Management of postpolio syndrome Henrik Gonzalez, Tomas Olsson, Kristian BorgLancet Neurol 2010; 9: 634–42 Postpolio syndrome is characterised by the exacerbation of existing or new health problems, most often muscle weakness
See Reﬂ ection and Reaction and fatigability, general fatigue, and pain, after a period of stability subsequent to acute polio infection. Diagnosis is based on the presence of a lower motor neuron disorder that is supported by neurophysiological ﬁ ndings, with exclusion Division of Rehabilitation of other disorders as causes of the new symptoms. The muscle-related eﬀ ects of postpolio syndrome are possibly Medicine, Department of associated with an ongoing process of denervation and reinnervation, reaching a point at which denervation is no Clinical Sciences, Danderyd longer compensated for by reinnervation. The cause of this denervation is unknown, but an inﬂ ammatory process is Hospital (H Gonzalez MD,
K Borg MD) and Department of possible. Rehabilitation in patients with postpolio syndrome should take a multiprofessional and multidisciplinary Clinical Neurosciences, Centre approach, with an emphasis on physiotherapy, including enhanced or individually modiﬁ ed physical activity, and muscle for Molecular Medicine training. Patients with postpolio syndrome should be advised to avoid both inactivity and overuse of weak muscles.
(T Olsson MD), Karolinska Institute, Stockholm, Sweden Evaluation of the need for orthoses and assistive devices is often required. Introduction
summary of the pathophysiology and clinical
12–20 million people worldwide have sequelae of characteristics of postpolio syndrome, outline diagnostic
poliomyelitis, according to Post-Polio Health and treatment options, and suggest future research
International. Postpolio syndrome is the most common strategies.
neuromuscular disorder in Sweden1 and the most
prevalent motor neuron disease in the USA.2
A common misconception is that people in developed Studies of motor units of patients with postpolio
For more on Post-Polio Health
countries who have had poliomyelitis are old. Large syndrome have revealed an ongoing denervation–
International see http://www.
epidemics were frequent in Europe and in the USA in reinnervation process.8,9 This is probably initiated after
the 1940s and during the ﬁ rst half of the 1950s when the acute poliomyelitis, and over time leads to increased vaccination programmes were launched,2,3 and many motor unit areas caused by collateral sprouting of people who have recovered from poliomyelitis infection adjacent motor neurons in the spinal cord in patients are still of working age. A global eradication of with postpolio syndrome; a process also evident during poliomyelitis is close to accomplishment; in a few years normal ageing, although not until the seventh decade of time there should be no new cases of the disorder. life.10 The motor unit area might increase by up to However, in several developing countries, many young 20 times, reaching a level at which further reinnervation people have recently contracted the disease. Although the
is no longer possible. Uncompensated denervation
number of people with sequelae of poliomyelitis will causes atrophy of muscle ﬁ bres and subsequently loss of decrease in Europe and the USA in the next few decades,
muscle strength.8,9 The underlying cause of the ongoing
many people in developing countries will be aﬀ ected for denervation resulting in the motor symptoms of at least a generation.
postpolio syndrome is unclear. Several hypotheses have
Many health-care workers believe that the sequelae of been proposed, as described below.
poliomyelitis do not change throughout a patient’s lifetime. However, more than a century ago the Stress or overuse of motor units development of new or exacerbated symptoms was Stress is a favoured hypothesis, proposed by Wiechers already reported long after the acute poliomyelitis and Hubbell,11 which attributes postpolio syndrome to infection.4 The existence of postpolio syndrome has been
degenerating terminal axonal sprouts and an inability to
questioned, but the late eﬀ ect of poliomyelitis, or maintain the increased metabolic demand from the postpolio syndrome, is generally accepted as a deﬁ ned enlarged motor unit. Overuse was suggested by Perry clinical entity.2,5,6 The prevalence of postpolio syndrome and colleagues12 in 1988. Overuse of remaining motor has been reported to be between 20% and 85% of people
units leads to activation of compensatory mechanisms:
who have had poliomyelitis.2,6,7 This disparity is most muscle ﬁ bre transition from fast to slow contracting probably caused by the use of diﬀ erent clinical diagnostic
muscle ﬁ bres and muscle ﬁ bre hypertrophy, that is,
criteria. In this context, it is important to remember that changes in contractile properties of the overused muscle people who have sequelae of poliomyelitis but who do ﬁ bres and an increase of the contractile tissue.8,13–15 not fulﬁ l diagnostic criteria for postpolio syndrome might
Compensatory changes in the muscle have negative
still have substantial loss of motor function and be in eﬀ ects, such as muscle pain and fatigue caused by lower need of therapeutic interventions.
capillarisation and changes in the contractile properties
Interest in postpolio syndrome has increased over the of the remaining muscle ﬁ bres. These changes favour
past two to three decades, with research varying in focus muscle strength before endurance,15 and thus a from molecular to clinical aspects, and health-related discrepancy between low energy resynthesis and a high quality of life. In this Review, we provide a comprehensive
energy utilisation in the overused muscle ﬁ bres, which is
www.thelancet.com/neurology Vol 9 June 2010
of importance for development of fatigue, was assumed. Nonetheless, results from longitudinal studies do not
Panel: Criteria for postpolio syndrome16
show that overuse leads to increased persistent muscle
1 Prior paralytic poliomyelitis with evidence of motor
neuron loss, as conﬁ rmed by history of the acute paralytic illness, signs of residual weakness and atrophy of muscles
on neurological examination, and signs of denervation on
The length of time between acute poliomyelitis and the
start of symptoms is a risk factor for postpolio syndrome,17
2 A period of partial or complete functional recovery after
and two studies independently concluded that age was a
acute poliomyelitis, followed by an interval (usually
confounding factor for the development of postpolio
15 years or more) of stable neurological function.
syndrome.17,18 However, the normal ageing process can
3 Gradual or sudden onset of progressive and persistent
also cause muscle weakness in patients with postpolio
new muscle weakness or abnormal fatigability (decreased
endurance), with or without generalised fatigue, muscle atrophy, or muscle and joint pain. (Sudden onset may
follow a period of inactivity, or trauma or surgery.) Less
Persistence of poliovirus fragments might cause postpolio
commonly, symptoms attributed to postpolio syndrome
syndrome. Mutated poliovirus genomic sequences have
include new problems with breathing or swallowing.
been detected in the CSF of some patients,19,20 but not in
the CSF of others.21 One study22 reported detection of
5 Exclusion of other neurological, medical, and orthopaedic
poliovirus genome fragments in all patients with
postpolio syndrome. Further study is clearly needed to prove the hypothesis of a persistent viral infection in postpolio syndrome.
If the neurodegeneration in postpolio syndrome is an
ongoing process caused by chronic inﬂ ammation,
Immunological factors and chronic inﬂ ammation
treatment of the disorder with drugs that modify the
Increasing interest in recent years has been devoted to immune response (eg, intravenous immunoglobulin and the immunological process underlying postpolio cortisone, as discussed later) should be possible. syndrome. Inﬂ ammatory changes have been described in the spinal cord23,24 and the CSF25 of patients with Genetics postpolio syndrome. Also, concentrations of several Some studies have attempted to ﬁ nd a genetic background cytokines, mainly those with proinﬂ ammatory actions to postpolio syndrome. Bartholdi and colleagues32 reported (eg, interferon-γ and tumour necrosis factor [TNF]), are that the SMN gene deletion, a cause of adult spinal high in the CSF of patients.26–28 These ﬁ ndings probably muscular atrophy, was not present in patients with reﬂ
ammation in the spinal cord postpolio syndrome. Polymorphisms in the Fc-gamma
parenchyma, with potential damage to motor neurons. receptor IIIA might be a risk factor for postpolio Further support for this scenario was obtained by use of syndrome.33 Further studies of possible gene variants that unbiased proteomics of the CSF. A small series of could predispose to both acute poliomyelitis and postpolio proteins and their fragments were found at high syndrome would be of interest. concentrations in the CSF only in patients with postpolio syndrome; the peptides were all involved in apoptosis Diagnosis and inﬂ ammation.29 Furthermore, peptide cleavage Several diagnostic criteria for postpolio syndrome have patterns were consistent with actions of TNF. A systemic
been proposed.8,34–36 Diﬀ erent criteria from diﬀ erent count-
proinﬂ ammatory response in postpolio syndrome is also
ries focus on muscle atrophy34 or muscle dysfunction,10 but
likely. High TNF concentrations in blood were associated
all are mainly based on those originally suggested by
with increased muscle pain.30 The ﬁ nding of high titres Halstead and Rossi.36 In 1991, Halstead added gradual or of poliovirus antibodies and high numbers of regulatory abrupt onset of new neurogenic muscular weakness as a T cells31 further supports the notion of an active criterion.37 In the criteria suggested by the 29th European immunological process.
Neuromuscular Centre workshop on postpolio muscle
The role of this chronic inﬂ ammation in postpolio dysfunction, clinical and neurophysiological ﬁ ndings,
syndrome is unclear and further study is needed. MRI, or both, compatible with a lower motor neuron lesion Potential causes include a late aberrant immune response
were included.8 At the March of Dimes international
to the original infection, a persistent immune response, conference on postpolio syndrome in 2000, diagnostic or persistence of viral particles (boosting of the response
criteria were recommended, including a criterion that
by non-polio enteroviruses might also be involved); a late
symptoms should persist for at least 1 year (panel).16
autoimmune complication of the original infection; and
Diagnosis of postpolio syndrome is based on clinical
an immune response secondary to ongoing neuro-
symptoms and signs (tables 1 and 2). To diagnose a patient
with postpolio syndrome not all symptoms and signs
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In a large cohort of patients with a reported history of
poliomyelitis, 5% had normal EMG.42 Sandberg and
Physical activity, muscle training, avoiding muscle
Stålberg42 suggested that, despite normal EMG, there was
overuse and disuse, and lifestyle changes
a transient functional loss without degeneration of
weakness in previously clinically unaﬀ ected muscle groups
anterior horn cells, making these cells more vulnerable
Symptomatic medication, physiotherapy, bracing,
weight reductionDecompression and pharmacological treatment for
Symptoms and signs
Because poliomyelitis aﬀ ects the anterior horn cells in
Physical activity, muscle training, rest, avoiding
the anterior part of the spinal cord (the ﬁ rst part of the
muscle overuse and disuse, lifestyle changes,
endurance. Mental fatigue can also weight reduction, and, if required, medication for
motor unit), postpolio syndrome is a lower motor neuron
restless legs syndrome, depression, and sleep
disorder. The symptoms in patients with postpolio
syndrome are muscle weakness and atrophy, and fatigue
Assisted ventilation and inspiratory muscle training
and pain from muscles and joints (table 1).2,37 Other
muscles and chest wall deformities, Invasive controlled mechanical ventilationobstructive apnoea, and central
muscle twitching and cramps, respiratory distress, and
Instruction on swallowing and voice therapy
On clinical investigation, signs of a lower motor neuron
Table 1: Symptoms and treatment of postpolio syndrome
disorder are apparent; the most typical is asymmetrical ﬂ accid paresis. Sensory deﬁ cits are not observed unless a secondary disorder is present, for example compression
Clinical signs Investigation
Weak or no muscle strength. Lower Clinical examination
Health-related quality of life has been investigated in
patients with postpolio syndrome in several studies.
Diﬀ erent questionnaires, mainly the SF-3643–46 and the
Nottingham health proﬁ le,47–51 have been used. But,
although diﬀ erent questionnaires were used, results
were comparable, with low health-related quality of life
Neurophysiology (nerve conduction velocity)
in physical domains, pain, and vitality; however, results
Investigation on oesophageal and laryngeal
from mental domains are similar to those reported by
control individuals. Patients with postpolio syndrome
Pulmonary function Weak respiratory muscles, chest
Pulmonary investigation, including complete
can have a high degree of independence with regard to
and sleep-disordered wall and spinal deformities
personal activities of daily living but typically have
culty with mobility.52–54 Overall morbidity is high in
Table 2: Clinical signs of postpolio syndrome
patients with postpolio syndrome compared with that in healthy control individuals.55 Besides, comorbidity and
need to be present. As stated previously, this is a diagnosis
ageing can cause further health problems in these
based on exclusion. The most common symptom of patients.44 postpolio syndrome is a triad of fatigue, deterioration in muscle strength, and pain (panel). Serum creatine Muscle weakness and atrophy phosphokinase concentrations are usually normal.2,3
In patients with postpolio syndrome new or increased
Diagnosis is supported by electrophysiological exam-
muscle weakness and atrophy can be permanent, because
ination including electromyography (EMG), which usually
of loss of motor units, or transient, because of muscle
reveals longstanding neurogenic signs. Macro-EMG can fatigue.2 Progression of muscle weakness is probably slow enable a more precise quantiﬁ cation of remaining motor but faster than in normal ageing.56 Stolwijk-Swüste and units and their size, thereby indicating the extent of the colleagues57 systematically analysed studies assessing the denervation and reinnervation process.38
course of functional status and muscle strength over time
Patients who had non-paralytic polio and those with in patients with postpolio syndrome. Only two studies that
clinically unaﬀ ected muscles and a history of polio-
myelitis might present with postpolio syndrome and they reported inconsistent results. Four studies that neuro
physiological signs of denervation.39,40 In people assessed muscle strength were of suﬃ
aged 60 years or over, loss of half of their motor units reported a decline in muscle strength and two reported no might not be associated with a decline in muscle change. Grimby and colleagues58 reported a decrease of strength;41 this could explain both why paresis might not muscle cross-sectional area in patients with poliomyelitis be recognised and the occurrence of new postpolio sequelae during a 4-year follow-up period58 and a 9–15% syndrome symptoms in extremities that were thought decrease in muscle strength during a follow-up period of not to have been aﬀ ected by poliomyelitis.
8 years.9 We recorded a 6% decrease in muscle power in a
www.thelancet.com/neurology Vol 9 June 2010
selected muscle in patients with postpolio myelitis over a age and time since the acute poliomyelitis) are non-6-month period.43 McComas and colleagues59 described a modiﬁ able, others (eg, stress and physical activity) are decrease in motor units of 13·4% in patients with previous
modiﬁ able, and hence they are important to consider in
poliomyelitis during a 2-year follow-up. Lower ﬁ gures the management of these patients. were reported by Sorensonand coworkers,60 with a yearly loss of 3% during a 15-year follow-up period, and Ivanyi Pain and colleagues61reported no decrease of muscle strength Pain is common in patients with postpolio syndrome; the during a follow-up period of about 2 years. Thus, as pain intensity is high76 and is more often located in parts pointed out by Stolwijk-Swüste and colleagues,57 long-term
of the body that were aﬀ ected by polio than in parts that
follow-up studies with unselected study populations and were not.77 Many patients with postpolio syndrome report age-matched control individuals are needed to shed cramping pain in the legs (most often the upper leg further light on this question.
musculature) and aching pain in the neck and shoulders.77
Loss of motor units and a decrease in muscle strength The pain has been reported to be widespread.78 Pain is
and endurance is not necessarily associated with physical most common in women with postpolio syndrome, young function, physical activity, or social participation. There is patients, or patients who have had a long stable period.79 no correlation between muscle strength and walking Although the pain can have variable origin, it is mostly ability in patients with postpolio syndrome.50,62 The associated with overload of muscles, tendons, and joints association is non-linear possibly because of compensatory
and is related to the amount of physical activity.77,79–82 10%
of patients with postpolio syndrome have neuropathic
Daily activity did not decrease during a 3-year follow-up
pain, caused by secondary disorders such as nerve
period63 and participation in walking activities was self-
compression or disc hernia that can be treated.83 Thorough
cient for daily life mobility by the clinical assessment of patients with postpolio syndrome
patients.64 Horemans and colleagues50 and Klein and who have neuropathic pain is therefore needed to exclude colleagues63 found that actual walking in daily life in concomitant and secondary disorders and to provide patients with postpolio syndrome was not only aﬀ ected adequate pain treatment. by walking capacity but also by social behaviour and personal lifestyle. Willen and colleagues65 reported that Hypoventilation there was a non-linear relation between walking speed Some patients with polio who had initial weakness of and muscle strength. Furthermore, Sorenson and respiratory muscles or other factors that might have colleagues66 concluded that there was no association decreased lung function (eg, chest deformity or between the amount of decline in motor units and the progression of scoliosis) experience new respiratory symptoms of this late muscle deterioration, but minor problems as a consequence of postpolio syndrome.84 changes in disability were seen during follow-up.
Furthermore, patients with postpolio syndrome are also
Increased muscle weakness can lead to reduced balance
at risk of nocturnal hypoventilation caused by sleep-
and increased numbers of falls in patients with previous disordered breathing (a general term used for diﬀ erent poliomyelitis.67 Patients with increased muscle weakness kinds of symptoms related to disorders of breathing might need to use assistive devices for walking or a during sleep, such as obstructive apnoea, central apnoea, wheelchair, and those with weak respiratory muscles or a mixed dyspnoea). Shortness of breath is the most might require ventilation.
common complaint, but patients might also present with non-speciﬁ c symptoms, such as daytime somnolence,
morning headache, and fatigue.84–87 In patients with a
Fatigue in patients with postpolio syndrome is multi-
history of these symptoms, hypoventilation and sleep-
dimensional68 and can be of general or mental character disordered breathing should always be investigated with derived from the CNS (caused by early neuronal damage tests of pulmonary function and polysomnography, in the brain in the acute poliomyelitis stage, overlapping respectively. Cardio pulmonary comorbidity should also psychological factors, or both) or muscular from the be considered. motor unit.69–71 Fatigue is probably the most disabling symptom of postpolio syndrome. Muscle weakness Other symptoms during fatigue is caused by slow recovery of the muscle Other symptoms and new health problems include cold and could reﬂ ect both central and peripheral fatigue.2,72,73
intolerance, cold sensitivity, muscular twitching, and
Fatigue in postpolio syndrome has a negative eﬀ ect on muscular cramps, as well as concentration problems and physical and psychosocial functioning but does not swelling of legs and feet.7,17,88,89 Bulbar muscle weakness impair mental health.74,75 Health-related quality of life for can lead to dysphagia and dysphonia.2,3,7,90,91 Investigation vitality is to a greater extent caused by physical of whether new health problems are caused by postpolio (eg, decreased physical endurance) than by mental syndrome, are secondary to postpolio syndrome, or are (eg, mental fatigue) parameters.75 According to Trojan and
caused by comorbidities is important because some
colleagues,68 although some risk factors for fatigue (eg, comorbidities require adequate intervention.
www.thelancet.com/neurology Vol 9 June 2010 Clinical management
today. Heavy resistance training was recommended for
No speciﬁ c treatment for postpolio syndrome exists. patients with postpolio syndrome who had near-normal Evaluation of the eﬃ
cacy of treatment regimens for muscle strength and no signs of reinnervation of the
patients with postpolio syndrome was initiated by motor unit.8,101 Submaximum endurance training, which the Cochrane Library in 2009. Patients with postpolio increases muscle strength and endurance,98 was syndrome often have a wide range of medical recommended for patients with moderate paresis and problems and may also have associated problems with signs of reinnervation of the motor unit.8,101 Patients with participation in society, such as need for technical aids severe paresis should avoid muscle training; however, at home and at work.
ﬁ nding a suitable physical activity for cardiovascular conditioning in these patients is important. Aerobic
Physiotherapy, physical activity, and muscle training
exercise, including bicycle ergometry, treadmill walking,
Physical activity forms the basis of management of patients
and swimming, are recommended.2 Aquatic exercise is
with postpolio syndrome. Most patients with postpolio also beneﬁ cial.102 syndrome beneﬁ t from appropriate physical activity and a large proportion beneﬁ t speciﬁ cally from individually Pharmacological treatment chosen muscle training. Lygren and colleagues78 noted that
A few controlled trials of pharmacological treatments
patients with postpolio syndrome who reported doing have been done in patients with postpolio syndrome. regular physical activity had fewer symptoms and a higher
Amantadine and high-dose prednisone were ineﬀ ective at
level of functioning than those who were not often reducing muscle weakness and fatigue.103,104 In one study, physically active. No prospective data show that increased no beneﬁ cial eﬀ ect on muscle function was reported after physical activity leads to muscle weakness.6
treatment with pyridostigmine.105 Conversely, another
Few randomised controlled trials have investigated the study reported a slight improvement in walking in
eﬀ ect of muscle training in patients with postpolio patients treated with pyridostigmine.106 In another syndrome. Because most patients with postpolio randomised controlled trial, there was no signiﬁ cant syndrome have asymmetrical muscle weakness and the diﬀ erence in muscle function between patients with degree of paresis diﬀ ers over time and between patients, postpolio syndrome who were having muscle training training programmes should be carefully customised and
and taking coenzyme Q-10 and those receiving placebo.107
planned by physiotherapists to avoid both overuse and Modaﬁ nil has proven ineﬀ ective for treatment of fatigue disuse, and the level of physical activity modiﬁ ed to in patients with postpolio syndrome in two randomised decrease pain.77,92 Patients should be carefully monitored controlled trials.108,109 However, a controlled study on the to identify signs of increasing muscle weakness and eﬀ ect of lamotrigine on pain, fatigue, and quality of life muscle pain, and thus to avoid adverse eﬀ ects, especially had promising results.110overuse of muscles that are clinically unaﬀ ected but were
Based on the notion of an inﬂ ammatory process in the
found clinically or by use of EMG to be aﬀ ected by polio CNS of patients with postpolio syndrome, intravenous infection.12,16 Overuse-induced weakness has been immunoglobulin has been tested. A single course of proposed,12–15 but there is no evidence that overuse high-dose intravenous immunoglobulin greatly reduced weakness permanently damages muscles aﬀ ected by the concentrations of proinﬂ ammatory cytokines in the poliomyelitis. Rather, the occurrence of overuse-induced CSF 2 months after treatment.27 The idea of a role for weakness could be explained by metabolic demands these cytokines in postpolio syndrome would be exceeding the individual muscle capacity or reparable strengthened if a clinical response was also seen, with intramuscular damage, similar to those in healthy amelioration of symptoms and signs. In a single patient,111 individuals.93 In this respect, one must also bear in mind in small open studies,27,112 and in two larger randomised that the energy cost of movement is higher in patients controlled trials,26,43 variable eﬀ
with postpolio syndrome than in control individuals.94,95
immunoglobulin on muscle strength, pain, physical
To save energy, reduction in activity and pacing as well activity, and quality of life have been described. These
as training in muscle conservation techniques are data encourage further controlled trials to more ﬁ rmly required; this approach remains the mainstay of treatment
establish if this treatment regimen should be used.
of postpolio syndrome.16,96 Cup and colleagues97 reviewed Furthermore, such trials should assess dosing and dosing studies dealing with exercise therapy in patients with intervals and ways to predeﬁ ne responders and non-postpolio syndrome and found evidence for eﬀ ectiveness responders to this treatment. of strengthening or aerobic exercise to be insuﬃ
Symptomatic treatment is of course important in
However, endurance98,99 and heavy resistance training100
postpolio syndrome. For example, restless legs syndrome
are eﬀ ective at increasing muscle strength and endurance
is a common complaint in patients with postpolio
in patients with postpolio syndrome. In 1994, the syndrome and can be successfully treated with dopamine European Neuromuscular Centre workshop8 on postpolio
agonists.113 As pointed out by Trojan and colleagues,68
muscle dysfunction and Grimby and Stålberg101
the most prominent symptom in postpolio syndrome,
recommended guidelines for exercise that are still valid fatigue, is multidimensional, and some of the con-
www.thelancet.com/neurology Vol 9 June 2010
tributing factors can be treated. Other symptomatic syndrome have a higher risk for late poliomyelitis-related pharmacological treatments that should be considered symptoms compared with active people with postpolio are analgesics and antidepressants.
syndrome.122 An active lifestyle should therefore be recommended. However, patients should be carefully
assessed to avoid both overexertion and inactivity.
Joint deformities, arthrosis, and limb-length inequality Lifestyle modiﬁ cations can be eﬀ ective in reducing may require surgery. Increased function can be achieved overuse symptoms.123 Workload and social interaction in by arthrodesis, tendon transfers, and muscle transplant-
the community68 should be assessed, and occupational
ation.114 For other secondary disorders, such as spinal and vocational interventions might be needed.124 Weight stenosis and disc hernia, surgical treatment can help. reduction or a programme to stabilise bodyweight may However, motor neurons of patients with postpolio be important.3,7 A weight reduction programme, when syndrome might be more sensitive to eﬀ ects of indicated, can reduce fatigue, improve respiratory anaesthetic drugs and thus patients should be carefully symptoms, and increase mobility. assessed before and monitored both during an operation
Occupational interventions, weight-control programmes,
group therapy (eg, water exercise125), and increased use of assistive devices should be considered and managed by
Orthoses and assistive devices
the multiprofessional rehabilitation team.126
Orthopaedic braces can restrict unwanted movements— supporting joints and muscles and reducing the impact Future perspectives of bodyweight, particularly in legs and feet. The use of Better distinction between postpolio syndrome and braces should improve mobility, reduce pain, and reduce
poliomyelitis-related secondary disorders by more
overuse of the still well functioning parts of the muscles,
thorough clinical analyses is important. Further studies
joints, tendons, and ligaments. Use of lightweight knee–
are needed to establish if there are clinical markers or risk
ankle–foot braces can have a beneﬁ cial eﬀ ect (measured factors that might predict the development of postpolio as decreased oxygen consumption during walking) and syndrome. If identiﬁ ed, measures for preventing post-save energy.116,117
polio syndrome could be started at an early stage. Further
Patients with postpolio syndrome should be supplied study of subgroups of patients with postpolio syndrome
with appropriate orthoses and braces on the basis of (eg, assessing rate of progression of muscle weakness individual needs.118 To further improve energy eﬃ
ciency, and diﬀ erent forms of fatigue) and identiﬁ cation of
carbon-composite material is preferred.116,117,119 Besides measures to distinguish these subgroups early and thus orthoses, assistive devices to increase functional activity be able to tailor treatment accordingly are also important. include crutches, manual and electrical wheelchairs, and
Pharmacological and rehabilitation interventions seem
eﬀ ective in patients with postpolio syndrome. The study
Thorén-Jönsson54 noted that, despite the need for of combinations of these diﬀ erent therapeutic strategies
assistance with mobility, patients with postpolio syndrome
will be important to achieve the best outcomes.
associated the use of assistive devices with negative
Postpolio syndrome is likely caused by ongoing
feelings. However, technical developments, including neurodegeneration, perhaps driven by aberrant chronic new lightweight and strong materials, have made orthoses and assistive devices more appealing to patients and therefore more useful. Kelley and DiBello118 have
Search strategy and selection criteria
developed a patient classiﬁ cation system that is useful for
References for this Review were identiﬁ ed through searches of
The Cochrane Library (1950 to April, 2010), Medline (1950 to April, 2010), Embase (1974 to May, 2009), the Allied and
Hypoventilation and ventilator support
Complementary Medicine Database (1985 to April, 2010),
Some patients with hypoventilation need ventilator
CINAHL (1984 to April, 2010), and Web of Science (1945 to
assistance. Non-invasive positive pressure ventilation or
April, 2010) with the search terms “post-poliomyelitis
non-invasive bi-level positive airway pressure ventilation
syndrome”, “poliomyelitis survivor”, “late onset poliomyelitis”,
improve quality of life and are preferred by patients,
“late eﬀ ect poliomyelitis”, “post-poliomyelitis”,
rather than invasive ventilators.120 Inspiratory muscle
“complications after poliomyelitis”, and “disabilities after
training can increase respiratory muscle endurance and
poliomyelitis”. The searches were broad and all the terms were
wellbeing; however, those patients with chronic
truncated and diﬀ erent proximity operators were used. No
respiratory failure are still treated with controlled
language restriction was made. Papers were also identiﬁ ed
mechanical ventilation through tracheostomy.121
through searches of the authors’ own ﬁ les. We mostly selected publications from the past 6 years, but we did not exclude
important older publications. The reference list was modiﬁ ed
Lifestyle changes are necessary for many patients with
according to recommendations from peer reviewers.
postpolio syndrome. Inactive patients with postpolio
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22 Baj A, Monaco S, Zanusso G, Dall’ora E, Bertolasi L, Toniolo A.
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23 Kaminski HJ, Tresser N, Hogan RE, Martin E. Spinal cord
HG has received fees as a senior consultant for Pharmalink. TO has
histopathology in long-term survivors of poliomyelitis. Muscle Nerve
received fees for consultancy from Sanoﬁ -Aventis, Merck Serono, and
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JA Delmonte Obesidad, insuficiencia cardíaca y rimonabant CARDIOMETABOLISMO Obesidad, insuficiencia cardíaca y rimonabant Introducción Heart . Se clasificaron a las personas con un IMC de 18,5 a24,9 como “normales” ; aquéllas con un IMC de 25,0 a 29,9En la actualidad, por una parte unos cinco millones de per-con “sobrepeso” ; y aquéllas con 30,0 ó más: “obesas