uncal and/or cerebellar tonsill herniation, with resulting life threatening brain stem compression. For details on other manifestations of increased intracranial pressure:
Main article: intracranial pressure
The triad (Hakim triad) of gait instability, urinary incontinence and dementia is a relatively typical manifestation of the distinct entity normal pressure hydrocephalus (NPH). Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located).
Main article: normal pressure hydrocephalus
[edit] Effects
Because hydrocephalus injures the brain, thought and behavior may be adversely affected. Learning disabilities are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However, the severity of hydrocephalus differs considerably between individuals and some are of average or above average intelligence. Someone with hydrocephalus may have motivation and visual problems, problems with coordination, and may be clumsy. They may hit puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy.
Because the problem resides inside the head, doctors rely heavily upon computer tomography scanning (CT scans), which may be used frequently to evaluate the condition of the disorder throughout the patient's life. Each CT scan exposes the patient to many times the level of x-ray radiation of a chest x-ray. See CT radiation exposure.
[edit] Treatment
Hydrocephalus treatment is surgical. It involves the placement of a ventricular catheter (a tube made of silastic), into the cerebral ventricles to bypass the flow obstruction/malfunctioning arachnoidal granulations and drain the excess fluid into other body cavities, from where it can be resorbed. Most shunts drain the fluid into the peritoneal cavity (ventriculo-peritoneal shunt), but alternative sites include the right atrium (ventriculo-atrial shunt), pleural cavity (ventriculo-pleural shunt), and gallbladder. A shunt system can also be placed in the lumbar space of the spine and have the CSF redirected to the peritoneal cavity (LP Shunt). An alternative treatment for obstructive hydrocephalus in selected patients is the endoscopic third ventriculostomy (ETV), whereby a surgically created opening in the floor of the third ventricle allows the CSF to flow directly to the basal cisterns, thereby shortcutting any obstruction, as in aqueductal stenosis. This may or may not be appropriate based on individual anatomy.
[edit] Shunt complications
Examples of possible complications include shunt malfunction, shunt failure, and shunt infection. Although a shunt generally works well, it may stop working if it disconnects, becomes blocked (clogged), infected, or it is outgrown. If this happens the cerebrospinal fluid will begin to accumulate again and a number of physical symptoms will develop (headaches, nausea, vomiting, photophobia/light sensitivity), some extremely serious, like seizures. The shunt failure rate is also relatively high (some sources site up to 45% chance of shunt failure in the first year following placement) and it is not uncommon for patients to have multiple shunt revisions within their lifetime.
The diagnosis of cerebrospinal fluid buildup is complex and requires specialist expertise.
Another complication can occur when CSF drains more rapidly than it is produced by the choroid plexus, causing symptoms -listlessness, severe headaches, irritability, light sensitivity, auditory hyperesthesia (sound sensitivity), nausea, vomiting, dizziness, vertigo, migraines, seizures, a change in personality, weakness in the arms or legs, strabismus, and double vision - to appear when the patient is vertical. If the patient lies down, the symptoms usually vanish in a short amount of time. A CT scan may or may not show any change in ventricle size, particularly if the patient has a history of slit-like ventricles. Difficulty in diagnosing overdrainage can make treatment of this complication particularly frustrating for patients and their families.
Resistance to traditional analgesic pharmacological therapy may also be a sign of shunt overdrainage or failure. Diagnosis of the particular complication usually depends on when the symptoms appear - that is, whether symptoms occur when the patient is upright or in a prone position, with the head at roughly the same level as the feet.
[edit] Shunts in Developing Countries
Since the cost of shunt systems is beyond the reach of common people in developing countries, most of them die without even getting a shunt. Worse is the rate of revision in shunt systems that adds to the cost of shunting many times. Looking at this point, a study done by Dr. Benjamin C. Warf comparing different shunt systems and highlighting the role of low cost shunt system in most of the developing countries. This study has been published in Journal of Neurosurgery: Pediatrics May 2005 issue. It is about comparing Chhabra shunt system to those of the shunt systems from developed countries. The study was done in Uganda and the shunts were donated by International Federation for Spina Bifida and Hydrocephalus.
[edit] Exceptional case
One interesting case involving a person with past hydrocephalus was a 44-year old French man, whose brain had been reduced to little more than a thin sheet of actual brain tissue, due to the buildup of fluid in his skull. The man, who had a shunt inserted into his head to drain away fluid (which was removed when he was 14), went to a hospital after he had been experiencing mild weakness in his left leg.
DWS: All of the black in the middle is cerebrospinal fluid and the brain matter is the rim of white along the outside of the skull. This is a screen shot from a Fox News report.
In July of 2007, Fox News quoted Dr. Lionel Feuillet of Hopital de la Timone in Marseille as saying: "The images were most unusual... the brain was virtually absent."[6] When doctors learned of the man's medical history, they performed a computed tomography (CT) scan and magnetic resonance imaging (MRI) scan, and were astonished to see "massive enlargement" of the lateral ventricles in the skull. Intelligence tests showed the man had an IQ of 75, below the average score of 100 but not considered mentally retarded or disabled, either.
Remarkably, the man was a married father of two children, and worked as a civil servant, leading a normal life, despite having little brain tissue. "What I find amazing to this day is how the brain can deal with something which you think should not be compatible with life," commented Dr. Max Muenke, a pediatric brain defect specialist at the National Human Genome Research Institute. "If something happens very slowly over quite some time, maybe over decades, the different parts of the brain take up functions that would normally be done by the part that is pushed to the side."[7]
To find out if I had this, we had to travel to Memphis, TN. Memphis is a three hour drive from where we lived but it was the nearest place to have a ct-scan machine. This was the only way of telling if I had hydrocephalus. The answer was no. There was a fluid issue but not to the extent of being hydrocephalus. The machine didn't show this but a 1977-1978 ct machine was very primitive. Twenty seven years later my son would go through the same testing based on the same fear and this would be his diagnosis so it was likely mine as well but back in the late 1970's things weren't as clear as they were in 2004.
My mom said the doctors placed me on therapy to strengthen my back and neck muscles and I hated it. While my two weeks older cousin was about to begin crawling, I was still not lifting my head off the floor. The exercises caught me up and I walked at 13 months old--a little late but no later than my dad who hadn't went through what I had.
The first years of my life were normal except for one thing. From about age 3 to age 9, I would wake up in the morning with a flat stomach and by the end of the day I looked like a starving Ethiopian kid from swelling. Doctors insisted it was me swallowing air. Mom said she never felt like that answer was good enough but took it until events went downhill enough for us to find the true cause of the swelling. Prior to this, I had my first true experience with something related to Cowden Syndrome. Though hemangiomas are rare, they do happen and in 1984 when I was 6, my mom found one.
She had no idea what it was. I will never forget the fear in her voice. My parents spoiled me and my mom was still washing my hair when I was 6. She liked to do it in the kitchen sink. I remember looking down the drain many times wondering when she would be done with washing my hair so I could play. This particular day was different. I heard her scared voice say "I have found a lump." She could see my pulse beating inside the lump. She had me put my finger up there and I felt it as well. I thought it was weird but didn't know why she was so scared. Though I had experience with kids becoming sick and dying at that point--my cousin lost her life in an accident the year prior to this, I thought kids always died by accident. I didn't understand the seriousness. I thought of it a lot like I did when my cousin and I were playing in the swingset that same year and I got hit in the head with the two seated swing. I was bleeding very badly and mom was set to take me to the emergency room but my aunt was there and she calmly took me to the restroom and once the blood was washed away it was obvious there was only a small scratch there. I thought mom was overreacting about the lump but went with her to see the doctor.
To rule out aneurysm (though at that point no one was known to have this problem in my family), I underwent my first operation in Jan. 1984 (a side note--my dad had aneurysm burst on his brain 10 years after this surgery and made it through it despite terrible odds).
It was held at Lebonheur Children's Hospital. I have very faded and dark memories of it. I remember the waiting room before going back. We had been allowed to pick out a gift and I can't remember what I chose though I think it was a necklace. The anesthesiologist asked me what "flavor" of gas I wanted. Strawberries have always been my favorite everything so that was the answer.
The last thing I remember was thinking "this tastes awful--nothing like strawberries" and then--darkness.
I don't remember recovery room and I praise the Lord for it because with all twenty something operations it has been the roughest part of the operation. I have a gap in my memory until right before I was allowed to leave. I was prancing up and down the hallway trying to release some of the six year old energy I had when I heard a small voice say "come in my room."
I have always been shy but back then it wasn't nearly as bad. Still, I hesitated. The voice sounded nice but I knew you never could tell. My dad had been with me and he told me to go in--so I did.
When I walked in, I saw a girl who looked about my own age in bed. She had her leg attached to something that was attached to the ceiling. I whispered to my dad and he said she apparently broke it. What she said next confirmed it. She seemed very chipper and was really nice. I almost hated going home but already a part of me hated Memphis, TN and I was ready to go. The little girl's name was Amanda and she was about 1 1/2 years older than me. We traded addresses. We kept in touch until not long before I would first be diagnosed with cancer. Our parents wrote our letters because neither of us could write very well. My dad told me that Amanda had spinal bifida. He tried to explain to me what that meant and that she might die young as my cousin had but a young mind has a way of blocking out the bad. I decided she quit writing because we grew apart though my dad did bring up she could have died. I was sure that wasn't it. Kids die in accidents and not by illness. As a matter of fact, a year later I told my Sunday school teacher that if someone sat home and didn't leave they couldn't have a car accident and die, if they ate right and exercised they would be healthy, etc--how does someone die if they do everything perfectly? By age 9, I would know.
The surgery showed an AV malformation. After it was done, I no longer had nosebleeds and life was normal. Until age 9 when things got very confusing for me and my parents world seemed to be crashing down on them.
Cowden syndrome is an inherited disorder characterized by multiple tumor-like growths called hamartomas and an increased risk of certain forms of cancer. Almost everyone with this condition has hamartomas. These small, noncancerous growths are most commonly found on the skin and mucous membranes (such as the lining of the mouth and nose), but can also occur in the intestinal tract and other parts of the body. People with Cowden syndrome have an increased risk of developing several types of cancer, including cancers of the breast, thyroid, and uterus. Indeed, women with Cowden syndrome have as much as a 25-50% lifetime risk of developing breast cancer. (Robbins & Cotran (2004). Pathological Basis of Disease, 7th Edition. Elsevier, 1134. ) Noncancerous breast and thyroid diseases are also common. Other signs and symptoms of Cowden syndrome can include an enlarged head, a rare noncancerous brain tumor called Lhermitte-Duclos disease.
[edit] Epidemiology
Because Cowden syndrome can be difficult to diagnose, the exact prevalence is unknown; however, it probably occurs in at least 1 in 200,000 people.
[edit] Genetics
Mutations in the PTEN gene cause Cowden syndrome. PTEN is a tumor suppressor gene, which means it helps control the growth and division of cells. Inherited mutations in the PTEN gene have been found in about 80 percent of people with Cowden syndrome. These mutations prevent the PTEN protein from effectively regulating cell survival and division, which can lead to the formation of tumors. Cowden syndrome is one of several inherited diseases caused by mutations in the PTEN gene.
In the other 20 percent of Cowden syndrome cases, the cause is not yet known. Some of these cases may be caused by mutations in a region of DNA that regulates the activity of the PTEN gene.
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, an affected person inherits the mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family. It is characterized by numerous hamartomas, among other symptoms.
The truly bizarre thing is that no one in my family has shown strong symptoms of this and even now we are just beginning to test to see which parent I inherited it from. There had been a strong history of colon cancer in my dad's family line. In late Dec 1976, my paternal grandfather died of metastic colon-rectal cancer at only 49 years old. Three weeks later my maternal grandfather died of a heart attack. My mom was pregnant with me at the time both grandfathers died. I always wondered if that caused all my weird problems---the stress she felt when she lost these important men but learning many years later that I definately have a genetic problem put those thoughts to rest.
When I was born, my neck and back muscles were very underdeveloped. Mom said it either came from my being born a little early or from being so cramped up in her uterus that I couldn't move to develop them. I also had a gigantic head. O.k., more large than gigantic but still large enough for the doctor to wonder if I had hydrocephalus
From wikipedia
Hydrocephalus (pronunciation IPA: /ˌhaɪˌdɹoʊˈsɛfələs/) is a term derived from the Greek words "hydro" meaning water, and "cephalus" meaning head, and this condition is sometimes known as "water on the brain". People with this condition have abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain. This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, and mental disability.
Hydrocephalus is usually due to blockage of CSF outflow in the ventricles or in the subarachnoid space over the brain. In a normal healthy person, CSF continuously circulates through the brain and its ventricles and the spinal cord and is continuously drained away into the circulatory system. In a hydrocephalic situation, the fluid accumulates in the ventricles, and the skull may become enlarged because of the great volume of fluid pressing against the brain and skull. Alternatively, the condition may result from an overproduction of the CSF fluid, from a congenital malformation blocking normal drainage of the fluid, or from complications of head injuries or infections.[1]
Infants and young children with hydrocephalus typically have abnormally large heads, because the pressure of the fluid causes the individual skull bones — which have yet to fuse — to bulge outward at their juncture points. Compression of the brain by the accumulating fluid eventually may cause convulsions and mental retardation. Hydrocephalus occurs in about one out of every 500 live births[2] and was routinely fatal until surgical techniques for shunting the excess fluid out of the central nervous system and into the blood or abdomen were developed.
Usually, hydrocephalus need not cause any intellectual impairment if recognized and properly treated. A massive degree of hydrocephalus rarely exists in normally functioning people, though such a rarity may occur if onset is gradual rather than sudden.[3]
Contents[hide]
1 History
2 Epidemiology
3 Pathology
4 Types of hydrocephalus and their etiologies
4.1 Communicating hydrocephalus
4.2 Non-communicating hydrocephalus
4.3 Congenital hydrocephalus
4.4 Acquired hydrocephalus
5 Symptoms
6 Effects
7 Treatment
7.1 Shunt complications
8 Shunts in Developing Countries
9 Exceptional case
10 See also
11 References
12 External links
//
[edit] History
Hydrocephalus was first described by the ancient Greek physician Hippocrates, but it remained an intractable condition until the 20th century, when shunts and other neurosurgical treatment modalities were developed. The condition has been often informally referred to as "water on the brain".
[edit] Epidemiology
Hydrocephalus affects one in every 500 live births, making it one of the most common birth defects, more common than Down syndrome or deafness.[2] According to the NIH website, there are an estimated 700,000 children and adults living with hydrocephalus, and it is the leading cause of brain surgery for children in the United States. There are over 180 different causes of the condition, one of the most common being brain hemorrhage associated with premature birth.
One of the most performed treatments for hydrocephalus, the cerebral shunt, has not changed much since it was developed in 1960. The shunt must be implanted through neurosurgery into the patient's brain, a procedure which itself may cause brain damage. An estimated 50% of all shunts fail within two years, requiring further surgery to replace the shunts. In the past 25 years, death rates associated with hydrocephalus have decreased from 54% to 5% and the occurrence of intellectual disability has decreased from 62% to 30%.
In the United States, the healthcare costs for hydrocephalus has exceeded $1 billion per year, but is still much less funded than research on other diseases including juvenile diabetes.[4]
[edit] Pathology
The elevated intracranial pressure may cause compression of the brain, leading to brain damage and other complications. Conditions among affected individual vary widely. Children who have had hydrocephalus may have very small ventricles, and presented as the "normal case". This is the problem with this condition.
If the foramina (pl.) of the fourth ventricle or the cerebral aqueduct are blocked, cereobrospinal fluid (CSF) can accumulate within the ventricles. This condition is called internal hydrocephalus and it results in increased CSF pressure. The production of CSF continues, even when the passages that normally allow it to exit the brain are blocked. Consequently, fluid builds inside the brain causing pressure that compresses the nervous tissue and dilates the ventricles. Compression of the nervous tissue usually results in irreversible brain damage. If the skull bones are not completely ossified when the hydrocephalus occurs, the pressure may also severely enlarge the head. The cerebral aqueduct may be blocked at the time of birth or may become blocked later in life because of a tumor growing in the brainstem.
Internal hydrocephalus can be successfully treated by placing a drainage tube (shunt) between the brain ventricles and abdominal cavity to eliminate the high internal pressures. There is some risk of infection being introduced into the brain through these shunts, however, and the shunts must be replaced as the person grows. A subarachnoid hemorrhage may block the return of CSF to the circulation. If CSF accumulates in the subarachnoid space, the condition is called external hydrocephalus. In this condition, pressure is applied to the brain externally, compressing neural tissues and causing brain damage. Thus resulting in further damage of the brain tissue and leading to necrotization
[edit] Types of hydrocephalus and their etiologies
Hydrocephalus can be caused by impaired cerebrospinal fluid (CSF) flow, reabsorption, or excessive CSF production.
The most common cause of hydrocephalus is CSF flow obstruction, hindering the free passage of cerebrospinal fluid through the ventricular system and subarachnoid space (e.g., stenosis of the cerebral aqueduct or obstruction of the interventricular foramina - foramina of Monro secondary to tumors, hemorrhages, infections or congenital malformations).
Hydrocephalus can also be caused by overproduction of cerebrospinal fluid (relative obstruction) (e.g., papilloma of choroid plexus).
Based on its underlying mechanisms, hydrocephalus can be classified into communicating, and non-communicating (obstructive). Both forms can be either congenital, or acquired.
[edit] Communicating hydrocephalus
Communicating hydrocephalus, also known as non-obstructive hydrocephalus, is caused by impaired cerebrospinal fluid resorption in the absence of any CSF-flow obstruction. It has been theorized that this is due to functional impairment of the arachnoid granulations, which are located along the superior sagittal sinus and is the site of cerebrospinal fluid resorption back into the venous system. Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis, Chiari malformation, and congenital absence of arachnoidal granulations (Pacchioni's granulations).
Normal pressure hydrocephalus (NPH) is a particular form of communicating hydrocephalus, characterized by enlarged cerebral ventricles, with only intermittently elevated cerebrospinal fluid pressure. The diagnosis of NPH can be established only with the help of continuous intraventricular pressure recordings (over 24 hours or even longer), since more often than not, instant measurements yield normal pressure values. Dynamic compliance studies may be also helpful. Altered compliance (elasticity) of the ventricular walls, as well as increased viscosity of the cerebrospinal fluid, may play a role in the pathogenesis of normal pressure hydrocephalus.
Main article: normal pressure hydrocephalus
Hydrocephalus ex vacuo also refers to an enlargement of cerebral ventricles and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in dementias), post-traumatic brain injuries and even in some psychiatric disorders, such as schizophrenia. As opposed to hydrocephalus, this is a compensatory enlargement of the CSF-spaces in response to brain parenchyma loss - it is not the result of increased CSF pressure.
[edit] Non-communicating hydrocephalus
Non-communicating hydrocephalus, or obstructive hydrocephalus, is caused by a CSF-flow obstruction (either due to external compression or intraventricular mass lesions).
Foramen of Monro obstruction may lead to dilation of one or, if large enough (e.g., in colloid cyst), both lateral ventricles.
The aqueduct of Sylvius, normally narrow to begin with, may be obstructed by a number of genetically or acquired lesions (e.g., atresia, ependymitis, hemorrhage, tumor) and lead to dilatation of both lateral ventricles as well as the third ventricle.
Fourth ventricle obstruction will lead to dilatation of the aqueduct as well as the lateral and third ventricles.
The foramina of Luschka and foramen of Magendie may be obstructed due to congenital failure of opening (e.g., Dandy-Walker malformation).
The subarachnoid space surrounding the brainstem may also be obstructed due to inflammatory or hemorrhagic fibrosing meningitis, leading to widespread dilatation, including the fourth ventricle.
[edit] Congenital hydrocephalus
The cranial bones fuse by the end of the third year of life. For head enlargement to occur, hydrocephalus must occur before then. The causes are usually genetic but can also be acquired and usually occur within the first few months of life, which include 1) intraventricular matrix hemorrhages in premature infants, 2) infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and stenosis, and 5) Dandy-Walker malformation.
Main articles: Arnold-Chiari malformation and Dandy-Walker malformation
In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th%. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position.
The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in his surroundings. Later on, the upper eyelids become retracted and the eyes are turned downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous. Papilledema is absent but there may be reduction of vision. The head becomes so enlarged that the child may eventually be bedridden.
About 80-90% of fetuses or newborn infants with spina bifida - often associated with meningocele or myelomeningocele - develop.[hydrocephalus.[5]
[edit] Acquired hydrocephalus
This condition is acquired as a consequence of CNS-infections, meningitis, brain tumors, head trauma, intracranial hemorrhage (subarachnoid or intraparenchymal) and is usually extremely painful for the patient.
[edit] Symptoms
Symptoms of increased intracranial pressure may include headaches, vomiting, nausea, papilledema, sleepiness, or coma. Elevated intracranial pressure may result in uncal and/or cerebellar tonsill herniation, with resulting life threatening brain stem compression. For details on other manifestations of increased intracranial pressure:
Main article: intracranial pressure
The triad (Hakim triad) of gait instability, urinary incontinence and dementia is a relatively typical manifestation of the distinct entity normal pressure hydrocephalus (NPH). Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located).
Main article: normal pressure hydrocephalus
[edit] Effects
Because hydrocephalus injures the brain, thought and behavior may be adversely affected. Learning disabilities are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However, the severity of hydrocephalus differs considerably between individuals and some are of average or above average intelligence. Someone with hydrocephalus may have motivation and visual problems, problems with coordination, and may be clumsy. They may hit puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy.
Because the problem resides inside the head, doctors rely heavily upon computer tomography scanning (CT scans), which may be used frequently to evaluate the condition of the disorder throughout the patient's life. Each CT scan exposes the patient to many times the level of x-ray radiation of a chest x-ray. See CT radiation exposure.
[edit] Treatment
Hydrocephalus treatment is surgical. It involves the placement of a ventricular catheter (a tube made of silastic), into the cerebral ventricles to bypass the flow obstruction/malfunctioning arachnoidal granulations and drain the excess fluid into other body cavities, from where it can be resorbed. Most shunts drain the fluid into the peritoneal cavity (ventriculo-peritoneal shunt), but alternative sites include the right atrium (ventriculo-atrial shunt), pleural cavity (ventriculo-pleural shunt), and gallbladder. A shunt system can also be placed in the lumbar space of the spine and have the CSF redirected to the peritoneal cavity (LP Shunt). An alternative treatment for obstructive hydrocephalus in selected patients is the endoscopic third ventriculostomy (ETV), whereby a surgically created opening in the floor of the third ventricle allows the CSF to flow directly to the basal cisterns, thereby shortcutting any obstruction, as in aqueductal stenosis. This may or may not be appropriate based on individual anatomy.
[edit] Shunt complications
Examples of possible complications include shunt malfunction, shunt failure, and shunt infection. Although a shunt generally works well, it may stop working if it disconnects, becomes blocked (clogged), infected, or it is outgrown. If this happens the cerebrospinal fluid will begin to accumulate again and a number of physical symptoms will develop (headaches, nausea, vomiting, photophobia/light sensitivity), some extremely serious, like seizures. The shunt failure rate is also relatively high (some sources site up to 45% chance of shunt failure in the first year following placement) and it is not uncommon for patients to have multiple shunt revisions within their lifetime.
The diagnosis of cerebrospinal fluid buildup is complex and requires specialist expertise.
Another complication can occur when CSF drains more rapidly than it is produced by the choroid plexus, causing symptoms -listlessness, severe headaches, irritability, light sensitivity, auditory hyperesthesia (sound sensitivity), nausea, vomiting, dizziness, vertigo, migraines, seizures, a change in personality, weakness in the arms or legs, strabismus, and double vision - to appear when the patient is vertical. If the patient lies down, the symptoms usually vanish in a short amount of time. A CT scan may or may not show any change in ventricle size, particularly if the patient has a history of slit-like ventricles. Difficulty in diagnosing overdrainage can make treatment of this complication particularly frustrating for patients and their families.
Resistance to traditional analgesic pharmacological therapy may also be a sign of shunt overdrainage or failure. Diagnosis of the particular complication usually depends on when the symptoms appear - that is, whether symptoms occur when the patient is upright or in a prone position, with the head at roughly the same level as the feet.
[edit] Shunts in Developing Countries
Since the cost of shunt systems is beyond the reach of common people in developing countries, most of them die without even getting a shunt. Worse is the rate of revision in shunt systems that adds to the cost of shunting many times. Looking at this point, a study done by Dr. Benjamin C. Warf comparing different shunt systems and highlighting the role of low cost shunt system in most of the developing countries. This study has been published in Journal of Neurosurgery: Pediatrics May 2005 issue. It is about comparing Chhabra shunt system to those of the shunt systems from developed countries. The study was done in Uganda and the shunts were donated by International Federation for Spina Bifida and Hydrocephalus.
[edit] Exceptional case
One interesting case involving a person with past hydrocephalus was a 44-year old French man, whose brain had been reduced to little more than a thin sheet of actual brain tissue, due to the buildup of fluid in his skull. The man, who had a shunt inserted into his head to drain away fluid (which was removed when he was 14), went to a hospital after he had been experiencing mild weakness in his left leg.
DWS: All of the black in the middle is cerebrospinal fluid and the brain matter is the rim of white along the outside of the skull. This is a screen shot from a Fox News report.
In July of 2007, Fox News quoted Dr. Lionel Feuillet of Hopital de la Timone in Marseille as saying: "The images were most unusual... the brain was virtually absent."[6] When doctors learned of the man's medical history, they performed a computed tomography (CT) scan and magnetic resonance imaging (MRI) scan, and were astonished to see "massive enlargement" of the lateral ventricles in the skull. Intelligence tests showed the man had an IQ of 75, below the average score of 100 but not considered mentally retarded or disabled, either.
Remarkably, the man was a married father of two children, and worked as a civil servant, leading a normal life, despite having little brain tissue. "What I find amazing to this day is how the brain can deal with something which you think should not be compatible with life," commented Dr. Max Muenke, a pediatric brain defect specialist at the National Human Genome Research Institute. "If something happens very slowly over quite some time, maybe over decades, the different parts of the brain take up functions that would normally be done by the part that is pushed to the side."[7]
To find out if I had this, we had to travel to Memphis, TN. Memphis is a three hour drive from where we lived but it was the nearest place to have a ct-scan machine. This was the only way of telling if I had hydrocephalus. The answer was no. There was a fluid issue but not to the extent of being hydrocephalus. The machine didn't show this but a 1977-1978 ct machine was very primitive. Twenty seven years later my son would go through the same testing based on the same fear and this would be his diagnosis so it was likely mine as well but back in the late 1970's things weren't as clear as they were in 2004.
My mom said the doctors placed me on therapy to strengthen my back and neck muscles and I hated it. While my two weeks older cousin was about to begin crawling, I was still not lifting my head off the floor. The exercises caught me up and I walked at 13 months old--a little late but no later than my dad who hadn't went through what I had.
The first years of my life were normal except for one thing. From about age 3 to age 9, I would wake up in the morning with a flat stomach and by the end of the day I looked like a starving Ethiopian kid from swelling. Doctors insisted it was me swallowing air. Mom said she never felt like that answer was good enough but took it until events went downhill enough for us to find the true cause of the swelling. Prior to this, I had my first true experience with something related to Cowden Syndrome. Though hemangiomas are rare, they do happen and in 1984 when I was 6, my mom found one.
She had no idea what it was. I will never forget the fear in her voice. My parents spoiled me and my mom was still washing my hair when I was 6. She liked to do it in the kitchen sink. I remember looking down the drain many times wondering when she would be done with washing my hair so I could play. This particular day was different. I heard her scared voice say "I have found a lump." She could see my pulse beating inside the lump. She had me put my finger up there and I felt it as well. I thought it was weird but didn't know why she was so scared. Though I had experience with kids becoming sick and dying at that point--my cousin lost her life in an accident the year prior to this, I thought kids always died by accident. I didn't understand the seriousness. I thought of it a lot like I did when my cousin and I were playing in the swingset that same year and I got hit in the head with the two seated swing. I was bleeding very badly and mom was set to take me to the emergency room but my aunt was there and she calmly took me to the restroom and once the blood was washed away it was obvious there was only a small scratch there. I thought mom was overreacting about the lump but went with her to see the doctor.
To rule out aneurysm (though at that point no one was known to have this problem in my family), I underwent my first operation in Jan. 1984 (a side note--my dad had aneurysm burst on his brain 10 years after this surgery and made it through it despite terrible odds).
It was held at Lebonheur Children's Hospital. I have very faded and dark memories of it. I remember the waiting room before going back. We had been allowed to pick out a gift and I can't remember what I chose though I think it was a necklace. The anesthesiologist asked me what "flavor" of gas I wanted. Strawberries have always been my favorite everything so that was the answer.
The last thing I remember was thinking "this tastes awful--nothing like strawberries" and then--darkness.
I don't remember recovery room and I praise the Lord for it because with all twenty something operations it has been the roughest part of the operation. I have a gap in my memory until right before I was allowed to leave. I was prancing up and down the hallway trying to release some of the six year old energy I had when I heard a small voice say "come in my room."
I have always been shy but back then it wasn't nearly as bad. Still, I hesitated. The voice sounded nice but I knew you never could tell. My dad had been with me and he told me to go in--so I did.
When I walked in, I saw a girl who looked about my own age in bed. She had her leg attached to something that was attached to the ceiling. I whispered to my dad and he said she apparently broke it. What she said next confirmed it. She seemed very chipper and was really nice. I almost hated going home but already a part of me hated Memphis, TN and I was ready to go. The little girl's name was Amanda and she was about 1 1/2 years older than me. We traded addresses. We kept in touch until not long before I would first be diagnosed with cancer. Our parents wrote our letters because neither of us could write very well. My dad told me that Amanda had spinal bifida. He tried to explain to me what that meant and that she might die young as my cousin had but a young mind has a way of blocking out the bad. I decided she quit writing because we grew apart though my dad did bring up she could have died. I was sure that wasn't it. Kids die in accidents and not by illness. As a matter of fact, a year later I told my Sunday school teacher that if someone sat home and didn't leave they couldn't have a car accident and die, if they ate right and exercised they would be healthy, etc--how does someone die if they do everything perfectly? By age 9, I would know.
The surgery showed an AV malformation. After it was done, I no longer had nosebleeds and life was normal. Until age 9 when things got very confusing for me and my parents world seemed to be crashing down on them.
To Little Rock-to Pocahontas-to Little Rock- to Pocahontas
My surgery for breast implants was nine days ago. Already I have been back to Little Rock. It was supposed to be twice actually--my geneticist appointment fell through due to him having a meeting. My dad will take me to Little Rock on Monday where I again have to bare my breasts (or what used to be my breasts--not sure what you say after you have a masectomy and reconstruction is mostly done) and hear about how they won't look like this in the end--thank you Jesus. I have ripples starting to form in one of them and I don't like it. However, I look at how it was fifty years ago when women couldn't have recontruction at all and feel blessed.
On each of these trips to and from Little Rock, I find myself lying down in the backseat wondering when it will end and looking up the backseat window at what has been big fluffy clouds each trip since coming home from the surgery. I have seen every thing you can imagine in those clouds. Mostly good things--butterflies and angels but when the pain comes in it turns more into bats and demons until the pain meds take away most of the pain and I fall asleep.
As Shawn and I sat waiting on Dr H for my first post-op appointment this past week, I told him if I had back all the time waiting on doctors, going through surgery and recovery time, time spent worrying over whether or not I would survive cancer and now Cowden's; I would be about 19 years old again. Would I want that time back? That's something I've been wondering. Always before I would have said yes but now I'm not so sure.
I've read some interesting things lately that make so much sense. If I had back that time--if my life had been normal as far as most people's lives are--where would I be? I read a quote that God has to break us down to build us back up again. If this is so, I am hoping that I am as broken down as it gets and I'm ready to be built back up again.
The psychological effects of the masectomy have started. This past surgery also involved the removal of my nipples because back in Feb when it was done we didn't realize cancer was being removed--we thought it was preventative. Two weeks later we found out it saved my life. It explained the nagging feeling I had for two years to get looked at because things were not normal in any way in there though I was being told fibrocystic was the issue. That was a whole other issue. Things had went bad in there and I was diagnosed with ductal carcinoma in situ in both breasts--affecting 70% of one and 60% of the other.
In situ meant the masectomy would have been recommended treatment anyway. If reconstruction hadn't been an option then I don't know if I would have had the "preventative" treatment. Because of all the cysts, they likely wouldn't have found the cancer until it had became invasive and my kids could have lost their mom before either of them even reached the age of 10.
I've had my thyroid gland removed, a kidney, an ovary, etc but those were different. Though I could see the scar on the outside the missing organs were from the inside and maybe in a way I have been trying to pretend I haven't lost them? Seeing my implants and myself without nipples brought it home to me that I have lost a lot more than just my breasts. I worry now about my extreme risk of other cancers but I'm trying to keep it under control. There's not a lot more of me that can be lost before that's it for this body. All due to a genetic fluke that happened some time in the fall of 1976 when I was conceived. A condition that approximately 1 in 250,000 people have and almost none of them have it affect them as severely as it has me--or at least as early as it has me. Most people present with skin tags in their late 20's. I had those skin tags (removed for now during the implant surgery) begin during my pregnancy with Hannah more than three years ago. Everything else began early. Starting in 1984 when I was 6.
On each of these trips to and from Little Rock, I find myself lying down in the backseat wondering when it will end and looking up the backseat window at what has been big fluffy clouds each trip since coming home from the surgery. I have seen every thing you can imagine in those clouds. Mostly good things--butterflies and angels but when the pain comes in it turns more into bats and demons until the pain meds take away most of the pain and I fall asleep.
As Shawn and I sat waiting on Dr H for my first post-op appointment this past week, I told him if I had back all the time waiting on doctors, going through surgery and recovery time, time spent worrying over whether or not I would survive cancer and now Cowden's; I would be about 19 years old again. Would I want that time back? That's something I've been wondering. Always before I would have said yes but now I'm not so sure.
I've read some interesting things lately that make so much sense. If I had back that time--if my life had been normal as far as most people's lives are--where would I be? I read a quote that God has to break us down to build us back up again. If this is so, I am hoping that I am as broken down as it gets and I'm ready to be built back up again.
The psychological effects of the masectomy have started. This past surgery also involved the removal of my nipples because back in Feb when it was done we didn't realize cancer was being removed--we thought it was preventative. Two weeks later we found out it saved my life. It explained the nagging feeling I had for two years to get looked at because things were not normal in any way in there though I was being told fibrocystic was the issue. That was a whole other issue. Things had went bad in there and I was diagnosed with ductal carcinoma in situ in both breasts--affecting 70% of one and 60% of the other.
In situ meant the masectomy would have been recommended treatment anyway. If reconstruction hadn't been an option then I don't know if I would have had the "preventative" treatment. Because of all the cysts, they likely wouldn't have found the cancer until it had became invasive and my kids could have lost their mom before either of them even reached the age of 10.
I've had my thyroid gland removed, a kidney, an ovary, etc but those were different. Though I could see the scar on the outside the missing organs were from the inside and maybe in a way I have been trying to pretend I haven't lost them? Seeing my implants and myself without nipples brought it home to me that I have lost a lot more than just my breasts. I worry now about my extreme risk of other cancers but I'm trying to keep it under control. There's not a lot more of me that can be lost before that's it for this body. All due to a genetic fluke that happened some time in the fall of 1976 when I was conceived. A condition that approximately 1 in 250,000 people have and almost none of them have it affect them as severely as it has me--or at least as early as it has me. Most people present with skin tags in their late 20's. I had those skin tags (removed for now during the implant surgery) begin during my pregnancy with Hannah more than three years ago. Everything else began early. Starting in 1984 when I was 6.
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