Case Study 4374

[4374] Journal of Neurological Inquiry Vol. 1 No. 1                              2011

A CASE OF EARLY CHILDHOOD ONSET PRIMARY PROGRESSIVE MULTIPLE SCLEROSIS ASSOCIATED WITH A BILATERAL BURNING CENTRAL NEUROPATHIC PAIN SYNDROME, NOTICABLE AT A VERY EARLY AGE, DUE TO PLAQUES THAT DEMYELINATED CERVICAL LEVEL PATHWAYS AND A SUBPOPULATION THAT WERE SEVERED BY A CHRONIC SPINAL CORD INJURY AT THE AGE OF FORTY SIX.

Mr. Antonio Domingo Valdez III, BS

This is a First Person Case Study

Journal of Neurological Inquiry Vol. 1 No. 1

Abstract:

I was born in September 20th of 1944. As a very young child I experienced burning sensations when I touched (glabrous skin) my mother’s silk, rayon or nylon fabrics in the crib and her bed (touch evoked tactile hyperalgesia), worse on my left side. Upon aging I experienced burning sensations when I applied pressure to touching objects, like holding down the frets on my brother’s guitar (mechanical pressure evoked hyperalgesia) worse on my left side. I also became aware that I was somewhat clumsy worse on my right side. At age 5-6 I developed new secondary areas of bilateral burning touch evoked tactile hyperalgesia from my hands up to my shoulders and from my feet up to my thighs (hairy skin), again a sensitivity to silk, rayon and nylon on hairy skin, most noticeable when I wore silk or rayon shirts, worse on my left side. Just before I left San Francisco, age seven or eight, polyester came out and I found that touching it was like touching a very hot object or getting electrocuted. In the mid 70’s around age early 30’s I developed burning sensations in my knees, worse in my right side. In my late 30’s and early 40’s I developed early sighs of urogenital problems ED and BPH. By 1964, age 20 I became aware that I was having bilateral difficulty in distinguishing between objects in my pockets, most noticeable on my right side. My tactile agnosia has never been complete, it is worse in my right hand.

In 1991, age 46, I was rear ended and experienced a severe whiplash and soon developed suicidal pain consisting of ever increasing burning spontaneous hyperalgesia on my glabrous skin, worse on my left side and in muscles inside my calves gastrocnemius muscle worse on the right side. I developed burning light touch tactile allodynia on my hairy skin where as a child experienced secondary areas of bilateral burning touch evoked tactile hyperalgesia, worse on my left side. I soon realized that if I shock my arms, hands, legs of feet my muscles within would burn (kinesthetic evoked hyperalgesia). My urogenital problem got worse to include hypertonic bladder with urgent urination with urinary leakage suggesting early demyelination and severing of the central canal. My burning pain became unbearable and I attempted suicide twice. The early appearance of my burning central pain syndrome, my diagnosis as having multiple sclerosis, and the lack of any “Relapses or Remissions” are evidence of very early childhood onset primary progressive multiple sclerosis.

Introduction

My first memories as a young child are of bilateral burning sensations in my fingers, glabrous skin, when I touched my mother’s silk, rayon or nylon fabrics in the crib and on her bed. These burning sensations were worse on my left side. I have clear memories of this burning sensation (touch evoked tactile hyperalgesia) years prior to my heart operation.

As child I knew before my heart operation (Tetrology of Fallot) at age five. [D109] that I was clumsy. As I grew my right leg became less dependable. When I returned home from my heart operation I stumbled down to stairs to my mother’s great distress.

I soon (age 5-6) developed secondary areas of bilateral burning touch evoked tactile hyperalgesia on hairy skin, from my hands up to my shoulders and from my feet up to my thighs, again a sensitivity to silk, rayon and nylon most noticeable when I wore silk or rayon shirts and worse on my left side.

When polyester fabric appeared in the 1950s, I discovered that it produced the most intense burning sensations (burning touch evoked hyperalgesia) of any substance that I have ever touched. I would do anything to avoid polyester clothing, a practice that I have followed throughout my life.

When I was a child I would not wear wool stockings as they irritated my skin (touch evoked tactile hyperalgesia).

While in grade school (age 6-11), I tried to play my brother’s guitar and the act of holding down the strings to the frets with my left hand produced an excruciating burning pain (mechanical pressure evoked hyperalgesia). I was told that calluses would form and I would not feel the burning pain. I never got to the point of calluses, as the burning pain was too extreme.

As a young child growing up in San Francisco (age 2-11) , I noticed that if I held a pencil too long my finger areas in contact with the pencil would tingle or even burn (mechanical pressure evoked hyperalgesia). Also, in grade school I noted that if I ran too far my feet would burn (mechanical pressure evoked hyperalgesia). All my life I would get watches but I would never wear them as they irritated my wrist (touch evoked tactile hyperalgesia and mechanical pressure evoked hyperalgesia).

Somewhere around 1950 to 1952, when I was six to eight years old, I was placed in a boarding school, where I helped to pile chopped wood. One time as I picked up a piece of wood, another child accidentally chopped the top of my head. This required hospitalization and stitches.

The earliest symptoms I brought to my doctor’s attention were after I moved up to Portland, Oregon from San Francisco (at age 11), I told him about a strange tingling (mechanical pressure evoked hyperalgesia) on my waist girdle the skin next to my pants, right or left, front or back, worse on my wallet side, my left side. He told me that I had “hip pocket syndrome” and that I needed to rotate things in my pockets. I later learned that there was no such thing as “hip pocket syndrome.”

When I worked I noticed that my hands and feet were prone to callus. I would cut them down with knives or razors.

Around 1960, I became active in sports and ran with the high school track team.  I wasn’t very good in the mile but I could do that same mile for miles and miles, so I ran cross-country. After a cross-country race I would sit in the locker room and complain about my “burning feet” while others complained about their “aching feet.”  This, too, I mentioned to my doctor, and was told to watch it, and if it ever changed for the worse to let him know.

After graduation I went into the Air Force Reserves.  Once I got out onto the rifle range my world changed for the better in a big way.  My rifle sergeant said I was an excellent shot but they would never let me have a gun, since I was hitting bull’s eyes into not only my targets, but also the targets of the airmen on either side of me. I got my first pair of glasses, diagnosed as having uncompensated strabismus, and found that I could then read for more than five minutes without getting a migraine headache.  I excelled in the Air Force Tech School, and when I got out of my six-month stint in the reserve I was allowed to enter Portland State College (PSC, now Portland State University) on probation in the performing arts program as a dance major.

By 1964, age 20, when I was in college, I became aware that I was having bilateral difficulty in distinguishing between objects in my pockets, most noticeable on my right side. I have never had a problem in thinking of a lighter, a set of keys or some change, as to their shape or purpose; I just have problems in distinguishing between these objects in my pockets. My tactile agnosia has never been complete, it is worse in my right hand.

I have never worn underpants to bed. If I could get away with it I would not wear them at all after my mid twenties.

As a child I loved to dance and skate. Even then I knew that my right leg was a little unpredictable. Nevertheless, I danced in all the school plays and went to every dance I could. While in the PSC dance program, I paid more attention to each movement and I became more concerned about my right leg.

In 1967, I got to know the Classical Indian musician Ali Akbar Khan (Khansahib), who was setting up his School Of Indian Music in Marin County, California. He saw me dance and I was offered a chance to go to India to study a form of classical Indian dance (Bharata Natyam). I spent a few days dancing at Winterland and the Fillmore, but I became convinced that I could not depend on my right leg and I had to decline Khansahib’s offer. That year I finally dropped out of the dance program at PSC because I knew that I had problems with my right leg.

Around 1965-68, age of 21 to 24, I noticed a tingling feeling that moved around like pins “on the go” on my shoulders and back (formications?) which appeared on and off for some years but have stopped for the last thirty five to forty years.

All of my life I’ve known that my memory wasn’t very good.  In fact, it was horrible and has continued to be a great embarrassment and inconvenience. However, I learned that if I crammed before tests, learned key ideas, studied things and made my notes like a relational database, I could do quite well. I intentionally avoided professors that gave pop-quizzes. In spite of my poor memory and in spite of the fact that I’ve always been a poor speller, I have managed to master subjects as diverse as philosophy, molecular biochemistry, physics, quantum chemistry, dance and theater with a 3.75 GPA.

In the mid 1970s, age of early 30’s, I noticed that if I held the black and white Xerox copies, (lots of toner), of articles that I was studying; my hands would start to tingle and burn (touch evoked tactile hyperalgesia). Since that time, this sensitivity has worsened.

Also in the mid 70’s I noticed a burning sensation in my knees I assumed was some forms of “dancer’s knees.” It is worse on my right side.

In the early 1980s I was diagnosed as having an enlarged prostate and experienced the beginnings of ED.
In the mid 1980s, I found that I was becoming increasingly clumsy. All my friends joked about how I would trip over anything. During that time as well, I started to experience increasing fatigue, increasing unsteadiness in walking, dancing and sensitivity to heat.  I went to Chronic Fatigue Syndrome meetings but found my situation did not fit the picture.

In the late 1980s, age of 43, I experienced two seizures in two days. I have never experienced another seizure since then.

In October of 1991, age 46, when I was going to work, the car behind me plunged into the rear end of my car and I received a severe whiplash. One morning, after the accident, when I was getting ready to put on my socks, I bent over and bent my head down to see what I was doing and a very sharp electric shock shot down my neck to my right leg and to my right foot. I went to my primary care physician and he told me that the shooting electric pain, Lhermitte’s sign could be the result of a number of different neurological problems (D72) 07/09/92. I had some additional X-rays and a MRI of my cervical spine, which revealed three hyperintensities.  I was told that I probably had MS or an AIDs related neuropathy. At this point I was referred to Richard Rosenbaum MD.

I had a series of MRIs done on my skull; and together with my physical signs I was provisionally diagnosed as having multiple sclerosis in August 1992 (D73). I next saw Robert J Grimm MD who performed sensory-evoked potentials. I had no problems with my visual or auditory pathways but there were significant delays in my somatosensory evoked potentials in my legs.

Since the accident I have not felt any pain in my viscera nor have I had any sense of hunger, thirst or satiation. Most unexplainable is the observation that I have also not hat a headache sence the accident.

About six months after the accident, I noticed that my feet (especially my toes), hands (especially my fingers) and the insides of my calf’s gastrocnemius muscle started burning all the time. The pain was slowly becoming stronger and stronger and become worse exponentially with time. The burning in my hands, feet and inner calf’s (burning spontaneous hyperalgesia) is similar to the touch evoked hyperalgesia in the same places, the calf’s were new, but are constant in time and not dependent on touching anything. These new burning spontaneous hyperalgesias were worse on my left side for glabrous skin and in my right calf’s gastrocnemius muscle.

I developed burning pain in my muscles when I shake my hands, feet, arms or legs. This phenomenon is most intense in my hands. If I shake or clap my hands, the muscles inside them burn (kinesthetic evoked hyperalgesia). This phenomenon is worse on my right side.

Areas of bilateral burning light touch tactile allodynia spread from my hands up to my shoulders and from my feet up to my thighs and buttocks. The same areas where I first experienced the appearance of bilateral areas of secondary burning touch evoked hyperalgesia on hairy skin on my arms and legs, worse on my left side, as a child.

After the accident, my touch evoked hyperalgesia and my mechanical pressure evoked hyperalgesia both got worse by orders of magnitude again worse on the left side of my body.

After the accident, my tactile agnosia got worse, worse in my right hand. Now I often need to take everything out of my pockets to get what I want since I cannot always feel the difference in items.

I developed chronic pelvic pain syndrome almost immediately after the accident. If I sit for any length of time, within seconds I develop chronic pelvic pain. If I consume cannabis required for pain relief my chronic pelvic pain worsens.

My urogenital problems: ED and benign prostate hyperplasia, both diagnosed prior to the accident, and hypertonic bladder after the accident suggest a possible of early demyelination of the central canal prior to the accident. After the accident urogenital problems, ED and benign prostate hyperplasia worsened. Hypertonic bladder and urinary urgency became very big problem. I have to have a bottle by my bed at night and if I have to go to a doctor’s appointment or if I want to go out I cannot have anything to drink because it goes through me like water through a sieve.

Putting my hands in warm water and massage (giving or getting) significantly reduces my bilateral burning spontaneous hyperalgesia, burning touch evoked tactile hyperalgesia, burning mechanical pressure evoked hyperalgesia and burning light touch tactile allodynia. Massage is a constant way of dealing with the above pains, especially my burning spontaneous hyperalgesia in my calves, which is as intense a pain as I have.

Most importantly, regarding my observed burning kinesthetic evoked hyperalgesia pain associated with shacking my hands, I cannot massage my pain away while shaking my hands and simultaneously massaging them together.

The most effective nondrug thing I can do is to not think of my pain. Significantly to think of a particular area (say my left index finger) as this will make the pain worse in that part of my body. This phenomena is not found on my right hand but on my left hand my little finger is nonresponsive to attention induced increase in pain, my ring finger is the weakest responder, and middle finger is next and my index finger  and my thumb is the most responsive. On my left foot, the large toe and the second toe are approximately equally sensitive to attention induced increases in pain where as the reaming toes are insensitive.

After the accident I gave away all of my socks, shoes, underwear and gloves. I only wear pants when I have to. I have a pair of sandals that I wear to go out in public but I take them off as soon as possible, during the winter people often ask me if my feet are not cold, I try not tell them that they are burning.

After about six months of constant worsening the pain over large parts of my body my pain got to 8-9 (in a 0 to 10 scale van Seventer R et al. (2011) <11539> Younger J et al. (2009) <11540>, where 10 is the pain I experience in the operation that corrected my uncompensated strabismus where I received four injections of xylocaine into my right eye) and I was suicidal.

When I went to the OHSU hospital I was given amitriptyline and several other tricyclic antidepressants.  I found that at low doses amitriptyline had some moderate antinociceptive properties but it was basically ineffective. In order to get very moderated pain relief I had to deal with very intense dry mouth, it was just not worth It.
I found my pain made it very hard to sleep, as there was no way I could lay in bed between the sheets without having my feet, thighs, arms and hands touch something that would make them burn. All I could do was lie there and burn and burn, no matter, which way I turned.  It increasingly became unacceptable. Getting into bed was like getting into a toaster and pushing down on the lever. I found that amitriptyline could not give me any significant relief. I started to use alcohol to help me get to sleep. Then I combined diazepam and alcohol.

My doctor did not like me combining diazepam and alcohol so I was put on morphine and Valium to allow me to get to sleep without alcohol, and I used morphine (40mg) and Valium (20mg) only at bedtime. Morphine had absolutely no effect on any of my pains and was only of use in helping me to get to sleep.  I did use excessive alcohol when I first was diagnosed and experienced the ever-increasing pain. I was without hope and my life was falling apart in front of my eyes.

I only wear sandals when I need to get somewhere outside but I take them off immediately when I get to where I’m going, like the wheelchair.  At home I don’t wear pants around as my care providers and some of my friends don’t care, with other people and for going out I wear cotton pants and live with the increased burning pain.

I believe that I suffer from a form of hypothermia. All of my care providers complain of the 76°F that I keep my home; I do only wear a short sleeve shirt, and no pants. No pants mean that I am experiencing very much less pain.

I have noticed that, like a lot of people with multiple sclerosis, hot temperatures knock me out; my ataxia is worst at high temperatures and gets better as the temperature lowers, but when I get to about 76°F I feel very comfortable, and if it goes lower I begin to get a chill at 75°F and at 74°F I start to fill a cold. When I go out, if it is not hot, I keep my coat on. I notice that I feel cold in environments that other people feel are fine.

The Multiples Sclerosis Society lent me a thermal vest that allows me to go out in hot summer days.

I initially slept on my left side as the burning light touch tactile allodynia is less intense on my right side and it is easier to get to sleep.

I soon realized that the only drug that helped was the use of large doses of marijuana. Marijuana was only effective at very large doses and even then it only reduced my pain from 8-9 to 8.

Dr. Kem Burchel told me that my condition was inoperable (D59) 05/31/94

I attempted suicide twice before I discovered, in 1994, a treatment for my neuropathic pain syndrome. Valdez III AD 1997[4375]
Because of my disabling pain and suicidal tendencies, I was rapidly accepted into social security and SDSD (Senior and Disabled Services Department) and am now receiving Medicaid and Medicare Parts A and B.

Carlton SM et al. (2009) “Following both complete and partial spinal lesions, chronic central pain syndromes develop in the majority of spinal cord injured (SCI) patients [Christensen MD and Hulsebosch CE (1997) <9247>], [Yezierski RP (1996) <9249>], usually within a month following injury [Richards JS et al. (1980) <9248>].” Carlton SM et al. (2009) <9246>

Carlton SM et al. (2009) “The pain so greatly affects the quality of life that depression and suicide frequently result [Cairns D et al. (1996) <9250>], [Segatore M (1994) <9251>].” Carlton SM et al. (2009) <9246>

Carlton SM et al. (2009) “This painful condition is permanent and because the lesion is often contained within the central nervous system (CNS), the condition is referred to as central neuropathic pain (CNP).” Carlton SM et al. (2009) <9246>

My burning sensations are similar to being burnt by a cigarette or being electrocuted. Before the accident the intensity was relatively minor but painful. After the accident the intensity was unimaginably horrible and extremely painful and frankly suicidal without the drug combinations that I describe in Valdez III AD 1997[4375] and Valdez III AD 1997[6549]. After the accident I developed pitting edema in my feet and hands, worse on the right side, my right foot and hand are cooler than on my right side. Over six to seven years of treatment with the drug combinations that I describe in Valdez III AD 1997[4375] and Valdez III AD 1997[6549] the pitting edema slowly reduced but still exists moderately worst on my right foot.

Immediately after the accident I experienced some sensory loss. Now I have developed extensive sensory loss over most of my body. Notable exceptions are my tongue and the inside of my buccal cavity. It is notable that I have few sensations when I have dental work, although some cavities are very painful.

I feel: cut, burn, and peripheral nerve pain like corn/callus pain in my feet, acute infection of a toe, but not pinprick, pinch, and blunt force injury. I have fallen many a time to later find a very large bruise having never felt it. I dislocated a finger and did not fill a thing. I developed an increased risk for getting large hematomas and I’ve had some big ones. Unfortunately I do not feel any pain and this puts me a risk for hurting myself and I take as many precautions as I can.

In 2007 I started using a tooth paste with whiteners. I soon developed burning mouth syndrome (BMS) characterized by what I thought was oral spontaneous hyperalgesia on my tongue and lips. I was terrified that my pain syndrome had evolved into my mouth.

After several months I mentioned this observation to my dentist and she told me that she was aware of some people having adverse reactions to whiteners. I discontinued the use of whiteners and my oral, what I came to realize, irritant evoked hyperalgesia slowly decreased and over a period of six to eight months they went away.

I live in my home and most of the time it is just me and my care provider that lives in my home. She does all of my paper work and cooking etc. I have two other care providers, one that cleans my living quarters, and fills in for the others when they need a hand, and one that brushes my teeth, shaves and bathes me, she also helps me with a few meals.

I can walk around the upper story of my home by firmly holding on to things, but I need to use a wheelchair to get around outside my home. I cannot use a cane because of burning pain. My wheelchair is controlled by a head sensor system, Magiteck, as I don’t like touching things, especially holding control devices. Holding something feels like holding an ever increasingly hot rod. I can hold onto things that I can massage.

Clinical Observations

MRI RESULTS:

“I have taken that scan to the radiologists and have reviewed it with the again because I saw some abnormalities on the scan that bothered me. The radiologists agreed that the scan is abnormal, and that there are at least three abnormalities in the cervical spine within the spinal cord itself. There are three bright spots on the scan that do not have any mass affect.” (D73)

“Multiple periventricular white matter hyperintensities are present;
including several involving the basal ganglia on the left are noted.  They
do not have any significant surrounding edema and no mass effect.  The
lesions vary in size and configuration and have slightly irregular margins. The largest ones are approximately 1 cm in size.  They are most likely secondary to multiple sclerosis. There is no hydrocephalus and no abnormal shift of the midline structures. There is no hemorrhage and no abnormal extracerebellar fluid collection. There also appears to be a lesion involving the posterior aspect of the cerebral peduncle on the right side and one of the basal ganglia lesions on the left is near the genu of the internal capsule. IMPRESSION: Multiple hyperintensities involving the brain stem on the right, the basal ganglia on the left and the periventricular white matter, most likely related to multiple sclerosis.” (D74).

A second reading of the MRI raised several questions as to diagnosis and interpretation: “Examination of the various MRIs (of the cervical spine – 5/7/92), lumbar spine (7/1/92) and head (7/22/92) reveal in the cervical spine views, e.g., upper thoracic, as well as the head view, T2 weighted roundy spots occasionally suggestive that they have rims scattered throughout the white matter of different size but without any suggestion of edema. Therein the white matter surrounds the ventricles but are not classically periventricular per se.  Importantly, high in one of the sagittal sections there are multiple of these little lesions scattered almost grape-shot like in the white matter, raising the question of whether this might be a vasculitis.” (D43)

CLINICAL VALUES:

The patient’s cerebrospinal fluid revealed 6 oligoclonal bands in the CSF and 0 in the serum.  Gamma globulin concentration was at the upper end of the normal range (14.0 mg/dl), as was the synthesis rate (+5.2 mg/day) the Index was above the normal range (0.89).  The results were interpreted as being consistent with an inflammatory and degenerative CNS disease (D42).

SOMATOSENSORY EVOKED POTENTIALS:

A series of average evoked potential measurements were done.  The Bilateral visual evoked potentials [VER] and the bilateral click evoked potentials [ABER] were normal.

Median Nerve Somatosensory Evoked Potential:

“Stimulation of the median nerve in the neutral position resulted in
reproducible waveforms on both sides except from the cervical response from the left.  Repeated trials failed to raise a clearly identifiable response. The intracord intervals (N10 – N20 norms: 9.1-10.7 msec) were 11.9 msec (L) and 10.6 msec (L).  The central conduction from Erb’s point to cortex (L) was markedly delayed, there was a minimal central delay between Erb’s point on to the recording point at C6-7.” (D44)

Posterior Tibial Nerve Somatosensory Response

“Stimulation of the posterior tibial nerves at each ankle 9- failed to
elicit clearly identifiable root entry response from either side; cortical
responses obtained were bilaterally markedly delayed (right) and 20.4 msec (left).” (D44)

Dr. Grimm (D44) gives his impression of the results.  “Multimodal EP studies were carried out in this cooperative man revealing normal VER and ABER responses. Both the cuneate and gracile fasiciular pathways reveal significant delays as demonstrated with median nerve and posterior tibial nerve stimulus points. This paces the lesions in the myelinated pathways between spinal cord and VPL of thalamus. As the ABER and VER responses are normal, these abnormalities are place at spinal cord levels.”(D44)

RNFL THICKNESS AVERAGE ANALYSIS REPORT

The results from my OTC scan are consistent with my lack of any VEP delays and my having primary progressive multiple sclerosis.

Henderson AP et al. (2008) “OCT measures of the RNFL thickness (RNFLT) and macular volume were studied in 23 patients with primary progressive multiple sclerosis (primary progressive MS) (13 male; 10 female; mean age 52 years; median EDSS 6.0; mean disease duration 11 years), and 27 patients with secondary progressive multiple sclerosis (secondary progressive MS) (8 male; 19 female; mean age 50 years; median EDSS 6; mean disease duration 22 years).” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “Twenty healthy controls (11 male; 9 female; mean age 46 years) had RNFLT and macular volume studied.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “The mean RNFL thickness and macular volume were significantly reduced in secondary progressive MS, but not in primary progressive MS when compared with control RNFL thickness and macular volume.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “RNFL loss was most evident in the temporal quadrant, where significant reduction was seen in primary progressive MS versus controls and in secondary versus primary progressive MS.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “There are significant global reductions in RNFLT and macular volume in the eyes of secondary progressive MS patients not previously affected by ON, but not in primary progressive MS patients, compared with controls.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “Of the patients with a primary progressive course, three had visual symptoms, predominantly blurred vision, and in two of these three patients glare sensitivity. The visual symptoms developed some time after the initial presentation, which in each case was a progressive spastic paraplegia. All of these patients had undergone a comprehensive visual assessment to exclude other causes of visual dysfunction. One further patient had an episode of difficulty perceiving moving objects that lasted 2 months, where she described moving objects as ‘smeared’, in the absence of ocular pain, scotoma or change in colour vision. She described her vision at the time of the study as normal. Twelve patients with a primary progressive course were judged on fundoscopy to have bilateral optic disc pallor, and a further four had unilateral disc pallor. ” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “The primary progressive MS patients had slightly worse logMAR and low-contrast acuity than controls but this was not significant. There was no significant difference between secondary progressive MS and primary progressive MS patients in terms of visual function.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “When both primary and secondary MS patients were analysed as a single group and compared with control values, there were significant reductions in mean RNFL thickness (patient–control difference 7.14 µm, P = 0.032, 95% CI: –13.63, –0.65), temporal quadrant RNFL thickness (patient–control difference –17.65 µm, P < 0.001, 95% CI: –25.61, –9.69) and macular volume (patient–control difference –0.27 mm3, P = 0.019, 95% CI: –0.50, –0.05). There was no significant difference between the pooled progressive patient group and controls in the superior quadrant RNFL thickness, nasal quadrant RNFL thickness or inferior quadrant RNFL thickness” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “If the primary progressive MS group was considered alone, the relationships remained significant for RNFL thickness and macular volume with all of the measures of visual acuity but not with visual field MD.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “The study demonstrates that there is retinal axonal loss in the eyes of progressive MS patients with no history of a previous episode of optic neuritis. The majority of these eyes were without visual symptoms. The mechanism for this axonal loss is not clear, but it may be that clinically silent demyelinating lesions within the optic nerve, associated with axonal damage with retrograde degeneration into the RNFL and macula have occurred. The visual evoked potential (VEP) obtained from the visually asymptomatic eyes of MS patients is frequently abnormal (Halliday A (1993) <8294>), suggesting that clinically silent demyelinating lesions are common in the optic nerves of patients with MS. ” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “The secondary progressive MS and primary progressive MS groups both had significantly lower temporal RNFL thicknesses than controls, and the secondary progressive MS group had significantly lower temporal quadrant RNFL when compared with the primary progressive MS group.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “In the primary progressive group, these measures were reduced, but this was not significantly different from either controls or the secondary progressive MS group. The smaller reductions in the primary progressive MS group than the secondary progressive MS group are in keeping with the clinical profile of primary progressive MS.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “There is little data that gives any indication of the frequency of optic nerve pathology in primary progressive MS.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “Our study was focused on typical cases of primary and secondary progressive MS, and the former tend to have predominant clinical involvement of the spinal cord and smaller brain MRI lesions loads than patients with secondary progressive MS.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “The primary insult in progressive MS is likely to be located in the optic nerve, and the RNFL atrophy reflects this. Whereas the ganglion cell bodies that lie within the macula might also be affected by optic nerve insults, the macular volume measurements include the full thickness of the retina, of which only part would be directly affected by an insult to the optic nerve.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “The standard deviation of the mean for RNFL in normal eyes is ~11% (Budenz DL et al. (2007) <8295>) and in our study the standard deviation of the mean for controls was 10.6% for RNFL thickness. This natural variation reduces the sensitivity of cross-sectional studies such as the current one to group-based change, suggesting that large cohorts will be required in order to detect small but potentially relevant differences. This is particular relevant when considering the OCT findings in primary progressive MS: it is notable that although this group did not have significantly smaller RNFL thickness than controls, there were significant correlations of the retinal and macular measures with visual function in the former but not latter group, suggesting that subtle but functionally relevant retinal axonal loss occurs in primary progressive MS.” Henderson AP et al. (2008) <8290>

Henderson AP et al. (2008) “In addition, the higher EDSS associated with progressive MS is also often substantially influenced by spinal cord disease including axonal loss, and this may be relatively dissociated from pathological changes in the optic nerve (and retinal nerve fibre layer) when compared with the earlier relapsing remitting phase of MS where predominantly inflammatory demyelinating lesions determine both OCT abnormality and EDSS.” Henderson AP et al. (2008) <8290>

In contrast to the primary progressive multiple sclerosis patients in Henderson AP et al. (2008) <8290> I have no subtle nor functionally relevant evidence of retinal axonal loss.

Non-clinical Observations

Birth defects

I have a number of birth defects including: A family history of multiple sclerosis [….], Tetralogy of Fallot and patient ductus [….], uncompensated strabismus (D109), ptosis of the eyelids (bilaterally), Multiple lipoma, keratosis pilaris, hyperkeratosis palmaris and plantaris (D110), milk protein allergy (producing nasal congestion), fermented grape protein allergy, sprouts, and soy protein allergy (producing dehydrating vomiting and diarrhea). I also have late onset allergies (starting in my mid 30s) to dander’s, pollens, etc., that have reduced with older age, unlike my food allergies that have remained dangerous in the case of soy that is in prepared food. If there is no label I do not eat it.

“Familial keratosis palmaris et plantaris (KPPF) is characterized by extreme keratinization and desquamation of the skin of the palmar and plantar surfaces of the hands and feet.” Rogaev EI et al. (1993) <8209> “We have mapped the causative genetic defect to an 8 cM interval on 17q12-24 in or close to the acidic keratin (type I) gene cluster.” Rogaev EI et al. (1993) <8209> “Some pedigrees with familial hyperkeratosis of the palms and soles have co-inherited diseases such as congenital malformations and familial cancers” Rogaev EI et al. (1993) <8209>. I have no history of familial cancers but I do have the Tetralogy of Fallot and patient ductus.

Family history of multiple sclerosis

I have two distant cousins on my father’s side of the family that had multiple sclerosis.[Dxxx]

Tetralogy of Fallot

I was born in September of 1944, a quiet and well-behaved baby. Too quiet and too well behaved.  When I was four I was diagnosed as having the Tetralogy of Fallot and patient ductus.  I was lucky enough to survive the condition. I received a life-saving heart operation at Stanford University Hospital (04/23/50, 05/07/50), by Doctor Emile Holeman (D109). The experience stunted my development in many ways. I grew almost three inches after graduating from high school. My pubic hairs didn’t start growing until I was a sophomore, and my lungs are very large.

Prior to the operation I was fascinated by the following observation and as a child I often did it for amusement. After my diagnosis my mother told me to stop doing it.

If I got down on my knees and then stood up rapidly (without hyperventilating) I would have hallucinations and simultaneously I would have a sensation of what I thought was “…like my blood flowing down my arms and legs…” on my hairy skin of my arms and legs. I would then pass out. I have no memories of my blood flowing down from my stomach, my back, nor from my head. I felt the blood flowing down sensations only in those areas that are consistent with my areas of secondary hyperalgesia that appeared soon after the age of five to six. When I returned home from the heart operation I tried to repeat the rapid standing up routine and found that it was no longer possible.

As a child, I became aware of my increasing clumsiness. Before my heart operation, my clumsiness was clear and upon returning from the hospital I stumbled down the stairs like I did many times as a young child. This could be understood as a reflection of the effect of congenital heart disease on functional abilities. Even after the heart operation, its long-term effects on functional abilities would be understandable. But as I aged my right leg became less and less dependable. Around the age of ten, playing in the schoolyard, I knew something was wrong with my right leg. In a study of functional abilities in young adults with congenital heart disease: Wright M et.al 1985 found in a study of patients with congenital heart disease, including Tetrology of Fallot, that.”Overall, physical function scores were slightly below average.” Wright M et.al. 1985 <6703>

Uncompensated strabismus

I was born with uncompensated strabismus. My double vision went undetected until I was in the Air Force.  From the start of my education, I complained of chronic headaches when I was required to read, but I was treated as if I was a troublemaker. I passed eye exams, which I’ve since learned were impossible for me to have passed.  I was put in the back of the class, where I could not see the black board.  I flunked out of the fifth grade and after that I was quietly allowed to slide by until I was out of school.

When I was in my early thirties, Dr. Andrea C. Tounge performed corrective surgery on my right eye and corrected the double vision (Uncompensated Strabismus). Luckily in a few years I developed depth perception (citation).  My daughter also inherited my uncompensated strabismus. Early patching and glasses successfully treated her vision problem.

Immunology

I have experienced an enterocolitis like food allergy to soy, sprouts or fermented grape as long as I can remember. As a child, soy, sprouts or fermented grape would produce dehydrating diarrhea, emesis, and irritability, dairy would cause sinuous congestion. “Dietary protein enterocolitis generally presents in the first year of life with diarrhea, emesis, and irritability.” Lake AM 2001 <6617> Lake AM also notes that “The offending antigen is usually cow’s milk protein or soy protein.”I have been hospitalization for dehydration due to fermented grape or soy over 20 times in my life, mostly due to soy as it is hardest to avoid due to the failure of producers to identify it in products. Unlike enterocolitis, my diarrhea is never bloody but the vomit and the stool have a very unique foul smell.

I have had contact dermatitis to grass all my life. Lying on grass as a child was unacceptable as it produced an extremely painful burning sensation on my hands, arms, feet and legs.

When I got older I had to work in many agricultural environments and found that wheat, alfalfa and been fields were irritating but that I would not work in berry (strawberry, raspberry or blue berry fields) as they produced burning skin dermatitis much like grass. Strawberries, raspberries, blue berries and poppy seed give me diarrhea, oral allergy symptoms of burning lips and tounge and increased mucus-like fine gritty material in my mouth especially noticeable on my teeth and difficulty in swallowing.

I eventually developed late onset allergies (late thirties, peaking in late forties and now tapering off) to danders and pollens

I still have unidentified food allergies as all my life I get people commenting on me smacking my lips and I suffer from oral allergy symptoms.

URGENCY

Overactive bladder (OAB)

From Appendix in Blaivas JG et al. (2007) <8234>

My answers to Blaivas JG et al. (2007) <8234> Appendix:

Appendix

1.What is the reason that you usually urinate?

X Because I have desperate urge (must stop what I am doing and go immediately)

2.Once you get the urge to urinate, how long can you usually postpone it comfortably?

X Must go immediately

3.How often do you get a sudden urge to urinate that makes you want to stop what you are doing and rush to the bathroom?

X Daily

4.How often do you get a sudden urge to urinate that makes you want to stop what you are doing and rush to the bathroom but you don’t get there in time (eg, you leak urine or wet pads)?

X Daily

5. In your opinion how good is your bladder control?

012345678910

perfect controlgood controlno control at all

I say 9 because I do not have total incontinence but I do have total urgency.

Mitra R et al. 2009 describe “A 79-year-old woman with a history of chronic back pain and urinary urgency.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “She described her sense of urgency as severe, and could delay urination for 10 min or less.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “She described her bladder control as 6 out of 10 on the urgency perception score (with 0 being perfect control Blaivas JG et al. (2007) <8234>).” Mitra R et al. 2009 <7841>

She was “Diagnosis Overactive bladder associated with severe central-canal stenosis at L4–5, in the setting of anterolisthesis.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “MRI of the lumbar spine revealed a grade 1 anterolisthesis of L4 on L5, with associated severe central-canal stenosis and bilateral subarticular stenosis.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “The patient was diagnosed with spinal stenosis, and was scheduled for a caudal epidural steroid injection for pain relief.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “The sacral spine was identified with the use of fluoroscopy in the lateral view, and the skin was prepared using aseptic technique. The sacral hiatus was palpated and marked. A 3.5 inch (8.9 cm) 22 gauge curved Tuohy spinal needle was slowly advanced through the sacral hiatus using the lateral view into the epidural space. Next, 1 ml of iohexol was injected, and revealed epidural spread. After negative aspiration, a 7.5 ml solution containing 60 mg of triamcinolone, 3 ml of 1% lidocaine hydrochloride, and 3 ml of normal saline was injected in increments. The stylet was reinserted and the needle was removed.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “The patient had immediate pain relief, and had an instant sense of relief of her urgency symptoms. At 1 month follow-up, the patient’s low back pain had diminished considerably; she had a VAS pain score of 1 out of 10. Her urinary urgency had greatly resolved, and her bladder control improved by 50% on the urgency perception score to 3 out of 10. Her main reason for urination after the injection was “out of convenience”, and she was able to postpone urination for longer than 60 min.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “This patient’s OAB was associated with spinal stenosis. Severe central-canal stenosis with cord compression is known to produce urinary retention (”cauda equina” syndrome); however, the relationship between spinal stenosis and OAB is not well defined. Spinal pathology may be a cause of OAB, as the S2 and S3 nerve roots are primary regulators of bladder function, and spinal stenosis may be a common and overlooked treatable cause of OAB. Again, no established algorithm for spinal evaluation of patients with the symptoms of OAB exists, and an unknown percentage of patients with a diagnosis of idiopathic OAB might actually have an identifiable underlying disorder. Patients with symptoms of OAB that are refractory to conventional management may benefit from diagnostic spinal imaging (e.g. lumbosacral MRI) to rule out clinically significant spinal central-canal stenosis. The assumption that the OAB was caused by the spinal stenosis in this patient was attributed to the dramatic change in urgency immediately after the epidural steroid injection, as well as the change in her urgency perception score.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “To our knowledge, urinary urgency successfully managed with lumbosacral steroid and anesthetic injections has not been reported to date. Although epidural steroid injections have traditionally been utilized in the management of pain disorders, they might also represent an option in the management of OAB in patients with spinal stenosis, and may be preferable to standard pharmacologic therapy.” Mitra R et al. 2009 <7841>

Mitra R et al. 2009 describe “As the patient improved with epidural steroid injection, this case indicates that an inflammatory component might be involved in urinary urgency. The other possibility is that the steroid–anesthetic mixture modulated sacral afferent pathways. Pre-injection and post-injection urodynamic studies may have helped shed better light on the phenomenon. Our Case Study was also limited by the short-term follow-up of 1 month.” Mitra R et al. 2009 <7841>

As demonstrated in the appendix above I have a bladder control of 9 out of 10 on the urgency perception score (with 0 being perfect control Blaivas JG et al. (2007) <8234>).” I have always had some issues with loss of bowel function. As my severing of the central canal is at the cervical level I have not found a Neurologist or an Urologist that could find a pharmacological or surgical solution to my urgency problem.”

THE ABILITY OF SURFACES T0 ACTIVATE MY SKIN RECEPTORS

The following is a partial list of objects ranked in the order of their intensity of inducing bilaterally my burning touch evoked tactile hyperalgesia:

Polyester >>rayon > silk,> nylon >Toner/Xerox copies > Wool > Copper > Paper > Silver > Nickel >>Cotton > Leather >Skin

The nature of the coating and the texture of the material change this order in complex ways.

For example:

Rough polyester sweater >> smooth polyester paint brush fibers.

Smooth paper >> rough paper

I discuss these observations elsewhere; see Valdez III AD 2009 [7911].

My opiate resistant neuropathic pain and the mirror-neuron system

One day after, my opiate resistant neuropathic pain syndrome had became fully developed and I was actively attempting suicide, I received a catalogue in the mail that was very painful to look at; it was a thick color catalogue of shoes, stockings and gloves. To this day I avoid looking at people’s feet or hands if their wearing gloves. If I see someone wearing shoes and stockings I feel their pain and although it is just “my problem” it stills burns.

A good friend of mine recently removed his shoes and stockings in front of me and my grimace turned to a smile of relief.

Jackson PL et al. (2005) “The results demonstrated that perceiving and assessing painful situations in others was associated with significant bilateral changes in activity in several regions notably, the anterior cingulate, the anterior insula, the cerebellum, and to a lesser extent the thalamus.” Jackson PL et al. (2005) <11812>

Jackson PL et al. (2005) “These regions are known to play a significant role in pain processing.” Jackson PL et al. (2005) <11812>

Jackson PL et al. (2005) “Finally, the activity in the anterior cingulate was strongly correlated with the participants’ ratings of the others’ pain, suggesting that the activity of this brain region is modulated according to subjects’ reactivity to the pain of others.” Jackson PL et al. (2005) <11812>

Jackson PL et al. (2005) “Our findings suggest that there is a partial cerebral commonality between perceiving pain in another individual and experiencing it oneself.” Jackson PL et al. (2005) <11812>

Jackson PL et al. (2005) “This study adds to our understanding of the neurological mechanisms implicated in intersubjectivity and human empathy.” Jackson PL et al. (2005) <11812>

Cheng Y et al. (2008) “Accumulating evidence demonstrates that similar neural circuits are activated during the first-hand experience of pain and the observation of pain in others.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “However, most functional MRI studies did not detect signal change in the primary somatosensory cortex during pain empathy.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “To test if the perception of pain in others involves the primary somatosensory cortex, neuromagnetic oscillatory activity was recorded from the primary somatosensory cortex in 16 participants while they observed static pictures depicting body parts in painful and non-painful situations.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “The left median nerve was stimulated at the wrist, and the poststimulus rebounds of the approximately 10-Hz somatosensory cortical oscillations were quantified.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “Compared to the baseline condition, the level of the approximately 10-Hz oscillations was suppressed during both of the observational situations, indicating the activation of the primary somatosensory cortex.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “Importantly, watching painful compared to non-painful situations suppressed somatosensory oscillations to a significant stronger degree.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “In addition, the suppression caused by perceiving others in the painful relative to the non-painful situations correlated with the perspective taking subscale of the interpersonal reaction index.” Cheng Y et al. (2008) <11828>

Cheng Y et al. (2008) “These results, consistent with the mirror-neuron system, demonstrate that the perception of pain in others modulates neural activity in primary somatosensory cortex and supports the idea that the perception of pain in others elicits subtle somatosensory activity that may be difficult to detect by fMRI techniques.” Cheng Y et al. (2008) <11828>

Ramachandran VS and Brang D (2009) “Sensations evoked in patients with amputation from watching an individual whose corresponding intact limb is being touched.” Ramachandran VS and Brang D (2009) <11829>

Ramachandran VS and Brang D (2009) “After amputation of a limb, the majority of patients experience phantom sensations, such as phantom pain. Such patients provide an opportunity for the exploration of the perceptual correlates of recently discovered “mirror neurons,” which fire not only when individuals move their own limb but when they watch the movements of the corresponding limb of another person. Similar neurons exist in the secondary somatosensory cortex for touch: they fire when the individual is touched or simply watches another person be touched. While these neurons cannot by themselves discriminate between the two, the mind is aware of the difference between feeling and watching; one does not confuse empathy with actual experience.” Ramachandran VS and Brang D (2009) <11829>

Ramachandran VS and Brang D (2009) “To investigate whether patients with amputation experience the sensations of another person in their own phantom limb during the mere observation of someone else being touched, owing to removal of the inhibition of the mirror neuron system that would have occurred had the limb been intact.” Ramachandran VS and Brang D (2009) <11829>

Ramachandran VS and Brang D (2009) “We report that 4 individuals with arm amputation, the mere watching of the intact hand of another being touched evokes vivid, precisely localized sensations in their own phantom hands.” Ramachandran VS and Brang D (2009) <11829>

Ramachandran VS and Brang D (2009) “We suggest these evoked sensations are owing to removal of neural signals from the hand that would have ordinarily inhibited the response of the mirror neurons and prevented their activity from reaching the threshold of conscious awareness.” Ramachandran VS and Brang D (2009) <11829>

Ramachandran VS and Brang D (2009) “Neurons in the prefrontal cortex send signals down the spinal cord that orchestrate skilled and semi-skilled movements such as putting food in the mouth, pulling a lever, pushing a button, etc.1 Mountcastle VB (1995) <11830> These are “ordinary” motor command neurons, but some of them, known as mirror neurons, also fire when one merely watches another person perform a similar act. It is as if the neuron (or, more strictly, the network of which the neuron is part) used the visual input to do a sort of “virtual reality simulation” of the actions of the other person. This allows one to empathize with the other person and view the world from his or her point of view.2 Rizzolatti G et al. (2006) <11831>, 3 Cattaneo L and Rizzolatti G (2009) <11832>, 4 Gallese V et al. (1996) <11777>, 5 Iaccoboni M (2008) <11833>” Ramachandran VS and Brang D (2009) <11829>

Ramachandran VS and Brang D (2009) “There are also “touch mirror neurons” in the secondary somatosensory cortex that fire not only when the skin is touched but also when one merely watches someone else being touched.5 Iaccoboni M (2008) <11833>, 6 Keysers C et al. (2004) <11834> This raises an interesting question: how does the neuron know what the stimulus is? Why does the activity of these neurons not lead one to literally experience the touch delivered to another person? How does “oneself” know who is being touched? One possibility is that the tactile receptors in the skin tell the other touch neurons in the cortex (the nonmirror neurons) that they are not being touched, and this null signal prevents touch sensations from reaching the threshold of conscious awareness. The net result is that one empathizes with but does not actually experience the touch quale.” Ramachandran VS and Brang D (2009) <11829>

Discussion

As a very young child, one of my earliest memories was of burning pain when I touched my mother’s silk, rayon or nylon fabrics in the crib and her bed (touch evoked tactile hyperalgesia). Then at age 46 I had a whiplash spinal cord injury to a prior existing condition. This evolved into suicidal pain.

I have a multifiber tract injury to my cervical spinal cord. The demyelination and severing of fiber tracts led to pain and visceral-urogenital problems.

I. The demyelination and severing of the central canal fiber tract led visceral-urogenital problems.

After the accident I have not felt any pain in my viscera nor have I had any sense of hunger, thirst or satiation. I also developed immediate urgency and a worsening of preexisting BPH and ED. I was eventually diagnosed with hypertonic bladder. As demonstrated in the appendix above I have a bladder control of 9 out of 10 on the urgency perception score (with 0 being perfect control Blaivas JG et al. (2007) <8234>). I have always had some issues with loss of bowel function.

My MRI’s, SSEP’s, loss of visceral sensations, and central neuropathic opioid resistant pain indicate that the dorsal column medial lemniscus pathways are sites of early demyelination.

Since the accident I have not felt any pain in my viscera nor have I had any sense of hunger, thirst or satiation. Willis WD et al. reported that “A limited midline myelotomy at T10 can relieve pelvic cancer pain in patients.” Willis WD et al. 1999 <6900>. Willis WD et al. further reported on a “… series of experiments, a balloon catheter was chronically implanted in the duodenum in rats through the stomach wall (Feng Y et al. 1998 <6901>). Graded distention of the duodenum in awake, behaving animals resulted in graded intensities of the writhing reflex. A lesion of the DC at C2 produced a dramatic reduction in the intensity of the writhing reflex … However, to be effective, the lesion had to include the region of the dorsal intermediate septum bilaterally.” Willis WD et al. 1999 <6900>

Honda CN found that “…in the sacral spinal cord many cells near the CC (central canal (CC)) receive primary afferent inputs converging from a wide range of receptor types in somatic and visceral structures. Such neurons are capable of integrating afferent information from somatic structures on both sides of the body with information originating in pelvic viscera and midline regions such as the genitals.” Honda CN 1985 <7852>

Mitra R et al. describe a 79-year-old woman with a history of chronic back pain and urinary urgency she could delay urination for 10 min or less very much like my situation. I do not drink fluids if I have to go outside, since when I get the sensation that I need to urinate I have less than one minute. Mitra R et al. made the diagnosis of “…overactive bladder associated with severe central-canal stenosis at L4-5, in the setting of anterolisthesis” Mitra R et al. 2009 <7841>.

“Lesions of the dorsal columns block pelvic cancer pain (Hirshberg RM et al., 1996 <4223>; Nauta HJ et al. 1997 <4219>), pain associated with pancreatitis … (Houghton AK et al. 1997 <5044>, Houghton AK et al. 2001 <7444>).” Ossipov MH et al. 2002 <6943>

“The excitation of neurons of the n. gracilis or of the ventroposterolateral nucleus of the thalamus elicited by colorectal distension or a noxious cutaneous pinch was blocked by lesions of the dorsal columns (Al-Chaer et al.  Al-Chaer ED et al. 1996a <4226>, Al-Chaer ED et al. 1996b <4227>).” Ossipov MH et al. 2002 <6943>

The above mentioned observations are consistent with the proposition that I have a severed central canal. This is consistent with my visceral loss of hunger, satiation and nociception, and my bladder (disruption of micturition reflex), and my ED.

My bladder problems are complicated by my use of baclofen, diazepam and cannabis in my pain treatment combination of drugs described in Valdez III AD 1997[4375].

Miyazato M et al. (2008) “The results of the present study indicate that intrathecal application of muscimol or baclofen decreases urethral pressure elevation during bladder contractions and changes a pattern from DSD (detrusor-sphincter dyssynergia) to detrusor-sphincter synergy in SCT(spinal cord transection) rats. These effects were apparently mediated by GABAA and GABAB receptors, since the actions of muscimol and baclofen were completely suppressed by the selective antagonists bicuculline and saclofen, respectively.” Miyazato M et al. (2008) <8240>

II. The demyelination and severing of fiber tracts in my cervical tracts led to my opiate resistant neuropathic pain syndrome.

Spencer PS and Schaumburg HH (1976) reported that in “Rats and cats intoxicated with hexacarbons displayed giant axonal swellings in vulnerable regions of the PNS degeneration in these animals was accompanied by pronounced endoneurial edema. In the CNS, rostral regions of long, ascending tracts (dorso-spino-cerebellar, gracile and, later, the cuneate) and the caudal end of long, descending tracts (lateral columns, ventrolateral and ventromedial tracts) of hexacarbon-treated animals were especially vulnerable. After prolonged intoxication of cats with MBK, giant axonal swelling was also found in preterminal and terminal axons in Rexed laminae V-VII at spinal levels C4 through S3-Neurofilament proliferation without giant axonal swelling was seen in CNS fibers of rats intoxicated with acrylamide.” Spencer PS and Schaumburg HH (1976) <37>

Spencer PS and Schaumburg HH (1976) defined the term “…central-peripheral distal axonopathy is introduced to emphasize the widespread, distal distribution of disease in these and in similar experimental conditions. It is suggested that certain human neuropathies (toxic, nutritional, uremic, diabetic and some hereditary polyneuropathies, and the neuropathy associated with multiple myeloma) are additional examples of central-peripheral distal axonopathies.” Spencer PS and Schaumburg HH (1976) <37>

Suzuki C et al. (2000) found that “Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT (central conduction time) abnormality does not coincide with lowering of the peripheral sensory conduction. The current results do not favor a hypothesis that a central-peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.” Suzuki C et al. (2000) <8223>

I have a central axonopathy similar to Spinal Cord Injury (SCI) where multiple fiber tracts are damaged.

Rance NE et al. (1988) described “Gracile tract degeneration in patients with sensory neuropathy and AIDS.” Rance NE et al. (1988) [22]

Rance NE et al. found that “At autopsy, four homosexual men with acquired immunodeficiency syndrome (AIDS) were found to have selective degeneration of the gracile tract, a finding previously unreported in AIDS.  Clinically, these patients had progressive lower extremity paresthesias and dysesthesias with reduced or absent ankle jerks, and eventually they developed dementia.  Postmortem examination of spinal cords showed a striking loss of both axons and myelin sheaths confined to the fasciculus gracilis, with the most severe involvement in upper thoracic or cervical segments.  Lumbar dorsal columns showed only a mild fiber loss, and no fiber loss was observed in lumbar dorsal roots.  Lumbar dorsal root ganglia were available from one patient and showed a mild sensory ganglionitis.  In all cases examined, micrtoglial nodules were present in the brain.  In 23 other individuals with AIDS who had autopsies consecutively with these four subjects, none had sensory neuropathy and the gracile tracts were normal.  The combination of distal sensory neuropathy and gracile tract degeneration suggests a ‘dying-back’ process of dorsal root ganglia neurons.” Rance NE et al. (1988) [22]

Rance NE et al. found that “The spinal cords from these four patients showed a common pathologic feature: degeneration of the gracile tracts.  Gracile tract degeneration was sufficiently marked in three subjects…as to be readily apparent in H-E stained section.  In all patients, pallor of the gracile tract was most prominent in the upper thoracic or cervical cord…and N-F silver stains confirmed loss of both myelin and axons with the upper part of the fasciculus gracilis.  Macrophages were present in these regions indicating that the changes were not postmortem artifact.” Rance NE et al. (1988) [22]

Rance NE et al. found that “The majority of ganglion cells appeared normal.  There appeared to be a mild reduction in the number of sensory neurons associated with nodules of satelite cells (nodules of Nageotte)…and infrequent giant axonal swellings.  A mild sensory ganglionitis (i.e., lymphocytic infiltration associated with some of these nodules) was noted, but there was no evidence of viral inclusions or opportunistic infection.  Electronmicroscopy of ganglia confirmed (1) the presence of occasional nodules of satelite cells (with surrounding basal lamina) in foci lacking neuronal perikarya; and (2) the existence of small numbers of neurofilament-filed giant axonal swellings.  No viral particles were seen.” Rance NE et al. (1988) [22]

Rance NE et al. found that “In all four patients, the rostral gracile tracts were severely affected, with little or no involvement of more caudal regions.  The lumbar dorsal roots showed no detectable loss of sensory nerve fibers…  This type of pathology is characteristic of distal axon degeneration of the central process of the primary sensory neurons, or a dying-back process involving dorsal root ganglion cells. (Spencer PS and Schaumburg HH (1976) <37>)  In these disorders, the distal regions of the longest axons are affected first.  With progression, these axons degenerate in a centripetal fashion, and shorter fibers become involved.” Rance NE et al. (1988) [22]

Rance NE et al. found that “…the four patients with gracile tract degeneration clearly had prominent sensory complaints, absent or reduced ankle reflexes, and abnormal sensory examinations consistent with a distal sensory neuropathy.” Rance NE et al. (1988) [22]

Rance NE et al. found that “Taken together, the clinical and autopsy findings suggest that sensory neuropathy with gracile tract degeneration represents distal axonal degeneration of sensory neurons in the lumbosacral ganglia.” Rance NE et al. (1988) [22]

Beric A et al. (1988) discussed the “Central dysesthesia syndrome in spinal cord injury patients.” Beric A et.al. (1988) [21]

Beric A et al. (1988) described …13 spinal cord injury patients with a complaint of diffuse, ongoing dysesthesias below the level of the lesion, which are burning in quality, and usually functionally limiting. Quantitative sensory and neurophysiological testing revealed relative preservation of the dorsal column functions in comparison to absence of spinothalamic system mediated functions. Beric A et.al. (1988) [21]

Beric A et al. (1988) concluded that On the basis of these findings, we are speculating that such an imbalance between the spinothalamic and dorsal column systems is the main underlying mechanism of dysesthesias as a central nervous system misinterpretation of residual peripheral input.Beric A et.al. (1988) [21]

Beric A et al. (1988)The results of quantitative sensory examination and neurophysiological testing showed that a common feature of most of our patients was the presence of vibratory and touch perception in contrast to absence of temperature and pain, indicating relative preservation of the dorsal column function with virtual abolition of the classical anterolateral, spinothalamic system function.Beric A et.al. (1988) [21]

Beric A et al. (1988)The difference between the involvement of dorsal column and the spinothalamic systems might be further emphasized by the observed worsening of the dysesthesia during SCS <spinal cord stimulation for spasticity via epidural electrodes> with 50-100 Hz.Beric A et.al. (1988) [21]

Beric A et al. (1988)This is in accordance with the fact that the dorsal columns are often degenerated in the population of severe SCI patients and thus the substrate for pain relieving stimulation is missing, resulting in negative general experience with SCS in SCI pain (Richardson RR et al. (1980) <36>)Beric A et.al. (1988) [21]

Beric A et al. (1988) “In analogy with the present findings, dysesthesias may occur after spinothalamic cordotomy.” Beric A et.al. (1988) [21]

Beric A et al. (1988) “Another high incidence of diffuse dysesthesias has been reported after the mesencephalic spinothalamic tractotomy operations performed for pain relief in the 1940’s (for review see Cassinari V and Pagni CA (1969)  <1569>).” Beric A et.al. (1988) [21]

Beric A et al. (1988) “Boivie et al. (Boivie J et al. (1987) [42]) observed in their series of stroke patients, that if the patient had a concomitant post-stroke pain or dysesthesias on quantitative sensory examination, there was invariably absence of ascending anterolateral system functions with preserved or even normal dorsal column system functions.” Beric A et.al. (1988) [21]

Beric A et al. (1988) discussed the “Furthermore, Pagni (Pagni CA (1976) <7893>) concluded on the basis of his own results and a thourough review of reported cases with central pain that lesions of the spinothalamic system regardless of the level they occur produce dysesthsias and pain while lesions of dorsal column system may produce only paresthesias.  Pagni also pointed out that the isolated lesions of the dorsal column-medial lemniscus system do not proudce pain (Pagni CA (1976) <7893>).” Beric A et.al. (1988) [21]

Beric A et al. (1988) discussed the “There is even a possible animal model to study the dysesthesias originating from spinal lesions.  Levitt and Levitt described unusual pain behavior in monkeys after anterolateral cordotomy (Levitt M and Levitt JH (1981) <1574>).” Beric A et.al. (1988) [21]

Beric A et al. (1988) discussed the “Occurrence of pain dysesthesias with loss of spinothalamic but preservation of dorsal column function is actually opposite to the expectations of the gate control theory (Melzack R and Wall PD (1965) <2950>, Wall PD Brain, 101 (1978) 1-18. <2292>), which postulates pain inhibition through large fiber systems.” Beric A et.al. (1988) [21]

Beric A et al. (1988) discussed the “We can speculate that the gate mechanism at the spinal level below the lesions is grossly intact in these patients, as there was no sign of dysfunction at the peripheral level as documented by normal LSEPs.  We propose that the pain producing dysfunction is located rostrally, at the lower brain-stem level or thalamus.  At least at the thalamic level there is an evidence of both functional and morphological convergence of spinothalamic and dorsal column systems (Boivie JJG and Perl ER (1975) <7894>, Ma W et al. (1987) <3337>).  Our speculation is that dysesthesias may result from central misinterpretation of residual dorsal column system input in the absence of suppression via integrated spinothalamic system activity.” Beric A et.al. (1988) [21]

Beric A et al. (1988) discussed the “We would propose to call the presence of spontaneous, uniform, diffuse, unpleasant, burning sensation in patients with disproportionate dysfunction of spinothalamic and dorsal column systems, the ‘central dysesthesia syndrome.’  ‘Central’ would indicate the apparent absence of dysfunction of the peripheral nervous system, suggesting a supraspinal dysfunction.  The term ‘dysesthesia’ is used because some patients, if not all of them, can differentiate between the unpleasant ongoing sensations and other pains that they have or have had in the past.  The distinction may help to separate the pains which may have a peripheral origin or at least peripheral triggering mechanisms.” Beric A et.al. (1988) [21]

Sandkühler J (2009) “Changes of signal processing in the nervous system may contribute to or may become the sole cause for hyperalgesia and allodynia.” Sandkühler J (2009) <8233>

Sandkühler J (2009) “central changes in the processing of nociceptive information may potentially outlast their trigger events for days, months, and perhaps years and may spread to sites somatotopically remote from the primary cause of pain.” Sandkühler J (2009) <8233>

Sandkühler J (2009) “…central mechanisms constitute one of the causes for pain chronicity and pain amplification in pain patients.” Sandkühler J (2009) <8233>

Wallerian degeneration

The axons below my cervical level spinal cord injury were subject to Wallerian degeneration and the target cells of these fibers loss of their input contributes to the complex nature of my neuropathic pain syndrome.

Shamash S et al. (2002) “Wallerian degeneration (WD) is the inflammatory response of the nervous system to axonal injury, primarily attributable to the production of cytokines, the mediator molecules of inflammation.” Shamash S et al. (2002) <9931>

Beirowski B et al. (2010) “Wallerian degeneration of the CNS is accompanied by axonal dystrophy or swelling.” Beirowski B et al. (2010) <9932>

Beirowski B et al. (2010) “Axons in ON, spinal cord dorsal column, and corpus callosum all showed marked gradients with more swellings in proximal regions of their distal stumps early after lesion.” Beirowski B et al. (2010) <9932>

Beirowski B et al. (2010) “Because axonal swellings are hallmarks of many neurodegenerative conditions, these data suggest that they are a manifestation of Wallerian-like degeneration in some cases. Thus, Wallerian-like degeneration may be a more common component mechanism in CNS diseases than previously thought.” Beirowski B et al. (2010) <9932>

CONCLUSIONS

An imbalance between the spinothalamic and dorsal column systems as the main underlying mechanism of spontaneous hyperalgesia as a central nervous system misinterpretation of peripheral input is reasonable. In my case I have relative preservation of the spinothalamic system and some loss of my dorsal column system. I have burning spontaneous hyperalgesia below the level of the injury, my cervical spinal cord, and a mixed picture of nociception.

I have the sensation of vibratory and touch perception and temperature and pain. Touch is abnormal and characterized by hyperalgesias and light touch tactile allodynia in my effected dermatomes to varying degrees. Temperature is abnormal characterized by thermal hyperalgesia. Pain is abnormal characterized by hyperalgesias, light touch tactile allodynia and sensory loss in the effected dermatomes except for my tongue and buccal cavity.

Gonçalves CE et al. (1998) found intradermal irritation of dental bleaching agents in rats.”Gonçalves CE et al. (1998) <8137> my tongue and lips developed irritant evoked hyperalgesia.

In multifiber tract injury (MFTI) any combination of fiber tract injuries can cause central hyperalgesias. The unique combination of tracts involved gives each central hyperalgesia syndrome its unique set of signs and symptoms.

Pfeifer MA et al. (1993) “…used a treatment algorithm based on anatomic site and neuropathophysiological source of the neuropathic pain” in a study of chronic painful diabetic peripheral neuropathies. Pfeifer MA et al. (1993) <8236>

Pfeifer MA et al. (1993) “A model that categorizes the types of pain into three groups (superficial, deep, and muscular) was applied in 75 diabetic patients with chronic (> 12 mo) painful distal symmetrical polyneuropathy in a controlled case series.” Pfeifer MA et al. (1993) <8236>

Pfeifer MA et al. (1993) “Twenty-two patients were untreated and 53 patients were treated with imipramine +/- mexiletine for deep pain, capsaicin for superficial pain, and stretching exercises and metaxalone +/- piroxican for muscular pain.” Pfeifer MA et al. (1993) <8236>

Pfeifer MA et al. (1993) “No significant differences were observed in initial pain scores, sleep scores, demographics, biochemistries, or physical findings between the two groups. After 3 mo a significant improvement in scores was noted in the treated but not the untreated patients. In addition, a significant difference was found in the change of scores between the treated and untreated patients: total pain (-18 +/- 2 vs. 0 +/- 2), deep pain (-7 +/- 1 vs. 0 +/- 1), superficial pain (-5 +/- 1 vs. 0 +/- 1), muscular pain (-6 +/- 1 vs. 0 +/- 1), and sleep (1.2 +/- 0.2 vs. 0.2 +/- 0.2), all P < 0.0001. In treated patients 21% became pain-free (total pain < 2), 66% had improvement (decrease in total pain > 5, but not total elimination of painful symptoms), and 13% were considered treatment failures (a decrease in total pain of < or = 5).” Pfeifer MA et al. (1993) <8236>

Pfeifer MA et al. (1993) “This study presents a new rationale and hypothesis for the successful treatment of chronic painful diabetic peripheral neuropathy. It uniquely bases the treatment algorithm on the types and sources of the pain.” Pfeifer MA et al. (1993) <8236>

Using a treatment algorithm based on anatomic site and neuropathophysiological source of the neuropathic pain for multifiber tract injuries of the spine has long been the basis for ablative attempts to control pain.

Slavik E (2006)  “Cordotomy is very effective in pain treatment and it may produce complete abolishment of pain, especially in patients suffering from neoplastic invasion of the brachial plexus (Pancoast’s syndrome) or lumbosacral plexus. Dorsal root entry zone operation is generally the only treatment option for pain due to root avulsion and segmental pain in spinal cord injury. Spinal cord stimulation is useful in management of pain following peripheral nerve injury. Deep brain stimulation is a promising treatment of central pain.” Slavik E (2006) <8237>

Cetas JS et al. (2008) “A total of 146 articles was included in the review. The large majority of studies (131) constituted Class III evidence. Eleven Class I and 4 Class II studies were found, of which nearly all (13 of 15) evaluated radiofrequency rhizotomies for different pain origins, including lumbar facet syndrome, cervical facet pain, and Type I or typical trigeminal neuralgia. Overall, support for ablative procedures for nonmalignant pain is derived almost entirely from Class III evidence; despite a long history of use in neurosurgery, the evidence supporting destructive procedures for benign pain conditions remains limited. CONCLUSIONS: Newly designed prospective standardized studies are required to define surgical indications and outcomes for these procedures, to provide more systematic review, and to advance the field. ”Cetas JS et al. (2008) <7884>

A pharmacological treatment algorithm based on anatomic site and neuropathophysiological source of the neuropathic pain for multifiber tract injuries of the spine has been long been ineffective because of a lack of knowledge of the complex pharmacology of multifiber tract injury involving sensory neurones.

The use of N-type calcium channel blockers has greatly changed this situation.

Much like spinal cord injury or AIDS related sensory neuropathy I have a multifiber tract injury (MFTI) to my spinal cord, with damage to multiple sensory nerve central processes and other afferent and efferent tracts that effect nociception. It is relevant to note that in AIDS related sensory neuropathy involving the dorsal column dysesthesias are found Rance NE et al. (1988) [22] whereas when the dorsal column is severed no pain is found. Pagni CA (1976) <7893>

If the argument is one of an imbalance between the spinothalamic and dorsal column systems Beric A et.al. (1988) [21] it would be reasonable to expect that the total imbalance of severing would result in pain, whereas changes of central signal processing in the nervous system as the sole cause for hyperalgesia and allodynia Sandkühler J (2009) <8233> would be consistent with AIDS related sensory neuropathy Rance NE et al. (1988) [22], my multifiber tract injury related hyperalgesias and allodynia and the absence of pain in the severing of the dorsal column-medial lemniscal pathways, which would be the total loss of signal processing. In normal individuals whiteners might cause irritation but I develop an irritant evoked hyperalgesia reflecting changes in central signal processing in my nervous system.

Consistent with Sandkühler J (2009) <8233>, “hyperalgesia in an area adjacent to or remote of the site of injury is secondary hyperalgesia,” my touch evoked hyperalgesia and my mechanical pressure evoked hyperalgesia in my glabrous skin are secondary hyperalgesia, in that the injury is in the cervical spinal cord.”

Together with MRI and SSEP data my phenomenon of bilateral burning sensations are consistent with a conjecture that at a very early age myelin plaques crossed my myelinated cervical level afferent pathways. These plaques led to my evolving bilateral burning neuropathy (touch evoked tactile hyperalgesia and mechanical pressure evoked hyperalgesia).

Irritation to the touch of silk, nylon and rayon has been with me all of my life. I can never remember a time in my life when those fabrics did not burn to the touch. More importantly, my earliest memories are of these unusual sensations.

Other than the automobile accident I have never had an exacerbation of my symptoms but only a slow progression of my evolving neuropathic pain syndrome. I have never had anything like a “relapsing remitting cycle,” only a steady slow progressive increase in plaque load and decrease in mobility with sparing of my retinal nerves.

My age of first unequivocal symptom of the disease occurred at age 0-3; my earliest memories are of abnormal burning sensations in my mother’s crib and bed when I touched rayon, silk or nylon fabrics. “Age at onset was calculated using the date on which the first unequivocal symptom of the disease had occurred.” Ford HL et al. 1998 <6488> See Sjöberg RL (2001) <8226> and Kropp P (2004) <8227> for discussions of pain and childhood memory.

Fitzgerald M and Beggs S (2001) “Invasive procedures that would be painful in children and adults are frequently performed on infants admitted to the neonatal intensive care unit.” Fitzgerald M and Beggs S (2001) <9149>

Fitzgerald M and Beggs S (2001) “First, the immaturity of sensory processing within the newborn spinal cord leads to lower thresholds for excitation and sensitization, therefore potentially maximizing the central effects of these tissue-damaging inputs.” Fitzgerald M and Beggs S (2001) <9149>

Fitzgerald M and Beggs S (2001) “Second, the plasticity of both peripheral and central sensory connections in the neonatal period means that early damage in infancy can lead to prolonged structural and functional alterations in pain pathways that can last into adult life.” Fitzgerald M and Beggs S (2001) <9149>

Vega-Avelaira D et al. (2009) “Differential regulation of immune responses and macrophage/neuron interactions in the dorsal root ganglion in young and adult rats following nerve injury.” Vega-Avelaira D et al. (2009) <9150>

Vega-Avelaira D et al. (2009) “The results show, for the first time, a major difference in the neuroimmune response to nerve injury in the dorsal root ganglion of young and adult rats. Differential analysis reveals a new set of immune related genes in the ganglia, that are differentially regulated in adult neuropathic pain, and that are consistent with the selective activation of macrophages around adult, but not young large A sensory neurons post injury. These differences may contribute to the reduced incidence of neuropathic pain in infants.” Vega-Avelaira D et al. (2009) <9150>

Vega-Avelaira D et al. (2009) “This observation suggests that the failure of macrophages in young animals to be attracted toward damaged A-neurons could be a key factor responsible for the lack of neuropathic behaviour. This could be due to the absence of released macrophage activation/chemoattractant factors. Our results are consistent with those of, Murphy et al, 1996 who described the presence of IL-6 in large and medium size neurons in axotomized adult DRGs [Fadel S and Sarzotti M (2000) <9151>]. Hence, the immature neuroimmune response to nerve injury and the consequent lack of neuropathic pain in young mammal may not be due to a deficient immunological capacity per se but to antigenic inexperience [Gilchrist RB et al. (2009) <9152>] which leads to macrophages failing to specifically target neurons in the DRGs.” Vega-Avelaira D et al. (2009) <9150>

Vega-Avelaira D et al. (2009) “Differential microarray analysis has revealed clear differences in the response in the dorsal root ganglia to peripheral nerve injury in adult and young rats which are likely to underlie the known age related differences in the onset of neuropathic pain. Genes involved in the immune system, many of which play a role in macrophage activity, are the most differentially regulated group following adult nerve injury relative to the younger animals. Consistent with this, macrophages are activated in the adult DRGs, in a characteristic pattern around large A sensory neurons following nerve injury but this pattern of activation does not occur in young rats. This study highlights the important contribution of the maturity of the immune system and neuron/macrophage interactions to the postnatal development of neuropathic pain.” Vega-Avelaira D et al. (2009) <9150>

Gwak YS et al. (2004a) “In this study, we evaluated behavioral responses to mechanical and thermal stimuli following SCI using three different age groups of adult Sprague-Dawley rats: young (40 days), adult (60 days), and middle-age (12 months).” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004a) “SCI was produced by unilateral hemisection of the spinal cord at T13.” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004a) “Behavioral measures of locomotor function were assayed in open field tests and somatosensory function by paw withdrawal frequency (PWF) to innocuous mechanical stimuli and paw withdrawal latency (PWL) to radiant heat stimuli on both the forelimbs and hindlimbs.” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004a) “Prior to hemisection, the PWF was not different between the three groups; however, the PWL of the young group was significantly greater than the adult and middle-age group.” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004a) “After spinal hemisection, spontaneous locomotor recovery occurred more rapidly in young and adult than in middle-age rats.” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004a) “In both forelimbs and hindlimbs, the young group displayed a significant increase in PWF and a significant decrease in PWL compared to presurgical and sham values or values from the adult and middle-age groups.” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004a) “These results indicate that younger rats developed more robust neuropathic behaviors than middle-age rats, indicating that age selection is an important factor in animal models of CCP syndromes following SCI.” Gwak YS et al. (2004a) <9341>

Gwak YS et al. (2004b) “We tested the effect of age at the time of spinal cord injury (SCI) on locomotor recovery, in open field tests, and mechanical hyperalgesia, using paw withdrawal frequency (PWF) in response to noxious mechanical stimuli, in male Sprague–Dawley rats after spinal hemisection at T13 in young (40 days), adult (60 days) and middle-age (1 year) groups.” Gwak YS et al. (2004b) <9340>

Gwak YS et al. (2004b) “Behavioral outcomes were measured weekly for 4 weeks in both SCI and sham groups.” Gwak YS et al. (2004b) <9340>

Gwak YS et al. (2004b) “Following SCI, the young and adult groups recovered significantly more locomotor function, at a more rapid rate, than did the middle-age group.” Gwak YS et al. (2004b) <9340>

Gwak YS et al. (2004b) “The PWF of the young group was significantly increased, the adult group was significantly decreased, and the middle-age group showed no significant change in fore- and hindlimbs when compared to other age groups, pre-injury and sham controls.” Gwak YS et al. (2004b) <9340>

These observations suggest that my early onset of burning hyperalgesias may have led to prolonged structural and functional alterations in my pain pathways, neural and associated immune cells that lasted into my adult life.

The phenomena of burning sensations to the touch of rayon, silk or nylon fabrics that I have felt from a very early age to this day and the above described sequela of burning pain sensations, urogenital functions and their evolution is a falsifiable conjecture for my infency onset of primary progressive multiple sclerosis.

Acknowledgement: The first formal draft of this text was started in 1998.

DOCUMENTS

D1    01/26/93  Wynn, Michael B.O. Resident (sig), Neurology and Bourdette,
Dennis Associate Professor, Neurology (sig)
Progress record “…self-referred for evaluation and second
opinion of multiple sclerosis.”
Dr. Michael Wynn and Dr. Dennis Bourdette, OHSU, multiple sclerosis
Clinic, 1-29-93
Dr. Dennis Bourdette, M.D.
Associate Professor, Neurology
Oregon Health Sciences University Hospital and Clinics
3181 S.W. Sam Jackson Park Road
Portland, Oregon 97201-3098

D42   Legacy Health system, “Cerebrospinal fluid (CSF) protein studies.”
9-8-92
09/08/92  Robert Grimm, M.D. (sig)
Good Samaritan Hospital & Medical Center
Outpatient Ambulatory Surgery Service Record
Procedure note
“spinal puncture”
Preliminary diagnosis:
“Myelopathy of unknown origin.”
Cerebrospinal fluid (CSF)
CSF:                 normal        Antonio Valdez
Gamma               7.0-14.0%          14.0%
IgG Index          0.36-0.56            0.89
Synthesis Rate  -14 to 5.6 mg/day    5.2 mg/day
Oligoclonal bands       0                 6
“The data are consistent with inflammatory and
degenerative CNS disease.”

D43   09/01/92  Robert Grimm, M.D., E.A.C.P., P.C.; Physician; Consultant in

Neurology (no sig)
Neurological Consultation
Dr. Robert J. Grimm, Consultant in Neurology, 9-1-92
Dr. Robert J. Grimm, M.D., F.A.C.P., P.C.
Physician, Consultant in Neurology
2455 N.W. Marshall – Suite 14
Portland, Oregon 97210

D44   09/15/92  Robert Grimm, M.D., E.A.C.P., P.C.; Physician; Consultant in

Neurology (sig)
Average Evoked Potential Measurements

Impression:

“Multimodal EP studies were carried out in this cooperative man revealing normal VER and ABER responses. Both the cuneate and gracile fasiciular pathways reveal significant delays as demonstrated
with median nerve and posterior tibial nerve stimulus points. This paces the lesions in the myelinated pathways between spinal cord and VPL of thalamus. As the ABER and VER responses are normal, these abnormalities are place at spinal cord levels.”

D59   05/31/94  Kim J. Burchiel, M.D.; John Raaf Professor and Head
School of Medicine, Division of Neurosurgery
Letter to Dennis Bourdette, M.D.
Dr. Kim Burchell
John Raaf Professor and Head
Oregon Health Sciences University Hospital and Clinics
3181 S.W. Sam Jackson Park Road
Portland, Oregon 97201-3098

D72   07/09/92  J. Thomas Hogard, M.D.
2647 N.E. 33rd
Portland, OR 97212
Letter to Dr. Richard Rosenbaum, M.D.
Request to evaluate Antonio Valdez

D73   07/20/92  Richard B. Rosenbaum, M.D.
510 N.E. 49th Avenue, #314
Portland, Oregon 97213-2975
Letter to Dr. Thomas Hoggard, M.D.
p.2       “I have taken that scan to the radiologists and have
reviewed it with the again because I saw some abnormalities on the
scan that bothered me. The radiologists agreed that the scan is
abnormal, and that there are at least three abnormalities
in the cervical spine within the spinal cord itself. There are three bright spots on the scan that do not have any mass affect.”

D74   07/22/92  Phillip Schilling, M.D.
Report to Dr. Richard B. Rosenbaum, M.D.
Dr. Phillip J. Schilling, Providence Medical Center, 7-22-92
Dr. Phillip Schilling, M.D.
Providence Medical Center
4805 N.E. Glisan street

D109   04/23/50  Stanford University Hospitals
Clay and Webster Sts.
San Francisco 15 California
Department C
05/07/50  Heart Operation

D110   9/25/2002 Dr. Steven G. Tillett
Dr. Steven G. Tillett
Ankle and Foot Center, PC
511 SW 10th Ave. Suite 811
Portland OR, 97205-2709
Letter to My PCP Dr. R. Houle
August 19, 2002
Re: Antonio Valdez

Dear Dr. Houle:
“I just wanted to drop you a note to touch base regarding Mr.Valdez. As you know, in addition to complications from MS, he also struggles with sequelae of diffuse hyperkeratosis palmaris and plantaris. We have recently made progress in improving his ambulation by slightly more frequent debridements. I feel this has improved his ability to perform his activities of daily living. We will continue to follow him closely and monitor his condition.
Thank you, Steven Tillett

[Dxxx] History of the Yong Moya Romero Valdez and related Families
(Compeleted and edited by Donie Alberta Nelson, issued in Bi-annual installments November 1990 5035 Overland Avenue Culver City, Ca  90230 213/204-6808
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