Skip Navigation

Rheumatology 2008 47(2):208-211; doi:10.1093/rheumatology/kem345
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Caro, X. J.
Right arrow Articles by Dumas, A. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Caro, X. J.
Right arrow Articles by Dumas, A. J.
Related Collections
Right arrow Fibromyalgia
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

A subset of fibromyalgia patients have findings suggestive of chronic inflammatory demyelinating polyneuropathy and appear to respond to IVIg

X. J. Caro, E. F. Winter and A. J. Dumas

Division of Rheumatology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

Correspondence to: X. J. Caro, 18350 Roscoe Blvd., Suite 418, CA 91325-4174, USA. E-mail: xjcaro{at}earthlink.net


   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Objectives. The aetiopathogenesis of the fibromyalgia syndrome (FMS) remains unknown. Recent reports, however, suggest that a subgroup of FMS subjects has an immune-mediated disease. Therefore, our primary objective was to study FMS subjects for evidence of an immune-mediated demyelinating polyneuropathy. Our secondary objective was to determine the effects of treating these FMS subjects with the immune modulator, intravenous immunoglobulin (IVIg).

Methods. Fifty-eight FMS subjects, 26 rheumatic non-FMS subjects and 52 non-rheumatic non-FMS subjects were studied. Subjective measures of paraesthesias, weakness, stocking hypaesthesia, pain, fatigue and stiffness were made. Objective measures of tenderness, proximal muscle strength and electrodiagnostic (EDX) evidence of polyneuropathy and demyelination were also made. Eleven other FMS subjects underwent sural nerve biopsy.

Results. Paraesthesias, subjective weakness and stocking hypaesthesia were more common in FMS than in rheumatic non-FMS (P ≤ 0.0001). Proximal muscle strength was less in FMS than in rheumatic non-FMS (P ≤ 0.0001). EDX demonstrated a distal demyelinating polyneuropathy, suggestive of chronic inflammatory demyelinating polyneuropathy (CIDP), in 33% of FMS subjects. No rheumatic non-FMS subject had polyneuropathy (P = 0.005), or demyelination (P = 0.05). Fifteen FMS/CIDP subjects were subsequently treated with IVIg (400 mg/kg each day for 5 days). Pain (P = 0.01), tenderness (P = 0.001) and strength (P = 0.04) improved significantly. Fatigue and stiffness trended towards improvement.

Conclusions. A significant subset of FMS subjects have clinical and EDX findings suggestive of CIDP. IVIg treatment shows promise in treating this subset. These observations have implications for better understanding and treating some FMS patients.

KEY WORDS: Fibromyalgia, IVIg, Chronic inflammatory demyelinating polyneuropathy


   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Results
 Discussion
 References
 
Clinical experience suggests the existence of a fibromyalgia syndrome (FMS) subgroup exhibiting features of immune dysregulation. Findings for this include Raynaud's phenomenon, sicca symptoms, livedo reticularis, the production of antinuclear and antipolymer antibodies, abnormalities in T-cell activation and CD4 : CD8 ratios, cytokine expression and cutaneous deposition of immunoreactants [1–11]. Since many FMS symptoms are neuropathic in nature we studied FMS, and non-FMS, patients for evidence of immune-mediated injury of the peripheral nervous system. We report here a surprisingly high prevalence of clinical and electrodiagnostic (EDX) abnormalities implying a demyelinating polyneuropathy, suggestive of chronic inflammatory demyelinating polyneuropathy (CIDP), in FMS. Furthermore, we report the amelioration of some FMS symptoms, in this subset, with intravenous immunoglobulin (IVIg), a known immune modulator.


   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Results
 Discussion
 References
 
Our FMS group was 58 consecutive rheumatic disease subjects (mean age 63 yrs, range 18–92 yrs; 53 females), meeting American College of Rheumatology FMS criteria [12]. Our rheumatic non-FMS group was 16 consecutive rheumatic disease patients (mean age 64 yrs, range 33–80 yrs; 11 males) who lacked FMS. Our non-rheumatic, non-FMS group was 52 subjects referred concurrently for EDX by other physicians. Ten other rheumatic non-FMS subjects (mean age 73 yrs, range 59–81 yrs; 7 males) also underwent comparison EDX examination. None of our EDX subjects had a medical, rheumatological or post-surgical condition that influenced EDX interpretation. The Northridge Hospital Institutional Review Board (IRB) approved this study. Written informed consent from all experimental subjects was obtained according to the Declaration of Helsinki.

Self-administered questionnaires assessed paraesthesias and subjective weakness. Stocking hypaesthesia was diagnosed by a Wartenberg pinwheel and 128 Hz tuning fork [13]. Proximal muscle strength was measured using modified Medical Research Council (MRC) [14] guidelines. Muscle groups were tested bilaterally: shoulder abductors, forearm flexors, hip flexors and knee flexors (total eight muscle groups). No attempt was made to isolate muscles more specifically, or to test distal extremity musculature. MRC results were converted to a ‘strength score’ for each subject.

EDX examinations consisted of EMG and nerve conduction studies (NCS) using a Neuro Diagnostic LBM machine. EMG studied right-sided extremities and associated paraspinal muscles. Bilateral NCS tested median, ulnar, peroneal, posterior tibial and sural nerves. A demyelinating polyneuropathy was defined as: two or more nerves, not including the median nerve, with conduction velocities 2 S.D., and often 3 S.D., below normal published values [15,16]. H-reflex, and F-wave measurements were included [17]. These EDX criteria most closely follow those suggested by the Inflammatory Neuropathy Cause and Treatment (INCAT) group [18], Saperstein et al. [19] and Rotta et al. [20]. No subject had another clinically apparent, congenital, nutritional, infectious or rheumatic disease (e.g. vasculitic) cause of their EDX findings. The prevalence of monoclonal gammopathies of undetermined significance (MGUS), as detected by immunofixation electropheresis (IFE) did not differ significantly between FMS subjects (9%) and rheumatic non-FMS subjects (6%). Carpal tunnel syndrome (CTS) was diagnosed if either median distal motor latency (measured to wave onset) ≥4.6 ms or median distal sensory latency ≥3.7 ms [15,16].

A CIDP-like illness was defined as: lower extremity stocking hypaesthesia, proximal muscle weakness in at least two extremities, and EDX evidence of a demyelinating polyneuropathy.

To further assess the nature of any neuropathic injury in FMS, 11 subsequent FMS subjects (9 females; mean age 61 yrs, range 42–81 yrs), who satisfied criteria for inclusion in the current study, underwent sural nerve biopsy. Three subjects had diagnosed conditions that could have influenced their biopsy results (one type 2 diabetes mellitus, two RA). All of the subjects had abnormal EDX examinations suggesting a demyelinating sensorimotor polyneuropathy. The same neuropathologist examined all biopsy specimens for morphometry, single fibre teasing and ultra-structural analysis (Neuromuscular Disease Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA).

Open-label IVIg (ZLB Inc., Burbank, CA, USA) treatment was provided to 15 FMS patients exhibiting demyelinating polyneuropathy, normal cardiovascular, renal and hepatic status, detectable serum IgA and vascular accessibility. To limit IVIg side-effects, subjects received a single i.m. injection of methylprednisolone acetate 40 mg, 2–7 days prior to IVIg infusion [21] and acetaminophen 1000 mg and loratidine 10 mg, as needed, at the time of infusion. IVIg was given at 400 mg/kg each day for 5 days (i.e. total of 2 gm/kg) [22].

Complaints of pain, fatigue, morning stiffness, objective tenderness and proximal strength were recorded pre-IVIG and 2–4 weeks post-infusion. Pain was rated on a 0–10 scale (10 being maximal). Fatigue was recorded as present or not, and morning stiffness was recorded in minutes (480 min maximal). One author (X.J.C.) assigned a tenderness score, ranging from 0 to 3 (3 being maximal tenderness).


   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Results
Discussion
 References
 
Clinical and EDX examination results are listed in Table 1. No subject had EDX evidence of any entrapment neuropathy other than CTS, or signs of a metabolic myopathy or myositis. Sural nerve biopsy results from 11 subsequent FMS subjects satisfying criteria for inclusion in the current study are shown in Table 2. Two subjects showed minor degenerative axonal changes (one had RA, the other type 2 diabetes mellitus). Two of 11 biopsies also showed some large myelinated fibre loss. None of the 11 biopsies showed amyloid deposits, vasculitis or nerve inflammatory infiltrates.


View this table:
[in this window]
[in a new window]

  		TABLE 1. Clinical and EDX results in study populations

 

View this table:
[in this window]
[in a new window]

  		TABLE 2. Summary of myelinated fibre findings in sural nerve biopsies from 11 FMS subjects

 
IVIg treatment results are given in Table 3. Mean proximal muscle strength scores are given in Table 3 for 14 of the 15 patients because post-IVIg strength was inadvertently not recorded in one. Three of nine patients had loss of their fatigue post-infusion. Nevertheless, this change in fatigue, as a group, did not reach statistical significance in our small population. No significant adverse effects of IVIg were seen.


View this table:
[in this window]
[in a new window]

  		TABLE 3. Clinical outcome of IVIg treatment in 15 FMS patients with a CIDP-like component to their clinical picture

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
References
 
The neuropathic nature of the painful symptoms commonly seen in FMS suggested to us the possibility of a coexisting CIDP-like illness. For example, 76% of our FMS subjects claimed paraesthesias, a feature commonly associated with CIDP [23–25]. Only 20% of our rheumatic non-FMS subjects had paraesthesias (P < 0.0001). This high prevalence of paraesthesias in our FMS subjects compares well with that of Simms and Goldenberg [26] who found that 84% of 161 FMS patients had such complaints. Martinez-Lavin et al. [27] also noted that 95% of their FMS patients described dysaesthetic sensory disturbances, compared with 30% of their RA patients (P < 0.0001).

We found a high prevalence of stocking distribution hypaesthesia in our FMS group (88%) but none in our rheumatic non-FMS group (P < 0.0001). Numbness and paraesthesias, often involving all four extremities, are reported in 85.5% of adult CIDP patients in Simmons and Albers’ review of CIDP [23], and 64–89% of patients in Hahn et al.'s review [25]. So far as we are aware, the finding of stocking distribution hypaesthesia, as a physical finding in FMS, has not been previously described.

Though pain remains the sine qua non of FMS, it is not often thought of as a component of CIDP. Nevertheless, Gorson et al. [28] found that 42% of their CIDP patients had prominent pain. Likewise, Hahn et al. [25] found that between 8% and 20% of CIDP patients had pain. Devor [29] has reviewed the role of injured, large myelinated nerve fibres, such as those classically affected in CIDP, in peripheral pain production. Scadding and Koltzenburg [30] point out that sensory lesions, in general and particularly those of unmyelinated nociceptors (often cutaneous) probably participate in most peripheral neuropathic states. Unmyelinated nerve fibre lesions have recently been described in CIDP [31].

We found that 90% of our FMS subjects had complaints of weakness, compared with only 13% of rheumatic non-FMS subjects (P < 0.0001). Furthermore, FMS patients were significantly weaker on examination than rheumatic non-FMS subjects (P < 0.0001). Muscle weakness has been reported in FMS [32, 33], and is common in CIDP [23, 28].

EDX is a relatively simple, readily available tool, which can be a sensitive, though not perfect, aid in the diagnosis of neuropathic illnesses. Simms and Goldenberg [26] reported minimal EDX abnormalities, mostly CTS, in their FMS subjects. Their study, however, was limited to a retrospective chart review of EDX findings, and was not intended to focus on the prospective EDX evaluation that we, and others, have carried out [34, 35]. By using a systematic EDX approach we were able to identify a polyneuropathy in 47% of our 58 FMS subjects, while only 5% of the 52 non-rheumatic, non-FMS subjects had such findings (P < 0.0001). Seventy percent of our FMS subjects with a polyneuropathy also had EDX evidence of demyelination, usually marked by conduction slowing, dispersion phenomena and/or abnormal H-wave reflexes [15–17]. The disadvantage of EDX is that it remains implicative, rather than discriminative, in the diagnosis of demyelination and CIDP.

Most agree that nerve biopsy in CIDP provides the single most definitive evidence for this diagnosis, both through the exclusion of other, sometimes confusing, neuropathic disorders and through the identification of subtle changes confirming the presence of a demyelinating condition [36]. It was impractical, however, to obtain such invasive testing on all of the FMS subjects in this clinical study, and unethical to consider such biopsies in our comparison groups. We did, however, perform sural nerve biopsies on 11 subsequent FMS subjects who would have fulfilled clinical and EDX criteria for inclusion in this study. While uncontrolled, this series of biopsies (Table 2) failed to provide any other obvious explanation for these patients’ EDX and clinical findings (e.g. no evidence of amyloidosis or vasculitis). Furthermore, a majority of them showed signs suggestive of myelin injury, including segmental de- and remyelination, and/or apparent, small myelinated nerve fibre drop out. Although ageing itself can cause some myelinated fibre loss in sural nerve biopsies, age-related changes alone seem an unlikely explanation for our subjects’ findings since age-related sural nerve fibre loss most prominently affects large myelinated fibres [37]. The lack of cellular infiltrate in our subjects’ sural nerve tissue is not unexpected since the presence of inflammatory cells involving sural nerve biopsies in CIDP is considered rare [37].

In this study, we took our clinical findings to their logical conclusion by treating 15 selected FMS subjects with IVIg, a biologic agent known to benefit CIDP [38]. A large percentage of this select FMS subset experienced significant short-term benefits from IVIg treatment, at least in terms of pain, tenderness and strength. Although it might be argued that our patients’ improvement was in some way tied to their infusion-related pre-medication with methylprednisolone, this seems unlikely. This medication was provided because of our concern for safety during this novel treatment programme [21]. There is no real evidence that low-dose steroids benefit FMS, and some published evidence that it does not [39]. Of course, we cannot exclude, on the basis of this preliminary study, the possibility that some other unrecognized clinical variable, such as age, gender or even a placebo effect might have significantly affected these subjects’ improvement with IVIg. A larger, blinded and placebo-controlled trial of IVIg in this subset of FMS subjects ought to better answer such questions.

It should also be emphasized that despite our FMS/CIDP patients’ relatively innocuous experience, IVIg is not altogether benign. The side-effects of IVIg may include headache, fever, myalgias, tachycardia, renal tubular necrosis, hyperviscosity (with potential for stroke and myocardial infarction), anaphylaxis (particularly in IgA-deficient individuals), haemolysis, hepatic injury, rashes, cutaneous vasculitis and thromboembolic events [40].

Finally, it is worth noting that we did not set out in this pilot study to provide proof of CIDP in FMS. In fact, research criteria for the diagnosis of CIDP can be rather restrictive, so instead, we attempted to merely ascertain the presence, and demyelinating nature, of the neuropathic process seen in a subset of FMS subjects. Nevertheless, we have been influenced by our FMS subjects’ clinical and laboratory findings, their apparent response to IVIg, and statements by leaders in the field, such as Latov [41], who notes that ‘... most acquired demyelinating neuropathies of otherwise unknown etiology are considered to be a form of CIDP’. For all of these reasons, we classified our FMS patients as having a disorder suggestive of CIDP.

In summary and conclusion, we have described a subset of FMS patients with findings suggestive of CIDP, a disorder known to be immune mediated. This FMS/CIDP subset may constitute a significant portion of the overall, non-homogeneous family of FMS. Furthermore, it is readily identifiable, and may be responsive to IVIg, a known immune modulator. This subset of FMS appears worthy of further study, and may afford medical scientists a new avenue of understanding and therapeutics in this enigmatic disorder.

Formula

Disclosure statement: The authors have declared no conflicts of interest.


   References
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

  1. Caro XJ. Immunofluorescent detection of IgG at the dermal-epidermal junction in patients with apparent primary fibrositis syndrome. Arthritis Rheum (1984) 27:1174–9.[CrossRef][Web of Science][Medline]
  2. Caro XJ. Is there an immunologic component to the fibrositis syndrome? Rheum Dis Clin North Am (1989) 15:169–86.[Web of Science][Medline]
  3. Dinerman H, Goldenberg DL, Felson DT. A prospective evaluation of 118 patients with fibromyalgia syndrome: prevalence of Raynaud's phenomenon, sicca symptoms, ANA, low complement, and Ig deposition at the dermal-epidermal junction. J Rheumatol (1986) 13:368–73.[Web of Science][Medline]
  4. Smart PA, Waylonis GW, Hackshaw KV. Immunologic profile of patients with fibromyalgia. Am J Phys Med Rehabil (1997) 76:231–4.[CrossRef][Web of Science][Medline]
  5. Salemi S, Rethage J, Wollina U, et al. Detection of interleukin 1 beta (IL-1beta), IL-6, and tumor necrosis factor-alpha in skin of patients with fibromyalgia. J Rheumatol (2003) 30:146–50.[Abstract/Free Full Text]
  6. Hernanz W, Valenzuela A, Quijada J, et al. Lymphocyte subpopulations in patients with primary fibromyalgia. J Rheumatol (1994) 21:2122–4.[Web of Science][Medline]
  7. Wallace DJ, Bowman RL, Wormsley SB, Peter JB. Cytokines and immune regulation in patients with fibrositis. Arthritis Rheum (1989) 32:1334–5.[CrossRef][Web of Science][Medline]
  8. Caro XJ, Wolfe F, Johnston WH, Smith AL. A controlled and blinded study of immunoreactant deposition at the dermal-epidermal junction of patients with primary fibrositis syndrome. J Rheumatol (1986) 13:1086–92.[Web of Science][Medline]
  9. Wilson RB, Gluck OS, Tesser JR, Rice JC, Meyer A, Bridges AJ. Antipolymer antibody reactivity in a subset of patients with fibromyalgia correlates with severity. J Rheumatol (1999) 26:402–7.[Web of Science][Medline]
  10. Shanklin DR, Stevens MV, Hall MF, Smalley DL. Environmental immunogens and T-cell-mediated responses in fibromyalgia: evidence for immune dysregulation and determinants of granuloma formation. Exp Mol Pathol (2000) 69:102–18.[CrossRef][Web of Science][Medline]
  11. Macedo JA, Hesse J, Turner JD, et al. Adhesion molecules and cytokine expression in fibromyalgia patients: increased L-selectin on monocytes and neutrophils. J Neuroimmunol (2007) 188:159–66.[CrossRef][Web of Science][Medline]
  12. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum (1990) 33:160–72.[Web of Science][Medline]
  13. DeJong RN. The neurologic examination: incorporating the fundamentals of neuroanatomy and neurophysiology. (1979) 4th edition. Cambridge: Harper and Row. 44–49, 67–68.
  14. Katirji B. Clinical assessment in neuromuscular disorders. In: Neuromuscular disorders in clinical practice—Katirji B, Kaminski HJ, Preston DC, Ruff RL, Shapiro BE, eds. (2002) Boston: Butterworth-Heinemann. 3–19.
  15. Oh SJ. Interpretation of nerve conduction data. In: In clinical electromyography and nerve conduction studies (2003) 3rd edition. New York: Lippincott Williams and Wilkins. 582–600. 623–33.
  16. Dumitru D, Amato AA, Zwarts M. Nerve conduction studies; needle electromyography; and acquired neuropathies. In: Electrodiagnostic medicine—Dumitru D, Amato AA, Zwarts M, eds. (2002) 2nd. Philadelphia: Hanley and Belfus. 159–223. 257–91, 937–1041.
  17. Fisher MA. H reflexes and F waves: physiology and clinical indications. AAEM Minimonograph #13. Muscle Nerve (1992) 15:1223–33.[CrossRef][Web of Science][Medline]
  18. Hughes R, Bensa S, Willison H, et al. Inflammatory Neuropathy Cause and Treatment (INCAT) Group. Randomized controlled trial of intravenous immunoglobulin versus oral prednisolone in chronic inflammatory demyelinating polyradiculoneuropathy. Ann Neurol (2001) 50:195–201.[CrossRef][Web of Science][Medline]
  19. Saperstein DS, Katz JS, Amato AA, Barohn RJ. Clinical spectrum of chronic acquired demyelinating polyneuropathies. Muscle Nerve (2001) 24:311–24.[CrossRef][Web of Science][Medline]
  20. Rotta FT, Sussman AT, Bradley WG, Ram Ayyar D, Sharma KR, Shebert RT. The spectrum of chronic inflammatory demyelinating polyneuropathy. J Neurol Sci (2000) 173:129–39.[CrossRef][Web of Science][Medline]
  21. Lederman HM, Roifman CM, Lavi S, Gelfand EW. Corticosteroids for prevention of adverse reactions to intravenous immune serum globulin infusions in hypogammaglobulinemic patients. Am J Med (1986) 81:443–6.[CrossRef][Web of Science][Medline]
  22. Ropper AH. Current treatments for CIDP. Neurology (2003) 60(Suppl. 3):S16–22.[Abstract/Free Full Text]
  23. Simmons Z, Albers JW. Chronic inflammatory demyelinating polyradiculoneuropathy and related disorders. In: Neuromuscular disorders in clinical practice—Katirji B, Kaminski HJ, Preston DC, Ruff RL, Shapiro BE, eds. (2002) Boston: Butterworth-Heinemann. 567–88.
  24. Kieseier BC, Kiefer R, Gold R, Hemmer B, Willison HJ, Hartung HP. Advances in understanding and treatment of immune-mediated disorders of the peripheral nervous system. Muscle Nerve (2004) 30:131–56.[CrossRef][Web of Science][Medline]
  25. Hahn AF, Hartung HP, Dyck PJ. Chronic inflammatory demyelinating polyneuropathy. In: Peripheral neuropathy—Dyck PJ, Thomas PK, eds. (2005) 2nd edition. Philadelphia: WB Saunders. 2221–53.
  26. Simms RW, Goldenberg DL. Symptoms mimicking neurologic disorders in fibromyalgia syndrome. J Rheumatol (1988) 15:1271–3.[Web of Science][Medline]
  27. Martinez-Lavin M, Lopez S, Medina M, Nava A. Use of the Leeds assessment of neuropathic symptoms and signs questionnaire in patients with fibromyalgia. Semin Arthritis Rheum (2003) 32:407–11.[CrossRef][Web of Science][Medline]
  28. Gorson KC, Allam G, Ropper AH. Chronic inflammatory demyelinating polyneuropathy: clinical features and response to treatment in 67 consecutive patients with and without a monoclonal gammopathy. Neurology (1997) 48:321–8.[Abstract/Free Full Text]
  29. Devor M. Response of nerves to injury in relation to neuropathic pain. In: Wall and Melzack's textbook of pain—McMahon SB, Koltzenburg M, eds. (2006) 5th. Philadelphia: Elsevier Churchill Livingstone. 905–27.
  30. Scadding JW, Koltzenburg M. Painful peripheral neuropathies. In: Wall and Melzack's textbook of pain—McMahon SB, Koltzenburg M, eds. (2006) 5th. Philadelphia: Elsevier Churchill Livingstone. 973–99.
  31. Bosboom WM, Van den Berg LH, Dieks HJ, et al. Unmyelinated nerve fiber degeneration in chronic inflammatory demyelinating polyneuropathy. Acta Neuropathol (2000) 99:571–8.[CrossRef][Medline]
  32. Jacobsen S. Chronic widespread musculoskeletal pain – the fibromyalgia syndrome. Danish Med Bulletin (1994) 41:541–64.
  33. Norregaard J, Bulow PM, Lykkegaard JJ, Mehlsen J, Danneskiold-Samsoe B. Muscle strength, working capacity and effort in patients with fibromyalgia. Scand J Rehab Med (1997) 29:97–102.[Web of Science][Medline]
  34. Ersoz M. Nerve conduction tests in patients with fibromyalgia: comparison with normal controls. Rheumatol Int (2003) 23:166–70.[CrossRef][Web of Science][Medline]
  35. Caro XJ, Winter E. Nerve conduction tests in patients with fibromyalgia syndrome. Rheumatol Int (2005) 25:77–8.[CrossRef][Web of Science][Medline]
  36. Bosboom WM, Van den Berg LH, Franssen H, et al. Diagnostic value of sural nerve demyelination in chronic inflammatory demyelinating polyneuropathy. Brain (2001) 124:2427–38.[Abstract/Free Full Text]
  37. Oh SJ. Color atlas of nerve biopsy pathology (2001) Boca Raton, FL: CRC Press. 36, 42.
  38. Dalakis MC. Autoimmune peripheral neuropathies. In: Clinical immunology principles and practice—Rich RR, Fleisher TA, Shearer WT, Kotzin BL, Schroeder HW Jr, eds. (2001) 2nd. Philadelphia: Mosby. 78.1–78.17.
  39. Clark S, Tindall E, Bennett RM. Double blind crossover trial of prednisone versus placebo in the treatment of fibrositis. J Rheumatol (1985) 12:980–3.[Web of Science][Medline]
  40. Brannagan TH III, Nagle KJ, Lange DJ, Rowland LP. Complications of intravenous immune globulin treatment in neurologic disease. Neurology (1996) 47:674–7.[Abstract/Free Full Text]
  41. Latov N. Diagnosis of CIDP. Neurology (2002) 59(Suppl. 6):S2–6.[Abstract/Free Full Text]
Submitted 1 August 2007; revised version accepted 19 November 2007.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Therapeutic Advances in Neurological DisordersHome page
M. Stangel
Review: New advances in the treatment of neurological diseases using high dose intravenous immunoglobulins
Therapeutic Advances in Neurological Disorders, September 1, 2008; 1(2): 115 - 124.
[Abstract] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Caro, X. J.
Right arrow Articles by Dumas, A. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Caro, X. J.
Right arrow Articles by Dumas, A. J.
Related Collections
Right arrow Fibromyalgia
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?