7/04/2016

VITALITY AMoNG SWEdISH PATIENTS WITH PoST-PoLIo: A PHYSIoLoGICAL PHENoMENoN*


J Rehabil Med 2008; 40: 709–714

ORIGINAL REPORT

Gunilla Östlund, MSci1, Åke Wahlin, PhD2, Katharina S. Sunnerhagen, MD, PhD3,4 and Kristian Borg, MD, PhD1
From the 1Divison of Rehabilitation Medicine, Karolinska Institutet, Department of Clinical Sciences at Danderyd Hospital, 2Department of Psychology, Stockholm University, Stockholm, 3Institute for Neuroscience and Physiology, Section for Clinical Neuroscience and Rehabilitation, Goteborg University, Goteborg, Sweden and 4Sunnaas Rehabilitation Hospital, Faculty of Medicine, University of Oslo, Oslo, Norway.

Objective: To evaluate vitality and fatigue in post-polio pa- tients, and the relative contributions of physiological and psychological parameters to the level of vitality. Design: Multi-centre study.

Subjects: One hundred and forty-three patients with post- polio syndrome.
Methods: 

Inventories of background, quality of life, fatigue and sleep quality were used. Pain was evaluated using a visual analogue scale. Descriptive statistics and correlations were used for all selected parameters. Hierarchical regres- sion models were constructed to examine predictors of varia- tions in vitality, pain, reduced activity and physical fatigue. 
Results: 

General fatigue accounted for 68% of the variation in vitality. Of this, 91% was accounted for by physiologi- cal indicators. After controlling for age, physiological para- meters accounted for 56.6% and 25%, if entered before and after the psychological parameters, respectively. The impact of the psychological parameters decreased after accounting for the physiological parameters. Physical fatigue, age and sleep quality were associated with variation in pain. Body mass index, pain and sleep quality accounted for differences in reduced activity and physical fatigue.

Conclusion: Vitality in post-polio patients depends on physio- logical parameters. Mental fatigue is not a prominent pre- dictor. Subgroups with or without fatigue, independent of age, need further study.

Key words: post-polio, fatigue, vitality, quality of life. J Rehabil Med 2008; 40: 709–714
Correspondence address: Gunilla Östlund, Department of Rehabilitation Medicine, Danderyd University Hospital, Building 39, 3rd Floor, SE-182 88 Stockholm, Sweden. E-mail: Gunilla.Ostlund@ki.se

Submitted September 21, 2007; accepted May 29, 2008

INTRoduCTIoN

Poliomyelitis leads to muscle weakness due to destruction of the anterior horn cells. After an initial recovery there is a phase
*This article has been fully handled by one of the Associate Editors, who has made the decision for acceptance, as it originates from the institute where the Editor-in-Chief is active.
© 2008 The Authors. doi: 10.2340/16501977-0253 Journal Compilation © 2008 Foundation of Rehabilitation Information.
of functional stability that usually lasts from 10 to 40 years. during this phase the life circumstances of polio survivors do not differ much from the general population with respect to work and family situation (1). However, after the stable phase deterioration may occur; a condition termed post-polio syndrome (PPS) (2). The most commonly reported symptoms of PPS are increased muscle weakness, fatigue and pain in the muscles and joints. The last epidemic of polio in Sweden was in 1953 when more than 5000 people contracted poliomyelitis. Today, the prevalence of polio-affected individuals in Sweden is estimated to be 186/100,000 (3). Reported estimates of polio survivors eventually developing PPS vary from 20% to 68% (2, 4). Thus, the majority of polio survivors in Sweden are now middle-aged or older, and consequently at risk of developing PPS. Risk factors for developing PPS include time since the acute polio infection (5), age at presentation of symptoms, muscle pain at exercise, recent weight gain, joint pain (6) and female gender.

During the last decade, increasing research interest has fo- cused on fatigue in patients with PPS (7). Jubelt & Agre (8) re- ported generalized fatigue as one of the most common symptoms in PPS. Mental, as well as physical, fatigue has been reported by both Bruno et al. (9) and Schanke & Stanghelle (10).
Interestingly, and related to mental fatigue, there are con- tradicting reports regarding cognitive dysfunction in patients with PPS. Difficulties with attention, word finding, maintaining wakefulness and ability to think clearly have been reported by Bruno et al. (11). However, in most other studies cognitive function is reported to be unaffected by mental fatigue (12, 13). Furthermore, fatigued polio survivors are reported to have more mental health problems than controls or polio survivors without severe fatigue (5). In a study by Conrady et al. (14) patients, both at a post polio-clinic and in a post-polio support group, experienced significantly elevated levels of psychologi- cal distress, such as somatization and depression. Gonzalez et al. (15) reported an increase in cytokines in the cerebrospinal fluid of patients with PPS, indicating an inflammatory proc- ess. 

The inflammatory processes were down-modulated by treatment with intravenous immunoglobulin followed by a clinical effect, especially on vitality, as evaluated by means of Short Form 36 (SF-36). This indicates that vitality has a central role in PPS that may be improved by means of phar- macological treatment. The subjective experience of vitality
ISSN 1650-1977J Rehabil Med 40
Neuropsychiatry, Neuropsychology, & Behavioral Neurology:
ORIGINAL ARTICLES: PDF Only
Post Polio Litaff, Association A.C _APPLAC Mexico

The Polio Crusade

THE POLIO CRUSADE IN AMERICAN EXPERIENCE A GOOD VIDEO THE STORY OF THE POLIO CRUSADE pays tribute to a time when Americans banded together to conquer a terrible disease. The medical breakthrough saved countless lives and had a pervasive impact on American philanthropy that ... Continue reading..http://www.pbs.org/wgbh/americanexperience/polio/

Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno

video

movie

movie2

A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.

On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.

Figure 1

The patient's legs, showing massive enlargement of the right calf and wasting on the left

Questions

1
What is that nature of the acute illness in infancy?
2
What is the nature of the subsequent deterioration?
3
What investigations should be performed?
4
What is the differential diagnosis of the cause of the progressive calf hypertrophy?

Answers

QUESTION 1

An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.

QUESTION 2

A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3

QUESTION 3

Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.

Figure 2

Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition

QUESTION 4

The differential diagnosis of the progressive calf hypertrophy is given in the box.

Causes of calf muscle hypertrophy

Chronic partial denervation

  • radiculopathy

  • peripheral neuropathy

  • hereditary motor and sensory neuropathy

  • spinal muscular atrophy

  • following paralytic poliomyelitis

    Neuromyotonia and myokymia

  • Isaac's syndrome

  • generalised myokymia

  • neurotonia

  • continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis

    Muscular dystrophies

    Myositis

    Infiltration

  • tumours

  • amyloidosis

  • cysticercosis

    Link here