Mar 27, 2012


Anne Carrington Gawne, M.D.
edited by Halstead & Grimby, © 1995
Hanley & Belfus, Inc., Philadelphia, PA.
Chapter 9, pp 141-164

Lincolnshire Post-Polio Library copy by kind permission of Dr. Gawne.
Appropriate exercises have been shown to improve muscular strength and endurance, improve range of motion, and reduce functional deficits associated with many disabilities. In dealings with the patient with a history of polio, however, several questions arise: How much exercise is enough, and when is it too much? What kinds of exercise are best? What kinds of exercise may he harmful? And are there any guidelines to prescribe a safe and effective exercise program? To answer these questions, it is helpful to first understand the basic principles of exercise physiology, as well as the pathophysiology involved in post-polio syndrome. Following a discussion of these issues is a review of the literature on the effects of exercise in neurologically intact and post-polio individuals. Finally, a new classification system is presented, which will facilitate the prescription of exercise regimens that are both safe and effective in this population.

The effects of exercise are seen at two levels. The first is the cellular level, or in the muscle fiber. The second is throughout the cardiovascular and respiratory systems to meet the physiologic demands of the muscle fibers. The two are discussed separately, looking first at muscle strength and then at cardiovascular endurance.
Muscular strength is the maximal force that can be exerted by a muscle.[21] An isometric contraction is one in which tension develops but in which the muscle stays the same length.[48] An isotonic contraction, or, more appropriately, a dynamic contraction, is one in which the muscle shortens (concentric) or lengthens (eccentric) against a constant resistance, with the muscle tension varying somewhat throughout the range of motion.[24,48] Anisokinetic contraction is one in which the tension, developed by the muscle as it shortens, is maximal at all joint angles over the full range of motion and in which the velocity remains constant.[56]
When the three types of contractions are compared, the isokinetic one theoretically leads to the greatest improvements in both strength and endurance because it activates a larger number of motor units.[56] However, because it requires special equipment and trained personnel to administer, it is much less readily available. Significant strength gains occur with both eccentric and concentric contractions, and exercise equipment to perform these contractions is easy to find and affordable.[23] The advantages of isometric exercises are limited as the development of strength and endurance is specific to the joint angle at which the muscle is trained. Isometric exercises do have a place with individuals who have joints immobilized secondary to surgery or casting.
The overload principle states that muscles increase in size and strength when forced to contract at tensions close to their maximum.[46] Physiologic changes accompanying increased strength include hypertrophy -- the increase in cross-sectional area of the muscle fibers. Hypertrophy is attributable to one or more of the following changes: increased number of myofibrils per muscle fiber; increased protein, especially in the myosin filament; increased capillary density per fiber; increased amounts and strength of connective tissue; and increased number of fibers from longitudinal fiber splitting.[48] These morphologic changes are seen more frequently with eccentric contractions.
Additional factors responsible for strength gains are central nervous system (CNS) adaptations. These include an increase in the number of motor units activated, an increase in the rate of activation, and increased synchronization of motor unit firing.[56] Such changes occur at the spinal cord level and are responsible for cross-education, a phenomenon seen commonly in a limb contralateral to the trained limb. In general, younger individuals (18 - 26 years old) increase their muscle strength due to hypertrophy, whereas strength gains by older individuals (67 - 72 years old) are predominantly due to CNS adaptations.[49,50]
Atrophy, or the reduction in size of a muscle, occurs with denervation or when an extremity is placed at rest. Morphological changes seen after a muscle has been immobilized include atrophy of type I muscle fibers, whereas atrophy associated with aging is predominantly limited to a decrease in type II fiber area.[56]

México a la vanguardia en el Síndrome de Post Polio

Mar 25, 2012

Molecular mechanisms of poliovirus persistence

CMLS, Cell. Mol. Life Sci. 54 (1998) 1385–14021420-682X:98:121385-18  1.500.20:0Verlag, Basel, 1998

Molecular mechanisms of poliovirus persistence: key role of
capsid determinants during the establishment phase.

I. Pelletier, G. Duncan, N. Pavio and F. Colbe`re-Garapin*
Groupe de Ge´ne´tique Virale, Unite´ de Neurovirologie et Re´ge´ne´ration du Syste`me Nerveux, Institut Pasteur,
25 rue du Dr. Roux, F-75724 Paris Cedex 15 (France), Fax 33 1 45 68 87 80, e-mail:
Received 2 June 1998; received after revision 28 July 1998; accepted 28 July 1998

Abstract. As viral persistence is of major medical im- strains can be used to study the PV-HEp-2 cell interportance.

Well-characterized, simple models are needed actions. The viral determinants of persistence have to improve our understanding of persistent infections. been investigated with this model, and PV determi .We have chosen to study the molecular mechanisms nants have proven to be of crucial importance for the of viral persistence with the poliovirus (PV), because establishment of persistence in HEp-2 cells. Precise dethis picornavirus is one of the best characterized ani- terminants of PV persistence have been identified for mal viruses, it infects the central nervous system PV serotypes 1 and 3, in capsid proteins VP1 andwhich is a target organ for viral persistence, and it VP2. These determinants modify the early steps of thebelongs to the Picorna6iridae family of viruses, which PV cycle, and in particular, the conformational modincludes several naturally persisting viruses. We have ifications of the capsid following virus adsorption developed models of PV persistence in neuronal and onto its receptor. These results permit us to propose epidermoid cells, and the present review will focus on several hypotheses concerning PV persistence and the latter one because both lytic and persistent PV early steps of the PV cycle.

Viral persistence is of major medical importance.

Many viruses are able to establish long-lasting, persistent Infections in their host, and some of them are even responsible for severe pathologies [1]. Retroviruses, and most DNA viruses including in particular herpesviruses,are known to establish persistent infections in their hosts. The acquired immunodeficiency syndrome results from the persistence of the human immunodeficiency virus [2], which, in turn, favours the reactivation of many other persistent viruses, with the appearance of the corresponding pathologies. Several non retrovirus RNA viruses also persist in their hosts [3]. For example, a common childhood infection caused by the measles virus can lead to a very rare but fatal pathology, subacute sclerosing panencephalitis, after a decade of persistent viral infection in the central nervous system (CNS). Another example is provided by the hepatitis C virus, which persists in humans very frequently after the primary infection, inducing chronic hepatitis which may finally provoke a hepatocarcinoma [4].

Moreover, several chronic pathologies are probably triggered by viral persistence. It has been 
proposed that a persistent coxsackievirus infection could be involved in cases of chronic heart disease and
in diabetes mellitus [5, 6]. Indeed, during viral persistence,housekeeping functions of the cell may not be
altered, whereas specialized functions, like the secretion of insulin, may be affected, resulting in pathology
at the level of the organism [7–9]. Other viruses, in particular retro-, corona- and herpesviruses, are proposed
to play a role in the development of autoimmune diseases such as multiple sclerosis [10–13].
These few examples provide evidence that viral persistence is of major medical importance. Thus, well-characterized,simple models are needed to improve our understanding of persistent infections. We have chosen
to study the molecular mechanisms of viral persistence with the poliovirus (PV), because this picornavirus is
one of the best-characterized animal viruses; it infects the CNS, which is a target organ for viral persistence
[3]; and it belongs to a family of viruses that include several naturally persisting viruses. Furthermore, in a
certain number of patients with a history of paralytic poliomyelitis, a second pathology, possibly resulting
from viral persistence, has been observed to develop several decades after the acute disease [14, 15]. It is
Therefore interesting to investigate the capacity of PV to establish persistent infections in human cells.

General mechanisms underlying viral persistence
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As viral persistence is of major medical importance, well-characterized, simple models are needed to improve our understanding of persistent infections. We have chosen to study the molecular mechanisms of viral persistence with the poliovirus (PV), because this picornavirus is one of the best characterized animal viruses, it infects the central nervous system which is a target organ for viral persistence, and it belongs to the Picornaviridae family of viruses, which includes several naturally persisting viruses. We have developed models of PV persistence in neuronal and epidermoid cells, and the present review will focus on the latter one because both lytic and persistent PV strains can be used to study the PV-HEp-2 cell interactions. The viral determinants of persistence have been investigated with this model, and PV determinants have proven to be of crucial importance for the establishment of persistence in HEp-2 cells. Precise determinants of PV persistence have been identified for PV serotypes 1 and 3, in capsid proteins VP1 and VP2. These determinants modify the early steps of the PV cycle, and in particular, the conformational modifications of the capsid following virus adsorption onto its receptor. These results permit us to propose several hypotheses concerning PV persistence and the early steps of the PV cycle.

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Mar 23, 2012

Polio vaccine creator Victor J. Cabasso dies

Dr. Victor J. Cabasso, a pioneer virologist and immunologist who worked on creating the polio vaccine and other vaccines against human and animal virus diseases, died Feb. 28 at Kaiser Permanente Medical Center in Walnut Creek. He was 96.
In his earliest days in America he became noted for his experiments in developing the altered live polio viruses that led to the live virus vaccine now widely used around the world.
Born in Port Said, Egypt, Dr. Cabasso came to the United States after World War II and was a leading researcher at two major research-based drug and vaccine companies before retiring in 1980 to teach French literature in local schools as a community volunteer.

When the German army invaded France at the beginning of World War II, Dr. Cabasso was a young research fellow at the Pasteur Institute in Paris. He earned his degree as a doctor of science in 1941 jointly from the famed Sor-bonne and the University of Algiers, and then fled to Tunis, where he continued his fellowship at the Pasteur Institute.
In 1944, he joined the United Nations Relief and Rehabilitation Agency, serving as head of bacteriology and laboratories in the Middle East and Greece. Dr. Cabasso arrived in United States in 1946 at the invitation of an American Army officer serving as a physician with UNRRA who recognized his expertise in the emerging field of virology.
Dr. Cabasso became a research virologist and later chief of immunologic virus research at the Lederle Laboratories in Pearl River,., where he worked until 1967.
In the Lederle lab he and Dr. Albert Sabin created two strains of live polio virus and developed methods for weakening one strain until it could not possibly cause the disease while retaining its complete structure - an achievement that would shortly become known as the Sabin live polio vaccine.
Later Dr. Cabasso joined the Cutter Laboratories in Emeryville to become director of microbiology research and then vice president for research and development before the firm was purchased by the German drug firm Bayer AG.
At Cutter, Dr. Cabasso led a laboratory team that developed the first human antirabies serum after six years of experiments - an achievement that became the first rabies vaccine.

Dr. Cabasso and his family lived in Moraga, and after retiring from Cutter he became director of the Moraga Public Library and took to designing tapestries drawn from sources as varied as Chinese flowers and electron microscope images. They have been widely displayed at local galleries and museums.
He is survived by his wife, Anna; daughter, Jacqueline of Oakland; and son, Phillip, of Sierra Madre (Los Angeles County).
A family celebration of Dr. Cabasso's life is being planned.

David Perlman is The San Francisco Chronicle's science editor.

Read more:

México a la vanguardia en el Síndrome de Post Polio

Mar 18, 2012

The Institute of Serology, Calcutta, detected the VDPV on March 2 this year,

Polio blow in Bengal with vaccine lesson

New Delhi, March 17: India has recorded its first case of polio caused by a vaccine-derived poliovirus (VDPV) this year in a five-month-old child in Murshidabad district of Bengal but the country remains free of the wild poliovirus.
A polio surveillance laboratory in Calcutta has found that the child from Lalbag block in Murshidabad was infected by VDPV, which occurs when the weakened virus in the oral polio vaccine (OPV) mutates over time, and regains the ability to cause paralysis.
Surveillance experts say VDPVs are extremely rare and typically occur in children with immunodeficiency or in populations with low levels of immunity. The child in Lalbag has had repeated episodes of infections, indicating the possibility of immunodeficiency, the polio surveillance programme run by the Union health ministry and the World Health Organisation said in an update on VDPVs.
The Institute of Serology, Calcutta, detected the VDPV on March 2 this year, about a week after the WHO deleted India from the list of polio-endemic countries after more than a year free of the wild poliovirus.

Public health experts say India remains free of wild polio, but the local response to VDPVs should be similar to the management of wild poliovirus outbreaks — rapid implementation of local mass immunisation campaigns.
Last year, the surveillance programme detected seven cases of VDPVs — one in a child with congenital immune deficiency in Dhamtari, Chhattisgarh, and the other six from areas with low routine immunisation coverage — Udaipur in Rajasthan, Ghaziabad and Badaun in Uttar Pradesh, Barnala in Punjab, Vidisha in Maharashtra, and Jajpur in Odisha. Rapid immunisation helped prevent the circulation of VDPVs that emerged in India during 2010 and 2011.
A VDPV is a risk associated with OPV that contains live, weakened vaccine virus. A child vaccinated with OPV excretes the vaccine virus for six to eight weeks and, rarely, a vaccine virus may genetically mutate and cause disease in vulnerable children.
“But even one case of VDPV should be viewed as the tip of an iceberg,” said Thekakarra Jacob John, former head of medical virology at the Christian Medical College, Vellore, and former member of a technical group that advises the government on polio.

“Each VDPV is a signal that the vaccine virus from OPV has become wild-like — and the rule in polio is that for every one infection detected, there are perhaps up to 1,000 silent infections,” John told The Telegraph.
The emergence of VDPVs, some of which have circulated and caused outbreaks, in several countries over the past decade, has prompted the WHO to rethink the polio eradication strategy and consider the option of introducing an inactivated polio vaccine (IPV), which contains killed viruses, and thus does not carry the risk of VDPV.

“There’s no alternative — the IPV will have to be introduced to intercept the emergence of VDPVs,” said John, who had in the late-1990s predicted the risks of trying to eradicate wild polio with OPV alone.
A report on VDPVs from the US Centres for Disease Control released last year said more than 400 cases of VDPV had been detected from countries in Africa, Asia and Europe between July 2009 and March 2011.
The Union health ministry has specific guidelines on following up each case of VDPV that include investigations on immunological conditions of each patient, efforts to determine if the VDPV is circulating in the community, and assess the population immunity in the immediate vicinity of the VDPV case.
The National Polio Surveillance Project says the OPV is a very safe and effective vaccine that is protecting millions of children from paralysis caused by the wild virus. The agency said the chance of an importation of the wild poliovirus remains “the larger threat to the children of India”.

México a la vanguardia en el Síndrome de Post Polio

Mar 5, 2012


          About postpolio syndrome
Decades after recovery from polio, many patients develop new muscle weakness and other symptoms that can lead to increased debility. Treatment is aimed at the most prominent symptoms. Medications may help, as well as physical therapy and a carefully paced exercise program. Screening for osteopenia and osteoporosis is recommended.
Postpolio syndrome affects an estimated 60% of “paralytic polio survivors, plus unknown numbers of patients who had subclinical polio.
Postpolio syndrome is a diagnosis of exclusion. Symptoms are related to new muscle weakness and may include muscle atrophy, myalgias, fatigue, and problems with swallowing and breathing.
No drugs specifically address postpolio syndrome. Pyridostigmine has had mixed results for treating weakness and fatigue, as have methylphenidate and bromocriptine. Modafinil may be helpful for fatigue. Nonsteroidal anti- inflammatory drugs are used to treat pain.
Rehabilitation professionals who have expertise in treating polio survivors can be va
Report #6779 4/9/96
People who have muscle and nerve diseases, such as post-polio syndrome and multiple sclerosis, usually do not exercise because their muscles hurt during exercise and they feel extremely tired after they exercise. A recent report in The American Journal of Physical Medicine and Rehabilitation shows that can benefit greatly from a program to strengthen their muscles.
Your muscles are made up of thousands of individual fibers. Each muscle fiber is innervated by a single nerve. When a nerve dies, the muscle fiber that is attached to that nerve lacks a stimulus to make it contract, so that fiber dies also. Multiple sclerosis and post-polio syndrome destroy nerves, causing muscle fibers to disappear. When such people exercise, their muscles have fewer fibers, so the remaining fibers have to work much harder, fatigue earlier and take far longer to recover. Strengthening the fibers allows a person with nerve damage to do more work before the muscles fatigue during exercise.
However, all people who have nerve damage become extraordinarily weak on the day after they exercise. To avoid long recovery periods after exercise, they can start out by lifting very light weights in 3 sets of ten and stop exercising immediately when they feel burning, heaviness and fatigue. 
They can try again at least 48 hours later, provided that their muscles do not feel heavy before they start. When they can perform 3 sets of 10 with a certain weight comfortably and feel fresh on the next day, they are ready to try a slightly heavier weight in their next workout.By Gabe Mirkin, M.D., for CBS Radio News
1) JC Agre, AA Rodriquez, TM Franke, ER Swiggum, RL Harmon, JT Curt. Low-intensity, alternate-day exercise improves muscle performance without apparent adverse affect in postpolio patients. American Journal of Physical Medicine & Rehabilitation. 1996(Jan-Feb);75(1):50-58. 
luable resources in preserving function and preventing deconditioning.

México a la vanguardia en el Síndrome de Post Polio

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