Powerful Personal Neuropathy Myeloma Account

Today's post from deludia.com is the third very recognisable personal account in a short time here on the blog about living with neuropathy as a result of multiple myeloma. Once again, there is no connection to HIV but neuropathy symptoms and living with them are common to so many people with the disease, irrespective of the cause, that this article will feel very familiar. The article goes into some detail about his treatment for myeloma and this will be useful for many others who are also living with cancer. Unfortunately people with HIV are also not immune to cancers of one sort or another.

Perpetual Neuropathy 

Bob Kirkpatrick: Friday, February 10th, 2012

Stop waving your hands out there. I see you, all ready to jump on me and say “Hey, Doofus, it’s Peripheral Neuropathy, not Perpetual.” Au Contraire, mon ami. For some of us, perpetual is exactly the right word. Let’s roll back a little: I have Multiple Myeloma. I’m in the 1% class. No, that doesn’t mean I’m rich and think contemptuous thoughts of the economically weaker. It means that the Myeloma eating me alive doesn’t manifest the proteins that Multiple Myeloma people speak of so often. An M-spike doesn’t have anything to do with me.

But when it comes to side effects, particularly neuropathy, we tend to be a part of the group that gets hit more severely than those in the more populated 99%. I am the perfect example of the leastmost population. While I haven’t the worries about damage to my kidneys, liver and other organs affected by the unwanted proteins, Multiple Myeloma dissolves my bones at a vastly greater rate than experienced by our community’s majority. It gives me a unique perspective on the cancer, and I grant readily that my views are often dim. I am told that I have matured significantly when it comes to my writing, but it’s also true that I have been able to “settle in” to having Multiple Myeloma; it’s going on five years since I was diagnosed –already at stage three when it was found. At the time of my diagnosis, my oncologist gave me six months to straighten out my affairs, and the prognosis did nothing to lighten my mood.

Hindsight is 20/20 as the expression goes, and I can attest to the validity of that statement. At least insofar as my cancer is concerned. As a non-secretor, my oncologist, a hematologist of 40 years experience put me on a regimen of Doxorubicin. My response (physical and emotional) was rather negative because it almost killed me on the first infusion. And then again on the second. When my oncologist tried to convince me to take a third shot at it, I declined, and rather vehemently –having grown tired of spending a week in ICU suffering near-lethal anaphylactic and toxic shock. So we tried a years worth of Velcade cycles. This did me no good, but it exposed me to the agonies of peripheral neuropathy in spades. Knowing what we do now, between my oncologist and I, we’d have probably chosen Thalidomide or Lenalidomide instead, considering that Velcade is an antiprotein therapy and not really suited to someone without the pesky proteins. But we went with Velcade, because of the conventional wisdom which says to treat non-secretory Multiple Myeloma the same as in all cases.

I lost the ability to use my feet and hands due to neuropathy. The pain was so severe that any attempt to stand or even grip a fork to eat with resulted in pain that literally caused me to scream because it was so profoundly painful. The fact that it was unrelenting, and for so long a time, I literally gave up and went in search of a physician who supported Death with Dignity. Washington, my home state las legislation permitting it under highly specific and controlled situations. None of the drugs like Gabapentin did anything to relieve the pain, it only compounded the discomfort by adding severe nausea to the discomfort menu. After a year with Velcade treatments, we finally abandoned the treatment because it was hurting me and taking more quality of life from me than the cancer ever did. And believe me, the cancer took a big chunk out of my mobility and comfort all on its own. I had to take radiation three times to kill off lesions/tumors that were exquisitely painful. The radiation worked wonderfully, I might add. With the Multiple Myeloma still rapidly progressing and the oncology team more vehemently ratifying a lethal prognosis, we decided to give Lenalidomide (Revlimid) a try. Sadly, with some patients, myself among them, neuropathy was very slow to wane away and would come back like gangbusters almost at the hint of any new treatments. The break in my therapy had nearly eliminated any neuropathic pain and so we elected to take another stab at slowing the cancer. I made it through a cycle and a half before we had to stop because of the disabling pain that rushed back to taunt me.

After a couple of months without further treatment, quite mysteriously, the progression of Myeloma seemed to stop, going into a holding pattern in early 2010. It took the entire year and a month or so of 2011 to leave me with reduced neuropathy in my feet –and the rest of the side effects gone at last. But to this day, my feet are still very sensitive to any pressure, and provide me with that ‘so cold its hot’ burning pain so common to those who get neuropathy. My oncologist and the teams in both the Spokane VA and the Seattle Cancer Consortium all agree that the current level of neuropathy I experience is permanent. As a result, to provide some lightness to the distress, we now refer to my symptoms as Perpetual Neuropathy. Things were pretty good from March 2011 until the end of December 2011, when the various symptoms that brought me to the doctor in the first place, returned. I have body aches, tremendous hot flashes, constant constipation, simple bruising that’s slow to heal, daily bloody noses, and bone pain emanating from my shoulders, neck, lower spine, hips, thighs and feet, and in my wrists and fingers. X-rays show lesions and areas of bone deterioration in all of those places. Nearly a third of my pelvis is just plain missing. Atop it all, the neuropathy of treatment is still there to make it all worse.

I am giving treatment some thought again. And oddly enough, considering a chemo plan that includes Doxorubicin, my old nemesis. My oncologist and I are requesting comments from Multiple Myeloma experts on the possibility of tiny dose Doxorubicin, perhaps augmented with low dose Lenalidomide. But because of my perpetual neuropathy, we’re moving very slowly and cautiously because a return of neuropathic pain could likely saddle me a with a greater level of pain that I would never get over. Sadly, I cannot tolerate steroids well, and so I don’t get the benefit it might provide to bolster the body against the toxic effects of chemotherapy. When we’ve heard back from the sources we’ve tapped for information, we’ll use it to decide whether to spin the cylinder in the chemotherapy six shooter for a game of chemo-roulette.

So those with their hands up and waving for my attention to correct my malapropism, relax. I was highly accurate in calling my side effects Perpetual Neuropathy. As the five year mark approaches, it makes me nervous to think of myself in the category of those who perish. But I bolster myself with the thinking that my cancer backed off once, perhaps my Multiple Myeloma can be convinced to do it again.

Some of us who undergo chemotherapy do so at a much greater disadvantage than others. It’s simply a matter of of circumstance. I’m a non-secretor sensitive to neuropathy and unable to tolerate steroids. The good news is that the vast majority of Multiple Myeloma patients don’t have to deal with therapeutic side effects at the level of people like me. We are the few, and our side effects can be as permanent as the rising sun. But in any treatment proposition, it pays to be informed and participatory. It is we patients who, bottom line, will take offered treatment or not. I can’t help but believe that had I been more informed about what Multiple Myeloma is, and what the chemicals used to treat it did, that I might have taken a different course. One that might not have had the permanent negative impact I suffer today.

http://www.deludia.com/?p=4149

Myeloma And Neuropathy A Personal Story

Today's post from multiplemyelomablog.com (see link below) is a personal story of living with the disease and the neuropathy that frequently comes with it. Myeloma is basically a cancer of the plasma cells and can have significant life-changing consequences. The writer has no connection with HIV but when you read about the experiences with the neuropathy treatment drugs, with which many of us are familiar, you may be able to relate it very closely to your own situation. Whatever the cause of your neuropathy (and there may be more than one potential cause), many of the experiences with both the disease and the neuropathy drugs are similar and that alone may help you feel less alone in coping with the problem.

Pat’s Medical Update: How do I feel?
Posted on February 19 2013 by Pat Killingsworth

How do I feel today? That depends on what you mean by “feel.” By feel do you mean my energy or pain levels? How about emotionally? Dropping Revlimid from my chemo regimen (still on weekly Velcade and 20 mg dex) has jump-started my numbers. All my blood counts are back to normal and my energy levels are up.

Great! Emotionally, my stress levels are relatively low. Money is tight but the bills are paid. Pattie and I are getting along just fine. Watchful waiting? I’m on cruise control, ignoring the fateful meeting I have set with my myeloma specialist, Dr. Alsina, in three weeks. Why fateful? Because that’s when I will learn if Velcade and dex alone are keeping my myeloma at bay, or if we will need to add Revlimid back into the mix as a temporary fix until we can decide which new therapy direction to go.

So energy levels are good–the best they’ve been since before my stem cell transplant 20 months ago. Emotionally things are fine. That leaves pain.

How do I feel? I’m hurting! A pair of old lesions have left big holes in my right hip which is now riddled with arthritis, making it difficult to walk. Nerve compression in my lower back hasn’t improved. If I sit and write, read or watch TV for longer than 10 minutes I can barely get up. I get headaches and stingers caused by previous damage to the vertebrae in my neck. And my peripheral neuropathy (PN), best I can tell caused by my myeloma and using Revlimid for the better part of six years hasn’t improved as much as I would have hoped since I stopped using Revlimid several months ago.

Small doses of oxycodone (20 mg spread throughout the day) works miraculously to dull pain in my back and hip. Without it I don’t think I could walk! It helps numb my PN, too.

Yesterday morning I forgot to take my Gabepentin. By mid-afternoon my hands and feet felt like they were on fire–a reminder that that medication is also working for me or things would be a lot worse.

I have written often about how difficult living with multiple myeloma can be for those of us that are fighting battles on two or more fronts. How about our myeloma brothers and sisters that have kidney issues. Think they feel good going through dialysis? Those of us with bone damage? Or patients and caregivers racked by anguish and depression?

I have trouble separating how I feel from those I hear from everyday. As you can plainly see, it makes it difficult for me to focus! Today’s post is supposed to be all about me!

I feel good when I’m laying down and sitting for short periods of time. I feel good once I’m up and moving for awhile. And I feel better if I take my meds as scheduled.

Like a lot of things in life, I guess what could or should be a simple question isn’t always so simple. My advice? Don’t ask me, “How are you?” unless you have a few minutes to sit-back, put your feet up and snooze. Ask a simple question and get a long-winded answer!

As always, you can ask questions or let me know how you feel by commenting here or emailing me:

Pat@HelpWithCancer.org

Feel good and keep smiling! Pat

http://multiplemyelomablog.com/2013/02/pats-medical-update-how-do-i-feel.html

A Personal Nightmare Of A Journey With Neuropathy

Today's very long post from blog.donnawilliams.net (see link below) is a perfect example of however bad you feel yourself, there's always someone else who's got it worse! This lady's story reads like a medical text book of everything to do with peripheral neuropathy and could perhaps help you feel better about your own situation in comparison. How she ever found the right doctors to diagnose her many problems is a wonder in itself but we can only wish her the best and hope that things improve with the advent of better treatments.
 

Peripheral Polyneuropathy: a case of the ‘perfect storm’?

Donna Williams, BA Hons, Dip Ed.
Author, artist, singer-songwriter, screenwriter.
Autism consultant and public speaker.
http://www.donnawilliams.net - See more at: http://blog.donnawilliams.net/2013/12/13/peripheral-neuropathy-a-theoretical-fruit-salad-of-eds-strep-herpes-simplex-haemophilus-docetaxel/#sthash.QraVjfyt.dpuf

Donna Williams BA Hons, Dip Ed.Author, artist, singer-songwriter, screenwriter. December13 2013

My journey with peripheral polyneuropathy has probably lasted my lifetime. It made itself known along the way but by 2009 its whisper was clearly audible, by 2011 it was shouting, by 2012 it was screaming at me. But what on earth had caused this autonomic then sensory, then by 2013 even the start of motor neuropathies?

I was born to an alcoholic who had attempted (failed) abortion twice with Quinine so peripheral nerve damage right from the start may well have been probable. By six months old I had recurrent infections (later diagnosed as primary immune deficiencies) and a number of viruses that could have caused it. I may have inherited salt wasting from my father and certainly did inherit a collagen disorder from my mother. Did I have symptoms of autonomic, sensory or motor neuropathies in early childhood? Autonomic, certainly, sensory, on and off, motor, maybe, episodically at different times throughout my life.

The closest we came to understanding why my polyneuropathy got to the level its now at was the theory that my collagen disorder – Ehlers Danlos Syndrome – had played a part; that collagen protects myelin which protects peripheral nerves and mine is degenerating. Another specialist suggested my autonomic neuropathy had developed as a result of chemo. But being immune deficient all my life, I wondered if this also played a part. And what of salt craving and my dramatic improvements when on high sodium intake? I knew chemo had tipped the balance and that Tomoxifen was implicated. But how to make sense of the puzzle, the fruit salad?

I could have accepted the word ‘idiopathic’ but maybe that’s just a word people have when they cannot find the ONE cause. But what if that’s because there actually were multiple, cumulative causes? This is what I came up with (together with cited associated medical studies):

1) SALT WASTING
I was a heavy salt craver all my life, as was my (rather autism spectrum) father who would coat his food until it was white and said if he didn’t keep up with salt he got headaches. I craved high salt foods, added salt and from mid childhood to my early teens drank saline on a daily basis. When, during chemo in 2011, I was told I had autonomic dysfunction I didn’t think to supplement salt because the chemo had already caused me to have a permanent taste in my mouth of salt. Following chemo and diagnosis of Orthostatic Hypotension, Arrythmia and Mixed Apnea, I read up about sodium and autonomic dysfunction and began to take 5 grams a day of sodium (around 10 grams of salt) which I took in addition to magnesium, calcium and citrulline supplementation. My autonomic dysfunction improved significantly though the hypoventilation continued. My sleep specialist suspected I had salt wasting and ordered electrolyte levels tested. On 5 grams of sodium a day my sodium levels (and other the electrolytes I was already supplementing) were ‘normal’. Before this, I have no idea.

I looked up salt wasting and found that whilst Barter’s Syndrome is almost always diagnosed in infancy, a related but usually milder condition, Gitelman’s Syndrome, can go undiagnosed into adulthood until a health crises exposes it. To test for Gitelman’s I’d have to come off sodium for 2 weeks. I dropped it to 2.5 grams a day and had severe polyuria. Gitelman’s is one cause of hypoventilation syndrome in children. My hypoventilation was probably happening since age 2-3, daytime hypopnea/bradypnea as long as I can recall, episodes of being ‘blue’ from age 2-3. Hypoventilation episodes can contribute to developmental disabilities and sensory perceptual disorders – I was diagnosed with autism at the age of 2.

Congenital central hypoventilation syndrome: Neurocognitive functioning in school age children

Frank A. Zelko; Michael N. Nelson; Sue E. Leurgans; Elizabeth M. Berry-Kravis; Debra E. Weese-Mayer (Profiled Authors: Frank A Zelko; Debra E Weese-Mayer)
Pediatric Pulmonology. 2010;45(1):92-98. Scopus
Abstract

Objective: Examine indices of neurocognitive functioning in children with PHOX2B mutation-confirmed neonatal onset congenital central hypoventilation syndrome (CCHS) and relate them to indices of PHOX2B genotype, demographics, and disease severity. Methods: Subjects were 20 patients with PHOX2B mutation-confirmed CCHS diagnosed as neonates who had undergone neurocognitive assessment in the course of clinical care at the Rush Children’s Hospital CCHS Center between 1990 and 2006. Neurocognitive variables of interest included Full Scale IQ (FSIQ) and Wechsler-derived marker indices (subtests) of verbal comprehension (Vocabulary), visuoperceptual reasoning (Block Design), working memory (Digit Span), and clerical/processing speed (Coding). Results: Single sample t-tests revealed participants’ general intelligence index (FSIQ; mean 84.9, SD 23.6) to be lower than the general population, though the range of FSIQ observed was broad. Visuoperceptual reasoning and clerical/visuographic speed marker indices were similarly depressed. These deficits were related to special education participation but not to PHOX2B genotype status or other demographic and clinical risk factors. Conclusions: PHOX2B mutation-confirmed CCHS confers risk for adverse neurocognitive outcome, though the range of functioning observed raises questions about factors that may contribute to neurocognitive variability. Visuoperceptual reasoning and clerical/visuographic speed appear particularly vulnerable. PHOX2B genotype and disease severity indicators were unrelated to neurocognitive indices, possibly due to our modest sample. Future research should employ comprehensive neurocognitive assessment emphasizing visuoperceptual ability, mental speed, attention, and information processing efficiency. Increased recognition and expedited diagnosis with PHOX2B testing should allow larger studies of the relationship between neurocognitive functioning, PHOX2B genotype/mutation, and disease severity and management. © 2009 Wiley-Liss, Inc.

PMID: 19960523

2) EPISODIC HYPOXIA
I was commonly blueish as a young child, always pale to the point I was called ‘Baby Legs’ and ‘Milk Bottle’. I was dizzy a lot of the time, it was normal for me to feel a little ‘out of it’ so I didn’t question it. I drowned twice at age 3, rescued from the bottom of the pool as I’d made no effort to breathe. Later I could spend more time underwater than any child I knew and easily swam the length of the Olympic pool on the bottom. So its fair to say that hypoventilation was probably my ‘norm’. When I was 2-3 years old I also experienced a year of being choked and suffocated by an abuser (I took to then sleeping under the bed, which ‘solved’ some of this). I’m sure this did my nerve health no favors whatsoever. Nevertheless, my brain MRI looks fine. So was their no damage? Or was the only damage to the peripheral nerves?

Peripheral Neuropathy in Sleep Apnea
A Tissue Marker of the Severity of Nocturnal Desaturation
PIERRE MAYER, MAURICE DEMATTEIS, JEAN LOUIS PÉPIN, BERNARD WUYAM, DAN VEALE, ANNICK VILA, and PATRICK LÉVY

ABSTRACT

Changes occur in peripheral nerves subjected to hypoxemia resulting from a low blood O2 concentration such as in chronic obstructive pulmonary disease (COPD), or to damage to the vasa nervorum causing ischemia, such as in diabetes. A modified tolerance of peripheral nerves to transient, experimentally induced limb ischemia has been reported in hypoxic COPD and diabetic patients (12, 13). This tolerance is characterized by abnormal persisting nerve conduction during ischemia. This resistance to ischemic conduction failure (RICF) seems to be the earliest abnormality of peripheral nerve function observed in diabetic patients who go on to develop an obvious neuropathy (14). The tolerance to ischemia may be an adaptative mechanism, since some electrophysiologic abnormalities have been reversed in hypoxic patients by improvement of oxygenation (12), and in diabetic rats by supplemental oxygen inhalation (15).

Chronic hypoxia is a well known cause of peripheral neuropathy (16-18). However, to our knowledge, no study has been done of peripheral neuropathy related to intermittent hypoxia except for the pharyngeal thermal hypoesthesia described in patients with OSA, which may be related to a pharyngeal neuropathy (19). The aim of the present study was therefore to assess peripheral nerve function with an ischemia test in OSA patients without a recognized cause of neuropathy. This type of dysfunction may represent an early and quantifiable tissue marker of the consequences of nocturnal hypoxemia.

Read More: http://www.atsjournals.org/doi/full/10.1164/ajrccm.159.1.9709051#.UqvKoI0YMck

3) EHLERS-DANLOS SYNDROME (EDS).
I was hypermobile since at least age 2-3, was turned into a ‘human pretzel’ by my mother for the entertainment of others and could easily put my feet to my head and rock, put my feet behind my head like a ‘frisbee’, do the splits and turn from one legs to the other. My history of progressive connective tissue degeneration is the usual for someone with EDS starting with diagnosis of juvenile arthritis in late childhood. It was only when I was diagnosed with Ehlers-Danlos Syndrome in 2013 that I learned I have 4 relatives on my mother’s side who have ruptured before the age of 40 – two with uterus rupture, one with spleen rupture, one with brain aneurysms. As such I’m thought to likely have EDS type IV. There is recent literature connecting EDS to some forms of autism.

Peripheral neuropathy in Ehlers-Danlos syndrome

Enrique Galan, MD, Boris G. Kousseff, MD
Received 18 July 1994; accepted 28 December 1994.
Abstract

Two unrelated male patients with clinical manifestations of Ehlers-Danlos syndrome type III and peripheral neuropathy are presented. At age 13 years, one developed bilateral brachial plexus palsy unrelated to trauma and 2 years later, a right lumbosacral plexopathy. The other presented at age 3 years with a left brachial plexopathy after sustaining a fracture of the lateral condyle of the right humerus. In both patients, nerve conduction velocities demonstrated conduction block across the brachial plexus and recovery was incomplete, indicating that peripheral neuropathy is a serious complication of Ehlers-Danlos syndrome. Its prompt diagnosis facilitates the care of patients with this syndrome. Increased ligament laxity/stretchability and mechanical trauma may play an important role in the pathogenesis of the neuropathy.

Neurology. 1976 Jun;26(6 PT 1):596-7.

4) IgG SUBCLASS DEFICIENCIES
I had recurrent infections from 6 months of age with my first 26 years regularly on antibiotics. I first became personally aware of my immune deficiencies when I was 17 and the nurse kept taking more and more blood samples because they couldn’t find any white cells. By the age of 38 I had my first normal white cell count but was then diagnosed with severe IgA deficiency (only trace). This improved but by my 40s remained mildly deficient. In 2009 I was found to be IgG2 deficient, and by 2011 also IgG4 deficient. The latter resolved but I remained IgG2 deficient.

Neurology. 1999 Jun 10;52(9):1902-5.
Recurrent multifocal demyelinating neuropathy with febrile illness and IgG subset deficiency.
Likosky DJ, Kraus EE, Yuen EC.
Source

Department of Neurology, University of Washington, Seattle 98195, USA.
Abstract

We describe a unique syndrome of recurrent multifocal demyelinating motor greater than sensory deficits in cranial and peripheral nerve distributions with rapid, spontaneous improvement. Three patients presented with episodes over a period of 7 to 24 years, largely accompanied by febrile illness. Variably decreased IgG1 and IgG3 subclass levels were found. We postulate an immune-mediated process based upon the clinical presentation and presence of decreased IgG subclass levels.

PMID:
10371544 [PubMed - indexed for MEDLINE]

IgG monoclonal paraproteinaemia and peripheral neuropathy.
A F Bleasel, S H Hawke, J D Pollard, and J G McLeod
Author information ► Copyright and License information ►
This article has been cited by other articles in PMC.
Abstract

Five patients with peripheral neuropathy and benign IgG monoclonal paraproteinemia are reported, all of whom had a sensorimotor neuropathy with a remitting and relapsing course. The serum paraprotein level did not correlate with the patient’s clinical status. Electrophsyiological studies showed marked slowing of conduction velocity and conduction block in four of the patients and mild slowing in the other. Sural nerve biopsies demonstrated a demyelinating neuropathy with inflammatory cell infiltrates in each of the five patients. Three of the patients had evidence of myelin/Schwann cell reactivity on immunofluorescence studies and in all nerves dense expression of major histocompatability complex class I and II molecules was evident within the endoneurium, on invading mononuclear cells, endothelial cells and Schwann cells. All the patients responded to treatment, plasmapheresis being particularly effective. Four patients have achieved prolonged remissions after all treatment had ceased. These five cases of peripheral neuropathy and IgG paraproteinaemia were identical in their clinical, electrophysiological and pathological features to patients with chronic inflammatory demyelinating polyneuropathy.

J Neurol Neurosurg Psychiatry. 1993 January; 56(1): 52–57.

5) STREP
I had Tourette’s since age 2 (part of my dx with autism at age 2 referred to my to Tourette’s tics) as part of constant Strep infections associated with IgG2 deficiency in a wider context of primary immune deficiencies.

Immune-mediated neuropathy and myopathy in post-streptococcal disease.

Sommer C, Schröder JM.
Source: Institut für Neuropathologie, Rheinisch-Westfälischen Technischen Hochschule Aachen, Germany.
Abstract

A 22-year-old man suffered from a complete flaccid tetraparesis and an immune complex-mediated rapid progressive glomerulonephritis after group A streptococcal infection. Serum creatine kinase was excessively elevated and myoglobinuria occurred. Nerve conduction studies revealed evidence of axonal neuropathy. Recovery was satisfactory within 18 months. Sural nerve and peroneus muscle biopsies were performed in the 4th and 14th week of the disease. Light microscopy of the sural nerve showed an incipient axonal type of neuropathy in the first biopsy. Ultrastructurally, Wallerian degeneration and endoneurial inflammatory cells were present. In the muscle biopsy, few atrophic fibers and altered blood vessels without further anomalies were found. In the second sural nerve biopsy, macrophages were numerous, some of which were immunoreactive for HLA-DR, and only a few myelinated and some unmyelinated nerve fibers remained. Muscle fibers in the second biopsy showed high-grade atrophy and myofibrillar abnormalities. Immunohistochemistry revealed diffuse endoneurial immunoglobulin deposition in the first sample, while in the later biopsy specimen, deposits of IgG, and kappa and lambda light chains were visible in circumscribed endoneurial areas. Immune-mediated neuropathy and myopathy are not well-known complications of streptococcal disease. This is, to our knowledge, the first detailed report on morphological findings in muscle and nerve in such a disorder.

PMID: 1318816 [PubMed - indexed for MEDLINE]

6) HERPES SIMPLEX
had Herpes Simplex since primary school, still get flare ups with cold sores now

Herpes simplex neuropathy.

Krohel GB, Richardson JR, Farrell DF.
Abstract

Atypical facial pain and permanent sensory loss in the second and third divisions of the trigeminal nerve developed in a patient who had had multiple attacks of herpes simplex neuralgia over a period of 8 years. Intravenous cytosine arabinoside failed to prevent a recurrence of the vasicular eruption, but carbamazepine produced symtomatic pain relief. This case demonstrates that herpes simplex can closely mimic herpes zoster as a cause of postherpetic neuralgia and suggests a possible etiology of atypical facial pain and/or trigeminal sensory neuropaty in some patients.

PMID: 945505 [PubMed - indexed for MEDLINE] Brain. 2000 Oct;123 ( Pt 10):2171-8.

7) HAEMOPHILUS
Autonomic (especially hypoventilation) and sensory-motor neuropathies escalated in 2010 following 7 mths of Haemophilus (am IgG2 deficient so was on Doxycycline ever since),

Haemophilus influenzae infection and Guillain-Barré syndrome.

Mori M, Kuwabara S, Miyake M, Noda M, Kuroki H, Kanno H, Ogawara K, Hattori T.
Source: Department of Neurology, Chiba University School of Medicine, Chiba, Japan. morim@olive.ocn.ne.jp
Abstract

It has been reported recently that Haemophilus influenzae can elicit an axonal form of Guillain-Barré syndrome. To investigate the incidence and features of H. influenzae-related Guillain-Barré syndrome, anti-H. influenzae antibody titres were measured by enzyme-linked immunosorbent assay (ELISA) in 46 consecutive Japanese patients with Guillain-Barré syndrome, 49 normal controls, 24 patients with multiple sclerosis and 27 patients with amyotrophic lateral sclerosis (ALS). Whole bacteria of non-encapsulated (non-typable) H. influenzae isolated from one of the Guillain-Barré syndrome patients was the antigen used. Elevated anti-H. influenzae antibodies for two or three classes of IgG, IgM and IgA were found in six (13%) Guillain-Barré syndrome patients, but not in the normal controls and patients with multiple sclerosis or ALS. The incidence was significantly higher in patients with Guillain-Barré syndrome than in the normal controls (P = 0.01) and patients with multiple sclerosis or ALS (P = 0.009). Western blot analysis confirmed that the H. influenzae-positive patients’ IgG recognized the lipopolysaccharides of H. influenzae. Guillain-Barré syndrome patients with anti-H. influenzae antibodies showed relatively uniform clinical and laboratory features: prodromal respiratory infection, less frequent cranial and sensory nerve involvement, pure motor axonal degeneration on electrophysiology, and positivity for IgG anti-GM1 antibodies. Although the features were similar to those in Guillain-Barré syndrome patients infected by Campylobacter jejuni, the recoveries seemed to be better in patients with H. influenzae-related Guillain-Barré syndrome. It is concluded that a form of Guillain-Barré syndrome occurs after respiratory infection by H. influenzae in the Japanese population. A particular strain of non-typable H. influenzae has a ganglioside GM1-like structure and elicits axonal Guillain-Barré syndrome similar to C. jejuni-related Guillain-Barré syndrome.

PMID: 11004133 [PubMed - indexed for MEDLINE] Neurology. 1996 Jan;46(1):108-11.

8) TAXOTERE
The autonomic neuropathy was out of control during chemo with Docetaxel in 2011 and post chemo

Peripheral neuropathy secondary to docetaxel (Taxotere)

New PZ, Jackson CE, Rinaldi D, Burris H, Barohn RJ.
Source: Department of Medicine/Neurology, University of Texas Health Science Center, San Antonio 78284-7883, USA. Comment in Docetaxel neuropathy. [Neurology. 1996]
Abstract

Docetaxel (Taxotere), a semisynthetic analogue of the antitumor agent paclitaxel, inhibits tubulin depolymerization. Paclitaxel produces a peripheral neuropathy. This study delineates clinically and electrophysiologically the characteristics of a peripheral neuropathy due to docetaxel. In 186 patients receiving docetaxel in phase I and phase II protocols, we performed serial neurologic exams. As patients became symptomatic, quantitative sensory testing and nerve conduction studies were done. Twenty-one patients developed mild to moderate sensory neuropathy on taxotere at a wide range of cumulative doses (50 to 750 mg/m2) and dose levels (10 to 115 mg/m2). Ten of these patients also developed weakness of varying degree in proximal and distal extremities. Nine of the 21 patients had received neurotoxic chemotherapy before; 16 were treated with docetaxel at a dose level of 100 to 115 mg/m2. In summary, docetaxel produced a sensorimotor peripheral neuropathy in 11% of our patient population.

PMID: 8559355 [PubMed - indexed for MEDLINE]

10) DEGENERATIVE LUMBAR SPINAL STENOSIS
 
Spine degeneration is usual with Ehlers Danlos Syndrome and I’d had sciatica since late childhood and regularly had challenges with my joints, neck, back. But I never envisioned that before the age of 50 I’d be diagnosed with degenerative spinal stenosis. Very shortly after chemo I had a severe bout of sciatica.

I’m so used to it I’d come off painkillers by my late teens and so I ignored it as usual. It was the worst episode I have ever had. The surging pains began stabbing from both sides, becoming almost circular around my torso. I was frozen with pain, couldn’t even scream.

Next I had four days of paralysis of my lumbar and thigh muscles. I could barely walk, couldn’t stand up from the toilet or sit up in bed, couldn’t get myself up off the floor or straighten after reaching down into a cupboard. An MRI revealed degenerative lumbar spinal stenosis.

My spinal cord was being squeezed by a thickened ligament (most likely in response to years of inflammation and scarring), I had several ruptured discs, and arthritis related damage limiting nerve exits and leaving nerves in contact and at risk of being damaged. I was told the four days of paralysis was due to a ‘sciatic storm’ triggering a neurological shutdown of movement to the lumbar and thigh muscles because I was ignoring the pain, a process called ‘pain inhibition’. I was told I’d need back surgery within a year.

I saw a physiotherapist, worked on all I could to regain abilities, took advice and made my desk a standing desk, bought ring cushions for the car, my seat at the dining table, a portable one for if out at the cinema, theatre, for dinner, and accepted the medical advice that I’d never jump from anything, would get rid of my trampoline and would never do another long haul flight unless it was laying down or sit for longer than 2 hours.

It did get harder and harder to walk after sitting but the ability would return after 30 seconds of walking. Two years post diagnosis I began to get buzzing surging up and down my legs, sudden loss of sensation to one or both legs, falling up steps, and sudden return of sensation with associated severe heaviness. Whilst I accepted that lumbar spinal stenosis could cause me peripheral neuropathy effecting the lower limbs, perhaps even the bladder and bowel, it did not account for the other forms of neuropathy I was having (MRI showed only the lumbar spine was significantly damaged). So even if it was part of the whole picture, it was not the whole.

Eur Neurol. 2004;52(4):242-9. Epub 2004 Dec 1.
The clinical syndrome associated with lumbar spinal stenosis.
Goh KJ, Khalifa W, Anslow P, Cadoux-Hudson T, Donaghy M.

Abstract

Lumbar spinal stenosis is well defined in patho-anatomical terms but its clinical features are heterogeneous. We carried out a comprehensive retrospective review of the clinical features, radiological changes and outcome of 75 patients with radiologically diagnosed lumbar spinal stenosis in order to define its clinical spectrum. The presenting complaints were of weakness, numbness/tingling, radicular pain and neurogenic claudication in almost equal proportions. The commonest symptom was numbness or tingling of the legs. Neurogenic claudication eventually occurred in only 61%. Ninety-three per cent showed abnormalities on neurological examination, but these were generally mild with reduced ankle jerks being commonest. Imaging of the lumbar spine showed that moderate to severe central spinal stenosis correlated with complaints of weakness and abnormal motor power on clinical examination. Patients were reviewed at a mean of 4 years after diagnosis and 65% had undergone surgical decompression; this was not a prospective comparison of different treatment modalities. Overall, a third of patients felt that their symptoms had improved while a quarter felt that they had worsened. More than half had satisfactory neurological function at the time of review. Thirty-nine per cent of those treated surgically, and 25% of those managed conservatively, reported improved symptoms. A poorer functional status at review correlated with complaints of motor weakness and associated comorbid disease. Degenerative lumbar stenosis is a clinically heterogeneous neurological disorder of the lower limbs in the elderly with variable longer-term outcome. A high index of suspicion is required and neuroimaging should be obtained to confirm the diagnosis.

2004 S. Karger AG, Basel. PMID: 15583458 [PubMed - indexed for MEDLINE]

10) TOMOXIFEN
Within weeks of starting Tomoxifen the autonomic neuropathy expanded into sensory neuropathies through 2012 and the start of motor neuropathies began in 2013.

Collagen protects myelin which protects peripheral nerves and collagen is an essential part of all connective tissue. The health of connective tissue is essential to both messages coming from the peripheral nerves to muscles, joints, ligaments, tendons etc, but also messages from tissues to the peripheral nerves. Collagen types 1 and 3 degenerate in EDS. Estrogen is essential to the health of collagen. It is reasonable to assume that blocking estrogen would theoretically accelerate or heighten estrogen depletion impacting collagen regeneration and tone.

Effect of estrogen on tendon collagen synthesis, tendon structural characteristics, and biomechanical properties in postmenopausal women.

Hansen M, Kongsgaard M, Holm L, Skovgaard D, Magnusson SP, Qvortrup K, Larsen JO, Aagaard P, Dahl M, Serup A, Frystyk J, Flyvbjerg A, Langberg H, Kjaer M.
Source: Institute of Sports Medicine, Bispebjerg Hospital, and Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. kontakt@mettehansen.nu
Abstract

The knowledge about the effect of estradiol on tendon connective tissue is limited. Therefore, we studied the influence of estradiol on tendon synthesis, structure, and biomechanical properties in postmenopausal women. Nonusers (control, n = 10) or habitual users of oral estradiol replacement therapy (ERT, n = 10) were studied at rest and in response to one-legged resistance exercise. Synthesis of tendon collagen was determined by stable isotope incorporation [fractional synthesis rate (FSR)] and microdialysis technique (NH(2)-terminal propeptide of type I collagen synthesis). Tendon area and fibril characteristics were determined by MRI and transmission electron microscopy, whereas tendon biomechanical properties were measured during isometric maximal voluntary contraction by ultrasound recording. Tendon FSR was markedly higher in ERT users (P < 0.001), whereas no group difference was seen in tendon NH(2)-terminal propeptide of type I collagen synthesis (P = 0.32). In ERT users, positive correlations between serum estradiol (s-estradiol) and tendon synthesis were observed, whereas change in tendon synthesis from rest to exercise was negatively correlated to s-estradiol. Tendon area, fibril density, fibril volume fraction, and fibril mean area did not differ between groups. However, the percentage of medium-sized fibrils was higher in ERT users (P < 0.05), whereas the percentage of large fibrils tended to be greater in control (P = 0.10). A lower Young's modulus (GPa/%) was found in ERT users (P < 0.05). In conclusion, estradiol administration was associated with higher tendon FSR and a higher relative number of smaller fibrils. Whereas this indicates stimulated collagen turnover in the resting state, collagen responses to exercise were negatively associated with s-estradiol. These results indicate a pivotal role for estradiol in maintaining homeostasis of female connective tissue.

PMID: 18927264 [PubMed - indexed for MEDLINE]

Of course one solution would be to come off estrogen blockers to aid collagen in replenishing so I can better protect my myelin and peripheral nerves. And that means risking the return of estrogen receptive breast cancer. This January I will finally see a neurologist who specialises in peripheral neuropathy. So until there’s other solutions all I can do it take solace in the fact that I do probably understand what I’m dancing with here, that it is not some unfathomable mystery, and this at least makes me feel in control of this quite out of control challenge. What’s this dance been like?

CHILDHOOD CONDITIONS, DIAGNOSES AND INFO:
 
Was born to an alcoholic mother who had twice attempted abortion with Quinine. Recurrent infections from 6mths old including fairly constant Strep, Measles (since age 3, recurrent for 10 mths in my 30s), Herpes Simplex since early childhood and EBV since my mid 20s. Antibiotics every few months for upper respiratory tract infections until age 26 (when dx’d with food allergies, off sugar, on probiotics, anti candida program, supplements). Dx’d with primary immune deficiencies (IgA, IgG2, Complement C3, neutropenic until 2001 then fluctuating neutropenia. On prophylactic Doxycycline since Feb 2010.
Was dx’d at St Elmos Hospital (Moreland, Vic) in 1965 with autism at age 2 (then called infantile psychosis), dx’d with language processing disorder at age 9 (gained functional speech by age 11), was born with collagen disorder of Ehlers-Danlos Syndrome (diagnosed 2013) with rupturing relatives indicating type 4. Salt craving since mid childhood (on saline and ate salt daily, father also saturated his food with salt and had dizziness if he didn’t have salt). People dx’d with autism on both sides of family.

Signs of autonomic dysfunction since at least early childhood. Hypoventilation (drowned twice at age 3, could swim the length of the Olympic pool on the bottom, commonly got dizzy from not coming up for breath), hyponeas and daytime central apneas since childhood (in early teens asked why other people’s brain keeps them breathing and mine keeps forgetting).

PRE- BREAST CANCER 2009-2010
SEPT 2009-FEB 2010: 7 mths of antibiotics for treatment resistant Haemophilus (I’m IgG2/IgA deficient),. By mid 2010 reported significant worsening of life long hypoventilation/central apnea, episodes of leg collapsing and recurrent severe multiple muscle spasms (legs, diaphragm).

POST BREAST CANCER
2011
APR-JULY 2011 Vertigo and significant increase in autonomic and mobility issues 3 mths before cancer dx
JULY 2011 dx’d with ER+ breast cancer
AUG 2011 left breast mastectomy and removal of sentinel node (right breast mastectomy FEB 2012 as cancer started as multifocal comedo which has high return rate including to unaffected breast)
SEPT- DEC 2011 4 rounds of chemotherapy (Taxotere, Cyclophosphamide)
DEC 2011-PRESENT on Tomoxifen

2012
JAN 2012 Severely painful feet on waking with progressive stiffening and clawing of hands. Episodes of acute stabbing pains in toes. Leading up to 2nd mastectomy so no action taken.
FEB 2012 dx degenerative lumbar spinal stenosis. Brain MRI normal. 2Nd mastectomy was done.
MAR 2012 dx’d Mixed (mostly Central) Apnea. Brain & Cervical spine MRI normal. Put on CPAP (later ASV). Responded well to sodium 5000mg, added magnesium. Sleep specialist suggested I had salt wasting.
APR 2012 Cardiologist dx’d Arrythmia and O.H, added Calcium and Citruline and arrythmia improved and daytime Central Apnea and bradypnea became relatively managed.
APR 2012 thyroid function (after supplementing, incl on 5000mg sodium) and electrolytes were normal. Reported polyuria and observes high sodium seemed to reduce it. Diabetes mellitus was tested and negative. It was then presumed part of autonomic dysfunction.
JUNE 2012 reported a few weeks of sleep attacks/flushing/nausea, then it subsided. No action. Episodes of surging dull pains travelling up upper arms – episodic so took no action. Had 1st episode of acute shooting pains up the back of my head on left side followed by very sore scalp (‘Trigeminal Neuralgia’?)- episodic so took no action.

2013
MAR 2013 dx’d Ehlers Danlos Syndrome (4 ruptured relatives so suspected to be type 4, the vascular type). Improved autonomic function on 8000mg sodium was taken to be part of self management with EDS/POTS.
MAR 2013 dx’d Inflammatory Tenosynovitis (of hands and feet) following MRI. Went onto Meloxicam 15mg and 14 days of Prednisolone to which it responded well. Rheumatologist ordered tests re markers for autoimmune disease/paraneoplastic syndrome (all ok) and tests to check re salt wasting. (on 8000mg sodium) serum sodium was normal and Urine sodium was in the normal range – 143mmol .Creatinine, protein both normal. eGFR 72 mL/min/1.73 (kidney function mildly impaired). Urine volumes were 1108ml and 3168ml
MAY 2013 Three days of severe back pain, presumed it was the lumbar spinal stenosis. Corresponded with nausea which I put down to the pain. The pain left after a few days but the nausea remained. ‘Sleep attacks’/somnolence with flushing recurred along with the nausea.
JUNE 2013 Sleep specialist ordered the urine and aldosterone/renin/cortisol tests repeated and ordered an MSLT test for narcolepsy. Results: Urine sodium on 8000mg sodium was now 289mmol but still not as high as expected. Creatinine and protein were normal. Kidney function again, only mildly impaired. Urine volume was 4080 ml
JUNE 2013 Came off Meloxicam (inflammatory tenosynovitis in remission) and reduced sodium to 2500mg. Developed progressively more severe polyuria, eventually up to 7L output a day (no polydipsia). D.I was ruled out following 14hr testing. Went from 59kg to 56kg on day of testing. Returned to 5000mg sodium next day and within 48 hrs weight was back at 59kg but no polyuria since.
JULY 2013 woke up in a (non-productive) coughing fit. Had three more coughing fits within 10 days, all set off by intense laughing and each time culminated in a choking episode. Lung X-Ray: normal. I still laugh but now don’t let myself get into intense laughter and now no further episodes.
SEPT 2013 had ultrasound of all major arteries as part of EDSIV screening . Vascular results all fine.
SEPT 2013 2nd episode of ‘Trigeminal Neuralgia’. Two days later lost sensation in end of thumb (returned), later same day lost sensation in my lips and last third of tongue. Next day severe burning sensation in lips and tongue with severe soreness and permanent ‘salt’ taste. GP who dx’d Neuropraxia/Burning Mouth Syndrome. Went on alphalipoic acid and in 4 weeks it resolved (Returned Nov)
SEPT 2013 sharp abdominal pain an inch below belly button, followed by hernia-like pulling sensation, then several weeks of what felt like uterine pains. Gynacologist’s ultrasound showed fibroids have grown, endometrium thickened (in a context of Tomoxifen) but not worrying enough yet to address. No further episodes.
SEPT 2013 progressive bone pain from the Ischial Tuberosity. After 4 weeks saw GP who dx’d Ischial Bursitis. Ongoing ever since, semi-managed with Meloxicam.
SEPT 2013 troubling clusters of central apneas (ie up to 5 min not breathing out of 9 min) and long hypopneas (up to 130 secs) lead to changing from CPAP Auto machine on to VPAP Adapt ASV machine. This resolved the clusters of centrals and the hypopneas reduced to max length so far of 60 secs. AHI is good and with VPAP insp/exp times normalised (previously insp time was double exp time, now exp time was double insp time) though EPAP (which helps with inhalation) pressures reduced from 14 (95% of the time) to 5-7 although IPAP (which helps with exhalation) went to pressures of 11-15. As a result temp dysregulation improved a lot and narcolepsy resolved completely (a GREAT relief).
OCT 2013 Increased episodic loss of sensation with legs… commonly in one or the other (since 2009 then especially since 2012), but now in both together. Ie: fell up stairs twice in a row, lost sensation followed by severe heaviness, ‘electric’ tingling running up and down legs following 30 min exercise. Noticed a few days after these episodes that a line up the sides of my thighs (and a line up the sides of my upper arms) were very sore to touch, as if bruised, and that I had lost strength in these. Inflammatory tenosynovitis in feet and hands returned (after 3 mths remission), low-moderate level at this stage as did mild nausea/vertigo (left after a week). This all coincided with being 4 weeks off Meloxicam, Q10 and Alpha Lipoic Acid=. Returned to Q10, alpha lipoic acid and increased omega 3s from 5000mg to 10,000mg… no improvement. Returned to Meloxicam and within 3-4 days had more strength in legs and arms and hands/feet less stiff, feet less sore.
NOV 2013 9/11/13 still on Meloxicam, buzzing in legs, bradypnea, flushing and stiffness returning in hands/feet. Came off Meloxicam 11/11/13, did fine until 22/11/13 (10 days) then hands/feet stiffness and pain returning together now with burning lips. Returned to Meloxicam 23/11/13 to limit progression of current PN flare. 48 hrs later, all good again.
DEC 2013 Came off Meloxicam on 7/12/13. Had 2nd sleep study 10/12/13. This confirmed there is still significantly slowed shallow breathing. Daytime episodes are also sometimes quite challenging sometimes causing dizziness and imbalance. 16/12/13 had a cold sore flare up which co-incided this time with another (though more minor) episode of ‘Trigeminal Neuralgia’. Started Lysine ASAP and cold sore and ‘Trigeminal Neuralgia’ both subsided within days. Have now continued Lysine daily as ongoing (as was on this daily for years and stopped post chemo.

 http://blog.donnawilliams.net/2013/12/13/peripheral-neuropathy-a-theoretical-fruit-salad-of-eds-strep-herpes-simplex-haemophilus-docetaxel/

Donna Williams, BA Hons, Dip Ed.
Author, artist, singer-songwriter, screenwriter.
Autism consultant and public speaker.
http://www.donnawilliams.net

- See more at: http://blog.donnawilliams.net/2013/12/13/peripheral-neuropathy-a-theoretical-fruit-salad-of-eds-strep-herpes-simplex-haemophilus-docetaxel/#sthash.QraVjfyt.dpuf

How To Finance Neuropathy And Other Medical Treatment Personal Story

Today's post from northwestgeorgianews.com (see link below) illustrates the problems many people have, especially in the US, with funding their illness. The costs of treatment and medication are of course artificially linked to so-called 'market forces' and therefore are often at the whim of profit-seeking medical companies and the pharmaceutical industry. If you're adequately insured, the bills don't affect you but if not, your recovery is severely tested through medical costs and demands. Many people find that they just can't meet those costs, especially if their illness turns out to be more complex or long-term. The family in this article (dealing with cancer and resulting neuropathy) turned to crowd-funding for help but it has to be a very bad turn of affairs, when the state cannot ensure that its citizens get the best possible care without it making them bankrupt. Most Europeans are universally insured (they don't have a choice) and many Americans are not. Unfortunately, thanks to financial strictures, many European health authorities are turning to a more American model but at least things are slowly changing for the better in the US.

Family starts GoFundMe account after dad stricken with cancer
 By Tonia Davis Staff Writer TDavis@calhountimes.com Posted: Friday, January 2, 2015 9:21 am | Updated: 12:12 pm, Fri Jan 2, 2015.

Bruce Taylor, who has cancer, asked his wife, Pam, to shave his head after he underwent chemotherapy treatments, which caused his hair to rapidly fall out.
Family starts GoFundMe fundraiser after dad stricken with cancer
 
Bruce Taylor, a 38-year-old native of Calhoun, has been a well known diesel mechanic with Shaw Industries for 16 years. He has taught Sunday School to seventh- and eighth-grade boys at Bethesda Baptist Church, been an active member of his community, and has a shop behind his house where he works on vehicles for friends and family. Unfourtunatly, Bruce has had to give up his hobbies, take medical leave from his job and focus on his health.

In July 2014, Bruce was diagnosed with testicular cancer. He underwent surgery to remove the cancer, and the surgeon realized Bruce was facing more than one cancerous cist. During recovery from the surgery, while discussing his treatment options, it was discovered that his kidneys were not strong enough to immediately proceed with chemotherapy, leaving his body defensless against the aggressive cancer.

After months of stregthening his kidneys, Taylor was able to finish the last of his chemotherapy treatments during the holidays. Doctors hoped to do a positron emission tomography or P.E.T. scan to check his body for any signs of cancerous cells soon before Christmas, but, after doing blood work, the doctors concluded that his blood was no longer healthy enough for the additive required for the scan.

The family did not get good news for Christmas; instead, they recieved no news of whether Bruce was free of cancer after the sickening rounds of chemotherapy, blood transfusions and countless medical bills.

The seasoned mechanic now suffers from chemotherapy-induced peripheral neuropathy, damage to the nerves that carry sensations to the hands and feet caused by the chemicals in chemotherapy drugs, and is on his seventh round of antibiotics trying to fight off continous blood infections with a weakened immune system.

“I know more about cancer now than I ever wanted to,” said Bruce’s wife, Pam, while describing her husbands recent medical history. She expressed concern about the new year beginning soon and how it means new deductibles to meet and more medical bills around the corner. She estimated that their medical bills are now well over $50,000 and are slowly being turned over to collections companies as months continue to go by without any changes in income, any financial leniencies or any developments in her husbands health.

The family says that the members of Bethesda Baptist Church have been a blessing to them; they have provided meals and have helped them with two mortgage payments at a desperate time in their lives.

“We are a family who has had to swallow our pride and admit that we need help,” said Pam. “We would use any donations to pay medical bills, help make our house payments, provide for our children and just to try to keep our heads above water. We appreciate donations from the bottom of our hearts; we’re very appreciative of people who are willing to help us. When we get back on our feet, we will most certainly be paying it forward.”

Bruce’s sister-in-law has set up a GoFundMe.com account to help the family collect donations for use in paying medical bills and day-to-day expenses.

Visit www.gofundme.com/brucetalor-ga to make donations to the family.

 http://www.northwestgeorgianews.com/calhoun_times/family-starts-gofundme-account-after-dad-stricken-with-cancer/article_8f5a15bc-928a-11e4-ba85-137143d01d61.html

Personal Account Battling Neuropathy

Today's personal story from (see link below) has no connection to HIV but is an account of living with neuropathy that many other sufferers will recognise. Reading about other people's experiences can be extremely enlightening because a) they remind you that you're not alone in feeling the way you do and b) they can tell you things you don't already know and maybe give you ideas as to how to improve your own situation. Once again, this is a neuropathy patient where the cause is diabetes but as regular readers will know, the end result, irrespective of the cause, is very often exactly the same. Never ignore an article about neuropathy because it has diabetes in the title, because the treatment paths are pretty much the same from the diagnosis onwards.

Battling Diabetic Neuropathy: A Personal Perspective by Rodric Johnson Last updated on July 1, 2014
 
Every night it is the same. My body decides that it wants to allow the daily routine of pain to occur. Some days it is not so bad, but every day is bad.

First the hands begin to feel tingly and slightly painful followed by the feet. Then the pain travels up the legs and up around the shoulders until it encompasses my entire body. It is a constant vibrating pain as if I were burning.

Occasionally I will experience a sharp jab of pain that causes me to yell out. It becomes so intense that I must remove all of my clothing and stop air from circulating around me so that I can find some sense of peace--it never comes. The pain lasts all night and most days.

I am used to feeling pain. In fact, as I type, I feel the pains in each of my fingers and my hand. It is enough to make life seem less important. It is enough to sap all hope and will to try more. It is enough to destroy ambition. The pain interferes with work and school. It interferes with family and marriage. It can be the source of so much emotional trauma for family members.

Each day I notice a few of the things that I did before become more difficult to do because the disease of diabetic neuropathy.

Diabetes
Diabetic Neuropathy means damage to the nerve endings caused by excessive high blood sugar levels due to diabetes. It is important to understand diabetes to understand diabetic neuropathy.

Diabetes is a disease caused by the pancreas not producing insulin, not producing enough insulin or cells in the body becoming insulin resistant.

Diabetes is a manageable disorder if strict adherence to glucose or sugar levels in the blood are maintained--between 80 and 120 mg. This is done by diet and exercise, medications, machine monitoring of glucose levels and a regular doctors visit to assess help.

Diabetes is a progressive disease that slowly damages the body over years. After 10 years of successful management of the disease, complication from having diabetes will arise generally between the tenth and twentieth years. Whether the glucose sugar levels are high or normal this will occur, but the severity of the complications developed depend on how well diabetics manage health.

I did not manage my health well at all when I was diagnosed one month after returning from my mission in the South Africa Cape Town mission December of 2000. I had been having symptoms since the last few months of my mission, but I did not know it. My missionary companion may have saved my life, Burkley Probst, because he insisted that we eat healthily. I had gained almost one hundred pounds on my mission. I was not actively exercising as a missionary and I would eat mountains of food.

Burkley Probst
Burkley would make us walk to places rather than drive each time and eat right. By the time he came along, it was too late for my health. One of the signs of having diabetes is frequent urination.

I remember when that started. My companion, Burkley and I were at a Born Again Christian's home in the middle of a prayer. The man would not stop praying and I was sweating bullets because I could not hold my urine! I bolted from the prayer circle when amen was said! I had to urinate just 30 minutes later thinking that whatever my companion had given me that day caused this sudden problem.

The plane ride to the United states was gruesome for me because I had to go to the restroom every 30 minutes for 12 hours! I sat in the window seat!

When I was at home, my mother, also a diabetic, took me to get tested and I thought my life was over. I at least knew what was wrong with me.

Dealing with the Pain
The pain is not an easy thing to deal with, even though I have suffered with it since 2008 when I was diagnosed with it after a trip to the emergency room and a consultation with a neurologist. I kept asking for morphine. It was right after Thanksgiving. I had come off of my four month diet plan to eat traditional Thanksgiving food. I had been doing P90X and my results were great. Going off the diet was not.

Following that episode in the hospital, my health steadily declined over the months until I came crashing down August of of 2010. My body completely betrayed me. I could no longer run or walk for long distances. I could no longer exercise. I could do none of the things I had done before.

Neuropathy had already started giving me pain, but now it cripples me. I can barely stand for any person to touch me sometimes. On top of that progressive pain, in 2010 my daughter passed away in a terrible manner and I had to quit my job because I could not perform it anymore.

The pain and depression really set in and that has been my lot since then--a round of pain here, depression there and endurance everywhere. Every sense is heightened and emotions run raw because of the constant pain. Hypertension increases because of pain. The immune system is taxed and stress levels run high because of the constant pain over all the skin. This is besides the other symptoms associated with other complications.

Each day I must rely on my faith to help me avoid lashing out at my family, which does not work everyday. I constantly need to remind my kids that they cannot jump on Daddy because I hurt.

I have to allow my wife to know when I can be touched because randomly showing me affection is not an option because I could be in pain. For years she was the only person to know about my pain until my health became serious in 2010.

Neuropathy not just in the feet
Neuropathy does not just occur in the feet. It can occur all over the body as it does with me. The nervous system basically starts to malfunction, similar to Fibromyalgia. The constantly overactive nervous system pain causes the most problems. Any person dealing with nerve pain alone has a difficult daily life, especially when medicines like Cymbalta only work partially to relieve the systems--I would rather have it than nothing at all. That is a whole other level of hell!

Cymbalta helps with the nerve pain and depression. Depression is a common companion for people dealing with chronic pain and health conditions. If you are accustomed to being the breadwinner and can no longer do so because of circumstance beyond your control like I am, life can be really hard to accept. It is important to be aware of your feelings and what is the root of negative feelings to avoid undue mental anguish. Because I know that I am prone to depression because of my health, I take steps to avoid slipping into depression bouts for long periods of time. It is a constant battle and I am not always successful.

Neuropathy, A small foot injury can cause a big hospital trip.
I went into the hospital because my blood pressure was 264/190 and my glucose levels were above 400 levels. The averages respectively are 120/80 and 80 to 120. I was on the verge of a stroke and a diabetic coma! I had gone to the emergency room by referral from the urgent care because of a swollen leg and foot. Apparently, due to my lack of feeling in certain parts of my foot, I had injured myself somehow.

Three days it took to get my blood pressure and glucose level under control, while I took morphine for pain--caused by my swollen leg. Each time in the past that I went to the hospital, no doctor would listen to me if my blood glucose levels were high because I am a diabetic.

They assumed that I ate irresponsibly. This time, I told them that my leg is swollen and painful, which is causing me to have high blood pressure. The pain prevents me from wanting to eat so I starve and my liver dumps sugar in my blood. No one would listen. It looked like I was about to be discharged once morphine took away the pain the insulin regulated my glucose levels enough for me to eat.I prayed all night that the nurse and doctors would notice my leg and foot, which I kept pointing out to them.

My wife called the nurses' station that very night and explained to the nurse to look at my foot. She did and saw nothing, but she felt impressed to call a wound nurse. The wound nurse saw a small dot on my foot and called the doctors. Four doctors saw my swollen foot and leg and three did not want to act while one adamantly suggested surgery.Three days these four doctors debated whether or not I should have an operation on my foot.

Three days I was made to lie in a hospital bed praying for something to be found wrong with me! I felt the pain and used the morphine. I knew something was wrong. I have the unfortunate face and body type that no one can look upon me and tell that I am ill. I look healthy no matter what I feel!

The doctors met on the third day discussing my situation. Two were against cutting into my flesh because it did not look like I needed it and all the tests and scans returned negative for a problem. Two thought something needed to be done other than elevating my foot. One of the two told the other three that he believes I had an infection that could be going towards the bone!.

Another day passed with the team of doctors in disagreement. I prayed more. One doctor, the one who knew that I had an infection, went to my room alone and asked me to sign a consent form to operate. He could not convince the other two anything was wrong because nothing showed on any test, but he was sure that he could see an infection--being that it was his specialty. The surgeon would not cut, so he decided he would. I gave him my consent and he cut open my flesh.

Out came a confluence of fluids that confirmed his suspicion. He had the nurse take pictures of the infection hidden behind my skin and removed the necrosis from my body.God answered my prayer by inspiring this doctor, Dr. Nwafor, to look beyond the machines and test and trust and impression.

God helped him find the problem so that he, God, could heal my disease. I spent the next month in a nursing home getting intravenous antibiotics. It was a strange experience being that I am so young to live in a nursing home, but God heard my prayer and gave me what I needed. And he did it for the entire month of September 2012 to the beginning of October 2012. The story with my foot does not end but continues through to 2014, but that's another article.

For information about Diabetes and how to increase awareness...
American Diabetes Association Home Page - American Diabetes Association
The American Diabetes Association is leading the fight against the deadly consequences of diabetes and fighting for those affected by diabetes.

Be Aware

Make sure if you have diabetes in your family tree that you take notice of your eating habits. You do not have to become a vegan, but you must eat a balanced healthy diet to avoid the early onset of diabetes.

Most people get diabetes in old age.

For
Native Americans,
Blacks
and Hispanics,

the rate of diabetes in younger people is exceptionally high.

Minorities are more likely to have the disease and must be aware of the genetic disposition. Native Americans are more susceptible than any other group.

Articles about Overcoming
Battles With My Body: Walking In Fear!
The worst part starts unexpectedly as I take the first step. I deliberately walk into the unknown each time I decide that I am independent enough to carry on without assistance.
Power in Prayer
But behold, I say unto you that ye must pray always, and not faint; that ye must not perform any thing unto the Lord save in the first place ye shall pray unto the Father in the name of Christ, that he will consecrate thy performance unto thee, that
Faith To Give Tithing
This tithing relationship with God is not one sided in nature. God expects us to show our devotion by giving back a tenth or ten percent of what he gives us annually. In return, he challenges us to test him. He challenges us to let him prove to us he
Scout Camp Revelation
A scout is honest and trustworthy still applies, though in that instance, that scout did not honor the rules of engagement in the game. Instead of judging the boy too harshly, I also reasoned that a person is not one good deed or one bad deed. A pers
Fibromyaliga: Say What?
Fibromyalgia means
Living with Chronic Pain: Psychological and Emotional Effects
Suffering with chronic pain is extremely difficult for the person with the pain, but also for the people around them. There are many psychological effects of chronic pain. This article discusses those effects.
Chronic Pain: How It Affects the Mind
Chronic pain is not merely harsh sensation but also an emotional experience. Avoid pain at all costs.
Living with Neuropathy and Other Chronic Pain Conditions
There are so many people that live with debilitating pain each and every day. It seems as if there are more and more of us all the time. I live with severe Peripheral Neuropathy, I have chronic pain 24/7. It may not be severe all the time but...

http://rodric29.hubpages.com/hub/Battling-Diabetic-Neuropathy