Thursday, 31 May 2012

SIP 2012_Impressions Trailer_F8 1Mbps.flv

http://youtu.be/KWrvT-HwXY4
Small You Tube video explaining Arachnoiditis

Tuesday, 29 May 2012

Pain-Topics.org News/Research UPDATES: Low Vitamin D Hinders Spine Health

Sunday, 27 May 2012

EU Road Map Monitor 2011

Preliminary Results now available!

tl_files/redakteur-bereich/Home/Cover_SIP Road Map Monitor Booklet_2011_06 02 2012lr.jpg

The European Road Map Monitor 2011 is an evaluation based on the EU policy document ‘A Road Map for Action’. It outlines seven concrete steps on how national governments and EU institutions can effectively address the societal impact of pain in Europe. The preliminary data give an initial overview of how the Road Map and its national and international implementation, is developing across the EU.

The research tool was established by EFIC® to provide politicians and health care decision-makers with a benchmark on national policy in pain care throughout Europe. View the full SIP European Road Map Monitor 2011.

Hi All,

SIP 2012 takes place next week where many of the EU's leading medical consultants will be making presentations. Some of the discussions that are available to view and follow live are listed below, however please note that you will need to follow a link which will only be published on the SIP web-site shortly before the symposium starts.

SIP 2012 live web streamed discussions are as follows:

· Wednesday, 30 May, 10.30-11:30 (English): Press Briefing from the International Press Centre under the Danish Ministry of Foreign Affairs

· Wednesday, 30 May, 13:00-18:00 (English): Workshop 1: Chronic Diseases: Chronic Pain as a disease in its own right

· Thursday, 31 May, 09:00-16:00: Plenary Sessions (English, Spanish, German, French, Italian & Danish)

To access the link to the live web-stream (published shortly before the SIP discussion commences) goto www.sip-platform.eu.

Friday, 25 May 2012

eu web portal video recommendation

eu web portal video recommendation:
EU European Patients Forum,
Nicola Bedington, recording at Brussells
Patient Involvement, research with rather than on Patients,

EPF stresses the importance of patient involvement in healthcare innovation

Anders Olauson, EPF President, and Nicola Bedlington, EPF Executive Director, participated in the conference “Innovation in Healthcare without borders”, on 16-17 April, in Brussels, Belgium. The main objective of the conference was to act as an innovation in healthcare policy forum involving the key actors and policy-makers. Mr Olauson highlighted his conviction that “Patients can play a key role in providing some answers to the question how to foster innovation and its adoption in healthcare in an equitable and sustainable way.”

This event brought together the key stakeholders involved in the innovation process of the healthcare sector in view of Europe 2020 and the Innovation Union Plan. It was organised by the services of the European Commission (DG Research and Innovation, DG Enterprise and Industry, DG Health and Consumers, DG for Regional Policy), in consultation with other relevant DGs, major health associations and stakeholders.

The conference sessions developed two tracks. Track A was entitled “Removing borders on the innovation in healthcare landscape” assessing achievements and remaining barriers. Mr Olauson raised the fact that patients have traditionally not been involved in the area of innovation in healthcare. He added that “innovation that does not reach the patient is not only wasteful, but is not innovation at all”.

As for Track B: "Overcoming barriers to equality and solidarity", the EPF President recommended meaningful involvement of patients as equal partners from inception to delivery, in order to foster innovation uptake and to ensure that final solutions are in line with patients’ needs and expectations. He also said that there needs to be a shift from technology-driven to more demand-driven and user-centred innovation at all levels. “User-driven innovation is key in closing the gap between innovation and market and between market and patients”, he concluded.

A key issue emerged: how to ensure the effective involvement of patients in healthcare innovation? There is a lot of work to be done in terms of creating the necessary conditions for patient involvement to take place, with particular regard to health literacy and patient empowerment. A remarkable step forward in this area is represented by the recently-launched EUPATI Patient Academy funded through the Innovative Medicines Initiative. Led by EPF and delivered though a sustainable partnership between patients, research institutions, and pharmaceutical industries, EUPATI aims to improve the availability of both patient-centric information as well as educated patient experts who will be able to contribute to pharmaceutical innovation at different levels.

This will ultimately help to ensure more patient-centred, transparent pharmaceutical research and innovation processes for the benefit of our healthcare systems.

Please follow this link to see Anders Olauson’s presentation online.

Please follow this link to see Nicola Bedlington’s presentation online.

Anders OLAUSON, President, European Patients' Forum

eu web portal video recommendation: eu web portal video recommendation
Innovation and Health Care Without Borders Brussels April 16th and 17th
Anders OLAUSON, President, European Patients' Forum

Why are Radiologists still saying Tarlov cysts are Incidental Findings on a MRI

Sacral Extradural Meningeal Cyst: Is It an Incidental Finding?2006

General Spine

Peter _ Yoo, MD, Non ASSR Member
Shane Lee, BA, Non ASSR Member
Nikhil Bhagat, MD, Non ASSR Member
Huey-Jen Lee, MD, Non ASSR Member

Scientific Paper

Purpose

(1) To determine the incidence of extradural meningeal cysts in adult patients who underwent routine magnetic resonance imaging (MRI) of the lumbar spine for lower back pain. (2) To describe the current classification of sacral meningeal cysts and its postulated pathophysiology. (3) Literature review of the clinical significance and management of sacral extradural meningeal cysts.

Methods & Materials

A total of 584 MRI studies of the lumber spine were retrospectively reviewed. The studies were performed for the evaluation of lower back pain and were performed between May 2005 and November 2005. Pediatric and trauma cases were excluded. Ages ranged from 18 years to 80 years. Routine MRI of the lumbar spine was performed on a 1.5 Tesla GE scanner. The study consists of sagittal T1, fast spin echo (FSE) and short TI inversion recovery (STIR) sequences of the lumbar and sacral spine. Axial proton and T2 weighted images of the disc spaces between L1 and S1 are also obtained. Post gadolinium axial and sagittal T1 weighted images are only obtained in post-spinal surgery patients.

Results

A total of 7 sacral extradural meningeal cysts were identified (1.2 %). 4 of the patients were male and 3 were female with a mean age of 49 years (range 32 years to 70 years). 5 were determined to be type I and 2 were indeterminate. All of the cysts occurred in the sacral spine. 4 cases also demonstrated coexistent disc disease of the lumbar spine and 1 case demonstrated a compression fracture of L5. 2 cases demonstrated no concurrent disc disease. Of these two patients, one patient presented with sacral and lower extremity pain with paresthesia while the other patient complained of nonspecific lower back pain.

Conclusion

The prevalence of sacral extradural meningeal cysts in our study is 1.2%. Sacral meningeal cysts have been classified into three categories: extradural cysts not containing nerve root fibers (Type I), extradural cysts containing nerve root fibers (Type II) and intradural cysts (Type III). The exact mechanism of formation of sacral extradural meningeal cysts is unknown. It has been postulated that the arachnoid membrane herniates through a dural defect, which is most likely congenital. Sacral extradural meningeal cysts are generally considered to be incidental findings. However, there are several published case reports that have attributed symptoms to these lesions and these patients have undergone surgical intervention. In our study, 2 out of the 7 cases demonstrated no coexistent disc disease. Therefore, the clinical symptoms may be related to the sacral cysts. In light of these reports and our findings, sacral extradural meningeal cysts should not be easily dismissed as an incidental finding.

References

1. Acosta FL Jr, Quinones-Hinojosa A, Schmidt MH, Weinstein PR.: Diagnosis and management of sacral Tarlov cysts. Case report and review of the literature.
Neurosurg Focus. 2003 Aug 15;15(2):E15.
2. Nabors MW, Pait TG, Byrd EB, Karim NO, Davis DO, Kobrine AI, Rizzoli HV.: Updated assessment and current classification of spinal meningeal cysts. J Neurosurg. 1988 Mar;68(3):366-77.
3. Sato K, Nagata K, Sugita Y.: Spinal extradural meningeal cyst: correct radiological and histopathological diagnosis. Neurosurg Focus. 2002 Oct 15;13(4):ecp1.
4. Rohrer DC, Burchiel KJ, Gruber DP.: Intraspinal extradural meningeal cyst demonstrating ball-valve mechanism of formation. J Neurosurg 78; 1993: 122-125.
5. Robinson Y, Reinke M, Haschtmann D, Ertel W, Heyde CE.:.Spinal extradural meningeal cyst with spinal stenosis. Spinal Cord. 2005 Nov 22; [Epub ahead of print]
6. Muthukumar N.: Sacral extradural arachnoid cyst: a rare cause of low back and perineal pain. Eur Spine J. 2002 Apr;11(2):162-6. Epub 2001 Jun 23. Review.
7. Uemura K, Yoshizawa T, Matsumura A, Asakawa H, Nakamagoe K, Nose T.: Spinal extradural meningeal cyst. Case report. J Neurosurg. 1996 Aug;85(2):354-6.
8. Langdown AJ, Grundy JR, Birch NC.: The clinical relevance of Tarlov cysts.
J Spinal Disord Tech. 2005 Feb;18(1):29-33.
9. Kendall BE, Valentine AR, Keis B.: Spinal arachnoid cysts: clinical and radiological correlation with prognosis. Neuroradiology. 1982;22(5):225-34.
10. Boukobza M, Sichez JP, Rolland E, Cornu P.: MRI evaluation of sacral cysts.
J Neuroradiol. 1993 Dec;20(4):266-71
11. Bartels RH, van Overbeeke JJ.: Lumbar cerebrospinal fluid drainage for symptomatic sacral nerve root cysts: an adjuvant diagnostic procedure and/or alternative treatment? Technical case report. Neurosurgery.1997 Apr;40(4):861-4

Images

www.psas.nl/en/onderzoek.asp
April 2012

revalence of sacral spinal (Tarlov) cysts in Persistent Genital Arousal Disorder

Barry R. Komisaruk, PhD1,2 & Huey-Jen Lee, MD2

1. Rutgers, The State University of New Jersey, Department of Psychology, Newark, New Jersey USA

2. University of Medicine and Dentistry of New Jersey, Department of Radiology, Newark, New Jersey USA

Abstract

Introduction:

Neither consistent etiology nor treatment have been established for Persistent Genital Arousal Disorder (PGAD), which is characterized by uninvited, unwelcome, and distressing genital sensation. Sacral (Tarlov) cysts, which form on dorsal (sensory) roots, most commonly of S2 and S3 in the sacral spine, are reported to produce genital symptoms that bear similarities to those described for PGAD.

Aims:

The present study ascertained the incidence of Tarlov cysts in the sacral spine of women with PGAD symptoms.

Methods:

Women in a PGAD internet support group were asked to submit MRIs of their sacral region to the investigators, who evaluated the MRIs for the presence or absence of Tarlov cysts.

Main Outcome Measures:

The presence or absence of Tarlov cysts at the level of the sacral spine.

Results:

Tarlov cysts were present in 12 of the first 18 (66.7%) MRIs submitted to the investigators by women who suffer from PGAD symptoms. By contrast to this incidence, that of Tarlov cysts reported in the literature for large samples of the population observed for various disorders (e.g., lumbosacral pain) is 1.2% - 9.0%.

Conclusion:

Tarlov cysts have been described in the literature as producing paresthesias and genital sensory disturbances. Hence, at least some cases of PGAD might be considered to be a Tarlov cyst-induced paresthesia. Based on the relatively high occurrence of Tarlov cysts currently observed in women who suffer from PGAD symptoms, it would seem advisable to suspect Tarlov cysts as a possible organic etiological factor underlying PGAD.

Introduction

Origin of a clue: This study began serendipitously. A colleague mentioned to one of us (BRK) that his wife, diagnosed with Persistent Genital Arousal Disorder, showed an incidental MRI finding of Tarlov cysts, and asked if they might produce pelvic vasocongestion and hence her discomfort. Sacral cysts, first described by I.M. Tarlov in 1938 [1] are occasionally found incidentally in the course of radiological examination of the lumbosacral spine for various disorders. Review of literature on Tarlov cysts (also termed, “sacral cysts” [2] indicated that they form characteristically at the S2 and S3 dorsal root ganglia, ballooning out as a result of filling with cerebrospinal fluid, contain dorsal root nerve fibers in the wall and/or internal portion of the cyst, and generate paresthesias. Because the S2 and S3 dorsal roots convey the sensory pudendal and pelvic nerves, which innervate the external and internal genitalia (for review, [3]), could they generate the abnormal sensations characteristic of PGAD?

What is Persistent Genital Arousal Disorder?: PGAD is a complex pathology with multiple etiologies and with variably effective therapies. It is a perplexing condition characterized by high levels of genital arousal occurring in the absence of subjective interest or desire. PGAD sufferers are women who experience intrusive, unsolicited and seemingly spontaneous genital arousal that can be unrelenting. This arousal can persist for hours, days or even longer, despite attempts to relieve it with sexual activity or orgasm, which at best provide only brief relief from the symptoms. Attempts to quell the genital arousal by engaging in masturbation or sexual activity may lead to brief relief, no relief, or even more arousal and activation. First characterized and termed Persistent Sexual Arousal Syndrome (PSAS) by Leiblum and Nathan [4, 5], the condition was later renamed PGAD by Leiblum [6] to clarify that the disorder was a problem of genital, rather than sexual, arousal.

The following five diagnostic features of the disorder were characterized by Leiblum and Nathan [4, 5]:

1) The physiological responses characteristic of sexual arousal persist for an extended period (hours to days) and do not completely subside on their own;

2) The signs of physiological arousal do not resolve with ordinary orgasmic experience, and may require multiple orgasms over hours or days to remit;

3) These physiological signs of arousal are usually experienced as unrelated to any subjective sense of sexual excitement or desire;

4) The persistent sexual arousal may be triggered not only by sexual activity, but also by seemingly nonsexual stimuli or by no apparent stimulus at all; and

5) The physiological signs of persistent arousal are experienced as uninvited, intrusive and unwanted.

A diagnosis of PGAD is made, based upon the presence of all five of the above features, when distress is rated as moderate or severe (a score of 2 or 3 on a scale in which 0 = no distress and 3 = extreme distress) [7]. Women who complain of PGAD can be severely distressed, especially when the symptoms continue for extended

duration without relief. This property of PGAD predisposes some women to become severely depressed and even suicidal [8]. As characterized by Goldstein et al. [9],

“In our experience, women affected with the condition are frequently suicidal, socially ostracized, isolated, frustrated, miserable, embarrassed, and extremely humiliated.” The shame and embarrassment attached to the symptoms has likely contributed to the phenomenon going previously unrecognized and underreported to health care providers, which could account, at least in part, for the absence of reliable data on the prevalence of PGAD.

By contrast with PGAD, some women experience persistent genital arousal as a normal, pleasant and even reassuring experience. However, those women differ from the PGAD sufferers in that their arousal is neither continuous nor unrelenting, and does not cause them distress [10, 11].

Sensations associated with PGAD: Complaints by PGAD sufferers have been described as clitoral tingling, irritation, vaginal congestion, vaginal contractions, throbbing, pressure, pain, and in some cases, spontaneous orgasms [12].

Sensations associated with Tarlov Cysts: Symptoms of Tarlov cysts include: pain in perineum, vagina, penis, buttock, leg, lower back, sacrum, or coccyx, dyspareunia, proctalgia, bladder dysfunction, urinary incontinence, micturition disorders, bowel incontinence, radicular pain (neuralgia), loss of sensibility, muscle weakness or paresis (partial paralysis), dysesthesias (abnormal sensations experienced in the absence of stimulation), paresthesias (burning, pricking sensations) of thigh or foot, retrograde ejaculation, and “impotence”, a description based on case reports and a limited sample size [13 -15]. Tarlov cysts smaller than 1.5cm diameter have been reported as asymptomatic. It seems plausible that despite differences in terminology, there is a degree of congruence between these two sets of symptomatology.

Characteristics of Tarlov Cysts: From the descriptions in the literature, Tarlov cysts evidently develop at the distal limits of the dural sheath, a thinned extension of the dura

mater, which encapsulates not only the brain and spinal cord, but also the dorsal and ventral nerve roots. The thinned dural sheath, which includes the epineurium, terminates just at, or distal to, the dorsal root ganglia. At that point, the perineurium, which is the distal continuation of the pia/arachnoid, balloons out under pressure of the cerebrospinal fluid (CSF), perhaps in part because of the absence of constraint by the proximally-overlying dura mater. The perineurial wall contains spinal nerve root fibers and ganglion cells [1, 16] and the fibers may be present in the cyst cavity itself [16]. It is described that the neck of this fluid-filled balloon structure is constricted, creating a one-way “ball-valve” structure that allows CSF to enter, but not leave readily. As the volume of CSF changes in response to postural and positional changes, e.g., from supine to sitting, or in response to the Valsalva maneuver, sensory nerve root fibers in the cyst wall can stretch or compress against adjacent bone or the nerve roots, thereby producing abnormal sensations [16]. As pointed out by Acosta et al. [16] “…a great deal of confusion continues to exist over the precise definition of Tarlov cysts and their distinction from other spinal cysts. Tarlov cysts have been referred to as perineurial cysts, nerve root diverticula, meningeal cysts, sacral cysts, arachnoid cysts, and arachnoid pouches.” For the present purpose, we refer to them as Tarlov or sacral cysts.

Present hypothesis: Tarlov cysts can generate PGAD symptoms: Missing from all the above considerations is that at least some cases of PGAD could be due to pathology of the dorsal spinal roots, which could generate abnormal, distressing genital sensations. Therapeutic procedures focused on pelvic organs or their innervation, e.g., clitoridectomy [17] or surgical relief of nerve entrapment or pudendal or pelvic nerve block [9, 18] would not provide relief if the symptoms are generated proximal to these interventions, e.g., at the dorsal spinal nerve roots near their entry to the spinal cord. That is, even if the clitoris is removed or anesthetic is administered as a nerve block to the distal portion of the nerve, direct Tarlov cyst-produced mechanical stimulation of the (unanesthetized portion of) the nerve where it enters the spine could still generate afferent action potentials that would be perceived as if originating in the genital region.

Based upon the above considerations, we hypothesized that Tarlov cysts can generate PGAD. We tested the hypothesis by contacting a specific PGAD internet support group, (Ms. Jeannie Allen, pers. comm.) asking the women in the group to send us MRIs of their lower back that they may have had taken for diagnostic purposes; we then evaluated the MRIs for existence of Tarlov cysts. In the general population, the incidence of Tarlov cysts has been reported as between 1.2% and 9.0%, based upon incidental findings of the cysts in thousands of cases and in a variety of conditions for which lumbosacral MRIs were obtained [2, 16, 18].

Methods

Approval was obtained from the Institutional Review Boards for the Protection of Human Subjects in Research of Rutgers University and the University of Medicine and Dentistry of New Jersey (Newark) for evaluating existing MRI records on a confidential basis, and each of the women gave written permission for publication of their MRI images to be made anonymously. We requested of women in the Internet PGAD support group hosted by Ms. Jeannie Allen to send us, postage prepaid, diagnostic MRIs that they had obtained of their sacral spinal region. Of the more than 300 women in the internet support group, we received 18 such MRIs, each of which we evaluated for the presence or absence of Tarlov cysts, which occur predominantly at the S2-S3 levels of the spine, and because they are filled with cerebrospinal fluid, appear bright on T2-weighted images and dark on T1-weighted images.

Results

Of the 18 sets of MRIs of the spinal region that we received from women suffering from PGAD, Tarlov cysts were clearly evident in 12 (i.e., 66.7%) (Figures 1 and 2). The MRIs of five women show one cyst, those of six women show two cysts, and those of one woman shows three cysts. Consistent with the classical location of Tarlov cysts, all of the 20 cysts in the 12 women were located at the S2 and/or S3 spinal levels; two of which (Figures a and j) were at the S1 and/or S2 level. The spheroidal-shaped cysts ranged in maximum diameter from 3mm to 20mm with a group mean maximum

diameter of 9.6mm +/- 5.1 (s.d). In the 13th woman, no Tarlov cyst was evident, but she had a spondylolisthesis, i.e., the L5 vertebra slid forward over the S1 vertebra by 25%, distorting the spinal nerve roots of the cauda equina. In the 14th woman, there was a severe stenosis at L2-3 compressing the cauda equina. No pathology was evident in the MRIs of the other 4 women.

Discussion

Limitations of the present methodology

We recognize that the validity of conclusions based on the present findings is tempered by the unconventional means by which the data were obtained. There was a self-selection process in which of more than 300 women in the PGAD support group who were notified via the internet of our request for MRI images of the lower back, only 18 women sent us their MRIs that included images of their sacral spinal region. Thus, we could not evaluate the MRI images by a blind procedure. We have no formal control group, but rather for comparison with our “convenience sample” of 18 women manifesting a 66.7% incidence of Tarlov cysts, we rely on the literature that reports a much lower incidence of Tarlov cysts (1.2%-9%) in the general population of thousands of patients with MRIs analyzed for lower back problems. As to whether small sacral cysts might have been be overlooked in those studies, a coauthor of the present study (H-JL) was also a coauthor on one of the above-mentioned studies [18] and counted even small sacral cysts, finding only 7cysts among 584 MRIs (1.2%). Despite the above limitations, we believe that the present findings indicate a sufficiently plausible etiological basis for PGAD to warrant further investigation.

PGAD not previously linked to Tarlov Cysts: A review of the literature on Tarlov cysts reveals no mention whatsoever of PGAD, despite multiple papers published on properties and surgical treatment of the cysts since 2001, when Leiblum and Nathan first characterized PGAD. On the other hand, a review of the literature on PGAD reveals no mention whatsoever of Tarlov cysts, even though physiological, as well as psychological, etiologies have been proposed.

Although multiple clinical reports claim that Tarlov cysts are asymptomatic unless they are at least 1.5cm in diameter, perhaps a less stringent criterion is required in the case of PGAD symptoms, which may be paresthetic rather than painful, and because of the potential under-reporting factor related to social factors. Leiblum et al [10] pointed out that PGAD patients often feel ashamed and embarrassed about revealing their symptoms. Embarrassment has been emphasized as a major factor in underreporting of sexual dysfunctions [19]. Tarlov cysts are frequently reported as just incidental findings, for they can be asymptomatic. However, if they produce PGAD, women may under-report the symptoms due to embarrassment, thus rendering the cysts only apparently asymptomatic. This could account, at least in part, for the lack of previous complaints of women diagnosed with Tarlov cysts reporting symptoms of PGAD, by contrast with the current finding that women who report PGAD symptoms have a relatively high incidence of previously undiagnosed Tarlov cysts. Thus, it should not be assumed, a priori, that a Tarlov cyst less than 1.5cm diameter would be too small to generate PGAD symptoms. At present, we cannot relate size of the cysts to individual women’s symptoms because we have only reviewed existing MRI records. Future research will evaluate the possible relationship between specific spectra of PGAD symptoms and the presence/size of Tarlov cysts.

Hypotheses of PGAD etiology: Leiblum [6] postulated that there may be two subtypes of PGAD: one more closely related to physiological factors (e.g., neurovascular or neurochemical), and the other to psychological factors. In the literature review by Leiblum et al. [7] the authors concluded that there are multiple hypotheses, but no consensus, regarding the etiology of PGAD. They summarized the hypotheses as: central neurological changes (e.g., post-surgical, post-injury brain lesion, seizure disorder), peripheral neurological changes (e.g., pelvic nerve hypersensitivity or entrapment), vascular changes (e.g., pelvic congestion or dilatation, or vascular pathology associated with chronic fatigue syndrome [20], mechanical pressure against genital structures, medication-induced changes (e.g. upon either initiation or cessation of SSRI or mood stabilizer therapy), psychological factors, (e.g., severe stress, the

perception and persistence of symptoms, anxiety and obsessive vigilance about physical symptoms, overall lower levels of sexual satisfaction, lower desire and greater pain), beginning menopause, physical inactivity [7], some combination of these, and/or idiopathic factors.

Other types of physical etiology were suggested by Waldinger and Schweitzer [17]; they observed a close association of PGAD with “restless legs syndrome (RLS)”, and characterized PGAD as “…the expression of a nonsexually driven hyperexcitability of the genitals and subsequent attempts to overcome it by genital manipulations”, the latter of which are an “…imperative urge to suppress dysesthesias and paresthesias.” Waldinger et al [21] related PGAD-like symptoms in two men to genital hypersensitivity, which they attributed to “small fiber sensory neuropathy” of the pudendal nerve. In light of the possible involvement of Tarlov cysts in producing PGAD symptoms, and the fact that the S1 and S2 spinal nerve roots control the posterior dermatomes of leg sensation and movement (e.g., [22]), the possibility should be considered that Tarlov cyst-induced irritation of the spinal nerve roots S1 and S2 could interact with, and contribute, at least in part, to the cerebral component of RLS. In a followup study, we plan to ascertain whether specific symptoms of PGAD, e.g., RLS, are correlated with the existence or absence of Tarlov cysts, at least in the women who comprise the sample in the current analysis.

Goldstein et al. [9] observed that “…persistent sexual arousal syndrome has much in common with stuttering or recurrent [clitoral] priapism” in women with idiopathic symptoms of the syndrome, and hypothesized an “unusual genital tissue biochemistry” as the etiology. But ultimately, they suggested that most patients with “persistent sexual arousal syndrome” should be classified into the category “idiopathic” because, “…for the most part, clearly recognized causes for the syndrome are limited” [9]. And in their own survey of 76 women who fulfilled all the criteria of PGAD, Leiblum et al [7] found “no evidence of specific major medical illness or pharmacological agents effects associated with the report of PGAD.” Thus, there appears to be no known unitary etiology for PGAD.

Current PGAD therapies: In a comprehensive literature review and recommendations for management of PGAD, Goldmeier et al [11, 23] emphasized taking: a) a psychiatric history, b) a full medical history including medications, c) a comprehensive genital and pelvic examination, and d) a pelvic ultrasound. They emphasized this approach in order to exclude local pathology, such as genital dermatosis and genital prolapse, and to exclude conditions such as pelvic or cerebral pathology. Regarding the latter, a speculation of a neurological epileptic basis for PGAD [9] was followed by a finding that epileptic activity was temporally associated with a patient’s symptoms, and anti-epileptic treatment suppressed both her orgasmic seizures and symptoms of PGAD [24]. Using a different approach, repeated sessions of electroconvulsive shock were reported to ameliorate PGAD symptoms [25]. Waldinger et al [26] reported, in two clinical cases, good therapeutic effects against PGAD and restless legs symptoms by using TENS stimulation. Perhaps in Waldinger’s two cases, the effectiveness against the symptoms was due to an effect originating at the same sacral region as that affected pathologically by Tarlov cysts.

Other therapeutic PGAD interventions have focused on symptom management. “Psychoeducation” and social support impress on the patients that they are not alone in their experience with PGAD. Patients were trained to distract themselves from focusing on their genital sensations and to become aware of the triggers that worsen symptoms. Cognitive-behavioral interventions have been used to enhance coping skills and assist in interrupting the cycle of anxiety and catastrophizing of the symptoms [7]. Anesthetizing agents have been applied to numb the genital area. Neither clitoridectomy [27], local anesthesia, nor peripheral pudendal nerve block would be expected to alleviate PGAD symptoms if the symptoms were generated proximally at the spinal level, e.g., by Tarlov cysts. Pelvic massage or stretching exercises provided by a specialist in pelvic floor physical therapy have been applied to reduce or eliminate the pelvic tension and break up connective tissue strictures that might contribute to the condition [6, 8]. Medication has been applied by trial and error, as certain medications may be associated paradoxically with either alleviation or activation of the symptoms.

Mood stabilizing, antiseizure medications such as valproic acid, or SNRIs (Selective Norepinephrine Reuptake Inhibitors) have been tried [6, 8]. In light of the current findings, it would seem advisable to add a diagnostic sacral spinal MRI to the PGAD therapy armamentarium. To our knowledge there are no reports in the literature of amelioration of PGAD symptoms by treatment of Tarlov cysts.

Potential value of MRI to test for presence of Tarlov Cysts in cases of PGAD: The present finding that 66.7% of the 18 women with PGAD who sent us their spinal MRIs have one or more Tarlov cysts in their sacral spine far exceeds the population average, which has been reported to range from 1.2% to 9% [2, 6, 18, 28]. Langdown et al [2] found that 54 of 3,535 (1.5%) patients showed Tarlov cysts in MRI scans for lumbosacral symptoms; 70% were women. Similarly, Oaklander et al. [28] reported that 1.8% of 1,305 lumbosacral scans showed Tarlov cysts, of which 75% were in women. In an international survey of persons with Tarlov cysts, women outnumbered men by 9:1; the predominant age of all respondents was 40-60 [29, 30]. While PGAD is likely to have a variety of etiologies, the prevalence of Tarlov cysts in the present population indicates that in the absence of any other identified pathology related to a woman’s PGAD symptoms, it would seem reasonable and advisable to test whether a Tarlov cyst is generating the PGAD symptoms.

Therapy for Tarlov Cysts

Probably the most convincing evidence as to whether a Tarlov cyst is generating the PGAD symptoms would be administration of an epidural anesthetic block at the sacral spinal level, which, if the Tarlov cyst is responsible for the PGAD symptoms, should eliminate the symptoms for the brief duration of the block, with return of the symptoms thereafter. If the PGAD symptoms are reversibly blocked by this epidural procedure, there are a number of long-term surgical procedures that could then be applied, although variable success has been claimed for surgical treatment of Tarlov cysts. As the most recent example, Murphy et al [31] surgically treated symptomatic Tarlov cysts by CT fluoroscopic-guided needle aspiration of the cerebrospinal fluid, followed by fibrin “glue” injection; they claim they have not had any case of aseptic meningitis as a

potential side effect of this procedure [31]. Other techniques for treating Tarlov cysts include subarachnoid drain, cyst fenestration and imbrication, muscle graft over the fenestrated cyst, cyst wall resection, and closure with myocutaneous flap reinforcement to prevent cyst recurrence or CSF leakage. A more drastic procedure is resection of the cyst and adjacent nerve roots, but this can result in neurological deficit [16]. For a concise summary of surgical treatments of Tarlov cysts, see Young [32]. A relatively recent procedure used in chronic pain patients is intrathecal catheterization with an implanted pump whose dose and timing of medication delivery is controlled by the patient [30]. This procedure has apparently not been reported to be used in the case of Tarlov cysts, but it would appear to be feasible if the cyst is situated superior to the filum terminale. There are risks associated with the procedure, e.g., movement of the catheter, CSF leakage, infection, etc. [30].

Characteristics of Tarlov Cysts and other spinal pathologies: Tarlov cysts are just one of several types of spinal cysts. While it is likely that the pathologies in the MRIs in Figures 1 and 2 are indeed Tarlov cysts, other, intraoperative and/or histological procedures, are necessary for differentiation of the several types of cyst. For example, Tarlov cysts show delayed filling on myelography because of their constricted, valve-like neck, which renders them non-compressible when tested intraoperatively [16]. They develop between the endoneurium and perineurium at, or distal to, the dorsal root ganglion. Their lining contains nerve fibers and /or ganglion cells. By contrast, meningeal diverticula freely communicate with the subarachnoid space, are situated proximal to the dorsal root ganglion, and possess a lining composed of arachnoid mater and dura mater devoid of neural tissue [16]. Histopathological examination of 8 specimens of Tarlov cysts demonstrated nerve fibers in 75%, ganglion cells in 25%, and evidence of old hemorrhage in 50% [13].

It is important to note that Tarlov cysts can occur in association with other spinal degenerative pathologies that could produce the symptoms, such as intervertebral disc prolapse or a stenosis that compresses the nerve root, sacral bone erosion which can produce an “insufficiency fracture,” spondylolisthesis (vertebral displacement), etc. [2].

Etiology and mechanism of action of Tarlov Cysts: No definitive etiology or mechanism of action has been established for Tarlov cysts; it has been suggested that they form as a result of congenital weakness of the meninges (perhaps more fundamentally related to connective tissue abnormalities) combined with subsequent acute physical trauma [33]. Trauma to the sacrum in the form of a skiing or motor vehicle accident, or heavy lifting or straining, were reported in the history of 5 of 10 patients who developed Tarlov cysts [13]. Perhaps the combination of the congenital and physical trauma factors can create a torsion defect specifically in the unique “weak-spot” just where the distal extension of the dura mater, i.e., the dural sheath, ends at the dorsal root ganglion, thus allowing the Tarlov cyst to form.

We are not aware of any direct evidence as to the mechanism(s) by which Tarlov cysts produce their symptoms. It would seem plausible that their sensory and/or motor (including autonomic, thus perhaps circulatory and/or vascular) effects could be produced by the mechanical irritation of sensory and/or motor nerve roots and/or the ganglion cells in the wall and/or the interior of the cyst, and/or by the cyst wall exerting force on the surrounding nerve roots, bone, or other tissue.

Conclusion: The lack of clear understanding of the etiology and mechanisms underlying PGAD has prevented the application of a rationale-based therapy. While PGAD may well be a complex pathology with multiple etiologies, the present findings provide a clue as to a plausible organic pathology – sacral (Tarlov) cysts -- that has evidently not been reported in the literature previously. It is too early to know whether, and if so which, symptoms of PGAD can be accounted for by these aberrant nerve fiber-containing cysts on the genital and leg sensory nerve roots in the sacral spine, but in the present study, the unusually high (66.7%) incidence of the cysts in women suffering from PGAD, much higher than the incidence of these cysts in the general population (up to 9%), strongly suggests that it would be worthwhile to test their possible role. In seeking the etiology and treatment for PGAD for a sufferer, it would seem advisable to test for – at the very least to rule out -- Tarlov cysts.

Figure Legend

Figures 1 & 2: MRI images submitted by 12 different women (a-l) showing evidence of sacral (Tarlov) cysts, out of 18 women with PGAD symptoms who submitted their sacral MRIs to us. All the images except (g) are T2-weighted; T1-weighted images are (also in some cases) shown in (g, h, i, and k). The arrows point to the cysts: Image a) sagittal view of three different cysts at the S1 and S2 levels ; b) sagittal and transaxial views of two different cysts at the S2 and S3 levels; c) sagittal and coronal views of one cyst at the lower S2 level; d) sagittal and transaxial views of one cyst at the S2-S3 junction; e) sagittal and transaxial view of a double cyst at the S2 and S3 levels; f) sagittal and coronal views of a pair of cysts at the lower S2 and upper S3 levels; g) T1-weighted images of sagittal and coronal views of three cysts. The T2-weighted images that were submitted did not include these sacral levels, so are not shown. The first two panels on the left show one cyst at the S2-S3 junction. The three panels on the left show two additional cysts, one (left side) at lower S2 and the other (right side) at upper S3; h) sagittal T1 and T2-weighted images of the same cyst at S2 and a T2-weighted transaxial view of this cyst (right panel); i) T1- and T2-weighted images of a large cyst at S2 (upper panels) and transaxial T1- and T2-weighted images of this cyst (lower panels); j) axial T2-weighted image of a cyst at the S1-2 level; not visible in sagittal view k) T1- and T2-weighted images of a cyst at the S2 level (upper panels) and coronal S2 and “STIR” images of the two cysts in this woman (bottom panels); l) sagittal T2-weighted image of a cyst at the S2 level.

Acknowledgement:

We dedicate this study to the pioneer of PGAD -- our dear friend and colleague, Professor Sandra Leiblum -- whose tragic and untimely death is a terrible loss. We gratefully acknowledge the excellent advice and helpful, critical commentary by Walter Fanburg, M.D., and Doctoral Candidates Nan Wise and Eleni Frangos

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dysfunction: study, diagnosis and treatment. London: Taylor and Francis; 2006, 674-685.

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12. Leiblum SR, and Seehuus M. FSFI scores of women with persistent genital arousal disorder compared with published scores of women with female sexual arousal disorder and healthy controls. J Sex Med 2009;6:469–473.

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Hi All,

SIP 2012 live web streamed discussions are as follows:

· Wednesday, 30 May, 10.30-11:30 (English): Press Briefing from the International Press Centre under the Danish Ministry of Foreign Affairs

· Wednesday, 30 May, 13:00-18:00 (English): Workshop 1: Chronic Diseases: Chronic Pain as a disease in its own right

· Thursday, 31 May, 09:00-16:00: Plenary Sessions (English, Spanish, German, French, Italian & Danish)

To access the link to the live web-stream (published shortly before the SIP discussion commences) goto www.sip-platform.eu.

Thursday, 24 May 2012

Yale team discovers unexpected source of diabetic neuropathy pain

Monday, 21 May 2012

Pain-Topics.org News/Research UPDATES: Neuropathy Inadequately Diagnosed & Treated

Saturday, 19 May 2012

From Medscape Medical News > Neurology

US Senate Investigates Pain Management Groups

Laird Harrison

Authors and Disclosures

May 18, 2012 — Leaders of the US Senate Finance Committee have asked pain specialty organizations to disclose any financial ties or collaborations with pharmaceutical companies that manufacture opioid medications. The committee's primary aim is to determine whether there has been any undue influence by these companies over research or practice guidelines governing opioid prescribing.

In letters sent to each organization, Sen. Max Baucus (D-MT), the committee's chair, and Sen. Chuck Grassley (R-IA), a senior member, have asked the American Pain Society (APS), the American Academy of Pain Medicine (AAPM), and 5 other medical groups to release details of any funding they may have received from opioid manufacturers.

Both the APS and the AAPM will supply the information requested, their spokespersons told Medscape Medical News.

In a news release, the senators said deaths from opioid overdose have tripled over the last decade, killing 14,800 Americans in 2008 — more than the number who died of heroin and cocaine overdose combined.

"The problem of opioid abuse is bad and getting worse," Sen. Grassley said in a statement. "Something has to change. A greater understanding of the extent to which drug makers underwrite literature on opioids is a good start. Doctors and patients should know if the medical literature and groups that guide the drugs' use are paid for by the drugs' manufacturers and if so, how much."

In letters to the APS, the AAPM, the American Pain Foundation, the Center for Practical Bioethics, the Wisconsin Pain and Policy Study Group, the Joint Commission on Accreditation of Healthcare Organizations, and the Federation of State Medical Boards, the senators ask for disclosure of any funding since 1997 and details of any collaborations producing informational materials for doctors or patients on use of opioids.

In addition, the senators wrote to Purdue Pharma, Johnson & Johnson, and Endo Pharmaceuticals asking them to disclose any financial or other relationships to the 7 organizations, as well as to the American Geriatrics Society, the Alliance of State Pain Initiatives, and Beth Israel Medical Center, Department of Pain Medicine and Palliative Care.

The letters are not subpoenas and no hearings have been scheduled, so the companies and organizations are only being asked to respond as a courtesy, Sen. Grassley's spokesperson, Jill Gerber, told Medscape Medical News. The senators have not announced plans for any legislation either, she said. "I don't think they have gotten that far yet."

In their statement, the senators also highlighted news reports, suggesting the increase in opioid use over the last decade "may be driven by misinformation and dubious marketing practices used by the pharmaceutical companies and the medical organizations they fund."

In their responses, both the APS and AAPM point out they are already working to discourage opioid drug abuse.

"APS also looks forward to sharing with the Committee its strong advocacy for a sound policy approach to addressing the problem of abuse and diversion of prescription analgesic medications," that organization said in a written statement. "As advocates for patients and their families, we seek to advance access to a wide range of safe and effective pain treatments, while supporting our need as a society to prevent and control drug abuse."

"Patient safety is the top priority of AAPM, which has long advocated responsible use of all appropriate pain medication, including opioids," said the AAPM's statement. "No outside entity influences the research or activities of AAPM, which gives us the independence to advocate for patients and the physicians who care for them."

No outside entity influences the research or activities of AAPM, which gives us the independence to advocate for patients and the physicians who care for them.

The American Pain Foundation has actually ceased operation, according to a statement on its Web site, "due to irreparable economic circumstances." The Board of Directors for the organization formally voted to dissolve the organization on May 3, 2012, the statement notes (www.painfoundation.org).

"As you unfortunately know, the need for public outcry around the needs of Americans struggling with pain conditions is greater today than ever before in light of the multi-front assault occurring daily on our right to dignified care," the statement adds. "Misguided state and federal policies are impeding access to appropriate and reasonable medical care for people struggling with pain, and deterring even the most compassionate medical providers from treating anyone with pain conditions."

Irish Healthcare; Is It Caring for Rare Disease?

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