Physiotherapy resources on bone mineral density loss prevention in patients with spinal cord injuries

Abstracts

Este trabalho é uma revisão bibliográfica sobre os tratamentos fisioterápicos destinados a prevenção, estabilização ou lentificação da perda da densidade mineral óssea em pacientes portadores de lesão medular. Foram encontrados poucos trabalhos que se destinaram aos tratamentos fisioterápicos para desmineralização óssea. Em relação aos tipos de tratamentos encontrados foram: estimulação elétrica funcional, estimulação elétrica funcional com bicicleta ergométrica, ortostatismo e deambulação. Estes tratamentos são bastante questionáveis não tendo um consenso na metodologia, apresentando muitas controvérsias em relação à eficácia dos tratamentos, que serão discutidos no decorrer deste trabalho.

Lesão medular; Osteoporose; Reabilitação

REVIEW ARTICLE

Physiotherapy resources on bone mineral density loss prevention in patients with spinal cord injuries

Daniele Rodrigues^I; Guilherme Herrera^II

^IPhysiotherapist by the Centro Universitário São Camilo

^IINeurology Specialist by UNIFESP - EPM, Masters in Health Science by UNIFESP — EPM

^{Correspondence}

SUMMARY

This work is bibliographic review about the physiotherapy treatments for the attenuation, prevention and stabilization or slowing down of the bone mineral density loss in spinal cord injured patients. There are few studies focusing the efficiency the physiotherapy treatment for bone demineralization. The kinds of treatments found were: functional electrical stimulation, functional electrical stimulation with an bycicle ergometry, orthostatic and deambulation. These treatments are much questionable, and with no consensus on the methodology, with the lot of controversies in relation to the efficacy of the treatments, which are going to be discussed in the development of this study.

Key words: Spinal cord injury; Osteoporosis; Rehabilitation.

INTRODUCTION

In Brazil, there are 130 thousand individuals bearers of spinal cord injury and every year its incidence is increasing due to the automobile accidents and mainly to the violence15. The individuals with spinal cord injury suffer the partial or total loss of the motive, sensitive, autonomous functions, and complications in the organic system, and one of them is the alteration of the bone metabolism, which, consequently, results in osteoporosis.

This bone loss (demineralization) is known in the literature, however its cause is not very clear, and it occurs during the first year after the spinal cord injury with the peak in the 4-6 month of lesion, attacking the proximal and distal areas of the bones preferring first the trabecular and then the compact layer of the bone.

With the demineralization, the fracture risk increases 8,20, occurring with as deformities, ulcerations, limitations for the rehabilitation, generating difficult handling situations, so much for sufferers as for their relatives or caretakers, besides the high economic costs due to the cares and with hospital admissions, because the cost of the fracture for osteoporosis is high, in the USA 13.8 billion dollars were spent with medical treatments29 and in France, the total cost was of approximately 200 million¹⁴.

Considering the several complications that follow after the fracture and the high cost for its treatment, it is interesting to prevent the bone mineral density's loss for the spinal cord injury patients, and the objective of this study is to review the literature to check the effectiveness of the physiotherapeutic treatments concerning the prevention, stabilization or slowing down of the loss of bone density.

DISCUSSION

The loss of the bone mineral density (BMD) in spinal cord injured patients is very well known. However its cause is not very clear. Initially we should consider some hypotheses regarding the loss of the bone mineral density:

There are authors that mention that the bone loss occurs due to an alteration of the sympathetic nervous system, reducing the blood flow in some areas of the bone, with that there are no gaseous exchanges and no nutrients, resulting in cellular necrosis, activating the osteoclastic cells, what explains the predominance of demineralization in the highly vascularized areas⁽⁴⁾.

It is believed that demineralization occurs due to the lack of mechanical force and lack of compression force, resulting in the increase of the bone reabsorption⁽¹⁾.

It is considered that the bone loss doe snot occur due to inactivity, but due to the absence of the longitudinal pressure of the long bones⁽²¹⁾. It was observed that paraplegic and tetraplegic individuals are not capable to sustain weight on their lower limbs and as such they are not exposed to the forces or to the necessary muscular tension to stimulate the bone formation, resulting in the triggering of the osteoclastic activities⁽¹²⁾.

The demineralization occurs during the first year after the spinal cord injury, with the peak in the fourth-sixth month from the injury, and it is evidenced in the first weeks after the injury. The trabecular bone is the more susceptible to osteoporosis, with the bone loss of 4%/month in the spongy bones and 2% in the cortical bones^(18,28) and the most affected bones are the ones that support more compression force⁽¹⁾. In the lower limbs the most affected areas are the distal epiphyses of the femur (70%) and the proximal epiphysis of the shinbone (52%) with predominance in highly vascularized areas in the long bones⁽⁴⁾. The bone loss is smaller in the proximal femur, because it is protected by some residual force exercised by the trunk while seated on the wheelchair⁽¹⁰⁾.

The decrease of the bone mineral density occurs in decreasing order: totally tetraplegic, not totally tetraplegic, totally paraplegic, not totally paraplegic¹⁶. According to Wilmet and cols⁽²⁸⁾ , it was observed that the spasticity was not enough to maintain the integrity of the skeleton, being the same for both, flaccid and spastic patients. However Demirel and cols.⁽³⁾ observed that there is no difference between tetraplegic and paraplegic, with more apparent loss in the patients with complete and flaccid injuries.

Few studies were found focused on the effectiveness of the physiotherapy treatments. In relation to the type of treatment used to fight bone demineralization we found:

• Functional electrical stimulation/ bycicle ergometry^{(1,7,13,24 )} ;

• Functional electrical stimulation (EEF)^(2,7);

• Orthostatism^(3,6,11,26);

• Deambulation^(3,9,19,22);

Considering the several types of treatments available, we checked the effectiveness of each one:

• Functional electrical stimulation / bycicle ergometry: not effective to revert, slow down or stabilize the bone demineralization in patients with spinal cord injury^(1,7,13,24);

• Functional electrical stimulation: not effective other hand⁽⁷⁾, there are authors that observed that the EEF was the responsible for the increase in the BMD⁽²⁾;

• Orthostatism: not effective to revert, slow down or stabilize the demineralization in spinal cord injured patients^(11,26). Other studies observed that it can prevent or delay the bone loss, and that the results were better for the groups that used osthesis^(3,6);

• Deambulation: prevents or delays the loss of bone mineral density^(3,9,19), but Shropshire and cols.⁽²²⁾ of the not agree with this because they could not observe an improvement of the BMD.

It is possible to observe that there is no consensus in the subject concerning the effectiveness of the different focus to prevent, slow down or stabilize the decrease of BMD, and we observe that there are many variables such as sample, gender, age, and time of injury and others that can interfere with the results.

The size of the sample that most used was the small quantity of patients, which may have interfered with the obtained results. Ogilvie and cols.⁽¹⁹⁾ mentioned that the number of patients observed in their study was small, and so the results were disregarded.

Another important factor that we observed in during this review was the heterogeneity of the samples for the items age and gender.

Concerning the age of the patients, only Leeds and cols.⁽¹³⁾ has the group of patients with the more homogenous age, limiting themselves to study adults. The other studies had very wide age variations, using young, young adults and elderly patients. This may interfere with the results, because the peak of bone mass is maintained up to the 40 years of age in normal individuals, and from that age on the decrease of bone mineral density starts, and this loss can be quicker if associated to imobilization^{(21, 23)}.

Concerning the gender of the patients, only four of the authors had the preoccupation to select the homogenous sample^(1,3,11), but the other authors dealt with both genders. However, it is widely known that women present the larger bone loss than men, which is accentuated after the menopause⁽²³⁾. In view of this scenario, women with spinal cord injury, depending on their age, show more tendencies to bone loss than men, and this can influence the results of the studies.

In view of the influence that age and gender may exert on BMD, we can infer that the large variation of these two categories can interfere with the results of the studies presented.

When we checked if the participants of the studies did undergo physiotherapeutic treatments, we observed that only one study mentioned that the patients did undergo physiotherapy. However it did not specify the type of exercise, the frequency of the therapy and the duration of the treatment⁽²⁴⁾.

Another point we believe is of critical importance in the reduction of BMD loss is the fact that the patients trained the gait or remained in orthostatism. We analyzed the literature and observed that only one group of authors commented that none of its patients were deambulators, and those ever remained in orthostatism⁽¹⁹⁾.

Concerning the exclusion criteria, the following individuals were not included:

• Post-menopausal women, youngsters with less than 20 years of age and patients taking bisphosphanate⁽⁶⁾;

• Patients with injuries to the inferior motoneuron^(7,22);

• Hepatic diseases of the liver, cardiovascular diseased. Fractures and the use of drugs that can interfere with the metabolism^{(2,7,9,11,22)};

When the type of spinal cord injury used in the studies were checked, we observed heterogeneity in relation to the type of injury:

• Traumatic and non-traumatic inuries⁽¹¹⁾

• Traumatic injuries^(2,13,19)

• Seven studies did not mention that the patients were sufferers of traumatic or non-traumatic spinal cord injury.

Another factor we think is of critical relevance for the decrease of BMD is the seriousness of the spinal cord injury. It was observed that the authors did not worry with the homogeneities of the seriousness of the injury, or with the deficiency scale of ASIA, mainly the incomplete spinal cord injuries. Four studies only leveled the patients according to the seriousness of the injury, leveling them as total injuries^(1,6,13,22) andfour studies used patients with non-total and total spinal cord injury^(2,3,7,24).

According to Demirel and cols.⁽⁵⁾ the individuals with total spinal cord injuries present a more apparent loss in comparison to the individuals with non-total spinal cord injuries.

Concerning the level of the spinal cord injury, it was observed that only Leeds and cols.⁽¹³⁾ selected the patients with closer levels of injury. The other authors used patients with high spinal cord injuries and low spinal cord injuries, this can interfere with the results of the studies presented.

Concerning the tonus of the patient bearer of the spinal cord injury, the authors stated that the spastic individuals have a lower loss of BMD as compared to the flaccid patients⁽⁵⁾. On the other hand, Wilmet and cols.⁽²⁸⁾ mentioned that the spasticity and maintenance of the muscular mass do not prevent the loss of the BMD as compared to the flaccid individuals. According to Goemaere and cols.⁽⁶⁾, the level of spasticity and the level of the injury do not affect the BMD.

Concerning the time from the injury, only three studies selected patients with early injuries, with less than 6 months of the injuries^(3,9,22). There were studies that used patients with a time from the injury above one year, with a very wide variation, with a possible interference in the results of the studies presented. The loss of the bone mineralization is known to occur in the first six months from the injury with a peak on the fourth month, and remaining stabilized during 12— 16 months after the spinal cord injury⁽²⁷⁾. This determines the importance of the early intervention.

Concerning the measuring techniques used in the studies, we found:

• DEXA^{(1,2,6,11,13,22,24,25,26)},

• QCT^(7,19,25);

• X RAYS^(17,25).

There was a wide variation concerning the site of the measurement of the bone mineral density:

• Lumbar spine^{(1,11,19,24,26)};

• Femur neck^{(1,6,11,13,19,22,24,26)}

• Trocanter^{(1,6,13,22,24)};

• Diaphysis of the femur^(2,6);

• Distal of the femur, diaphysis and proximal of the tíbia^(2,7).

According to Dauty and cols.(4), the most affected are with loss of the BMD is the metaphysis and the epiphysis of the femur distal and proximal of the tibia.

Kiratli and cols.⁽¹⁰⁾ mention that the bone demineralization of the lumbar spine and of the proximal femur are smaller due to the residual force excerpted by the trunk when seating on a wheelchair.

There was no uniformity in the studies in what refers to the duration, frequency and the type of study used.

It was observed that only Goemare and cols.⁽⁶⁾, compared the effectiveness of the 3 orthostatism inventions for BMD in spinal cord injured patients, using the orthesis, standing frame and the wheelchair that remains in orthostatism. The orthesis was the equipment with a better discharge, among the three equipments, due to the axial weight it supplies, and thus being the more efficient in the reduction of the loss of the BMD.

CONCLUSION

According to the bibliographical review, the loss of bone mineral density in the paralyzed areas is well known, and is one of the major complications for the spinal cord injured patients. However, which is the factor that results in this loss is not clearly established.

Concerning the objective of the study, it was concluded that we cannot mention which are the exercises that were effective, or not, because there were no consistent results concerning prevention or slowing down of the loss of the BMD. It was observed that the majority of the studies reviewed did not determine an adequate methodology, presenting major flaws referring mainly to the inclusion criteria.

We believe that new studies should be performed, with well defined inclusion criteria, such as, for example: the time from the injury, type of the injury (total or non-total), level of the injury (cervical, high thoracic, low thoracic, lumbar), age, gender, under physiotherapeutic treatment, type of treatment, orthesis bearers that enable orthostatism or gait training.

ACKNOWLEDGEMENTS

Guilherme Herrera, professor and advisor for this study. Marta Damasceno, professor and coordinator. Centro Universitário São Camilo and to the Selma Foundation.

REFERÊNCIAS BIBLIOGRÁFICAS

Trabalho recebido em 19/02/2004.

Aprovado em 18/06/2004.

Work performed São Camilo University Center

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Publication Dates

• Publication in this collection
  15 May 2007
• Date of issue
  Sept 2004

History

• Received
  19 Feb 2004
• Accepted
  18 June 2004