FIBROMYALGIA,UNMYELINATED NERVE CELLS

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March 27, 2008

Unmyelinated nerve fibres in Fibro patients – a preliminary study

Posted by linzworld under Fibro research, Uncategorized | Tags: Fibro,

Fibromyalgia, FM, FMS, korean, myelin, nerve, schwann, unmyelinated |

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Results of a Korean study announced last year that found changes in unmyelinated

nerve cells in Fibro patients have now been published in the journal Clinical

Rheumatology. The article `Characteristic electron microscopic findings in the

skin of patients with fibromyalgia–preliminary study' is by researchers at

Dongguk University College of Medicine in South Korea.

The aim of the blinded study was to determine whether there are any abnormal

electron microscopic (EM) findings in the skin of fibromyalgia syndrome (Fibro)

patients, which might contribute to or be due to the increased pain sensitivity

seen with the condition.

During the study, skin biopsy samples were obtained from 13 Fibro patients and 5

control subjects. Five skin biopsies from healthy controls showed relatively

even distribution of variegated sized unmyelinated axons sheathed well by

complicatedly folded Schwann cell membranes. In tissues from 9 of the 13 Fibro

patients, unmyelinated Schwann cells were noted to be ballooned, whereas this

finding was not noted in any controls. Schwann cells are a kind of cell that

mainly provide myelin insulation to axons (nerve fibres) in the peripheral

nervous system. According to wikipedia " the nervous system relies on this myelin

sheath for insulation and as a method of decreasing membrane capacitance in the

axon, thus allowing for [nerve] conduction to occur. Non-myelinating Schwann

cells are involved in maintenance of axons and are crucial for neuronal

survival. "

Axons in most of the Fibro patients trended towards being localized near the

edge of the unmyelinated Schwann cell sheaths. This peripheral localization of

axons in the unmyelinated Schwann cell sheaths had a strong relationship with

the ballooning of the Schwann cells, simplified folding of the Schwann cell

sheaths and smaller axons. Myelinated nerve fibers were unremarkable.

Unmyelinated nerve fibres in the peripheral nerves (C fibres) are bundled

together by unmyelinating Schwann cells to form Remak bundles of C fiber axons.

The free nerve ending of C fibres are pain-sensing nociceptors that respond to

all kinds of physiological changes in the body, including thermal, mechanical,

and chemical stimuli. C fibers respond to a stronger intensity of stimulus that

the nervers responsible for the sharp first pains and are responsible for the

slow, dull, longer-lasting, second pain. C fibers are involved in the process of

central sensitisation that can occur after nerve damage causes neuropathic pain.

The researchers concluded that:

" The EM findings seen in the skin of [Fibro] patients show unusual patterns of

unmyelinated nerve fibers as well as associated Schwann cells. If these findings

are replicated in a larger study, these abnormalities may contribute to, or be

due to, the lower pain threshold seen in [Fibro] patients. "

http://linzworld.wordpress.com/2008/03/27/unmyelinated-nerve-fibres-in-fibro-pat\

ients-a-preliminary-study/

UNMYELINATED NERVE FIBERS IN FIBROMYALGIA PATIENTS

2008 Mar;13(3 Suppl 5):12-7.

Psychophysical and neurochemical abnormalities of pain processing in

fibromyalgia.

Staud R, Spaeth M.

Division of Rheumatology and Clinical Immunology, McKnight Brain Institute,

University of Florida, Gainesville, FL 32610-0221, USA. staudr@...

Fibromyalgia pain is frequent in the general population, but its pathogenesis is

only partially understood. Patients with fibromyalgia lack consistent tissue

abnormalities but display features of hyperalgesia (increased sensitivity to

painful stimuli) and allodynia (lowered pain threshold). Many recent

fibromyalgia studies have demonstrated central nervous system (CNS) pain

processing abnormalities, including abnormal temporal summation of pain. In the

CNS, persistent nociceptive input from peripheral tissues can lead to

neuroplastic changes resulting in central sensitization and pain. This mechanism

appears to represent a hallmark of fibromyalgia and many other chronic pain

syndromes, including irritable bowel syndrome, temporomandibular disorder,

migraine, and low back pain. Importantly, after central sensitization has been

established, only minimal peripheral input is required for the maintenance of

the chronic pain state. Additional factors, including pain-related negative

affect and poor sleep have been shown to significantly contribute to clinical

fibromyalgia pain. Better understanding of these mechanisms and their

relationship to central sensitization and clinical pain will provide new

approaches for the prevention and treatment of fibromyalgia and other chronic

pain syndromes.

PMID: 18323768 [PubMed - indexed for MEDLINE]

2009;4(4):e5224. Epub 2009 Apr 21.

Mapping brain response to pain in fibromyalgia patients using temporal analysis

of FMRI.

Pujol J, López-Solà M, Ortiz H, Vilanova JC, on BJ, Yücel M, Soriano-Mas

C, Cardoner N, Deus J.

Institut d'Alta Tecnologia-PRBB, CRC Corporació Sanitària, Barcelona, Spain.

jpujol@...

BACKGROUND: Nociceptive stimuli may evoke brain responses longer than the

stimulus duration often partially detected by conventional neuroimaging.

Fibromyalgia patients typically complain of severe pain from gentle stimuli. We

aimed to characterize brain response to painful pressure in fibromyalgia

patients by generating activation maps adjusted for the duration of brain

responses. METHODOLOGY/PRINCIPAL FINDINGS: Twenty-seven women (mean age: 47.8

years) were assessed with fMRI. The sample included nine fibromyalgia patients

and nine healthy subjects who received 4 kg/cm(2) of pressure on the thumb. Nine

additional control subjects received 6.8 kg/cm(2) to match the patients for the

severity of perceived pain. Independent Component Analysis characterized the

temporal dynamics of the actual brain response to pressure. Statistical

parametric maps were estimated using the obtained time courses. Brain response

to pressure (18 seconds) consistently exceeded the stimulus application (9

seconds) in somatosensory regions in all groups. fMRI maps following such

temporal dynamics showed a complete pain network response (sensory-motor

cortices, operculo-insula, cingulate cortex, and basal ganglia) to 4 kg/cm(2) of

pressure in fibromyalgia patients. In healthy subjects, response to this low

intensity pressure involved mainly somatosensory cortices. When matched for

perceived pain (6.8 kg/cm(2)), control subjects showed also comprehensive

activation of pain-related regions, but fibromyalgia patients showed

significantly larger activation in the anterior insula-basal ganglia complex and

the cingulate cortex. CONCLUSIONS/SIGNIFICANCE: The results suggest that

data-driven fMRI assessments may complement conventional neuroimaging for

characterizing pain responses and that enhancement of brain activation in

fibromyalgia patients may be particularly relevant in emotion-related regions.

PMID: 19381292 [PubMed - indexed for MEDLINE]

PMCID: PMC2667672

Publication Types, MeSH Terms

2009;32:1-32.

Neuropathic pain: a maladaptive response of the nervous system to damage.

Costigan M, Scholz J, Woolf CJ.

Neural Plasticity Research Group, Department of Anesthesia and Critical Care,

Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts

02129, USA. mcostigan@...

Neuropathic pain is triggered by lesions to the somatosensory nervous system

that alter its structure and function so that pain occurs spontaneously and

responses to noxious and innocuous stimuli are pathologically amplified. The

pain is an expression of maladaptive plasticity within the nociceptive system, a

series of changes that constitute a neural disease state. Multiple alterations

distributed widely across the nervous system contribute to complex pain

phenotypes. These alterations include ectopic generation of action potentials,

facilitation and disinhibition of synaptic transmission, loss of synaptic

connectivity and formation of new synaptic circuits, and neuroimmune

interactions. Although neural lesions are necessary, they are not sufficient to

generate neuropathic pain; genetic polymorphisms, gender, and age all influence

the risk of developing persistent pain. Treatment needs to move from merely

suppressing symptoms to a disease-modifying strategy aimed at both preventing

maladaptive plasticity and reducing intrinsic risk.

PMID: 19400724 [PubMed - indexed for MEDLINE]

2009 Sep;10(9):895-926.

Central sensitization: a generator of pain hypersensitivity by central neural

plasticity.

Latremoliere A, Woolf CJ.

Neural Plasticity Research Group, Department of Anesthesia and Critical Care,

Massachusetts General Hospital and Harvard Medical School, town,

Massachusetts, USA.

Central sensitization represents an enhancement in the function of neurons and

circuits in nociceptive pathways caused by increases in membrane excitability

and synaptic efficacy as well as to reduced inhibition and is a manifestation of

the remarkable plasticity of the somatosensory nervous system in response to

activity, inflammation, and neural injury. The net effect of central

sensitization is to recruit previously subthreshold synaptic inputs to

nociceptive neurons, generating an increased or augmented action potential

output: a state of facilitation, potentiation, augmentation, or amplification.

Central sensitization is responsible for many of the temporal, spatial, and

threshold changes in pain sensibility in acute and chronic clinical pain

settings and exemplifies the fundamental contribution of the central nervous

system to the generation of pain hypersensitivity. Because central sensitization

results from changes in the properties of neurons in the central nervous system,

the pain is no longer coupled, as acute nociceptive pain is, to the presence,

intensity, or duration of noxious peripheral stimuli. Instead, central

sensitization produces pain hypersensitivity by changing the sensory response

elicited by normal inputs, including those that usually evoke innocuous

sensations. PERSPECTIVE: In this article, we review the major triggers that

initiate and maintain central sensitization in healthy individuals in response

to nociceptor input and in patients with inflammatory and neuropathic pain,

emphasizing the fundamental contribution and multiple mechanisms of synaptic

plasticity caused by changes in the density, nature, and properties of

ionotropic and metabotropic glutamate receptors.

PMID: 19712899 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19712899?ordinalpos=1 & itool=EntrezSystem2.PEn\

trez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA & linkpo\

s=1 & log$=relatedreviews & logdbfrom=pubmed

JOINT AND MUSCLE PROBLEMS WITH FUNGAL EXPOSURE

http://www.mold-survivor.com/fibromyalgia.html

ELECTRICITY ALWAYS TAKES THE PATH OF LEAST RESISTANCE.