Legendary Aussie rocker Chrissy Amphlett has died, aged 53.

She passed away overnight in New York, where she lived with her husband.

Amphlett battled multiple sclerosis for almost 15 years and suffered from breast cancer in 2010.

In a statement, her cousin Patricia “Little Pattie” Thompson and family said: “Our beloved Chrissy peacefully made her transition this morning.

“Christine Joy Amphlett succumbed to the effects of breast cancer and multiple sclerosis, diseases she vigorously fought with exceptional bravery and dignity.

“She passed gently, in her sleep, surrounded by close friends and family, including husband of 14 years, musician Charley Drayton, her sister, Leigh, nephew, Matt, and cousin Patricia Thompson.

“Chrissy’s light burns so very brightly. Hers was a life of passion and creativity; she always lived it to the fullest.

“With her force of character and vocal strength she paved the way for strong, sexy, outspoken women.

“Best remembered as the lead singer of the ARIA Hall of Fame inductee, Divinyls, last month she was named one of Australia’s top 10 singers of all time.

“Chrissy expressed hope that her worldwide hit I Touch Myself would remind women to perform annual breast examinations.

“Chrissy was a true pioneer and a treasure to all whose lives her music and spirit touched.”

Amphlett shot to fame as the lead singer of the Divinyls, whose hits, including I Touch Myself and Pleasure and Pain, topped Aussie charts in the 1980s, and led to worldwide fame.

In 2006, the Divinyls were inducted into the ARIA Hall of Fame, alongside Australian icons Icehouse and Daddy Cool.

Amphlett pursued a solo career after the Divinyls’ break-up in 1997, appearing on an Aussie soap and as Judy Garland in the original production of The Boy from Oz, which won her a Helpmann Award nomination for best female actor.

It was during this time that she noticed symptoms of multiple sclerosis.

Speaking to Sunday Night, she said the disease took years to reveal its full effects on her body.

English: Paolo Zamboni (Photo credit: Wikipedia)

Source: Journal of Cerebral Blood Flow And Metabolism © 2013 International Society for Cerebral Blood Flow & Metabolism (04/03/13)

Abstract

In 2006, Zamboni reintroduced the concept that chronic impaired venous outflow of the central nervous system is associated with multiple sclerosis (MS), coining the term of chronic cerebrospinal venous insufficiency (‘CCSVI’).

The diagnosis of ‘CCSVI’ is based on sonographic criteria, which he found exclusively fulfilled in MS. The concept proposes that chronic venous outflow failure is associated with venous reflux and congestion and leads to iron deposition, thereby inducing neuroinflammation and degeneration.

The revival of this concept has generated major interest in media and patient groups, mainly driven by the hope that endovascular treatment of ‘CCSVI’ could alleviate MS. Many investigators tried to replicate Zamboni’s results with duplex sonography, magnetic resonance imaging, and catheter angiography.

The data obtained here do generally not support the ‘CCSVI’ concept. Moreover, there are no methodologically adequate studies to prove or disprove beneficial effects of endovascular treatment in MS. This review not only gives a comprehensive overview of the methodological flaws and pathophysiologic implausibility of the ‘CCSVI’ concept, but

English: ccsvi stenosys Italiano: stenosi ccsvi (Photo credit: Wikipedia)

also summarizes the multimodality diagnostic validation studies and open-label trials of endovascular treatment.

In our view, there is currently no basis to diagnose or treat ‘CCSVI’ in the care of MS patients, outside of the setting of scientific research.

This work was supported by the German Research Council (DFG Exc 257 to FP). The MS Center Amsterdam is funded by the Stichting MS Research, Voorschoten, The Netherlands.

Full article

I guess this is a blow to many who saw this a s a miraculous way forward. Tell me what you think

Related articles

• Low Incidence Of Venous Insufficiency In MS
• ‘Liberation’ treatment offers no improvement for MS patients, may do harm: study

Introduction

In many cases, living with MS leads family members to be even more appreciative and attentive to each other but families are not always able to maintain a positive adjustment to MS – sometimes the relationship between a person with MS and their family caregiver can deteriorate so that the relationship becomes abusive.

This can happen for any number of reasons including

• The physical or emotional stress
  of the caregiver,
• The difficulty of the person with
  MS to adjust to increasing disability
• Difficulties that the spouse or
  partner caregiver may have in managing both the intimate aspects of their
  relationship and caregiving needs ( which may include bowel and bladder
  management)
• Dealing with cognitive
  dysfunction.- it can be very frustrating to the caregiver when a seemingly
  normal adult doesn’t seem to know what’s going on in their life

Caregiver stress is an internal experience that can result from the physical or emotional burden of caregiving. When a caregiver
responds to that stress and isolation by inflicting harm on the person with MS they care for, it becomes abuse.

Different types of abuse

Abuse can be split into a number
of different types:

• Adult physical abuse – substantial physical injury
  experienced by an adult that result from cruel and inhumane treatment or an
  intentionally harmful act committed by any person.
• Sexual abuse – any form of forced sex or sexual
  degradation. This includes forcing an individual to participate in or observe
  sexual behaviours.
• Emotional abuse – this is the most difficult form
  of abuse to concretely define or detect  but it is generally considered the most
  harmful because of the long-term effects
• Neglect – failure of a
  responsible person to provide a minimal
  level of care includes health, nutrition, shelter, supervision, affection or
  attention.
• Exploitation and theft – misappropriation of money or
  property, theft, and coercion to sign legal documents that benefit the
  offender.

In a study of people with MS at the Mellen MS Center, Dr Jack Conomy and colleagues concluded that “. . . domestic violence among persons with MS appears common [and] . . . no age, race, gender, or socioeconomic group of people with MS is immune from personal violence.”

No one living with MS is immune to the possibility of abuse. There is little doubt that people with MS are victims of neglect or
violence, but the extent is not clearly known. We believe that the pattern of abuse in families with a history of domestic violence (pre-dating the MS diagnosis) will continue and may escalate as the disease worsens. Just as importantly, families with no previous history of domestic violence may find themselves in abusive relationships as a result of the stresses of living with
MS.

When family, friends or health care professionals are concerned about the potential for abuse or neglect in a family living with MS,
the first step is to acknowledge concern. Try empathising with the caregiver by saying something such as “Everyone has a limit as to how much stress and responsibility they can take – how close do you think you are to your limit?”,

Since the laws around reporting neglect and abuse differ between countries, it is important that family members and health care
professionals understand their responsibilities and know the relevant authorities to contact if they have any concerns.

It is well known that epilepsy occurs more frequently in people with MS than in the general population. (Mean prevalence in MS 2.3% and in general population ranges between 0.27 and 1.7%). Seizures have often been the only or first manifestation of MS.

In this study RRMS patients with epilepsy were found to have a higher number of cortical lesions and a decreased cortical thickness than those without epilepsy. Epilepsy in this subgroup seems to be consequence of rapidly
evolving cortical pathology – both in terms of number of lesions and cortical atrophy.  This subgroup of patients was also seen to have a higher degree of cognitive impairment and more physical disability.

This study shows that this subgroup of RRMS patients constitutes a group of MS patients whose cortical pathology needs further investigation.

This may be frustrating to hear beacuse it says lets look at it but hasn’t done it yet. Clearly these things need to have this initial study first to find out if there’s anything worth investigating and now that there is they neeed to find funding to take it further.

Why not visit A Voice For MS Facebook Page

A study has reported that Viagra given to mice with the animal model of MS showed  staggering results in 50% of the animals.

Daily treatment with Sildenafil (Viagra) rapidy reduced MS-like symptoms so that after 8 days there was an almost complete recovery.

For the first time it was shown how the drug reduced the infiltration of inflammatory cells into the white mattter of the spinal chord. This threrfore reduced the damage to the axons making myelin repair easier for the myelin-making cells.

Recent studies had already pointed to the fact that as well as vasodilation this drug seems to have neroprotective actions so can be used in MS, stroke and Alzheimers.

Researcher are confident that clinical trails in humas will soon be carried out.

Already a study , in the USA , has shown that bloodflow to the brain can be increased in both men and women who have MS using Viagra.

Have you used Viagra and did you find any change in your MS symptoms

Why not visit A Voice For MS Facebook Page

Please let me know if this makes life easier or if you would like any other changes.

Thanks

Kath

Some people with MS may experience a progression of their
symptoms over time. However, the exact mechanisms underlying this progression are not fully understood and it is difficult to predict whose symptoms will worsen and whose will remain stable. The authors of tis report studied a group
of people with MS, with and without clinical signs of motor dysfunction, and agroup of healthy controls, using transcranial magnetic stimulation (TMS).

TMS is a physiological test which measures the damage of
motor pathways of the central nervous system by measuring the speed of nerve
fibre conduction and other related parameters. They found that people with MS had abnormal results in the TMS compared to the controls. The authors also found that people with a higher level of disability had more severe TMS abnormalities. The results demonstrate that TMS may be a useful tool in measuring progression in MS and better understanding the underlying processes responsible for disability in MS.

authors:

Santón A, Cristóbal E, Aparicio M, Royuela A,Villar LM,

Alvarez-Cermeño JC.

source: Mult Scler. 2011 Jul 14. [Epub ahead of print]

A paper was published this month which examines the hypothesis of a causal
link between Epstein-Barr virus (EBV) infection and MS. It  compares the frequencies of types 1 and 2 EBV and co-infections in both people with MS and healthy controls.

Eostein Barr Virus

There are two  strains of Epstein Barr virus, labelled EBV-1 and EBV-2 (also known as type A and type B). However , although there are some differences, the acute illnesses caused by the 2 strains are apparently identical. Both strains are prevalent throughout the world and can
simultaneously infect the same person. The common names for these infections are Glandular fever or  herpes simples ( cold sores and genital herpes)

EBV was detected in 93% of the people with MS and 66% of controls. Interestingly,
dual infection with strains 1 and 2 was seen in 90% of the group with MS but
only 37% of controls (p<0.001) suggesting that co-infection with dual
strains of EBV may be important.

This study provides molecular evidence associating co-infection of type 1
and 2 EBV with MS.

Have you had glandular fever or are you plagued by cold sores ? Please levae a comment and let us know. I had glandular fever when I was about 12 or 13 but fortunately have  never had a cold sore although my mother has and one of my sons has.

ScienceDaily (June 1, 2011) — Environmental and inherited risk factors associated with multiple sclerosis — previously poorly understood and not known to be connected — converge to alter a critical cellular function linked to the chronic neurologic disease, researchers with the UC Irvine Multiple Sclerosis Research Center have discovered.

---

UCI neurologist Dr. Michael Demetriou is associate director of the Multiple Sclerosis Research Center. (Credit: Steve Zylius / University Communications)

The findings, which appear in the online, open-access journal Nature Communications, suggest that a unifying mechanism may be responsible for multiple sclerosis and point to therapies personalized according to genetic factors.

“MS results from complex interactions between an individual’s genetics and his or her environment,” said study leader Dr. Michael Demetriou, a UCI neurologist and associate director of the Multiple Sclerosis Research Center. “Defining how these come together to induce the disease is critical for developing a cure. We’ve taken a giant first step toward understanding this.”

Using blood samples from about 13,000 people, Demetriou and colleagues identified the way environmental factors — including metabolism and vitamin D3, obtained through either sunlight exposure or diet — interact with four genes (interleukin-7 receptor-alpha, interleukin-2 receptor-alpha, MGAT1 and CTLA-4) to affect how specific sugars are added to proteins regulating the disease.

Earlier work on mice by Demetriou revealed that changes in the addition of these specific sugars to proteins engender a spontaneous MS-like disease. They also found that N-acetylglucosamine (GlcNAc), a dietary supplement and simple sugar related to glucosamine, is able to suppress this process.

The current research shows that both vitamin D3 and GlcNAc can reverse the effects of four human MS genetic factors and restore the normal addition of sugars to proteins. “This suggests that oral vitamin D3 and GlcNAc may serve as the first therapy for MS that directly targets an underlying defect promoting disease,” Demetriou said.

Virtually all proteins on the surface of cells, including immune and nervous system cells, are modified with complex sugars of variable lengths and composition. This adds information to proteins separate from that directly defined by the genome. The sugars interact with specific sugar-binding proteins on the cell, forming a molecular lattice that controls the clustering, signaling and surface expression of critical receptors and transporters, such as the T cell receptor and CTLA-4. Reducing sugar modification weakens the lattice and enhances growth and activity of immune system T cells in such a way that they increase neural degeneration — a hallmark of MS.

Production of the complex sugars is regulated by both metabolic and enzymatic functions, the latter altered by genetic MS risk factors and vitamin D3. Demetriou pointed out that the MGAT1 genetic variant linked to MS increases or decreases the sugars attached to proteins depending on metabolism — one possible explanation for why people with the same genetic risk factor may or may not develop MS.

These sugars have also been implicated in many other chronic diseases, such as diabetes and cancer, Demetriou added, so this work could open up entirely new areas of medicine.

Haik Mkhikian, Ani Grigorian, Carey F. Li, Hung-Lin Chen, Barbara Newton, Raymond W. Zhou, Sevan Torossian, Gevork Grikor Tatarian, Sung-Uk Lee, Christine Beeton, K. George Chandy and Zhaoxia Yu of UCI and Ken Lau, Erin Walker, Katherine A. Siminovitch and James W. Dennis of the Samuel Lunenfeld Research Institute in Toronto participated in the study, which received support from the National Institute of Allergy & Infectious Diseases and the National Multiple Sclerosis Society, among others.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by