Journal of Bodywork & Movement Therapies (2012) 16, 364e368
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/jbmt
PREVENTION & REHABILITATION: CLINICAL METHODS
Analysis of electromyographic activity in spastic biceps brachii muscle following neural mobilization
PREVENTION & REHABILITATION: CLINICAL METHODS
´ssica Castilho a, Luiz Alfredo Braun Ferreira a, Wagner Menna Pereira a, Je ´ Geraldo da Silva Morelli b, Danielle Brandalize a, Hugo Pasini Neto b, Jose Ivo Ilvan Kerppers a, Claudia Santos Oliveira, PhD b,* a b
Universidade Estadual do Centro-Oeste (UNICENTRO), Brazil Universidade Nove de Julho (UNINOVE), Brazil
Received 6 October 2011; received in revised form 15 November 2011; accepted 13 December 2011
KEYWORDS Neural mobilization; Electromyography; Spasticity
Summary Introduction: Hypertonia is prevalent in anti-gravity muscles, such as the biceps brachii. Neural mobilization is one of the techniques currently used to reduce spasticity. Objective: The aim of the present study was to assess electromyographic (EMG) activity in spastic biceps brachii muscles before and after neural mobilization of the upper limb contralateral to the hemiplegia. Materials and Methods: Repeated pre-test and post-test EMG measurements were performed on six stroke victims with grade 1 or 2 spasticity (Modified Ashworth Scale). The Upper Limb Neurodynamic Test (ULNT1) was the mobilization technique employed. Results: After neural mobilization contralateral to the lesion, electromyographic activity in the biceps brachii decreased by 17% and 11% for 90 flexion and complete extension of the elbow, respectively. However, the results were not statistically significant (p gt; 0.05). Conclusions: When performed using contralateral techniques, neural mobilization alters the electrical signal of spastic muscles. ª 2011 Elsevier Ltd. All rights reserved.
Introduction
* Corresponding author. Rua Itapicuru 380 apto CEP05006000-Sa ˜o Paulo, Brazil. E-mail address:
[email protected] (C.S. Oliveira).
111,
Cerebral vascular accident (stroke) is defined by the World Health Organization as a clinical sign of the rapid development of a focal disturbance in brain function that persists beyond 24 h (Cesa ´rio et al., 2006). The sensory, motor and/or cognitive sequelae of a stroke can lead to impaired functional capacity, diminished independence and a reduction in
1360-8592/$ - see front matter ª 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.jbmt.2011.12.003
quality of life (Aguiar et al., 2008). The incidence of stroke doubles every decade after 55 years of age, with prevalence values ranging from 0.5% to 0.7% of the population worldwide (Rodgers, 2004). Due to compromised neurons in the corticospinal plexus, contralateral paresis is one of the most common manifestations of a stroke. Approximately 50% of affected individuals recover functional independence after six months, whereas the remaining half experience hemiparesis or hemiplegia (partial and complete loss of voluntary movements, respectively) stemming from the event, which can lead to mild, moderate or severe motor disability (Marcucci et al., 2007). Spasticity is another characteristic consequence of central nervous system injuries (Pontes et al., 2000). This motor disorder is characterized by an increase in resistance to passive muscle stretching, dependent on the velocity of the stretch, causing hyper-excitability of the stretch reflex, elastic hypertonia and changes in proprioceptive sensitivity, often accompanied by clonus, flexor and/or extensor spasms and contractures. Spasticity can lead to incapacity, affecting the musculoskeletal system and limiting normal motor functions (Felice and Santana, 2009). Secondary disturbances related to spasticity include the extreme difficulty of muscle function rehabilitation, joint disorders, pain and compensatory movements (Corre ˆa et al., 2005). Spasticity among hemiplegic patients is clinically recognized by predominant hypertonia in the anti-gravity muscles. The hemiplegic upper limb generally remains in a position of adduction and internal rotation of the shoulder, elbow flexion, forearm pronation and finger flexion (Teive et al., 1998). Neural mobilization is one of the techniques currently used to reduce spasticity in individuals suffering from neurological disorders (Marinzeck, 2010). The term refers to a group of techniques the aim of which is to place the neuraxis in tension and stretch it by means of appropriate mobilization through certain postures, followed by the application of slow, rhythmic movements directed toward the peripheral nerves and spinal cord. These treatment techniques evolved from the diagnostic tests proposed by Elvey to assess adverse neural tension (Butler, 2003; Junior and Teixeira, 2007). When a nerve is mobilized, its cross-sectional area is gradually reduced and this deformation affects the intraneural microvascular flow, causing an improvement in neural function; moreover, the length of the spinal canal undergoes a change during movement (Walsh, 2005). Damaged nerves cause adverse tension in the entire nervous system, which limits movement and affects the adaptation capacity of the entire body and not only the injured area (Zamberlan and Kerppers, 2007). Davies (1997) stresses the importance of early treatment and the prevention of adaptive injuries to the peripheral nervous system following a stroke. The aim of the present pilot study was to determine the influence of neural mobilization on spasticity in patients with stroke sequelae.
Materials and methods The present study was conducted in compliance with the Brazilian National Health Council guidelines contained in
365 Resolution 196/96 and received approval from the local Human Research Ethics Committee. All participants were properly informed regarding the objectives and procedures of the study and signed a statement of informed consent. The participants in the present pilot study were enrolled at the CEFISIO Physiotherapy Clinic of the Universidade Estadual do Centro-Oeste (Brazil). The sample consisted of six adults with stroke sequelae (four men and two women) with a mean age and standard deviation of 54.16 7.9 years, height of 1.70 0.09 m, body mass index (BMI) of 24 6.5 kg/ m2 and an average of four years elapsed since the stroke. The inclusion criterion was a diagnosis of stroke with spasticity in the elbow flexors, according to the modified Ashworth Scale, which quantitatively evaluates the degree of passive movement during muscle stretching and determines the degree of spasticity in stroke victims through a scale ranging from 0 to 4, subdivided into Grade 0, Grade 1, Grade 1þ, Grade 2, Grade 3 and Grade 4, with 0 denoting an absence of resistance to passive stretching and 4 denoting joint rigidity and no range of motion. The exclusion criteria were joint deformities of the upper limb and cognitive deficiency that would impede the testing procedures. Volunteers first underwent an anthropometric examination and an assessment of the degree of spasticity in the elbow flexor muscles using the Modified Ashworth Scale. A score of 1e4 was awarded for passive movement of elbow flexionextension (Bohannon and Smith, 1987). An electromyographic assessment of the biceps brachii muscle of the affected upper limb was also carried out. Trichotomy and skin cleansing with ethyl alcohol (70%) were performed to reduce bioimpedance at the sites on which the electrodes were to be placed, as recommended by Surface Electromyography for the NonInvasive Assessment of Muscles (Hermens et al., 1999). Electromyographic studies were performed using an 8-channel signal recording system (EMG System Brasil LTDA) connected to a data acquisition and analysis system (WinDaqXL). The signal was then submitted to a 20e500 Hz band filter, amplified 1000 times and converted by an A/D plate with a sampling frequency of 2000 Hz per channel and input variation of 5 mV. Active bipolar electrodes were used, separated by a distance of 20 mm (De Luca, 1997). The root mean square (RMS) electronic media was used to measure the amplitude of the electromyographic signal. All procedures used to capture and analyze the electromyographic signals in this study are recommended by the International Society of Electrophysiology and Kinesiology (Solomonow, 1995). Electromyographic signals were recorded under two conditions: 90 flexion (F) and maximal extension (E). Under the first condition (F), the patients were instructed to lie in the supine position with the affected upper limb held passively at 90 elbow flexion. Under the second condition (E), the individuals remained in the supine position and actively extended the elbow, seeking the maximal range of motion. The procedure lasted 30 s under both conditions. As the biceps brachii muscle has fast muscle fiber characteristics, the 30-second collection time was based on the principle that the central nervous system does not affect the inhibition of Gamma hyperactivity regarding myoelectrical activity. The capturing of the electromyographic signals was performed in an isolated location following the neural mobilization procedure by a single operator with skill in handling both the hardware and software.
PREVENTION & REHABILITATION: CLINICAL METHODS
Neural mobilization in spasticity
PREVENTION & REHABILITATION: CLINICAL METHODS
366
J. Castilho et al.
After the initial electromyographic activity was recorded, neural mobilization of the median nerve was carried out (Upper Limb Neurodynamic Test or ULNT1) on the nonaffected upper limb. According to Elvey apud Butler (2003), this procedure can alter symptoms in the limb undergoing treatment. Neural mobilization of the affected limb was not performed in the present study in order to avoid the tendency toward a reduction in electrical activity due to the positioning of the spastic limb in a muscle stretching situation. The neural mobilization was performed by a professional physiotherapist with experience in this technique. To attain the required tension and neural mobilization, the patients were instructed to begin with passive depression of the shoulder girdle, 90 shoulder abduction, hands and forearms in a neutral position, wrist extension in the neutral position, forearm in supination, external rotation of the shoulders and elbow extension. These movements were performed consecutively without allowing the anterior segment to return to its original position. After holding this position, neural mobilization was performed with oscillations of slow, rhythmic wrist flexion and extension. Twenty oscillations were performed per minute for 3 min, repeated three times in the same session, with 1 min of rest between each effort (Butler, 2003). All procedures were conducted by the same investigator. The electromyographic signal of the biceps brachii muscle of the affected upper limb was recorded again after neural mobilization (at 90 flexion and maximal extension). For the statistical analysis, the percentage difference in RMS before and after neural mobilization was determined using the following calculation: percentage difference Z 100 (RMS value pre-neural mobilization e RMS value post-neural mobilization)/ original RMS value (Stell, 1997). The data were then analyzed using the Origin 7.0 program. The D’Agostino and Pearson test was used to assess the normality of the data, followed by Student’s t-test. The significance level was set at 5% (p 0.05) (Figure. 1).
Results
Figure 2 Mean electromyographic activity of biceps brachii muscle under two data acquisition conditions (90 flexion and maximal extension)
respectively, after neural mobilization of the unaffected limb. However, these changes were not statistically significant (p Z 0.27 and p Z 0.30, respectively). Figure. 3 displays the mean values in relation to the degree of spasticity. Individuals with grade 1 þ spasticity exhibited decreased electromyographic activity (from 16.03 mV to 14.77 mV) during elbow flexion after neural mobilization and increased electromyographic activity (from 29.60 mV to 30.13 mV) during elbow extension after neural mobilization. This small increase in myoelectrical activity may have been generated by facilitation of the biceps brachii muscle in the stretched position. Patients with grade 2 spasticity exhibited decreased electromyographic activity (from 13.95 mV to 13.05 mV) during elbow flexion after neural mobilization and decreased
Figure. 2 displays the mean electromyographic activity of the biceps brachii muscle before and after mobilization of the median nerve (at 90 flexion and maximal extension). Electromyographic activity in the biceps brachii muscles decreased by 17% and 11% during flexion and extension,
Figure 1
Application of Upper Limb Neurodynamic Test 1
Figure 3
Mean values among degrees of spasticity
Neural mobilization in spasticity
Discussion The present pilot study demonstrated that the application of the technique did not result in significant differences. A reduction in myoelectrical activity was found in the individuals submitted to the neural mobilization technique on the side contralateral to the stroke sequela. However, an increase in myoelectrical activity was found when the signal capturing was performed with the arm in extension. This corroborates the statement by Butler (2003) that the central and peripheral nervous systems are considered a single continuous system upheld by three dimensions: mechanical continuity, as evident in the transmission of forces and movements generated by connective tissue sheaths in nerve cells; electrical continuity, maintained by neurons and transmitted from one part of the body to another; and chemical continuity, maintained by central and peripheral neurotransmitters and axoplasmic flow, the function of which is to ensure that nutrients from the nervous system are guided into the axon. The same author reports that, since the tissue tract is continuous, any limb movement has mechanical consequences in the neuroaxis. This statement is supported by the change in electrical activity of the spastic biceps brachii muscle following neural mobilization contralateral to the lesion. Neural mobilization works on the nervous system as a whole, which could be one of the reasons the technique obtains positive results in the treatment of a range of conditions, as musculoskeletal disorders can cause a “crushing” or “double crushing” of peripheral nerves, which is related to spasticity. This crushing leads to reductions in nerve conductibility, axoplasmic flow within the neurons and somatic activity (Butler, 2003; Marinzeck, 2010). Santos (2004) reports that many disorders and responses to treatment are associated with axonal transport systems. The aim of mobilization is to normalize mechanical and physiological functions of the nervous system as well as to remedy impairments in this system and associated disorders in musculoskeletal structures (Ellis and Hing, 2008). The application of Upper Limb Neurodynamic Test 1 (ULNT1) is thought to improve retrograde axoplasmic flow, which is abnormal in spasticity, thereby providing the alleviation of nerve tension, a reduction in restrictions and adhesions of the nerve to surrounding tissues and an improvement in conditions for the enhancement of activities and muscle nutrition (Marinzeck, 2010). According to Walsh (2005), it is often necessary to begin neural mobilization contralateral to the lesion when treating irritable disorders without causing or aggravating symptoms and to proceed to the specific site as tolerated by the patient. The same author states that restoring mobility or improving tolerance to tension in a remote site helps alleviate nerve tension and reduce symptoms. Examining patients with hemiplegia stemming from head trauma and cerebral palsy, Davies (1997) found that the
range of motion in one part of the body was altered by passive movements in another part of the body distant from where the original movement occurred, stating that performing ULNT1 on the healthy upper limb may assist movement of the plegic limb. The findings of the present study corroborate this report, as a change in the electromyographic activity of the spastic biceps brachii muscle was found following neural mobilization of the contralateral limb, demonstrating that neural mobilization using contralateral techniques influences the affected limb.
Conclusion The present study on the effect of neural mobilization using the Upper Limb Neurodynamic Test 1 demonstrates a reduction in myoelectrical activity in certain cases of spasticity and an increase in activity in other cases. The small number of individuals in the sample may have contributed to the lack of statistically significant results. Thus, there is a need for studies involving a larger number of individuals in a more homogeneous sample with both males and females in order to determine whether the mobilization of the median nerve through neural mobilization on the side contralateral to the sequela can truly be used for the control of different degrees of spasticity. Although the application of this technique did not result in significant differences, a reduction in electrical activity was found in the spastic muscle after neural mobilization of the contralateral limb, demonstrating that this technique could be an additional tool in the control of spasticity, particularly in cases of lesser intensity.
References Aguiar, P.T., Rocha, T.N., Oliveira, E.S., 2008. Escalas de controle de tronco como progno ´stico funcional em pacientes apo ´s acidente vascular encefa ´lico. Acta Fisiatrica 15 (3), 160e164. Bohannon, B.W., Smith, M.B., 1987. Interrater ratability of a modified Ashwort scale of a muscle spasticity. Physical Therapy 67 (2), 206e207. Butler, D.S., 2003. Mobilizac ¸a ˜o do sistema nervoso. Manole, Sa ˜o Paulo. Cesa ´rio, C.M.M., Penasso, P., Oliveira, A.P.R., 2006. Impacto da disfunc ¸a ˜o motora na qualidade de vida em pacientes com acidente vascular encefa ´lico. Neurocie ˆncias 14 (1), 6e9. Corre ˆa, F.I., Soares, F., Andrade, D.V., Gondo, R.M., Peres, J.A., Fernandes, A.O., Corre ˆa, J.C.F., 2005. Arquivo de Neuropsiquiatria 63 (3-B), 847e851. Davies, P.M., 1997. Recomec ¸ando Outra Vez: Reabilitac ¸a ˜o precoce apo ´s Lesa ˜o Cerebral Trauma ´tica ou outra Lesa ˜o Cerebral Severa. Manole, Sa ˜o Paulo. De Luca, C.J., 1997. Use of the surface electromyography in biomechanics. Journal of Applied Biomechanics 13, 135e163. Ellis, R.F., Hing, W.A., 2008. Neural Mobilization: a systematic review of randomized controlled trials with an analysis of therapeutic efficacy. The Journal of Manual & Manipulative Therapy 16 (1), 8e22. Felice, T.D., Santana, L.R., 2009. Recursos Fisioterape ˆuticos (Crioterapia e Termoterapia) na espasticidade: revisa ˜o de literatura. Revista Neurociencie ˆncias 17 (1), 57e62. Hermens, H.J., Frekis, B., Merletti, R., Stegman, D., Blok, J., Rau, G., Klug, G., Ha ¨gg, C.D., 1999. SENIAM - European Recommendations for Surface Electromyography. Results of the SENIAM project. Roessingh Research and Development, Enschede, Netherlands.
PREVENTION & REHABILITATION: CLINICAL METHODS
electromyographic activity (from 33.70 mV to 30.85 mV) during elbow extension after neural mobilization. Moreover, patients with grade 1 spasticity exhibited decreased electromyographic activity (from 36.50 mV to 23.30 mV) during elbow flexion after neural mobilization and decreased electromyographic activity (from 46.60 mV to 30 mV) during elbow extension after neural mobilization.
367
368
PREVENTION & REHABILITATION: CLINICAL METHODS
Junior, H.F.O., Teixeira, A.H., 2007. Mobilizac ¸˜ ao do sistema nervoso: avaliac ¸a ˜o e tratamento. Revista Fisioterapia em Movimento 20, 41e53. Marcucci, F.C.I., Cardoso, N.S., Berteli, K.S., Garanhani, M.R., Cardoso, J.R., 2007. Alterac ¸o ˜es eletromiogra ´ficas dos mu ´sculos do tronco de pacientes com hemiparesia apo ´s acidente vascular encefa ´lico. Arquivo Neuropsiquiatria 65, 900e905. Marinzeck, S., 2010. Mobilizac ¸a ˜o Neural - Aspectos Gerais [cited 03/04/2010]. Available in: http://www.terapiamanual.com.br/ br/artigos.php?vZ1&pgZartigos/mobilizacaoneural.htm. Pontes, L.S., Fontes, S.V., Botelho, L.A.A., Fukujima, M.M., 2000. Toxina botulı´nia tipo A em pacientes com hemiplegia e/ou hemiparesia espa ´stica: uma abordagem fisioterape ˆutica. Revista de neurocie ˆncias 8, 99e102. Rodgers, H., 2004. Risk factors for-first ever stroke in older people in the North East of England: a population based study. Stroke 35, 7e11.
J. Castilho et al. Santos, V.R., 2004. A influe ¸a ˆncia da mobilizac ˜o do sistema nervoso na ca ˆimbra do escriva ˜o. Revista Terapia Manual 2 (4), 166e171. Solomonow, MA. Practical Guide to Electromyography International Society of Biomechanics. Proceedings of the 15th JyVaskyla, International Society of Biomechanics Congress. Finland, 5 July, 1995. p. 96. Stell, R.G.D., 1997. Principles and procedures of statistics. A Biometrical Approach. McGraw-Hill Companies, Inc., New York. Teive, H.A.G., Zonta, M., Kumagai, Y., 1998. Tratamento da espasticidade, uma atualizac ¸a ˜o. Arquivo Neuropsiquiatria 56 (4), 852e858. Walsh, M.T., 2005. Upper limb neural tension testing and mobilization. Journal of Hand Therapy 18, 241e258. Zamberlan, A.L., Kerppers, I.I., 2007. Mobilizac ¸˜ ao neural como um recurso fisioterape ¸a ˆutico na reabilitac ˜o de pacientes com acidente vascular encefa ´lico. Revista Salus 1 (2), 185e191.