Since as of September 7, 2017, there are three hurricanes in the Atlantic Basin in the United States (Hurricane Irma, Hurricane Jose, and Hurricane Katia), and it’s fairly certain that Hurricane Irma will affect the southeast coast from Florida to North Carolina, after devastating the Caribbean, and caregiving for our loved ones doesn’t stop just because of weather, here are some tips to help you throughout the crisis (hurricane recovery is long-term). Continue reading
Today, July 11, 2017, marks a strange anniversary for me personally.
It is the day that marks the genesis of Going Gentle Into That Good Night (although it would not officially be launched until about three years later) and of the books that I have written about the dementia journey.
Seven years ago today, I got a phone call at 7:15 am that I was expecting. The eight or so months preceding this phone call had been hell for both Mama and me (not all the time, but most of it).
It became apparent in those months that something was clearly wrong. Mama knew it and it scared her, and that made her defensive, hostile, and combative. I knew it, but didn’t know exactly what it was or how and what I could do about it.
Mama lived ready to fight. I lived ready to catch her when she fell, walking on eggshells, trying to keep things as sane, as calm, and as peaceful as was within my power.
These months took their tolls on Mama and me both in very different ways.
Fortunately, that phone call I received early in the morning seven years ago today helped relieve the toll on Mama in ways that she needed. I, on the other hand, still bear a lot of open, gaping wounds that may never heal from the toll it had on me.
Dementias change everybody who is involved and many of those changes, especially for those of us directly in the war zone with our loved ones, can’t be undone.
I’ve had people who’ve never been through any of this and who have not lived my life tell me they know what it’s like and they’ve walked in my shoes. And then the “I know what’s wrong and how you need to fix it because nothing will change until you do this” follows with condemnation and criticism instead of empathy and compassion.
In my opinion, there is nothing is more insulting, insensitive, or hurtful than having this happen to a person. I have to forgive – and I have – because that’s my responsibility. But wisdom must accompany forgiveness and wisdom says that it’s not healthy to keep these kinds of people in any kind of close proximity in our lives.
I’d give my life for any of them. I’d help them with my last breath if they needed it. I love them, but to keep them near or in my life isn’t possible because it’s not healthy for me nor, frankly, is it healthy for them. That time will come, but that time is not now.
My 7:15 am phone call seven years ago today was from a psychiatrist at a local hospital. She said Mama had been transported, after she called 911, at 3:30 am to the ER. The psychiatrist was going to involuntarily commit Mama to a geriatric psychiatric hospital and wanted my permission (I was Mama’s medical power of attorney).
I gave my permission because that’s where Mama and I were in our journey through dementias. I knew that’s where she needed to be, even though it broke my heart to think about it.
The psychiatrist gave me instructions on how to change the commitment to voluntary and told me what to bring for Mama at the psychiatric facility later that afternoon.
I hung up the phone, knowing that our lives had just permanently changed forever. And I got to work immediately adapting to that change.
Within the space of the next two weeks, we had a diagnosis of mid-to-late-stage vascular dementia and Alzheimer’s Disease (I also realized Mama had Lewy Body dementia after her release from the psychiatric hospital because I researched all the things I was seeing beyond the other two types of dementia).
The most harrowing part of all of this was the geriatric psychiatric hospital.
When I was admitted for the first time the afternoon of July 11, 2010 to change Mama’s commitment to voluntary, with me as the responsible party, and to deliver her bag, my immediate reaction was to rescue Mama and take her home (she actually wasn’t there yet and was rolled up in a wheelchair while I was completing her admission, but she didn’t see me and I don’t know, as bad as her psychosis was then, that she would have recognized me anyway).
It was Bedlam.
The stench from urinary and bowel incontinence from the people walking agitatedly or sitting and screaming in wheelchairs around me literally took my breath away.
The intense chaos and high noise level was so uncomfortable for me that I wanted to take Mama and run far, far away.
The deep compassion and empathy for these people, despite all the other stuff, made my heart break even further and it took all I had not to just melt down into a sobbing mess.
But I held it together for Mama. I was there every day at the times I was allowed to visit. I called every morning first thing and every night last thing to make sure Mama either had a good night or was in bed safely tucked away.
Two weeks of that routine and that place left its indelible mark on me. I can barely think of now without shedding tears.
But the two weeks that followed this day seven years ago got Mama on a medication regimen that alleviated many of the symptoms of her dementias and, all in all, made life more bearable and easier for her.
And for that I’m profoundly grateful. It makes everything before and after worth enduring.
Because in the end, it was always about my Mama, and never about me.
Daddy and Mama were married at Unaka Baptist Church in Johnson City, TN on June 9, 1956 by Howard T. Rich. It was a small wedding, with close family and like-family attending.
Harry Aiken, my mama’s cousin closest to her in age, gave her away in marriage to my daddy. Lois Aiken, Harry’s wife, made the wedding cake.
Jennings Berry, my daddy’s lifetime best friend, served as Daddy’s best man.
Aunt Velva, who wrote the wedding invitation, was my Mama’s mother’s sister. Continue reading
She went into what would be her death sleep around 1 pm on Sunday, August 12, 2014, with her last words of “I guess they’re going to throw me out now,” suffering, I think, the final heart attack that led to her death.
I assured her that I was not throwing her out, that she was home, and I loved her. It took me several months and writing Fields of Gold: A Love Story before I realized that Mama was back at nursing school at East Tennessee State University, unable to follow all the instructions she was given because of a congenital hearing loss, about to be dismissed from the program because she could not hear the doctors when her back was turned to them (she compensated for her hearing impairment by masterfully reading lips, even with hearing aids, most of her life). Continue reading
This is my fourth Mother’s Day without my mom. Although the immediate excruciating pain of losing her has subsided into a dull constant ache and longing punctuated by sudden and unexpected moments of intense grief, often triggered by a memory or something externally that I associate with Mama, I still miss her terribly.
But time and space has allowed me to grow into a deeper understanding, a greater respect, and a more complete love of this incredible woman that I was blessed to have as my mama. Continue reading
In my profile of William Shakespeare’s character, King Lear, from the play of the same name, it was clear that Lear was suffering from dementia and, most probably, Lewy Body dementia.
So I thought I’d share my review of The Year of Lear: Shakespeare in 1606 by James Shapiro to get a wider perspective on the year that saw Shakespeare give a title character in one of his plays many of the behaviors and symptoms of advanced cognitive impairment and Lewy Body dementia.
This book explores how the world around Shakespeare (beginning with the Gunpowder Plot on November 5, 1605 – now commemorated annually in England as “Guy Fawkes’ Day” – which had deep political and religious roots) during the early part of the reign of King James I, with an especially tumultuous year in 1606, influenced his writing that year.
Much of what was going on politically, socially, and emotionally in England at the time is reflected in the lines of King Lear, Macbeth, and Antony and Cleopatra, all of which are among Shakespeare’s tragedy plays and all of which Shakespeare wrote in 1606.
The Gunpowder Plot in late 1605 triggered much of the political and religious climate that overshadowed 1606. The plot, engineered by English Catholics who feared greater persecution – they got it – and more “do-or-die” pressure to abandon their Catholicism – a prescient fear even they didn’t realize the extent or depths of of James I – underscored the continued intense subterranean battle between England’s Catholics and Protestants.
While the plot was thwarted by the usual treachery and intrigue (it would have obliterated much of the heart of London government – buildings and people – and would have significantly changed the overall physical landscape of London), James I – as King of Scotland first, he was viewed as an interloper by much of the English population – reacted ferociously with a wide net that touched every English citizen, including Shakespeare, determined to have his will – the union of Scotland and England under one umbrella – no matter what he had to do to make it happen.
It seems James I did everything he could to alienate his English subjects, including moving, by disinterring, the graves of the royals in Westminster Abbey.
Most notably, he disinterred Elizabeth I and buried her on top of Mary I (“Bloody Mary,” the religiously-fanatical daughter of Henry VIII and Catherine of Aragon, whose main accomplishment on the throne was a religious pogrom against Protestants, of whom Elizabeth I was one), then moved his mother, Mary, Queen of Scots (one of Elizabeth’s staunchest rivals for the English throne), into Elizabeth’s grave and giving her a greater position of status in the cemetery.
Shakespeare, who lived in the heart of London most of the year, had a front row seat to all of this as part of the King’s Men, who were patronized by the crown, as they had been during Elizabeth I’s reign.
1606 was a year of fear (the plague hit London particularly hard during 1606, adding to the political and religious fear that was rampant in the city) and division (political and religious) and nostalgia (although by the end of her long reign the English believed Elizabeth I’s rule had become stagnant, the actions of James I made them long for her “good old days”) that punctuated the year.
I highly recommend this book even for people who may not know or really appreciate the incredible talent and acute, heart-of-the-matter insight that Shakespeare brought as a writer to his plays. Perhaps it will be a catalyst to go and read at least these three plays through the eyes of 1606.
Most dementias – Lewy Body dementia, vascular dementia, early-onset dementias, alcohol-related dementia, and Alzheimer’s Disease among them – appear seemingly suddenly as primary and distinct neurodegenerative processes without definitive causes (except in the case of genetic inheritance, which primarily occurs in rare dementias like Corticobasal Degeneration, Progressive Supranuclear Palsy, and Fatal Familial Insomnia and some of the early-onset dementias).
However, there are a group of neural disorders, which are caused by the same genetic mutation that affects lipid storage in the body, that often have dementia as a secondary symptom as the diseases progress.
These neural disorders (all these have sphingolipid metabolism dysfunction in common) – which include Niemann-Pick disease, Tay Sachs disease, and Gaucher disease – are characterized by by increased levels of a particular type of sphingolipid.
There is no cure for these neural disorders and they are all fatal (in many cases, during childhood).
Spingolipids are the biological product of a chemical process that creates a protective layer on nerve cell membranes and ensures proper – and protective – cell signaling and are critical to optimal brain function.
The genesis of sphingolipids are long-chain – also known as sphingoid – bases that normally have a length of 18 carbons, although they can also have lengths of 16 or 20 carbons. The length of long-chain bases is determined by serine palmitoyltransferase (STP), a multiprotein enzyme.
In neural disorders like Niemann-Pick disease, Tay Sachs disease, and Gaucher disease, a mutation (known as Stellar) in one of the proteins that makes up STP creates an abnormally high number of 20 carbon long-chain bases, which dramatically interferes with sphingolipid metabolism.
This causes neurodegeneration to occur. In all these neural disorders, much of the neurodegeneration begins soon after birth.
In Tay Sachs disease, neurodegeneration of the brain and spinal cord begins at about six months of age. The average lifespan is four years.
Gaucher disease has three subtypes.
In Type 1 Gaucher disease, symptoms, which include anemia, bone deterioration, and liver and spleen impairment, are non-neurological and do not materialize until middle age. The average life expectancy for Type 1 is 68 years.
Type 2 and Type 3 Gaucher disease are both neuropathic forms of the disease. Neurodegenerative symptoms include abnormal eye movements, seizures, and systemic brain damage.
In Type 2 Gaucher disease, the onset of symptoms is within three to six months of age. Deterioration is rapid; the average life expectancy is about two years of age.
Type 3 Gaucher disease is a slower onset and involving version of Type 2. The average onset of neurological involvement is late childhood into adolescence. Life expectancy ranges from the mid-twenties to, in extremely rare cases, the early forties.
Niemann-Pick disease has four types: Type A, Type B, Type C1 and Type C2.
Niemann-Pick disease Type A occurs in infants. Symptoms include enlargement of the liver and spleen (around three months of age) and a failure to thrive during the first year of life. At one year, widespread damage to the lungs occurs, and there is a progressive loss of neurological and motor function.
Along with Tay Sachs disease, Niemann-Pick disease Type A also has a common eye deformity consistent with neurometabolic disease, known as a cherry spot, that occurs within the macula and is often what initially identifies the two neural disorders.
While most children born with Niemann-Pick disease Type A die in infancy, a few may live as long as four years.
Niemann-Pick disease Type B includes most of the same symptoms as Type A (motor skills are not usually affected), but the onset of symptoms is during adolescence. Most people with Niemann-Pick disease Type B survive into adulthood, but mortality rates climb dramatically between twenty and thirty years of age.
Niemann-Pick disease Type C (C1 and C2 are caused by different gene mutations, but the symptoms are the same) is characterized by severe liver disease, severe pulmonary infections, progressive neurodegeneration, and increasing difficulty with speech and swallowing that deteriorates completely over time.
The onset of Niemann-Pick disease Type C can be at any age, but it is most commonly seen by the age of five. The life expectancy with this type is under twenty years of age when symptoms appear in childhood. When symptoms appear later, the life expectancy is ten to twenty years after symptoms begin.