Transcutaneous electrical nerve stimulation for spasticity: A systematic review. / Estimulación eléctrica nerviosa transcutánea como tratamiento de la espasticidad: una revisión sistemática.

INTRODUCTION: Although transcutaneous electrical nerve stimulation (TENS) has traditionally been used to treat pain, some studies have observed decreased spasticity after use of this technique. However, its use in clinical practice is still limited. Our purpose was twofold: to determine whether TENS is effective for treating spasticity or associated symptoms in patients with neurological involvement, and to determine which stimulation parameters exert the greatest effect on variables associated with spasticity. DEVELOPMENT: Two independent reviewers used PubMed, PEDro, and Cochrane databases to search for randomised clinical trials addressing TENS and spasticity published before 12 May 2015, and selected the articles that met the inclusion criteria. Of the initial 96 articles, 86 were excluded. The remaining 10 articles present results from 207 patients with a cerebrovascular accident, 84 with multiple sclerosis, and 39 with spinal cord lesions. CONCLUSIONS: In light of our results, we recommend TENS as a treatment for spasticity due to its low cost, ease of use, and absence of adverse reactions. However, the great variability in the types of stimulation used in the studies, and the differences in parameters and variables, make it difficult to assess and compare any results that might objectively determine the effectiveness of this technique and show how to optimise parameters.

Myotonometry as a measure to detect myofascial trigger points: an inter-rater reliability study.

OBJECTIVE: Several diagnostic methods have been used in the identification of mechanical properties of skeletal muscle, including myofascial trigger points (MTrPs), however, they are not suitable for daily clinical use. Myotonometry offers an easy noninvasive alternative to assess these muscle properties. Nevertheless, previous research has not yet studied the mechanical properties of MTrPs by myotonometry. The purposes of this study were (1) to analyze the differences in the mechanical properties between latent MTrPs and their taut bands by myotonometry, (2) to investigate the inter-rater reproducibility of myotonometric measurements, and (3) to examine the association between myotonometry and passive isokinetic dynamometry. APPROACH: Fifty individuals (58% male; age 24.6 ± 7.9 years) with a latent medial MTrP of the right soleus muscle participated. The mechanical properties of this MTrP area of soleus muscle and its taut band area were measured using a myotonometer (MyotonPRO). Additionally, passive resistive torque and extensibility of triceps surae muscle were assessed using a Kin-Com dynamometer. MAIN RESULTS: Statistical analysis indicated higher values for the stiffness parameter in the taut band with respect to the MTrP (P < 0.05). The inter-rater reliability of the myotonometric measurements was good for all variables (ICC3,1 > 0.75). The standard error of measurement (SEM) and minimal detectable difference (MDD) indicated a small measurement error for frequency and stiffness variables (SEM% < 10%; MDD95% < 20%). Significant fair correlations between myotonometric parameters and passive isokinetic parameters ranged from -0.29 to 0.48 (P < 0.05). SIGNIFICANCE: The myotonometer was demonstrated to be a reliable tool and was able to quantify differences in the mechanical properties of myofascial tissues. The potential of this method for the assessment of myofascial pain syndromes requires further investigation.

Modular control of gait after incomplete spinal cord injury: differences between sides.

STUDY DESIGN: This is an analytical descriptive study. OBJECTIVES: The main goal of this study was to compare the modular organization of bilateral lower limb control in incomplete spinal cord injury (iSCI) patients during overground walking, using muscle synergies analysis. The secondary goal was to determine whether the similarity between the patients and control group correlate with clinical indicators of walking performance. SETTING: This study was conducted in National Hospital for Spinal Cord Injury (Toledo, Spain). METHODS: Eight iSCI patients and eight healthy subjects completed 10 walking trials at matched speed. For each trial, three-dimensional motion analysis and surface electromyography (sEMG) analysis of seven leg muscles from both limbs were performed. Muscle synergies were extracted from sEMG signals using a non-negative matrix factorization algorithm. The optimal number of synergies has been defined as the minimum number needed to obtain variability accounted for (VAF) ⩾90%. RESULTS: When compared with healthy references, iSCI patients showed fewer muscle synergies in the most affected side and, in both sides, significant differences in the composition of synergy 2. The degree of similarity of these variables with the healthy reference, together with the composition of synergy 3 of the most affected side, presented significant correlations (P<0.05) with walking performance. CONCLUSION: The analysis of muscle synergies shows potential to detect differences between the two sides in patients with iSCI. Specifically, the VAF may constitute a new neurophysiological metric to assess and monitor patients' condition throughout the gait recovery process.

Abnormal cutaneous flexor reflex activity during controlled isometric plantarflexion in human spinal cord injury spasticity syndrome.

STUDY DESIGN: Although abnormal cutaneous reflex (CR) activity has been identified during gait after incomplete spinal cord injury (SCI), this activity has not been directly compared in subjects with and without the spasticity syndrome. OBJECTIVES: Characterisation of CR activity during controlled rest and 'ramp and hold' phases of controlled plantarflexion in subjects with and without the SCI spasticity syndrome. DESIGN: Transverse descriptive study with non-parametric group analysis. SETTING: SCI rehabilitation hospital. METHODS: Tibialis Anterior (TA) reflexes were evoked by innocuous cutaneous plantar sole stimulation during rest and ramp and hold phases of plantarflexion torque in non-injured subjects (n=10) and after SCI with (n=9) and without (n=10) hypertonia and/or involuntary spasm activity. Integrated TA reflex responses were analysed as total (50-300 ms) or short (50-200 ms) and long-latency (200-300 ms) activity. RESULTS: Total and long-latency TA activity was inhibited in non-injured subjects and the SCI group without the spasticity syndrome during plantarflexion torque but not in the SCI spasticity group. Furthermore, loss of TA reflex inhibition during plantarflexion correlated with time after SCI (ρ=0.79, P=0.009). Moreover, TA reflex activity inversely correlated with maximum plantarflexion torque in the spasticity group (ρ=-0.75, P=0.02), despite similar non-reflex TA electromyographic activity during plantarflexion after SCI in subjects with (0.11, 0.08-0.13 mV) or without the spasticity syndrome (0.09, 0.07-0.12 mV). CONCLUSIONS: This reflex testing procedure supports previously published evidence for abnormal CR activity after SCI and may characterise the progressive disinhibition of TA reflex activity during controlled plantarflexion in subjects diagnosed with the spasticity syndrome.

Spinal cord compression injury in lysophosphatidic acid 1 receptor-null mice promotes maladaptive pronociceptive descending control.

BACKGROUND: Although activation of the lysophosphatidic acid receptor 1 (LPA1) is known to mediate pronociceptive effects in peripheral pain models, the role of this receptor in the modulation of spinal nociception following spinal cord injury (SCI) is unknown. AIM: In this study, LPA1 regulation of spinal excitability mediated by supraspinal descending antinociceptive control systems was assessed following SCI in both wild-type (WT) and maLPA1-null receptor mice. METHODS: The effect of a T8 spinal compression in WT and maLPA1-null mice was assessed up to 1 month after SCI using histological, immunohistochemical and behavioural techniques analysis including electrophysiological recording of noxious toes-Tibialis Anterior (TA) stimulus-response reflex activity. The effect of a T3 paraspinal transcutaneous electrical conditioning stimulus on TA noxious reflex temporal summation was also assessed. RESULTS: Histological analysis demonstrated greater dorsolateral funiculus damage after SCI in maLPA1-null mice, without a change in the stimulus-response function of the TA noxious reflex when compared to WT mice. While T3 conditioning stimulation in the WT group inhibited noxious TA reflex temporal summation after SCI, this stimulus strongly excited TA reflex temporal summation in maLPA1-null mice. The functional switch from descending inhibition to maladaptive facilitation of central excitability of spinal nociception demonstrated in maLPA1-null mice after SCI was unrelated to a general change in reflex activity. CONCLUSIONS: These data suggest that the LPA1 receptor is necessary for inhibition of temporal summation of noxious reflex activity, partly mediated via long-tract descending modulatory systems acting at the spinal level.

Oral 2-hydroxyoleic acid inhibits reflex hypersensitivity and open-field-induced anxiety after spared nerve injury.

BACKGROUND: Recently, fatty acids have been shown to modulate sensory function in animal models of neuropathic pain. In this study, the antinociceptive effect of 2-hydroxyoleic acid (2-OHOA) was assessed following spared nerve injury (SNI) with reflex and cerebrally mediated behavioural responses. METHODS: Initial antinociceptive behavioural screening of daily administration of 2-OHOA (400 mg/kg, p.o.) was assessed in Wistar rats by measuring hindlimb reflex hypersensitivity to von Frey and thermal plate stimulation up to 7 days after SNI, while its modulatory effect on lumbar spinal dorsal horn microglia reactivity was assessed with OX-42 immunohistochemistry. In vitro the effect of 2-OHOA (120 µM) on cyclooxygenase protein expression (COX-2/COX-1 ratio) in lipopolysaccharide-activated macrophage cells was tested with Western blot analysis. Finally, the effects of 2-OHOA treatment on the place escape aversion paradigm (PEAP) and the open-field-induced anxiety test were tested at 21 days following nerve injury compared with vehicle-treated sham and pregabalin-SNI (30 mg/kg, p.o.) control groups. RESULTS: Oral 2-OHOA significantly reduced ipsilateral mechanical and thermal hypersensitivity up to 7 days after SNI. Additionally 2-OHOA decreased the COX-2/COX-1 ratio in lipopolysaccharide-activated macrophage cells and OX-42 expression within the ipsilateral lumbar spinal dorsal horn 7 days after SNI. 2-OHOA significantly restored inner-zone exploration in the open-field test compared with the vehicle-treated sham group at 21 days after SNI. CONCLUSIONS: Oral administration of the modified omega 9 fatty acid, 2-OHOA, mediates antinociception and prevents open-field-induced anxiety in the SNI model in Wistar rats, which is mediated by an inhibition of spinal dorsal horn microglia activation.

Impact of specific symptoms of spasticity on voluntary lower limb muscle function, gait and daily activities during subacute and chronic spinal cord injury.

BACKGROUND: Although the spasticity syndrome is an important sensorimotor disorder, the impact of grade of lower limb muscle hypertonia, spasm and clonus activity on voluntary muscle function, gait and daily activities has not been systematically analysed during subacute and chronic spinal cord injury (SCI). OBJECTIVE: To determine the prevalence of spasticity signs and symptoms during SCI, and to assess their impact on motor function and activities. METHODS: A descriptive transverse study of sixty-six subjects with SCI was performed by assessing injury characteristics, spasticity (modified Ashworth scale, Penn scale, SCATS scale) and motor function (lower limb manual muscle scores, WISCI II, spinal cord injury spasticity evaluation tool). RESULTS: Most subjects with the spasticity syndrome presented lower limb hypertonia and spasms during both subacute and chronic SCI, interfering with daily life activities. Subjects with incomplete SCI and hypertonia revealed a loss of voluntary flexor muscle activity, while extensors spasms contributed strongly to loss of gait function. The Penn spasms scale no correlated with muscle function or gait. CONCLUSIONS: Specific diagnosis of spasm activity during subacute SCI, and its impact on lower limb voluntary muscle activity, gait function and daily activities, is required to develop a more effective neurorehabilitation treatment strategy.

Sensory function after cavernous haemangioma: a case report of thermal hypersensitivity at and below an incomplete spinal cord injury.

STUDY DESIGN: Case report of a 42-year-old woman with non-evoked pain diagnosed with a cavernous C7-Th6 spinal haemangioma. OBJECTIVES: To assess the effect of intramedullary haemorrhage (IH) on nociception and neuropathic pain (NP) at and below an incomplete spinal cord injury (SCI). SETTING: Sensorimotor Function Group, Hospital Nacional de Parapléjicos de Toledo (HNPT). METHODS: T2*-susceptibility weighted image (SWI) magnetic resonance imaging (MRI) of spinal haemosiderin and a complete pain history were performed 8 months following initial dysaesthesia complaint. Thermal pain thresholds were assessed with short 1 s stimuli, while evidence for central sensitization was obtained with psychophysical electronic Visual Analogue Scale rating of tonic 10 s 3 °C and 48 °C stimuli, applied at and below the IH. Control data were obtained from 10 healthy volunteers recruited from the HNPT. RESULTS: Non-evoked pain was present within the Th6 dermatome and lower legs. T2*-SWI MRI imaging detected extensive haemosiderin-rich IH (C7-Th5/6 spinal level). Cold allodynia was detected below the IH (left L5 dermatome) with short thermal stimuli. Tonic thermal stimuli applied to the Th6, Th10 and C7 dermatomes revealed widespread heat and cold allodynia. CONCLUSION: NP was diagnosed following IH, corroborated by an increase in below-level cold pain threshold with at- and below-level cold and heat allodynia. Psychophysical evidence for at- and below-level SCI central sensitization was obtained with tonic thermal stimuli. Early detection of IH could lead to better management of specific NP symptoms, an appreciation of the role of haemorrhage as an aggravating SCI physical factor, and the identification of specific spinal pathophysiological pain mechanisms.

Voluntary ankle flexor activity and adaptive coactivation gain is decreased by spasticity during subacute spinal cord injury.

Although spasticity has been defined as an increase in velocity-dependent stretch reflexes and muscle hypertonia during passive movement, the measurement of flexor muscle paresis may better characterize the negative impact of this syndrome on residual motor function following incomplete spinal cord injury (iSCI). In this longitudinal study Tibialis Anterior (TA) muscle paresis produced by a loss in maximal voluntary contraction during dorsiflexion and ankle flexor muscle coactivation during ramp-and-hold controlled plantarflexion was measured in ten patients during subacute iSCI. Tibialis Anterior activity was measured at approximately two-week intervals between 3-5 months following iSCI in subjects with or without spasticity, characterized by lower-limb muscle hypertonia and/or involuntary spasms. Following iSCI, maximal voluntary contraction ankle flexor activity was lower than that recorded from healthy subjects, and was further attenuated by the presence of spasticity. Furthermore the initially high percentage value of TA coactivation increased at 75% but not at 25% maximal voluntary torque (MVT), reflected by an increase in TA coactivation gain (75%/25% MVT) from 2.5+/-0.4 to 7.5+/-1.9, well above the control level of 2.9+/-0.2. In contrast contraction-dependent TA coactivation gain decreased from 2.4+/-0.3 to 1.4+/-0.1 during spasticity. In conclusion the adaptive increase in TA coactivation gain observed in this pilot study during subacute iSCI was also sensitive to the presence of spasticity. The successful early diagnosis and treatment of spasticity would be expected to further preserve and promote adaptive motor function during subacute iSCI neurorehabilitation.